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.


Several cases of cardiac adverse reactions related to vinorelbine (VNR) have been reported in the literature. In order to quantify the incidence of these cardiac events, we performed a meta-analysis of clinical trials comparing VNR with other chemotherapeutic agents in the treatment of various malignancies. Randomized clinical trials comparing VNR with other drugs in the treatment of cancer were searched in Medline, Embase, Evidence-based Medicine Reviews databases and the Cochrane library from 1987 to 2002. Outcomes of interest were severe cardiac events, toxic deaths and cardiac event-related deaths reported in each publication. We found 19 trials, involving 2441 patients treated by VNR and 2050 control patients. The incidence of cardiac events with VNR was 1.19% [95% confidence interval (CI) (0.75; 1.67)]. There was no difference in the risk of cardiac events between VNR and other drugs [odds ratio: 0.92, 95% CI (0.54; 1.55)]. The risk of VNR cardiac events was similar to vindesine (VDS) and other cardiotoxic drugs [fluorouracil, anthracyclines, gemcitabine (GEM) em leader ]. Even if it did not reach statistical significance because of a few number of cases, the risk was lower in trials excluding patients with cardiac history, and seemed to be higher in trials including patients with pre-existing cardiac diseases. Vinorelbine-related cardiac events concern about 1% of treated patients in clinical trials. However, the risk associated with VNR seems to be similar to that of other chemotherapeutic agents in the same indications.

Organic compounds that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.


2',2'-DFDC 2',2'-difluoro-2'-deoxycytidine 2',2'-difluorodeoxycytidine 2'-deoxy-2',2''-difluorocytidine-5'-O-monophosphate 2'-deoxy-2'-difluorocytidine Gemzar LY 188011 LY-188011 dFdCyd gemcitabine hydrochloride (D-threo-pentafuranosyl)-isomer (alpha-D-threo-pentofuranosyl)-isomer (beta-D-threo-pentafuranosyl)-isomer


Pathological conditions involving the HEART including its structural and functional abnormalities.


5'-nor-anhydrovinblastine KW 2307 KW-2307 Navelbine vinorelbine tartrate


MRI findings of hypoxic cortical laminar necrosis in a child with hemolytic anemia crisis.

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.


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).


We present magnetic resonance imaging findings of a 5-year-old girl who had a rapidly installing hemolytic anemia crisis induced by trimethoprim-sulfomethoxazole, resulting in cerebral anoxia leading to permanent damage. Magnetic Resonance imaging revealed cortical laminar necrosis in arterial border zones in both cerebral hemispheres, ischemic changes in subcortical white matter of left cerebral hemisphere, and in the left putamen. Although cortical laminar necrosis is a classic entity in adulthood related to conditions of energy depletions, there are few reports available in children. A wide review of the literature is also presented.


Abactrim Bactifor Bactrim Biseptol 480 Biseptol-480 Biseptol480 Centran Centrin Co Trimoxazole Co-Trimoxazole Cotrimoxazole Drylin Eslectin Eusaprim Insozalin Kepinol Forte Lescot Metomide Oriprim Septra Septrin Sulfamethoxazole Trimethoprim Combination Sulfamethoxazole-Trimethoprim Sulprim Sumetrolim TMP SMX TMP-SMX Trimedin Trimethoprim-Sulfamethoxazole Trimethoprimsulfa Trimezole Trimosulfa

This drug combination has proved to be an effective therapeutic agent with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.


Anoxia Brain Cerebral Anoxic Damage Encephalopathies Encephalopathy Hypoxic Hypoxia

A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.


The natural history of Vigabatrin associated visual field defects in patients electing to continue their medication.

