Catatonic Rigidity Cogwheel Rigidities Extensor Extrapyramidal Gegenhalten Gegenhaltens Muscle Muscular Nuchal

Continuous involuntary sustained muscle contraction which is often a manifestation of BASAL GANGLIA DISEASES. When an affected muscle is passively stretched, the degree of resistance remains constant regardless of the rate at which the muscle is stretched. This feature helps to distinguish rigidity from MUSCLE SPASTICITY. (From Adams et al., Principles of Neurology, 6th ed, p73)


Previous studies demonstrated that both ketamine and morphine induced analgesia and catalepsy in the rat. Pre-treatment with ketamine produced cross-tolerance to morphine, whereas pretreatment with morphine did not induce cross-tolerance to ketamine but rather augmented the cataleptic response; this augmentation was attributed to residual morphine in the brain. The present studies explored the duration of the loss of righting reflex induced by sub-effective doses of ketamine and morphine, administered simultaneously. There was mutual potentiation between sub-effective doses of ketamine and morphine, but sub-effective doses of ketamine partly antagonized fully-effective doses of morphine. Latency to the loss of righting reflex, rigidity and behavior on recovery, reflected the relative predominance of ketamine or morphine in each combination. Naloxone inhibited the induced cataleptic effects. The degree and time course of development of tolerance to daily administration of sub-effective dose combinations of ketamine and morphine were similar. Rats, tolerant to ketamine-dominant combinations, were cross-tolerant to both drugs, while those tolerant to morphine-dominant combinations were cross-tolerant to morphine but showed either no cross-tolerance or an augmented response to ketamine. While the mutual potentiation, antagonism and tolerance suggest common mechanisms for the induced catalepsy, differences in latency, rigidity and behavior, asymmetry of cross-tolerance and a widely-different ID50 for naloxone would argue against an action at a single opioid site.

Abello Brand of Naloxone Hydrochloride Boots Bristol Myers Squibb Bristol-Myers Curamed Naloxon Dihydride Endo Hydrobromide Lamepro MRZ 2593 Br 2593-Br 2593Br MRZ-2593 MRZ2593 Nalone ratiopharm Naloxon-ratiopharm (5 beta,9 alpha,13 alpha,14 alpha)-Isomer Naloxonratiopharm Narcan Narcanti SERB United Drug

A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.


Acute renal failure in patients with AIDS on tenofovir while receiving prolonged vancomycin course for osteomyelitis.

Acute Kidney Failure Failures Injuries Injury Insufficiencies Insufficiency Renal

Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.


AIDS Acquired Immune Deficiency Syndrome Immuno Immuno-Deficiency Syndromes Immunodeficiency Immunologic

An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive T-lymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993.


(R)-9-(2-phosphonylmethoxypropyl)adenine 9-(2-phosphonomethoxypropyl)adenine 9-(2-phosphonylmethoxypropyl)adenine (+-)-isomer (R)-isomer (S)-isomer 9-PMPA (tenofovir) tenofovir


AB-Vancomycin Abbott Brand of Vancomycin Hydrochloride Azupharma Chiesi Combino Dakota Diatracin Dista Eli Lilly Hexal MIP Norman Sulfate VANCO-cell Vanco Vanco-saar Vancocin HCl Vancocine Vancomicina Phar Phosphate (1:2) Decahydrate Vancomycin-ratiopharm Vancomycine cell pharm curasan ratiopharm

Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.


Renal failure developed after a prolonged course of vancomycin therapy in 2 patients who were receiving tenofovir disoproxil fumarate as part of an antiretroviral regimen. Tenofovir has been implicated in the development of Fanconi syndrome and renal insufficiency because of its effects on the proximal renal tubule. Vancomycin nephrotoxicity is infrequent but may result from coadministration with a nephrotoxic agent. Clinicians should be aware that tenofovir may raise the risk of renal failure during prolonged administration of vancomycin.

Failure Kidney Renal Failures Insufficiency Insufficiencies

Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.


Adult Fanconi Syndrome Bickel De Toni-Debre-Fanconi Diabete Pseudo-Phlorizin Diabetes Renotubular with Intestinal Malabsorption and Galactose Intolerance without Cystinosis Renal Type Glycogenosis Fanconi-Bickel Syndromes Glycogen Storage Disease XI Hepatic Amino Aciduria Glucosuria Nephropathy Hepatorenal Idiopathic Lignac Lignac-Fanconi Luder Sheldon Luder-Sheldon Neonatal Primary Proximal Tubular Dysfunction Pseudo Phlorizin

A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.


Pathological processes of the KIDNEY or its component tissues.


Delayed leukoencephalopathy with stroke-like presentation in chemotherapy recipients.

CACH Syndrome Syndromes CACH/VWM Centralis Diffusa Myelinosis Diffusas Childhood Ataxia with Central Nervous System Hypomyelination Hypomyelinization Diffuse Cree Leukoencephalopathies Leukoencephalopathy Disease White Matter Diseases Vanishing Leukodystrophy

Any of various diseases affecting the white matter of the central nervous system.


Acute Cerebrovascular Accident Accidents Stroke Strokes Apoplexy Brain Vascular CVA (Cerebrovascular Accident) CVAs Cerebral

A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)


BACKGROUND: A transient leukoencephalopathy mimicking cerebrovascular accident has been described as a complication of chemotherapy, most commonly in recipients of intrathecal methotrexate for childhood leukaemia. Recently published neuroimaging data suggest a common pathophysiology associated with a variety of chemotherapy agents and modes of administration. METHODS: We reviewed the medical literature for single reports and case series of patients presenting with stroke-like episodes while receiving systemic or intrathecal chemotherapy. We only included studies providing detailed neuroimaging data. Patients with cerebrovascular accidents were excluded. RESULTS: We identified 27 reports of toxic leukoencephalopathy in patients treated with methotrexate (intrathecal, systemic), 5-fluorouracil and its derivative carmofur, and capecitabine. Diffusion weighted imaging (DWI) of all patients revealed well demarcated hyperintense lesions within the subcortical white matter of the cerebral hemispheres and the corpus callosum, corresponding to areas of decreased proton diffusion on apparent diffusion coefficient (ADC) maps (available in 21/27 patients). Lesions exceeded the confines of adjacent vascular territories. Complete resolution of symptoms within 1-4 days was accompanied by normalisation of ADC abnormalities. However, fluid attenuated inversion recovery (FLAIR) sequences frequently revealed persistent white matter abnormalities. CONCLUSIONS: Several pathophysiological models of delayed leukoencephalopathy after exposure to intrathecal or systemic chemotherapy have been proposed. DWI findings in this cohort are indicative of cytotoxic oedema within cerebral white matter and lend support to an at least partially reversible metabolic derangement as the basis for this syndrome.


Anterior Choroidal Artery Infarction Cerebral Left Hemisphere Right Infarctions Subcortical Posterior

The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).


Amethopterin Dicesium Salt Methotrexate Hydrate Sodium (D)-Isomer (DL)-Isomer Disodium Mexate

An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.


Leucocythaemia Leucocythaemias Leucocythemia Leucocythemias Leukemia Leukemias

A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)


5 FU Lederle medac Fluorouracil biosyn HU Hexal 5-FU 5-Fluorouracil 5-Fluorouracil-biosyn 5-HU 5FU Adrucil Allergan Brand of CSP Carac Dakota Fluorouracile Dermatech Dermik Efudex Efudix Ferrer Fluoro Uracile ICN Fluoro-Uracile Fluoroplex GRY Mononitrate Monopotassium Salt Monosodium Potassium Teva Fluorouracil-GRY Fluorouracilo Far Fluoruracil Fluracedyl Flurodex Gry Haemato fu Haemato-fu Neocorp Neofluor Onkofluor Onkoworks Pharmachemie Ribofluor Riemser Roche ribosepharm

A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.


1-hexylcarbamoyl-5-fluorouracil HCFU Mifurol N-hexylcarbamoyl-5-fluorouracil carmofur


lesions within the subcortical white matter


cytotoxic oedema within cerebral white matter

Brain Edema Cytotoxic Vasogenic Swelling Swellings Cerebral Edemas Intracranial

Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)


Down-regulation of norepinephrine transporter function induced by chronic administration of desipramine linking to the alteration of sensitivity of local-anesthetics-induced convulsions and the counteraction by co-administration with local anesthetics.

Abbott Brand of Levophed Bitartrate Arterenol Aventis Norepinephrine Hydrochloride Noradrenaline Levarterenol Levonor Levonorepinephrine Noradrénaline tartrate renaudin Norepinephrin d-Tartrate (1:1) (+)-Isomer (+,-)-Isomer l-Tartrate Monohydrate (1:2) Renaudin

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.