Acid gamma-Vinyl-gamma-Aminobutyric Aventis Brand of Vigabatrin Hoechst Sabril Sabrilex Yamanouchi gamma Vinyl GABA Aminobutyric gamma-Vinyl-GABA

An analogue of GAMMA-AMINOBUTYRIC ACID. It is an irreversible inhibitor of 4-AMINOBUTYRATE TRANSAMINASE, the enzyme responsible for the catabolism of GAMMA-AMINOBUTYRIC ACID. (From Martindale The Extra Pharmacopoeia, 31st ed)


Blindness Day Disabilities Vision Disability Disorder Visual Disorders Hemeralopia Hemeralopias Impairment Impairments Macropsia Macropsias Metamorphopsia Metamorphopsias Micropsia Micropsias

Visual impairments limiting one or more of the basic functions of the eye: visual acuity, dark adaptation, color vision, or peripheral vision. These may result from EYE DISEASES; OPTIC NERVE DISEASES; VISUAL PATHWAY diseases; OCCIPITAL LOBE diseases; OCULAR MOTILITY DISORDERS; and other conditions (From Newell, Ophthalmology: Principles and Concepts, 7th ed, p132).


PURPOSE: To determine the natural history of visual field defects in a group of patients known to have Vigabatrin-associated changes who elected to continue the medication because of good seizure control. METHODS: All patients taking Vigabatrin alone or in combination with other antiepileptic drugs for at least 5 years (range 5-12 years) were entered into a visual surveillance programme. Patients were followed up at 6-monthly intervals for not less than 18 months (range 18-43 months). In all, 16 patients with unequivocal defects continued the medication. Following already published methodology (Eye 2002; 16;567-571) monocular mean radial degrees (MRDs) to the I/4e isopter on Goldmann perimetry was calculated for the right eye at the time of discovery of a visual field defect and again after not less than 18 months follow-up. RESULTS: Mean right eye MRD at presentation was 36.98 degrees (range 22.25-51.0), compared to 38.40 degrees (range 22.5-49.75) after follow-up; P=0.338 unpaired t-test. Only one patient demonstrated a deterioration in visual field during the study period and discontinued treatment. CONCLUSION: Established visual field defects presumed to be due to Vigabatrin therapy did not usually progress in spite of continuing use of the medication. These data give support to the hypothesis that the pathogenesis of Vigabatrin-associated visual field defects may be an idiosyncratic adverse drug reaction rather than dose-dependent toxicity.


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."


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.


Induction of rosaceiform dermatitis during treatment of facial inflammatory dermatoses with tacrolimus ointment.


Dermatoses Facial Dermatosis Elastoidoses Nodular Elastoidosis Elastoses Elastosis Favre Racouchot Syndrome Favre-Racouchot


Anhydrous Tacrolimus Cilag Brand of FK 506 FK-506 FK506 FR 900506 FR-900506 FR900506 Fujisawa Janssen Prograf Prograft

A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.


BACKGROUND: Tacrolimus ointment is increasingly used for anti-inflammatory treatment of sensitive areas such as the face, and recent observations indicate that the treatment is effective in steroid-aggravated rosacea and perioral dermatitis. We report on rosaceiform dermatitis as a complication of treatment with tacrolimus ointment. OBSERVATIONS: Six adult patients with inflammatory facial dermatoses were treated with tacrolimus ointment because of the ineffectiveness of standard treatments. Within 2 to 3 weeks of initially effective and well-tolerated treatment, 3 patients with a history of rosacea and 1 with a history of acne experienced sudden worsening with pustular rosaceiform lesions. Biopsy revealed an abundance of Demodex mites in 2 of these patients. In 1 patient with eyelid eczema, rosaceiform periocular dermatitis gradually appeared after 3 weeks of treatment. In 1 patient with atopic dermatitis, telangiectatic and papular rosacea insidiously appeared after 5 months of treatment. CONCLUSIONS: Our observations suggest that the spectrum of rosaceiform dermatitis as a complication of treatment with tacrolimus ointment is heterogeneous. A variety of factors, such as vasoactive properties of tacrolimus, proliferation of Demodex due to local immunosuppression, and the occlusive properties of the ointment, may be involved in the observed phenomena. Future studies are needed to identify individual risk factors.


A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)


Acne Rosacea Erythematotelangiectatic Granulomatous Ocular Papulopustular Phymatous

A cutaneous disorder primarily of convexities of the central part of the FACE, such as FOREHEAD; CHEEK; NOSE; and CHIN. It is characterized by FLUSHING; ERYTHEMA; EDEMA; RHINOPHYMA; papules; and ocular symptoms. It may occur at any age but typically after age 30. There are various subtypes of rosacea: erythematotelangiectatic, papulopustular, phymatous, and ocular (National Rosacea Society's Expert Committee on the Classification and Staging of Rosacea, J Am Acad Dermatol 2002; 46:584-7).


Dermatitides Periocular Perioral Dermatitis

A papular eruption of unknown etiology that progresses to residual papular erythema and scaling usually confined to the area of the mouth, and almost exclusively occurring in young women. It may also be localized or extend to involve the eyelids and adjacent glabella area of the forehead (periocular dermatitis). (Dorland, 28th ed)


A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors.


Dermatitides Eczematous Dermatitis Eczema Eczemas

A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed).


Atopic Dermatitides Dermatitis Eczema Neurodermatitides Neurodermatitis Disseminated Infantile

A chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. It is manifested by lichenification, excoriation, and crusting, mainly on the flexural surfaces of the elbow and knee. In infants it is known as infantile eczema.


Structural abnormalities in the brains of human subjects who use methamphetamine.

Abbott Brand of Methamphetamine Hydrochloride Deoxyephedrine Desoxyephedrine Desoxyn Langly Madrine Metamfetamine Methylamphetamine N N-Methylamphetamine

A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.


We visualize, for the first time, the profile of structural deficits in the human brain associated with chronic methamphetamine (MA) abuse. Studies of human subjects who have used MA chronically have revealed deficits in dopaminergic and serotonergic systems and cerebral metabolic abnormalities. Using magnetic resonance imaging (MRI) and new computational brain-mapping techniques, we determined the pattern of structural brain alterations associated with chronic MA abuse in human subjects and related these deficits to cognitive impairment. We used high-resolution MRI and surface-based computational image analyses to map regional abnormalities in the cortex, hippocampus, white matter, and ventricles in 22 human subjects who used MA and 21 age-matched, healthy controls. Cortical maps revealed severe gray-matter deficits in the cingulate, limbic, and paralimbic cortices of MA abusers (averaging 11.3% below control; p < 0.05). On average, MA abusers had 7.8% smaller hippocampal volumes than control subjects (p < 0.01; left, p = 0.01; right, p < 0.05) and significant white-matter hypertrophy (7.0%; p < 0.01). Hippocampal deficits were mapped and correlated with memory performance on a word-recall test (p < 0.05). MRI-based maps suggest that chronic methamphetamine abuse causes a selective pattern of cerebral deterioration that contributes to impaired memory performance. MA may selectively damage the medial temporal lobe and, consistent with metabolic studies, the cingulate-limbic cortex, inducing neuroadaptation, neuropil reduction, or cell death. Prominent white-matter hypertrophy may result from altered myelination and adaptive glial changes, including gliosis secondary to neuronal damage. These brain substrates may help account for the symptoms of MA abuse, providing therapeutic targets for drug-induced brain injury.

Acute Brain Injuries Injury Contusion Contusions Diffuse Focal Traumatic Laceration Lacerations Trauma Traumas Cortical Encephalopathies Post-Concussive Post-Traumatic Encephalopathy Post Concussive Mild TBI (Traumatic Injury) TBIs

Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.


Disease Metabolic Diseases Thesaurismoses Thesaurismosis

Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)


Cognition Disorders Disorder Overinclusion

Disturbances in the mental process related to thinking, reasoning, and judgment.


abnormalities in the cortex, hippocampus, white matter, and ventricles


General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).


Age Related Memory Disorders Age-Related Disorder Cognitive Retention Deficit Deficits Semantic Spatial Loss Losses

Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.


The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.


Disease Nervous System Diseases Disorder Neurologic Neurological Disorders

Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.