Apo-Desipramine Apotex Brand of Desipramine Hydrochloride Aventis Behring Demethylimipramine Desmethylimipramine Norpramin Novartis Novo-Desipramine Novopharm Nu Pharm Nu-Desipramine Nu-Pharm PMS-Desipramine Pertofran Pertofrane Pertrofran Petylyl Pharmascience Ratiopharm Rhône Poulenc Rorer Rhône-Poulenc Temmler ratio-Desipramine

A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.


Auditory Seizure Seizures Clonic Convulsion Non Epileptic Non-Epileptic Convulsions Convulsive Focal Generalized Gustatory Jacksonian Motor Olfactory Sensory Somatosensory Tonic Tonic-Clonic Vertiginous Vestibular Visual

Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."


Alterations of norepinephrine transporter (NET) function by chronic inhibition of NET in relation to sensitization to seizures induce by cocaine and local anesthetics were studied in mice. Daily administration of desipramine, an inhibitor of the NET, for 5 days decreased [(3)H]norepinephrine uptake in the P2 fractions of hippocampus but not cortex, striatum or amygdalae. Co-administration of lidocaine, bupivacaine or tricaine with desipramine reversed this effect. Daily treatment of cocaine increased [(3)H]norepinephrine uptake into the hippocampus. Daily administration of desipramine increased the incidence of appearance of lidocaine-induced convulsions and decreased that of cocaine-induced convulsions. Co-administration of lidocaine with desipramine reversed the changes of convulsive activity of lidocaine and cocaine induced by repeated administration of desipramine. These results suggest that down-regulation of hippocampal NET induced by chronic administration of desipramine may be relevant to desipramine-induced sensitization of lidocaine convulsions. Inhibition of Na(+) channels by local anesthetics may regulate desipramine-induced down-regulation of NET function. Repeated administration of cocaine induces up-regulation of hippocampal NET function. Desipramine-induced sensitization of lidocaine seizures may have a mechanism distinct from kindling resulting from repeated administration of cocaine.


An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.


2-(Diethylamino)-N-(2,6-Dimethylphenyl)Acetamide 2-2EtN-2MePhAcN Astrazeneca Brand of Lidocaine Dalcaine Jenapharm Lidocanine Hydrochloride Carbonate (2:1) Hydrocarbonate Monoacetate Monohydrochloride Monohydrate Sulfate (1:1) Lignocaine Novocol Octocaine Strathmann Xylesthesin Xylocaine Xylocitin Xyloneural

A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.


1-Butyl-N-(2,6-dimethylphenyl)-2-piperidinecarboxamide Abbott Brand of Bupivacaine Hydrochloride Anhydrous Astra AstraZeneca Aventis Braun Bupivacaina Bupivacain Janapharm RPR Bupivacain-RPR Carbonate Monohydrochloride Monohydrate Buvacaina Carbostesin Dolanaest Inibsa Jenapharm Marcain Marcaine Pisa Sensorcaine Strathmann Svedocain Sin Vasoconstr


MS-222 Metacaine ethyl m-aminobenzoate methanesulfonate tricaine hydrochloride methane sulfonate (CH3SO4)


A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.


Definition and management of anemia in patients infected with hepatitis C virus.

A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.


Hepatitis C Viral Non-A Non-B Parenterally-Transmitted PT-NANBH Parenterally Transmitted Non A Non B

INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.


Chronic infection with hepatitis C virus (HCV) can progress to cirrhosis, hepatocellular carcinoma, and end-stage liver disease. The current best treatment for HCV infection is combination therapy with pegylated interferon and ribavirin. Although this regimen produces sustained virologic responses (SVRs) in approximately 50% of patients, it can be associated with a potentially dose-limiting hemolytic anemia. Hemoglobin concentrations decrease mainly as a result of ribavirin-induced hemolysis, and this anemia can be problematic in patients with HCV infection, especially those who have comorbid renal or cardiovascular disorders. In general, anemia can increase the risk of morbidity and mortality, and may have negative effects on cerebral function and quality of life. Although ribavirin-associated anemia can be reversed by dose reduction or discontinuation, this approach compromises outcomes by significantly decreasing SVR rates. Recombinant human erythropoietin has been used to manage ribavirin-associated anemia but has other potential disadvantages. Viramidine, a liver-targeting prodrug of ribavirin, has the potential to maintain the virologic efficacy of ribavirin while decreasing the risk of hemolytic anemia in patients with chronic hepatitis C.

INFLAMMATION of the LIVER in humans that is caused by HEPATITIS C VIRUS lasting six months or more. Chronic hepatitis C can lead to LIVER CIRRHOSIS.


Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.


Adult Liver Cancer Cancers Carcinoma Hepatocellular Cell Carcinomas Hepatoma Hepatomas

A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.


Chronic Liver Failure Failures End Stage Disease

Final stage of a liver disease when the liver failure is irreversible and LIVER TRANSPLANTATION is needed.


Proteins secreted by vertebrate cells in response to a wide variety of inducers. They confer resistance against many different viruses, inhibit proliferation of normal and malignant cells, impede multiplication of intracellular parasites, enhance macrophage and granulocyte phagocytosis, augment natural killer cell activity, and show several other immunomodulatory functions.


Dermatech Brand of Ribavirin Essex Grossman ICN 1229 ICN-1229 ICN1229 Merck Pfizer Rebetol Ribamide Ribamidil Ribamidyl Ribasphere Ribovirin Three Rivers Pharmaceuticals Tribavirin Vilona Viramide Virazide Virazole

A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses.


Acquired Hemolytic Anemia Microangiopathic

A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).


The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.


Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.


1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamidine TCNR ribamidine ribavirin amidine taribavirin viramidine


Calcium carbonate toxicity: the updated milk-alkali syndrome; report of 3 cases and review of the literature.

Aragonite Calcite Calcium Carbonate Milk Chalk Limestone Marble of Vaterite

Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.


Drug-Related Side Effects and Adverse Reactions

Adverse Drug Event Events Reaction Reactions Related Side Effects and Effect Toxicities Toxicity Drug-Related Drugs of

Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.


Hypercalcemia Hypercalcemias Milk Alkali Syndrome Milk-Alkali

Abnormally high level of calcium in the blood.


OBJECTIVE: To describe 3 patients with calcium carbonate-induced hypercalcemia and gain insights into the cause and management of the milk-alkali syndrome. METHODS: We report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium > or = 14 mg/dL) and review the pertinent literature on milk-alkali syndrome. RESULTS: The 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH-related peptide, and 1,25-dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classification, pathophysiologic features, and treatment of milk-alkali syndrome and summarize the cases reported from early 1995 to November 2003. CONCLUSION: Milk-alkali syndrome may be a common cause of unexplained hypercalcemia and can be precipitated by small amounts of orally ingested calcium carbonate in susceptible persons. Treatment with hydration, furosemide, and discontinuation of the calcium and vitamin D source is adequate. Pamidronate treatment is associated with considerable risk for hypocalcemia, even in cases of initially severe hypercalcemia.


A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.


Acute Kidney Failure Failures Injuries Injury Insufficiencies Insufficiency Renal

Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.


A pathological condition that removes acid or adds base to the body fluids.


Errolon Frusemid Frusemide Furanthril Furantral Furosemide Monohydrochloride Monosodium Salt Fursemide Fusid Lasix Salix (brand of furosemide)

A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.


(3-amino-1-hydroxypropylidene)-1,1-biphosphonate (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate 1-hydroxy-3-aminopropane-1,1-diphosphonic acid AHPrBP APD Aredia Novartis brand of pamidronate disodium salt amidronate amino-1-hydroxypropane-1,1-diphosphonate aminohydroxypropylidene diphosphonate aminopropanehydroxydiphosphonate calcium monosodium


Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)


A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.


Management strategies for ribavirin-induced hemolytic anemia in the treatment of hepatitis C: clinical and economic implications.


INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.


OBJECTIVES: Recently published studies have demonstrated increased efficacy and cost-effectiveness of combination therapy with interferon and alpha-2b/ribavirin compared with interferon-alpha monotherapy in the treatment of chronic hepatitis C (CHC). Combination therapy is associated with a clinically important adverse effect: ribavirin-induced hemolytic anemia (RIHA). The objective of this study was to evaluate the direct health-care costs and management of RIHA during treatment of CHC in a clinical trial setting. METHODS: A systematic literature review was conducted to synthesize information on the incidence and management of RIHA. Decision-analytic techniques were used to estimate the cost of treating RIHA. Uncertainty was evaluated using sensitivity analyses. RESULTS: RIHA, defined as a reduction in hemoglobin to less than 100 g/L, occurs in approximately 7% to 9% of patients treated with combination therapy. The standard of care for management of RIHA is reduction or discontinuation of the ribavirin dosage. We estimated the direct cost of treating clinically significant RIHA to be  170 per patient receiving combination therapy per 48-week treatment course (range  68- 692). The results of the one-way sensitivity analyses ranged from  57 to  317. In comparison, the cost of 48 weeks of combination therapy is  16,459. CONCLUSIONS: The direct cost of treating clinically significant RIHA is 1% ( 170/ 16,459) of drug treatment costs. Questions remain about the optimal dose of ribavirin and the incidence of RIHA in a real-world population. Despite these uncertainties, this initial evaluation of the direct cost of treating RIHA provides an estimate of the cost and management implications of this clinically important adverse effect.