Disruption of hepatic lipid homeostasis in mice after amiodarone treatment is associated with peroxisome proliferator-activated receptor-alpha target gene activation.

ASTA Medica Brand of Amiodarone Hydrochloride Alphapharm Amiobeta Amiodarex Amiodarona Amiohexal Aratac Armstrong Berenguer Infale Betapharm Braxan Corbionax Cordarex Cordarone G Gam Hexal Kordaron L 3428 L-3428 L3428 Leurquin Ortacrone Pharma Investi Rytmarone SKF 33134 A 33134-A 33134A Sanofi Winthrop Tachydaron Trangorex Wyeth

An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.


Amiodarone, an efficacious and widely used antiarrhythmic agent, has been reported to cause hepatotoxicity in some patients. To gain insight into the mechanism of this unwanted effect, mice were administered various doses of amiodarone and examined for changes in hepatic histology and gene regulation. Amiodarone induced hepatomegaly, hepatocyte microvesicular lipid accumulation, and a significant decrease in serum triglycerides and glucose. Northern blot analysis of hepatic RNA revealed a dose-dependent increase in the expression of a number of genes critical for fatty acid oxidation, lipoprotein assembly, and lipid transport. Many of these genes are regulated by the peroxisome proliferator-activated receptor-alpha (PPARalpha), a ligand-activated nuclear hormone receptor transcription factor. The absence of induction of these genes as well as hepatomegaly in PPARalpha knockout [PPARalpha-/-] mice indicated that the effects of amiodarone were dependent upon the presence of a functional PPARalpha gene. Compared to wild-type mice, treatment of PPARalpha-/- mice with amiodarone resulted in an increased rate and extent of total body weight loss. The inability of amiodarone to directly activate either human or mouse PPARalpha transiently expressed in human HepG2 hepatoma cells indicates that the effects of amiodarone on the function of this receptor were indirect. Based upon these results, we conclude that amiodarone disrupts hepatic lipid homeostasis and that the increased expression of PPARalpha target genes is secondary to this toxic effect. These results provide important new mechanistic information regarding the hepatotoxic effects of amiodarone and indicate that PPARalpha protects against amiodarone-induced hepatotoxicity.


Acute Liver Injury Drug Induced Drug-Induced Disease Diseases Hepatitides Hepatitis Injuries Toxic

A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.


Anhydrous Dextrose D Glucose D-Glucose Monohydrate (DL)-Isomer (L)-Isomer (alpha-D)-Isomer (beta-D)-Isomer L L-Glucose

A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.


Acids Aliphatic Esterified Fatty Saturated

Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)


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.


Safety and compliance with once-daily niacin extended-release/lovastatin as initial therapy in the Impact of Medical Subspecialty on Patient Compliance to Treatment (IMPACT) study.


Niacin extended-release/lovastatin is a new combination product approved for treatment of primary hypercholesterolemia and mixed dyslipidemia. This open-labeled, multicenter study evaluated the safety of bedtime niacin extended-release/lovastatin when dosed as initial therapy and patient compliance to treatment in various clinical practice settings. A total of 4,499 patients with dyslipidemia requiring drug intervention was enrolled at 1,081 sites. Patients were treated with 1 tablet (500 mg of niacin extended-release/20 mg of lovastatin) once nightly for 4 weeks and then 2 tablets for 8 weeks. Patients also received dietary counseling, educational materials, and reminders to call a toll-free number that provided further education about dyslipidemia and niacin extended-release/lovastatin. Primary end points were study compliance, increases in liver transaminases to >3 times the upper limit of normal, and clinical myopathy. Final study status was available for 4,217 patients (94%). Compliance to niacin extended-release/lovastatin was 77%, with 3,245 patients completing the study. Patients in the southeast and those enrolled by endocrinologists had the lowest compliance and highest adverse event rates. Flushing was the most common adverse event, reported by 18% of patients and leading to discontinuation by 6%. Incidence of increased aspartate aminotransferase and/or alanine aminotransferase >3 times the upper limit of normal was <0.3%. An increase of creatine phosphokinase to >5 times the upper limit of normal occurred in 0.24% of patients, and no cases of drug-induced myopathy were observed. Niacin extended-release/lovastatin 1,000/40 mg, dosed as initial therapy, was associated with good compliance and safety and had very low incidences of increased liver and muscle enzymes.