2 Interferon-alpha D Leif IFN alpha alpha5 IFN-alpha IFN-alpha-2 IFN-alpha5 Interferon Alfa 1 17 4 5 7 88 A J T alpha-1 alpha-17 alpha-2 alpha-4 alpha-5 alpha-7 alpha-88 alpha-A alpha-J alpha-T alpha4 Leukocyte Lymphoblast Lymphoblastoid LeIF I alpha-Interferon

One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells. In addition to antiviral activity, it activates NATURAL KILLER CELLS and B-LYMPHOCYTES, and down-regulates VASCULAR ENDOTHELIAL GROWTH FACTOR expression through PI-3 KINASE and MAPK KINASES signaling pathways.


INFLAMMATION of the LIVER in humans that is caused by HEPATITIS C VIRUS lasting six months or more. Chronic hepatitis C can lead to LIVER CIRRHOSIS.


Effects of amine pretreatment on ketamine catatonia in pinealectomized or hypophysectomized animals.

A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)


2-(2-Chlorophenyl)-2-(methylamino)cyclohexanone CI 581 CI-581 CI581 Calipsol Calypsol Kalipsol Ketalar Ketamine Hydrochloride Ketanest Ketaset

A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.


Catatonia Lethal Malignant Organic Schizophreniform Catatonias Catatonic Disorder Disorders

A neuropsychiatric disorder characterized by one or more of the following essential features: immobility, mutism, negativism (active or passive refusal to follow commands), mannerisms, stereotypies, posturing, grimacing, excitement, echolalia, echopraxia, muscular rigidity, and stupor; sometimes punctuated by sudden violent outbursts, panic, or hallucinations. This condition may be associated with psychiatric illnesses (e.g., SCHIZOPHRENIA; MOOD DISORDERS) or organic disorders (NEUROLEPTIC MALIGNANT SYNDROME; ENCEPHALITIS, etc.). (From DSM-IV, 4th ed, 1994; APA, Thesaurus of Psychological Index Terms, 1994)


The present studies were designed to clarify the role of catecholamines and pineal idolamines on ketamine-induced catatonia in the intact, pinealectomized or hypophysectomized chick and rat. In the pinealectomized chick, pretreatment with dopamine increased the duration of catatonia (DOC) after ketamine, but pretreatment with norepinephrine did not. The pineal indolamines exhibited mixed actions. Serotonin and N-acetyl serotonin which augmented ketamine DOC, did not do so in the absence of the pineal gland, whereas melatonin potentiated the ketamine DOC in both the intact and pinealectomized chick. Ketamine was more potent in the hypophysectomized chick and the circadian rhythm noted in the intact chick was absent; furthermore, melatonin did not augment the ketamine DOC whereas dopamine continued to do so. This study did not demonstrate a species difference regarding the role of the amines on the pineal in spite of the immature blood-brain barrier in the young chick and the intact barrier in the rat. In addition, these data indicate a direct role of the pituitary in the augmentation of ketamine DOC induced by melatonin. Furthermore, dopamine appeared to act on systems more closely involved with the induction of ketamine catatonia rather than directly on the pituitary.

A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.


3,4 Dihydroxyphenethylamine 3,4-Dihydroxyphenethylamine 4-(2-Aminoethyl)-1,2-benzenediol Dopamine Hydrochloride Hydroxytyramine Intropin

One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.


Abbott Brand of Levophed Bitartrate Arterenol Aventis Norepinephrine Hydrochloride Noradrenaline Levarterenol Levonor Levonorepinephrine Noradrénaline tartrate renaudin Norepinephrin d-Tartrate (1:1) (+)-Isomer (+,-)-Isomer l-Tartrate Monohydrate (1:2) Renaudin

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.


3-(2-Aminoethyl)-1H-indol-5-ol 5 Hydroxytryptamine 5-HT 5-Hydroxytryptamine Enteramine Hippophaine Serotonin

A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.


A biogenic amine that is found in animals and plants. In mammals, melatonin is produced by the PINEAL GLAND. Its secretion increases in darkness and decreases during exposure to light. Melatonin is implicated in the regulation of SLEEP, mood, and REPRODUCTION. Melatonin is also an effective antioxidant.


Multicenter, double-blind, multiple-dose, parallel-groups efficacy and safety trial of azelastine, chlorpheniramine, and placebo in the treatment of spring allergic rhinitis.

4-((4-chlorophenyl)methyl)-2- (hexahydro-1-methyl-1H-azepin-4-yl)-1(2H)- phthalazinone HCl 4-(p-chlorobenzyl)-2-(N-methylperhydroazepinyl-(4))-1-(2H)-phthalazinone A 5610 A-5610 ASTA Medica brand of azelastine hydrochloride Afluon Allergodil Astelin Azeptin Bayer Corifina Dagra Loxin Mann Muro Optilast Optivar Orion Rhinolast Sanfer Viatris Vividrin akut Azelastin Wallace


Aller-Chlor Antihistaminico Llorens Bayer Brand of Chlorpheniramine Maleate Chlo-Amine Chlor-100 Chlor-Trimeton Chlor-Tripolon Chlorphenamine Tannate Chlorpro Chlorprophenpyridamine Chlorspan 12 Chlortab-4 Cloro-Trimeton Efidac 24 Halsey Drug Hogil 1 2 Intra Kloromin Piriton Rugby Schein Schering Schering-Plough Stafford-Miller Teldrin Vortech 3

A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.


Allergic Rhinitides Seasonal Rhinitis Allergies Pollen Allergy Fever Hay Hayfever Pollinoses Pollinosis

Allergic rhinitis that occurs at the same time every year. It is characterized by acute CONJUNCTIVITIS with lacrimation and ITCHING, and regarded as an allergic condition triggered by specific ALLERGENS.


Azelastine, a novel antiallergic medication, was compared with chlorpheniramine maleate and placebo for efficacy and safety in the treatment of spring allergic rhinitis in a multicenter, double-blind, multiple-dose, parallel-groups study. One hundred fifty-five subjects participated. Subjects ranged in age from 18 to 60 years of age and had at least a 2-year history of spring allergic rhinitis, confirmed by positive skin test to spring aeroallergens. Medications were given four times daily; the azelastine groups received 0.5, 1.0, or 2.0 mg in the morning and evening with placebo in the early and late afternoon; the chlorpheniramine group received 4.0 mg four times daily. Daily subject symptom cards were completed during a screening period to assess pretreatment symptoms and during a 4-week treatment period while subjects received study medications. Individual symptoms, total symptoms, and major symptoms were compared to determine efficacy of medication. Elicited, volunteered, and observed adverse experiences were recorded for each subject and compared among groups. Vital signs, body weights, serum chemistry values, complete blood cell counts, urine studies, and electrocardiograms were obtained for each subject and compared among groups. Symptoms relief in the group receiving the highest concentration of azelastine (2.0 mg twice daily) was statistically greater than in the placebo group during all weeks of the study. Lower doses of azelastine were statistically more effective than placebo only during portions of the first 3 weeks of the study. In contrast, although the chlorpheniramine group did have fewer symptoms than the placebo group during the study, the difference never reached statistical significance during any week of the study. There were no serious side effects in any of the treatment groups. Drowsiness and altered taste perception were increased significantly over placebo only in the high-dose azelastine group. Azelastine appears to be a safe, efficacious medication for seasonal allergic rhinitis.