Elevated Cholesterol Hypercholesteremia Hypercholesteremias Hypercholesterolemia Hypercholesterolemias

A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.


Dyslipidemia Dyslipidemias Dyslipoproteinemia Dyslipoproteinemias

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.


3 Pyridinecarboxylic Acid 3-Pyridinecarboxylic Nicotinic Aluminum Salt Niacin Ammonium Calcium Enduracin Hydrochloride Induracin Lithium Nicotinate Magnesium Cobalt (2+) Copper Iron Hemihydrate Manganese Potassium Sodium Tartrate Tosylate Zinc Nicamin Nico 400 Nico-400 Nico400 Nicobid Nicocap Nicolar Wampocap

A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.


1 alpha-Isomer Lovastatin 6 Methylcompactin 6-Methylcompactin (1 alpha(S*))-Isomer alpha Isomer MK 803 MK-803 MK803 Mevacor Mevinolin Monacolin K

A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.


Muscle Disorder Disorders Muscular Disease Diseases Myopathic Condition Conditions Myopathies Myopathy

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


A transient reddening of the face that may be due to fever, certain drugs, exertion, stress, or a disease process.


(+-)-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.


Abufène Alanine Doms-Adrian Brand L Isomer L-Isomer Doms Adrian of L-Alanine

A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases IMMUNITY, and provides energy for muscle tissue, BRAIN, and the CENTRAL NERVOUS SYSTEM.


An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as CREATININE in the urine.


Protective effect of Terminalia chebula against experimental myocardial injury induced by isoproterenol.

Concentrated pharmaceutical preparations of plants obtained by removing active constituents with a suitable solvent, which is evaporated away, and adjusting the residue to a prescribed standard.


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).


4-(1-Hydroxy-2-((1-methylethyl)amino)ethyl)-1,2-benzenediol Euspiran Hydrochloride Isoproterenol Isadrin Isadrine Isoprenaline Isopropyl Noradrenaline Isopropylarterenol Isopropylnoradrenaline Isopropylnorepinephrine Sulfate Isuprel Izadrin Norisodrine Novodrin

Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.


Cardioprotective effect of ethanolic extract of Terminalia chebula fruits (500 mg/kg body wt) was examined in isoproterenol (200 mg/kg body wt) induced myocardial damage in rats. In isoproterenol administered rats, the level of lipid peroxides increased significantly in the serum and heart. A significant decrease was observed in the activity of the myocardial marker enzymes with a concomitant increase in their activity in serum. Histopathological examination was carried out to confirm the myocardial necrosis. T. chebula extract pretreatment was found to ameliorate the effect of isoproterenol on lipid peroxide formation and retained the activities of the diagnostic marker enzymes.


A group of compounds that contain a bivalent O-O group, i.e., the oxygen atoms are univalent. They can either be inorganic or organic in nature. Such compounds release atomic (nascent) oxygen readily. Thus they are strong oxidizing agents and fire hazards when in contact with combustible materials, especially under high-temperature conditions. The chief industrial uses of peroxides are as oxidizing agents, bleaching agents, and initiators of polymerization. (From Hawley's Condensed Chemical Dictionary, 11th ed)


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.


A case of postoperative anxiety due to low dose droperidol used with patient-controlled analgesia.