DOES (Disorders of Excessive Somnolence) DOESs Disorders Somnolence Disorder Hypersomnia Recurrent Hypersomnias Hypersomnolence Primary Secondary

Disorders characterized by hypersomnolence during normal waking hours that may impair cognitive functioning. Subtypes include primary hypersomnia disorders (e.g., IDIOPATHIC HYPERSOMNOLENCE; NARCOLEPSY; and KLEINE-LEVIN SYNDROME) and secondary hypersomnia disorders where excessive somnolence can be attributed to a known cause (e.g., drug affect, MENTAL DISORDERS, and SLEEP APNEA SYNDROME). (From J Neurol Sci 1998 Jan 8;153(2):192-202; Thorpy, Principles and Practice of Sleep Medicine, 2nd ed, p320)


Metallic Taste Tastes Primary Disorder Disorders Secondary Anterior Tongue Posterior Bitter Salt Sweet

Conditions characterized by an alteration in gustatory function or perception. Taste disorders are frequently associated with OLFACTION DISORDERS. Additional potential etiologies include METABOLIC DISEASES; DRUG TOXICITY; and taste pathway disorders (e.g., TASTE BUD diseases; FACIAL NERVE DISEASES; GLOSSOPHARYNGEAL NERVE DISEASES; and BRAIN STEM diseases).


One case of acute hypercalcaemia and two of recurrent nephrolithiasis are reported in patients who had regularly consumed large amounts of calcium carbon-ate-sodium bicarbonate powders for more than 20 years. The powders had been obtained from pharmacists unknown to the patients' medical practitioners. It is suggested that these preparations were responsible for the patient's problems, and that such powders should no longer be freely obtainable.

Abnormally high level of calcium in the blood.


Aragonite Calcite Calcium Carbonate Milk Chalk Limestone Marble of Vaterite

Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.


Baking Soda Bicarbonate Sodium Carbonic Acid Monosodium Salt Hydrogen Carbonate

A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.


Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids.

Palsies Palsy Paralyses Paralysis Todd Todd's Plegia Plegias Todds

A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)


nondepolarizing neuromuscular blocking agents

Agents Curare-Like Neuromuscular Nondepolarizing Blockers Curare Like Curariform Drugs Muscle Relaxants Non Depolarizing Non-Depolarizing Blocking Competitive

Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants.


Adrenal Cortex Hormones Corticoids Corticosteroids


The long-term use of nondepolarizing neuromuscular blocking agents (ND-NMBA) has recently been implicated as a cause of prolonged muscle weakness, although the site of the lesion and the predisposing factors have been unclear. We report 3 patients (age 37-52 years) with acute respiratory insufficiency who developed prolonged weakness following the discontinuation of ND-NMBAs. Two patients also received intravenous corticosteroids. Renal function was normal but hepatic function was impaired in all patients, and all had acidosis. Electrophysiologic studies revealed low amplitude compound motor action potentials, normal sensory studies, and fibrillations. Repetitive stimulation at 2 Hz showed a decremental response in 2 patients. The serum vecuronium level measured in 1 patient 14 days after the drug had been discontinued was 172 ng/mL. A muscle biopsy in this patient showed loss of thick, myosin filaments. The weakness in these patients is due to pathology at both the neuromuscular junction (most likely due to ND-NMBA) and muscle (most likely due to corticosteroids). Hepatic dysfunction and acidosis are contributing risk factors.


A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)


Depressions Ventilatory Respiratory Depression Failure Insufficiency

Failure to adequately provide oxygen to cells of the body and to remove excess carbon dioxide from them. (Stedman, 25th ed)


A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.


Bromide Vecuronium Citrate Hydrobromide Hydrochloride Maleate NC 45 NC-45 NC45 Norcuron ORG ORG-NC ORG-NC-45 ORG-NC45 ORGNC ORGNC45 Phosphate Quaternary Ion

Monoquaternary homolog of PANCURONIUM. A non-depolarizing neuromuscular blocking agent with shorter duration of action than pancuronium. Its lack of significant cardiovascular effects and lack of dependence on good kidney function for elimination as well as its short duration of action and easy reversibility provide advantages over, or alternatives to, other established neuromuscular blocking agents.


Muscle Disorder Disorders Muscular Disease Diseases Myopathic Condition Conditions Myopathies Myopathy

Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.


pathology at both the neuromuscular junction

Amyotonia Congenita Benign Fasciculation-Cramp Syndrome Syndromes Cramp Fasciculation Cramp-Fasciculation Foley Denny Brown Foley-Denny-Brown Neuromuscular Disease Diseases Oppenheim Oppenheim's Oppenheims

A general term encompassing lower MOTOR NEURON DISEASE; PERIPHERAL NERVOUS SYSTEM DISEASES; and certain MUSCULAR DISEASES. Manifestations include MUSCLE WEAKNESS; FASCICULATION; muscle ATROPHY; SPASM; MYOKYMIA; MUSCLE HYPERTONIA, myalgias, and MUSCLE HYPOTONIA.


Disease Liver Diseases Dysfunction Dysfunctions


Prostaglandin E2-induced bladder hyperactivity in normal, conscious rats: involvement of tachykinins?

Dinoprostone E2 alpha Prostaglandin E2alpha Gel Prepidil PGE2 PGE2alpha Prostenon

The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.


Bladder Overactive Detrusor Function Urinary

Symptom of overactive detrusor muscle of the URINARY BLADDER that contracts with abnormally high frequency and urgency. Overactive bladder is characterized by the frequent feeling of needing to urinate during the day, during the night, or both. URINARY INCONTINENCE may or may not be present.


A family of biologically active peptides sharing a common conserved C-terminal sequence, -Phe-X-Gly-Leu-Met-NH2, where X is either an aromatic or a branched aliphatic amino acid. Members of this family have been found in mammals, amphibians, and mollusks. Tachykinins have diverse pharmacological actions in the central nervous system and the cardiovascular, genitourinary, respiratory, and gastrointestinal systems, as well as in glandular tissues. This diversity of activity is due to the existence of three or more subtypes of tachykinin receptors.


In normal conscious rats investigated by continuous cystometry, intravesically instilled prostaglandin (PG) E2 facilitated micturition and increased basal intravesical pressure. The effect was attenuated by both the NK1 receptor selective antagonist RP 67,580 and the NK2 receptor selective antagonist SR 48,968, given intra-arterially, suggesting that it was mediated by stimulation of both NK1 and NK2 receptors. Intra-arterially given PGE2 produced a distinct increase in bladder pressure before initiating a micturition reflex, indicating that the PG had a direct contractant effect on the detrusor smooth muscle. The effect of intra-arterial PGE2 could not be blocked by intra-arterial RP 67,580 or SR 48,968, which opens the possibility that the micturition reflex elicited by intra-arterial PGE2 was mediated by pathways other than the reflex initiated when the PG was given intravesically. The present results thus suggest that intra-arterial PGE2, given near the bladder, may initiate micturition in the normal rat chiefly by directly contracting the smooth muscle of the detrusor. However, when given intravesically, PGE2 may stimulate micturition by releasing tachykinins from nerves in and/or immediately below the urothelium. These tachykinins, in turn, initiate a micturition reflex by stimulating NK1 and NK2 receptors. Prostanoids may, via release of tachykinins, contribute to both urge and bladder hyperactivity seen in inflammatory conditions of the lower urinary tract.


7,7-diphenyl-2-(1-imino-2-(2-methoxyphenyl)ethyl)perhydroisoindol-4-one RP 67580 68651 RP-67580 RP-68651


(S)-N-methyl-N(4-(4-acetylamino-4-phenylpiperidino)-2-(3,4-dichlorophenyl)butyl)benzamide SR 48965 48968 48968C SR-48968 SR-48968C SR48968 SR48968C saredutant


A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.


Thiazide diuretics, hypokalemia and cardiac arrhythmias.

Heterocyclic compounds with SULFUR and NITROGEN in the ring. This term commonly refers to the BENZOTHIADIAZINES that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS.


Hypokalemia Hypokalemias Hypopotassemia Hypopotassemias

Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)


Arrhythmia Cardiac Arrhythmias Arrythmia Dysrhythmia

Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.


Thiazide diuretics are widely accepted as the cornerstone of antihypertensive treatment programs. Hypokalemia is a commonly encountered metabolic consequence of chronic thiazide therapy. We treated 38 patients (22 low renin, 16 normal renin) with moderate diastolic hypertension with hydrochlorothiazide (HCTC) administered on a twice daily schedule. Initial dose was 50 mg and the dose was increased at monthly intervals to 100 mg, 150 mg and 200 mg daily until blood pressure normalized. The serum K during the control period was 4.5 +/- 0.2 mEq/l an on 50, 100, 150 and 200 mg HCTZ daily 3.9 +/- 0.3, 3.4 +/- 0.2, 2.9 +/- 0.2, and 2.4 +/- 0.3 mEq/l, respectively. Corresponding figures for whole body K were 4107 +/- 208, 3722 +/- 319, 3628 +/- 257, 3551 +/- 336, and 3269 +/- 380 mEq, respectively. In 13 patients we observed the effects of HCTZ therapy (100 mg daily) on the occurrence of PVC's during rest as well as during static and dynamic exercise. During rest we observed 0.6 +/- 0.08 PVC beats/min +/- SEM and during static and dynamic exercise 0.6 +/- 0.06 and 0.8 +/- 0.15, respectively. Corresponding figures during HCTZ therapy 100 mg daily were 1.4 +/- 0.1, 3.6 +/- 0.7 and 5.7 4/- 0.8, respectively. The occurrence of PVC's correlated significantly with the fall in serum K+ observed r = 0.72, p less than 0.001. In conclusion we found that thiazide diuretics cause hypokalemia and depletion of body potassium. The more profound hypokalemia, the greater the propensity for the occurrence of PVC's.


Dichlothiazide Dihydrochlorothiazide Esidrex Esidrix HCTZ HydroDIURIL Hydrochlorothiazide Hypothiazide Oretic Sectrazide

A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.


An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.


Diuretics, potassium and arrhythmias in hypertensive coronary disease.


Blood Pressure High Pressures Hypertension

Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.


An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.


It has been proposed that modest changes in plasma potassium can alter the tendency towards cardiac arrhythmias. If this were so, patients with coronary artery disease might be especially susceptible. Thus, myocardial electrical excitability was measured in patients with mild essential hypertension and known coronary artery disease after 8 weeks of treatment with a potassium-conserving diuretic (amiloride) and a similar period on a potassium-losing diuretic (chlorthalidone) in a randomised study. Plasma potassium concentrations were on average 1 mmol/L lower during the chlorthalidone phase compared to amiloride therapy. Blood pressure and volume states as assessed by bodyweight, plasma renin and noradrenaline (norepinephrine) concentrations were similar on the 2 regimens. Compared to amiloride treatment, the chlorthalidone phase was associated with an increased frequency of ventricular ectopic beats (24-hour Holter monitoring) and a higher Lown grading, increased upslope and duration of the monophasic action potential, prolonged ventricular effective refractory period, and increased electrical instability during programmed ventricular stimulation. The above results indicate that because potassium-losing diuretic therapy can increase myocardial electrical excitability in patients with ischaemic heart disease, even minor falls in plasma potassium concentrations are probably best avoided in such patients.


Arterioscleroses Coronary Arteriosclerosis Artery Disease Diseases Atheroscleroses Atherosclerosis

Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.


Alphapharm Brand of Amiloride Hydrochloride Amidal Amiduret Trom Amiloberag Anhydrous Amrad Berolina Cahill May Roberts Douglas Kaluril Merck Sharp & Dohme Midamor Midoride Modamide Trommsdorff

A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705)


Chlorphthalidolone Chlortalidone Chlorthalidone Hygroton Oxodoline Phthalamudine Thalitone

A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.


Abbott Brand of Levophed Bitartrate Arterenol Aventis Norepinephrine Hydrochloride Noradrenaline Levarterenol Levonor Levonorepinephrine Noradrénaline tartrate renaudin Norepinephrin d-Tartrate (1:1) (+)-Isomer (+,-)-Isomer l-Tartrate Monohydrate (1:2) Renaudin

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.


Ectopic Beat Ventricular Beats Extrasystole Premature Complex Contraction Contractions Extrasystoles Complexes

A type of cardiac arrhythmia with premature contractions of the HEART VENTRICLES. It is characterized by the premature QRS complex on ECG that is of abnormal shape and great duration (generally >129 msec). It is the most common form of all cardiac arrhythmias. Premature ventricular complexes have no clinical significance except in concurrence with heart diseases.


Disease Ischemic Heart Diseases Ischemia Myocardial Ischemias

A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).


GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

4 Aminobutanoic Acid Aminobutyric 4-Aminobutanoic 4-Aminobutyric Hydrochloride gamma-Aminobutyric Aminalon Aminalone GABA Lithium Gammalon gamma Monolithium Salt Monosodium Calcium (2:1) Zinc

The most common inhibitory neurotransmitter in the central nervous system.


Abello Brand of Naloxone Hydrochloride Boots Bristol Myers Squibb Bristol-Myers Curamed Naloxon Dihydride Endo Hydrobromide Lamepro MRZ 2593 Br 2593-Br 2593Br MRZ-2593 MRZ2593 Nalone ratiopharm Naloxon-ratiopharm (5 beta,9 alpha,13 alpha,14 alpha)-Isomer Naloxonratiopharm Narcan Narcanti SERB United Drug

A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.


Diaphragmatic Paralysis Muscle Paralyses Respiratory

Complete or severe weakness of the muscles of respiration. This condition may be associated with MOTOR NEURON DISEASES; PERIPHERAL NERVE DISEASES; NEUROMUSCULAR JUNCTION DISEASES; SPINAL CORD DISEASES; injury to the PHRENIC NERVE; and other disorders.


Abbott Brand of Thiopental Sodium Altana Pharma Bomathal Braun Merial Nesdonal Nycomed Penthiobarbital Pentothal Sodico Pharmtech Pisa Rhone Merieux Sodipental Thiomebumal Thionembutal Thiopentobarbital Thiopentone Tiobarbital Trapanal

A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.


No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.


Aluminum L Glutamate L-Glutamate D D-Glutamate Potassium Glutamic Acid (D)-Isomer L-Glutamic

A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.


(+-)-Aspartic Acid (R,S)-Aspartic Ammonium Aspartate Magnesium Hydrochloride Calcium Dipotassium Disodium Monopotassium Monosodium Potassium Sodium Aspartic Salt Hydrobromide (1:1) Trihydrate (2:1) Magnesium-Potassium (2:1:2) L L-Aspartate L-Aspartic Magnesiocard Mg 5 Longoral Mg-5-Longoral Mg5Longoral

One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.


Acid Aminoacetic Calcium Salt Glycine Cobalt Copper Carbonate (1:1) Monosodium (2:1) Monolithium Monopotassium Hydrochloride Phosphate Sulfate (3:1) Monoammonium Monopotasssium Sodium Hydrogen

A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.


N-aminothiourea thiocarbamylhydrazine thiosemicarbazide hydrochloride monohydrochloride


Depressions Ventilatory Respiratory Depression Failure Insufficiency

Failure to adequately provide oxygen to cells of the body and to remove excess carbon dioxide from them. (Stedman, 25th ed)


Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.


National project on the prevention of mother-to-infant infection by hepatitis B virus in Japan.

INFLAMMATION of the LIVER in humans caused by a member of the ORTHOHEPADNAVIRUS genus, HEPATITIS B VIRUS. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.


In Japan, a nationwide prevention program against mother-to-infant infection by hepatitis B virus (HBV) started in 1985. This program consists of double screenings of pregnant women and prophylactic treatment to the infants born to both hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive mothers. These infants are treated with two injections of hepatitis B immune globulin (HBIG) and at least three injections of plasma derived hepatitis B vaccine. We sent questionnaires about the numbers of each procedure or examination during nine months of investigation period to each local government in 1986 and 1987. 93.4% pregnant women had the chance to be examined for HBsAg, and the positive rate was 1.4 to 1.5%. The HBeAg positive rate in HBsAg positive was 23 to 26%. The HBsAg positive rate in neonates and in infants before two months were 3% and 2% respectively. Some problems may arise, because 27 to 30% of infants need the fourth vaccination in some restricted areas.


Antigen Australia HBsAg Hepatitis B Surface Antigens

Those hepatitis B antigens found on the surface of the Dane particle and on the 20 nm spherical and tubular particles. Several subspecificities of the surface antigen are known. These were formerly called the Australia antigen.


Antigens Hepatitis Be e HBe Ag-1 Ag-2 HBeAg B

A closely related group of antigens found in the plasma only during the infective phase of hepatitis B or in virulent chronic hepatitis B, probably indicating active virus replication; there are three subtypes which may exist in a complex with immunoglobulins G.


Vaccines or candidate vaccines containing inactivated hepatitis B or some of its component antigens and designed to prevent hepatitis B. Some vaccines may be recombinantly produced.


Nociceptive effects induced by intrathecal administration of prostaglandin D2, E2, or F2 alpha to conscious mice.

11 Dehydroprostaglandin F2 alpha F2alpha 11-Dehydroprostaglandin D2 Prostaglandin PGD2

The principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.


The effects of intrathecal administration of prostaglandins on pain responses in conscious mice were evaluated by using hot plate and acetic acid writhing tests. Prostaglandin D2 (0.5-3 ng/mouse) had a hyperalgesic action on the response to a hot plate during a 3-60 min period after injection. Prostaglandin E2 showed a hyperalgesic effect at doses of 1 pg to 10 ng/mouse, but the effect lasted shorter (3-30 min) than that of prostaglandin D2. Similar results were obtained by acetic acid writhing tests. The hyperalgesic effect of prostaglandin D2 was blocked by simultaneous injection of a substance P antagonist (greater than or equal to 100 ng) but not by AH6809, a prostanoid EP1-receptor antagonist. Conversely, prostaglandin E2-induced hyperalgesia was blocked by AH6809 (greater than or equal to 500 ng) but not by the substance P antagonist. Prostaglandin F2 alpha had little effect on pain responses. These results demonstrate that both prostaglandin D2 and prostaglandin E2 exert hyperalgesia in the spinal cord, but in different ways.