Anxiety Disorder Disorders Neuroses State Neurotic States


Dehidrobenzperidol Dehydrobenzperidol Droleptan Droperidol Inapsine Janssen Brand of Kern Taylor

A butyrophenone with general properties similar to those of HALOPERIDOL. It is used in conjunction with an opioid analgesic such as FENTANYL to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593)


A multiparous woman in good psychological health underwent urgent caesarean section in labour. Postoperatively, she was given a patient-controlled analgesia device delivering boluses of diamorphine 0.5 mg and droperidol 0.025 mg. Whilst using the device she gradually became anxious, the feeling worsening after each bolus. The diagnosis of droperidol-induced psychological disturbance was not made straight away although on subsequent close questioning the patient gave a very clear history. After she had received a total of only 0.9 mg droperidol, a syringe containing diamorphine only was substituted and her unease resolved completely. We feel that, although the dramatic extrapyramidal side effects of dopaminergic antiemetics are well known, more subtle manifestations may easily be overlooked.

APS Brand of Heroin Hydrochloride Diacetylmorphine Diagesil Diamorf Diamorphine Evans Vaccines Min I Jet Morphine Sulphate Min-I-Jet

A narcotic analgesic that may be habit-forming. It is a controlled substance (opium derivative) listed in the U.S. Code of Federal Regulations, Title 21 Parts 329.1, 1308.11 (1987). Sale is forbidden in the United States by Federal statute. (Merck Index, 11th ed)


Accurate patient history contributes to differentiating diabetes insipidus: a case study.

A disease that is characterized by frequent urination, excretion of large amounts of dilute URINE, and excessive THIRST. Etiologies of diabetes insipidus include deficiency of antidiuretic hormone (also known as ADH or VASOPRESSIN) secreted by the NEUROHYPOPHYSIS, impaired KIDNEY response to ADH, and impaired hypothalamic regulation of thirst.


This case study highlights the important contribution of nursing in obtaining an accurate health history. The case discussed herein initially appeared to be neurogenic diabetes insipidus (DI) secondary to a traumatic brain injury. The nursing staff, by reviewing the patient's health history with his family, discovered a history of polydipsia and long-standing lithium use. Lithium is implicated in drug-induced nephrogenic DI, and because the patient had not received lithium since being admitted to the hospital, his treatment changed to focus on nephrogenic DI. By combining information from the patient history, the physical examination, and radiologic and laboratory studies, the critical care team demonstrated that the patient had been self-treating his lithium-induced nephrogenic DI and developed neurogenic DI secondary to brain trauma. Thus successful treatment required that nephrogenic and neurogenic DI be treated concomitantly.

ADH-Resistant Diabetes Insipidus Acquired Nephrogenic Congenital Renalis Autosomal Type 1 I II X-Linked Vasopressin-Resistant

A genetic or acquired polyuric disorder characterized by persistent hypotonic urine and HYPOKALEMIA. This condition is due to renal tubular insensitivity to VASOPRESSIN and failure to reduce urine volume. It may be the result of mutations of genes encoding VASOPRESSIN RECEPTORS or AQUAPORIN-2; KIDNEY DISEASES; adverse drug effects; or complications from PREGNANCY.


Acute Brain Injuries Injury Contusion Contusions Diffuse Focal Traumatic Laceration Lacerations Trauma Traumas Cortical Encephalopathies Post-Concussive Post-Traumatic Encephalopathy Post Concussive Mild TBI (Traumatic Injury) TBIs

Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.


Excessive thirst manifested by excessive fluid intake. It is characteristic of many diseases such as DIABETES MELLITUS; DIABETES INSIPIDUS; and NEPHROGENIC DIABETES INSIPIDUS. The condition may be psychogenic in origin.


An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight [6.938; 6.997]. Salts of lithium are used in treating BIPOLAR DISORDER.


Factors contributing to ribavirin-induced anemia.

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.