A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.


Ache Aches Burning Pain Pains Crushing Migratory Radiating Splitting Physical Suffering Sufferings

An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.


Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed)


Allodynia Mechanical Tactile Thermal Allodynias Hyperalgesia Primary Secondary Hyperalgesias Hyperalgesic Sensations

An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.


Dinoprostone E2 alpha Prostaglandin E2alpha Gel Prepidil PGE2 PGE2alpha Prostenon

The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.


6-isopropoxy-9-oxoxanthene-2-carboxylic acid AH 6809 AH-6809 AH6809


9alpha,11beta PGF2 9alpha,11beta-PGF2 Dinoprost Enzaprost F Estrofan F2 alpha Prostaglandin F2alpha PGF2alpha

A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.


Swallowing-induced atrial tachyarrhythmia triggered by salbutamol: case report and review of the literature.

A generic expression for any tachycardia that originates above the BUNDLE OF HIS.


2-t-Butylamino-1-(4-hydroxy-3-hydroxy-3-hydroxymethyl)phenylethanol Albuterol Sulfate Proventil Salbutamol Sultanol Ventolin

A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.


CASE: A 49-year-old patient experienced chest discomfort while swallowing. On electrocardiogram, episodes of atrial tachyarrhythmia were recorded immediately after swallowing; 24-hour Holter monitoring recorded several events. The arrhythmia resolved after therapy with atenolol, but recurred a year later. The patient noticed that before these episodes he had been using an inhalator of salbutamol. After stopping the beta-agonist, and after a week with the atenolol, the arrhythmia disappeared. DISCUSSION: Swallowing-induced atrial tachyarrhythmia (SIAT) is a rare phenomenon. Fewer than 50 cases of SIAT have been described in the literature. This article summarizes all the cases published, creating a comprehensive review of the current knowledge and approach to SIAT. It discusses demographics, clinical characteristics and types of arrhythmia, postulated mechanisms of SIAT, and different treatment possibilities such as medications, surgery, and radiofrequency catheter ablation (RFCA). CONCLUSION: Salbutamol is presented here as a possible trigger for SIAT. Although it is difficult to define causality in a case report, it is logical to think that a beta-agonist like salbutamol (known to induce tachycardia) may be the trigger of adrenergic reflexes originating in the esophagus while swallowing and that a beta-blocker such as atenolol (that blocks the adrenergic activity) may relieve it.


Arrhythmia Cardiac Arrhythmias Arrythmia Dysrhythmia

Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.


Atenolol ICI 66082 ICI-66082 ICI66082 Tenormin Tenormine

A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.


Tachyarrhythmia Tachyarrhythmias Tachycardia Tachycardias

Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.


Coenzyme Q10 treatment ameliorates acute cisplatin nephrotoxicity in mice.

2,3-dimethoxy-5-methyl-6-decaprenylbenzoquinone Bio-Quinone Q10 CoQ 10 CoQ10 Q-ter co-enzyme coenzyme (Z,Z,Z,Z,Z,Z,E,E,E)-isomer ion (1-) (all-E)-isomer ubidecarenone ubiquinone 50 ubisemiquinone radical


Biocisplatinum Cisplatin Diamminodichloride Platinum Dichlorodiammineplatinum NSC-119875 Platidiam Platino Platinol cis Diamminedichloroplatinum cis-Diamminedichloroplatinum cis-Diamminedichloroplatinum(II) cis-Dichlorodiammineplatinum(II) cis-Platinum

An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.


Pathological processes of the KIDNEY or its component tissues.


The nephroprotective effect of coenzyme Q10 was investigated in mice with acute renal injury induced by a single i.p. injection of cisplatin (5 mg/kg). Coenzyme Q10 treatment (10 mg/kg/day, i.p.) was applied for 6 consecutive days, starting 1 day before cisplatin administration. Coenzyme Q10 significantly reduced blood urea nitrogen and serum creatinine levels which were increased by cisplatin. Coenzyme Q10 significantly compensated deficits in the antioxidant defense mechanisms (reduced glutathione level and superoxide dismutase activity), suppressed lipid peroxidation, decreased the elevations of tumor necrosis factor-alpha, nitric oxide and platinum ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cisplatin administration. Also, histopathological renal tissue damage mediated by cisplatin was ameliorated by coenzyme Q10 treatment. Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the cisplatin-induced overexpression of inducible nitric oxide synthase, nuclear factor-kappaB, caspase-3 and p53 in renal tissue. It was concluded that coenzyme Q10 represents a potential therapeutic option to protect against acute cisplatin nephrotoxicity commonly encountered in clinical practice.


Acute Kidney Failure Failures Injuries Injury Insufficiencies Insufficiency Renal

Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.


The urea concentration of the blood stated in terms of nitrogen content. Serum (plasma) urea nitrogen is approximately 12% higher than blood urea nitrogen concentration because of the greater protein content of red blood cells. Increases in blood or serum urea nitrogen are referred to as azotemia and may have prerenal, renal, or postrenal causes. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)


Glutathione Reduced gamma L Glu L Cys Gly Glutamyl Cysteinylglycine gamma-L-Glu-L-Cys-Gly gamma-L-Glutamyl-L-Cysteinylglycine

A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.


Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.


Benign Neoplasm Neoplasms Cancer Cancers Neoplasia Tumor Tumors

New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.


The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. Distinguish it from APOPTOSIS which is a normal, regulated cellular process.


Endogenous Nitrate Vasodilator Endothelium-Derived Nitric Oxide Mononitrogen Monoxide Nitrogen Endothelium Derived

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.


Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae".


An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE.


A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with ANEMIA, short stature, HYPOGONADISM, impaired WOUND HEALING, and geophagia. It is known by the symbol Zn.


Metformin prevents experimental gentamicin-induced nephropathy by a mitochondria-dependent pathway.

Dimethylbiguanidine Dimethylguanylguanidine Glucophage Metformin

A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)


G Myticin G-Myticin GMyticin Garamycin Gentacycol Gentamicin Sulfate (USP) Gentamicins Gentamycin Gentamycins Gentavet Genticin

A complex of closely related aminoglycosides obtained from MICROMONOSPORA purpurea and related species. They are broad-spectrum antibiotics, but may cause ear and kidney damage. They act to inhibit PROTEIN BIOSYNTHESIS.


The antidiabetic drug metformin can diminish apoptosis induced by oxidative stress in endothelial cells and prevent vascular dysfunction even in nondiabetic patients. Here we tested whether it has a beneficial effect in a rat model of gentamicin toxicity. Mitochondrial analysis, respiration intensity, levels of reactive oxygen species, permeability transition, and cytochrome c release were assessed 3 and 6 days after gentamicin administration. Metformin treatment fully blocked gentamicin-mediated acute renal failure. This was accompanied by a lower activity of N-acetyl-beta-D-glucosaminidase, together with a decrease of lipid peroxidation and increase of antioxidant systems. Metformin also protected the kidney from histological damage 6 days after gentamicin administration. These in vivo markers of kidney dysfunction and their correction by metformin were complemented by in vitro studies of mitochondrial function. We found that gentamicin treatment depleted respiratory components (cytochrome c, NADH), probably due to the opening of mitochondrial transition pores. These injuries, partly mediated by a rise in reactive oxygen species from the electron transfer chain, were significantly decreased by metformin. Thus, our study suggests that pleiotropic effects of metformin can lessen gentamicin nephrotoxicity and improve mitochondrial homeostasis.


Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.


Adverse Drug Event Events Reaction Reactions Related Side Effects and Effect Toxicities Toxicity Drug-Related Drugs of

Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.


An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.


Sedation depth during spinal anesthesia and the development of postoperative delirium in elderly patients undergoing hip fracture repair.

Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.


Delirium of Mixed Origin Subacute Deliriums

A disorder characterized by CONFUSION; inattentiveness; disorientation; ILLUSIONS; HALLUCINATIONS; agitation; and in some instances autonomic nervous system overactivity. It may result from toxic/metabolic conditions or structural brain lesions. (From Adams et al., Principles of Neurology, 6th ed, pp411-2)


Fractures Hip Intertrochanteric Subtrochanteric Trochanteric

Fractures of the FEMUR HEAD; the FEMUR NECK; (FEMORAL NECK FRACTURES); the trochanters; or the inter- or subtrochanteric region. Excludes fractures of the acetabulum and fractures of the femoral shaft below the subtrochanteric region (FEMORAL FRACTURES).


OBJECTIVE: To determine whether limiting intraoperative sedation depth during spinal anesthesia for hip fracture repair in elderly patients can decrease the prevalence of postoperative delirium. PATIENTS AND METHODS: We performed a double-blind, randomized controlled trial at an academic medical center of elderly patients (>or=65 years) without preoperative delirium or severe dementia who underwent hip fracture repair under spinal anesthesia with propofol sedation. Sedation depth was titrated using processed electroencephalography with the bispectral index (BIS), and patients were randomized to receive either deep (BIS, approximately 50) or light (BIS, >or=80) sedation. Postoperative delirium was assessed as defined by Diagnostic and Statistical Manual of Mental Disorders (Third Edition Revised) criteria using the Confusion Assessment Method beginning at any time from the second day after surgery. RESULTS: From April 2, 2005, through October 30, 2008, a total of 114 patients were randomized. The prevalence of postoperative delirium was significantly lower in the light sedation group (11/57 [19%] vs 23/57 [40%] in the deep sedation group; P=.02), indicating that 1 incident of delirium will be prevented for every 4.7 patients treated with light sedation. The mean +/- SD number of days of delirium during hospitalization was lower in the light sedation group than in the deep sedation group (0.5+/-1.5 days vs 1.4+/-4.0 days; P=.01). CONCLUSION: The use of light propofol sedation decreased the prevalence of postoperative delirium by 50% compared with deep sedation. Limiting depth of sedation during spinal anesthesia is a simple, safe, and cost-effective intervention for preventing postoperative delirium in elderly patients that could be widely and readily adopted.


Amentia Amentias Dementia Familial Dementias Senile Paranoid

An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.


2,6 Diisopropylphenol 2,6-Bis(1-methylethyl)phenol 2,6-Diisopropylphenol Abbott Brand of Propofol Alpha Aquafol Astra AstraZeneca Braun Curamed Diprivan Disoprivan Disoprofol Fresenius Kabi Fresofol ICI 35,868 35868 ICI-35,868 ICI-35868 ICI35,868 ICI35868 Ivofol Juste Parnell Pisa MCT Rovi Propofol-Lipuro Recofol Schering Zeneca

An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.


Behavior Disorders Diagnosis Psychiatric Disorder Mental

Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function.


Sorafenib-induced acute myocardial infarction due to coronary artery spasm.

4-(4-(3-(4-chloro-3-trifluoromethylphenyl)ureido)phenoxy)pyridine-2-carboxyllic acid methyamide-4-methylbenzenesulfonate BAY 43-9006 545-9085 BAY-545-9085 Nexavar sorafenib N-oxide tosylate


Cardiovascular Stroke Strokes Infarct Myocardial Infarction Infarctions Infarcts

NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).


Spasm of the large- or medium-sized coronary arteries.


A 65-year-old man with advanced renal cell carcinoma was admitted due to continuing chest pain at rest. Two weeks before his admission, sorafenib had been started. He was diagnosed with non-ST-elevation myocardial infarction by laboratory data and electrocardiogram. Enhanced heart magnetic resonance imaging also showed subendocardial infarction. However, there was no stenosis in coronary arteries on angiography. Coronary artery spasm was induced by a provocative test. Cessation of sorafenib and administration of Ca-channel blocker and nitrates ameliorated his symptoms, but relapse occurred after resumption of sorafenib. Addition of oral nicorandil reduced his symptoms and maintained stable angina status. We report the first case of sorafenib-induced coronary artery spasm. Sorafenib is a multikinase inhibitor that targets signaling pathways necessary for cellular proliferation and survival. On the other hand, the Rho/ROCK pathway has an important role in the pathogenesis of coronary artery spasm. Our report may show an adverse effect on the Rho/ROCK pathway by sorafenib use.

Adenocarcinoma Of Kidney Renal Cell Adenocarcinomas Cancer Cancers Carcinoma Collecting Duct (Kidney) Hypernephroid Nephroid Carcinomas Chromophil Chromophobe Clear of the Grawitz Tumor Hypernephroma Hypernephromas Papillary Sarcomatoid

A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.


Pressure, burning, or numbness in the chest.


A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.


Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.


2 Nicotinamidethyl Nitrate Nicotinamidoethyl 2-Nicotinamidethyl 2-Nicotinamidoethyl Adancor Aventis Brand of Nicorandil Pharma Dancor Ikorel Merck Lipha Santé Rhône Poulenc Rorer Rhône-Poulenc SG 75 SG-75 SG75

A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.


Angina Pectori Stable Pectoris Chronic Anginas

Persistent and reproducible chest discomfort usually precipitated by a physical exertion that dissipates upon cessation of such an activity. The symptoms are manifestations of MYOCARDIAL ISCHEMIA.


Anxiogenic potential of ciprofloxacin and norfloxacin in rats.

Anhydrous Ciprofloxacin Hydrochloride Bay 09867 Bay-09867 Bay09867 Ciprinol Cipro Monohydrochloride Monohydrate

A broad-spectrum antimicrobial carboxyfluoroquinoline.


AM 0715 715 AM-0715 AM-715 AM0715 MK 0366 366 MK-0366 MK-366 MK0366 MK366 Merck Brand of Norfloxacin Noroxin

A synthetic fluoroquinolone (FLUOROQUINOLONES) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA GYRASE.


INTRODUCTION: The possible anxiogenic effects of fluoroquinolones, namely ciprofloxacin and norfloxacin, were investigated in adult Charles Foster albino rats of either sex, weighing 150-200 g. METHODS: The drugs were given orally, in doses of 50 mg/kg for five consecutive days and the experiments were performed on the fifth day. The tests included open-field exploratory behaviour, elevated plus maze and elevated zero maze, social interaction and novelty-suppressed feeding latency behaviour. RESULTS: The results indicate that ciprofloxacin- and norfloxacin-treated rats showed anxious behaviour in comparison to control rats in all the parameters studied. However, ciprofloxacin- and norfloxacin-treated rats did not differ significantly from each other in various behavioural parameters. CONCLUSION: The present experimental findings substantiate the clinically observed anxiogenic potential of ciprofloxacin and norfloxacin.

A group of QUINOLONES with at least one fluorine atom and a piperazinyl group.


Anxiety Disorder Disorders Neuroses State Neurotic States


Myocardial Fas ligand expression increases susceptibility to AZT-induced cardiomyopathy.

3' Azido 2',3' Dideoxythymidine deoxythymidine 3'-Azido-2',3'-Dideoxythymidine 3'-Azido-3'-deoxythymidine AZT (Antiviral) Antiviral Azidothymidine BW A509U BWA 509U BWA-509U BWA509U Retrovir Zidovudine

A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.


Cardiomyopathies Primary Secondary Cardiomyopathy Disease Myocardial Diseases Myocardiopathies Myocardiopathy

A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).


BACKGROUND: Dilated cardiomyopathy (DCM) and myocarditis occur in many HIV-infected individuals, resulting in symptomatic heart failure in up to 5% of patients. Highly active antiretroviral therapy (HAART) has significantly reduced morbidity and mortality of acquired immunodeficiency syndrome (AIDS), but has resulted in an increase in cardiac and skeletal myopathies. METHODS AND RESULTS: In order to investigate whether the HAART component zidovudine (3'-azido-2',3'-deoxythymidine; AZT) triggers the Fas-dependent cell-death pathway and cause cytoskeletal disruption in a murine model of DCM, 8-week-old transgenic (expressing Fas ligand in the myocardium: FasL Tg) and non-transgenic (NTg) mice received water ad libitum containing different concentrations of AZT (0, 0.07, 0.2, and 0.7 mg/ml). After 6 weeks, cardiac function was assessed by echocardiography and morphology was assessed by histopathologic and immunohistochemical methods. NTg and untreated FasL Tg mice showed little or no change in cardiac structure or function. In contrast, AZT-treated FasL Tg mice developed cardiac dilation and depressed cardiac function in a dose-dependent manner, with concomitant inflammatory infiltration of both ventricles. These changes were associated with an increased sarcolemmal expression of Fas and FasL, as well as increased activation of caspase 3, translocation of calpain 1 to the sarcolemma and sarcomere, and increased numbers of cells undergoing apoptosis. These were associated with changes in dystrophin and cardiac troponin I localization, as well as loss of sarcolemmal integrity. CONCLUSIONS: The expression of Fas ligand in the myocardium, as identified in HIV-positive patients, might increase the susceptibility to HAART-induced cardiomyopathy due to activation of apoptotic pathways, resulting in cardiac dilation and dysfunction.

1A Dilated cardiomyopathy 1As Cardiomyopathies Congestive Familial Idiopathic Cardiomyopathy 1a Autosomal Recessive CMD1A LMNA With Conduction Defect 1 with Deffect1

A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.


Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.


HIV Infection Infections HTLV III LAV HTLV-III HTLV-III-LAV T Lymphotropic Virus Type Human T-Lymphotropic

Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).


Cardiac Failure Congestive Heart Decompensation Left Sided Left-Sided Right Right-Sided Myocardial

A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.


AIDS Acquired Immune Deficiency Syndrome Immuno Immuno-Deficiency Syndromes Immunodeficiency Immunologic

An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive T-lymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993.


Dilated cardiomyopathy, neutropenia, skeletal myopathy, and abnormal mitochondria

Dilated cardiomyopathy neutropenia skeletal myopathy and abnormal mitochondria


Valproate-induced chorea and encephalopathy in atypical nonketotic hyperglycinemia.

2 Propylpentanoic Acid 2-Propylpentanoic Acetate Dipropyl Propylisopropylacetic Valproic Calcium Valproate Convulsofin Depakene Depakine Depakote Divalproex Sodium Ergenyl Magnesium Semisodium Salt (2:1) Vupral

A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.


Benign Hereditary Chorea Choreas Disorder Disorders Syndrome Syndromes Chronic Progressive Rheumatic Senile Sydenham Sydenham's Choreatic Choreic Movement Movements Choreiform Dyskinesia Paroxysmal Dyskinesias Without Dementia St. Vitus Dance Vitus's Dances Vituss Sydenhams

Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as CHOREATIC DISORDERS. Chorea is also a frequent manifestation of BASAL GANGLIA DISEASES.


Brain Disease Diseases Disorder Disorders CNS Intracranial Central Nervous System Encephalon

Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.


Encephalopathies Glycine Encephalopathy Hyperglycinemia Non-ketotic Nonketotic Type I II III Hyperglycinemias Non ketotic

An autosomal recessive metabolic disorder caused by deficiencies in the mitochondrial GLYCINE cleavage system.


Nonketotic hyperglycinemia is a disorder of amino acid metabolism in which a defect in the glycine cleavage system leads to an accumulation of glycine in the brain and other body compartments. In the classical form it presents as neonatal apnea, intractable seizures, and hypotonia, followed by significant psychomotor retardation. An important subset of children with nonketotic hyperglycinemia are atypical variants who present in a heterogeneous manner. This report describes a patient with mild language delay and mental retardation, who was found to have nonketotic hyperglycinemia following her presentation with acute encephalopathy and chorea shortly after initiation of valproate therapy.


Amino Acid Metabolism Disorders Inborn Error Errors Inherited Acidopathies Congenital Acidopathy of

Disorders affecting amino acid metabolism. The majority of these disorders are inherited and present in the neonatal period with metabolic disturbances (e.g., ACIDOSIS) and neurologic manifestations. They are present at birth, although they may not become symptomatic until later in life.


Acid Aminoacetic Calcium Salt Glycine Cobalt Copper Carbonate (1:1) Monosodium (2:1) Monolithium Monopotassium Hydrochloride Phosphate Sulfate (3:1) Monoammonium Monopotasssium Sodium Hydrogen

A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.


A transient absence of spontaneous respiration.


Auditory Seizure Seizures Clonic Convulsion Non Epileptic Non-Epileptic Convulsions Convulsive Focal Generalized Gustatory Jacksonian Motor Olfactory Sensory Somatosensory Tonic Tonic-Clonic Vertiginous Vestibular Visual

Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."


Decreased Muscle Tone Flaccid Flaccidity Muscular Floppy Muscles Hypomyotonia Hypotonia Neonatal Unilateral Hypotonias Hypotony Atonic Atonics Poor Flaccidities

A diminution of the skeletal muscle tone marked by a diminished resistance to passive stretching.


Developmental Psychomotor Disorder Disorders Impairment Impairments

Abnormalities of motor function that are associated with organic and non-organic cognitive disorders.


Auditory Processing Disorder Central Delay Speech Delays Development Language Developmental or Disorders Semantic Pragmatic Semantic-Pragmatic

Conditions characterized by language abilities (comprehension and expression of speech and writing) that are below the expected level for a given age, generally in the absence of an intellectual impairment. These conditions may be associated with DEAFNESS; BRAIN DISEASES; MENTAL DISORDERS; or environmental factors.


Deficiencies Mental Deficiency Disabilities Intellectual Disability Idiocy Retardation Psychosocial Retardations

Subnormal intellectual functioning which originates during the developmental period. This has multiple potential etiologies, including genetic defects and perinatal insults. Intelligence quotient (IQ) scores are commonly used to determine whether an individual has an intellectual disability. IQ scores between 70 and 79 are in the borderline range. Scores below 67 are in the disabiled range. (from Joynt, Clinical Neurology, 1992, Ch55, p28)


Microinjection of ritanserin into the CA1 region of hippocampus improves scopolamine-induced amnesia in adult male rats.

6-(2-(4-(Bis(4-fluorophenyl)methylene)-1-piperidinyl)ethyl)-7-methyl-5H-thiazolo(3,2-a)pyrimidin-5-one R 55667 R-55667 R55667 Ritanserin Hydrochloride Tartrate

A selective and potent serotonin-2 antagonist that is effective in the treatment of a variety of syndromes related to anxiety and depression. The drug also improves the subjective quality of sleep and decreases portal pressure.


Alcon Brand of Scopolamine Hydrobromide Boro Scopol Boro-Scopol BoroScopol Bull Cooper Hamilton Hope Hyoscine Inibisa Isopto Kwells Novartis Consumer Health Renaudin Roche Scoburen Scopace Scopoderm TTS Transderm Scop V Transderm-V Travacalm HO Vorigeno Winzer Borate

An alkaloid from SOLANACEAE, especially DATURA and SCOPOLIA. Scopolamine and its quaternary derivatives act as antimuscarinics like ATROPINE, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in URINARY INCONTINENCE, in MOTION SICKNESS, as an antispasmodic, and as a mydriatic and cycloplegic.


Amnesia Memory Loss Dissociative Global Hysterical Tactile Temporary Amnesia-Memory Losses Amnesias Amnestic State States

Pathologic partial or complete loss of the ability to recall past experiences (AMNESIA, RETROGRADE) or to form new memories (AMNESIA, ANTEROGRADE). This condition may be of organic or psychologic origin. Organic forms of amnesia are usually associated with dysfunction of the DIENCEPHALON or HIPPOCAMPUS. (From Adams et al., Principles of Neurology, 6th ed, pp426-7)


The effect of ritanserin (5-HT2 antagonist) on scopolamine (muscarinic cholinergic antagonist)-induced amnesia in Morris water maze (MWM) was investigated. Rats were divided into eight groups and bilaterally cannulated into CA1 region of the hippocampus. One week later, they received repeatedly vehicles (saline, DMSO, saline+DMSO), scopolamine (2 microg/0.5 microl saline/side; 30 min before training), ritanserin (2, 4 and 8 microg/0.5 microl DMSO/side; 20 min before training) and scopolamine (2 microg/0.5 microl; 30 min before ritanserin injection)+ritanserin (4 microg/0.5 microl DMSO) through cannulae each day. Animals were tested for four consecutive days (4 trial/day) in MWM during which the position of hidden platform was unchanged. In the fifth day, the platform was elevated above the water surface in another position to evaluate the function of motor, motivational and visual systems. The results showed a significant increase in escape latencies and traveled distances to find platform in scopolamine-treated group as compared to saline group. Ritanserin-treated rats (4 microg/0.5 microl/side) showed a significant decrease in the mentioned parameters as compared to DMSO-treated group. However, scopolamine and ritanserin co-administration resulted in a significant decrease in escape latencies and traveled distances as compared to the scopolamine-treated rats. Our findings show that microinjection of ritanserin into the CA1 region of the hippocampus improves the scopolamine-induced amnesia.


DMSO Dimethyl Sulfoxide Sulphoxide Dimethylsulfoxide Dimethylsulphinyl Dimethylsulphoxide Dimexide Merckle Brand of Research Ind. Corp. 1 2 Rheumabene Rimso 100 Rimso-50 Sclerosol Shire Sulfinylbis(methane)

A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.


Hypoxia in renal disease with proteinuria and/or glomerular hypertension.

Anoxemia Anoxemias Anoxia Anoxias Deficiencies Oxygen Deficiency Hypoxemia Hypoxemias Hypoxia Hypoxias

Relatively complete absence of oxygen in one or more tissues.


Pathological processes of the KIDNEY or its component tissues.


The presence of proteins in the urine, an indicator of KIDNEY DISEASES.