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


BACKGROUND AND AIM: Interferon and ribavirin combination therapy for chronic hepatitis C produces hemolytic anemia. This study was conducted to identify the factors contributing to ribavirin-induced anemia. METHODS: Eighty-eight patients with chronic hepatitis C who received interferon-alpha-2b at a dose of 6 MU administered intramuscularly for 24 weeks in combination with ribavirin administered orally at a dose of 600 mg or 800 mg participated in the study. A hemoglobin concentration of <10 g/dL was defined as ribavirin-induced anemia. RESULTS: Ribavirin-induced anemia occurred in 18 (20.5%) patients during treatment. A 2 g/dL decrease in hemoglobin concentrations in patients with anemia was observed at week 2 after the start of treatment. The hemoglobin concentration in patients with > or =2 g/dL decrease at week 2 was observed to be significantly lower even after week 2 than in patients with <2 g/dL decrease (P < 0.01). A significant relationship was observed between the rate of reduction of hemoglobin concentrations at week 2 and the severity of anemia (P < 0.01). Such factors as sex (female), age (> or =60 years old), and the ribavirin dose by body weight (12 mg/kg or more) were significant by univariate analysis. CONCLUSIONS: Careful administration is necessary in patients > or =60 years old, in female patients, and in patients receiving a ribavirin dose of 12 mg/kg or more. Patients who experience a fall in hemoglobin concentrations of 2 g/dL or more at week 2 after the start of treatment should be monitored with particular care.

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.


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).


Oxidative damage precedes nitrative damage in adriamycin-induced cardiac mitochondrial injury.

Adriablastin Adriablastine Adriamycin Adriblastin Adriblastina Adriblastine Adrimedac Baxter Brand of Doxorubicin Hydrochloride Bedford Bristol-Myers Squibb Columbia DOXO cell DOXO-cell Doxolem Hexal NC Doxorubicina Ferrer Farm Funk Tedec Doxorubicine Doxotec Elan Farmiblastina Kenfarma Lemery Myocet Neocorp Onkodox Onkoworks Pfizer Prasfarma Ribodoxo Rubex Meiji Urokit Doxo Doxo-cell pharm medac ribosepharm

Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.


Deficiencies Oxidative Phosphorylation Respiratory Chain Deficiency Disease Mitochondrial Disorder Disorders Electron Transport Diseases

Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.


The purpose of the present study was to determine if elevated reactive oxygen (ROS)/nitrogen species (RNS) reported to be present in adriamycin (ADR)-induced cardiotoxicity actually resulted in cardiomyocyte oxidative/nitrative damage, and to quantitatively determine the time course and subcellular localization of these postulated damage products using an in vivo approach. B6C3 mice were treated with a single dose of 20 mg/kg ADR. Ultrastructural damage and levels of 4-hydroxy-2-nonenal (4HNE)-protein adducts and 3-nitrotyrosine (3NT) were analyzed. Quantitative ultrastructural damage using computerized image techniques showed cardiomyocyte injury as early as 3 hours, with mitochondria being the most extensively and progressively injured subcellular organelle. Analysis of 4HNE protein adducts by immunogold electron microscopy showed appearance of 4HNE protein adducts in mitochondria as early as 3 hours, with a peak at 6 hours and subsequent decline at 24 hours. 3NT levels were significantly increased in all subcellular compartments at 6 hours and subsequently declined at 24 hours. Our data showed ADR induced 4HNE-protein adducts in mitochondria at the same time point as when mitochondrial injury initially appeared. These results document for the first time in vivo that mitochondrial oxidative damage precedes nitrative damage. The progressive nature of mitochondrial injury suggests that mitochondria, not other subcellular organelles, are the major site of intracellular injury.

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.


An element with the atomic symbol N, atomic number 7, and atomic weight [14.00643; 14.00728]. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells.


Cardiac Toxicities Toxicity Cardiotoxicities Cardiotoxicity

Damage to the heart or its function secondary to exposure to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.


4-HNE cpd 4-hydroxy-2,3-nonenal 4-hydroxy-2-nonenal (E)-isomer 4-hydroxynonen-2-al 4-hydroxynonenal


3-mononitrotyrosine 3-nitro-L-tyrosine 3-nitrotyrosine (DL)-isomer (L)-isomer nitrotyrosine


Sotalol-induced coronary spasm in a patient with dilated cardiomyopathy associated with sustained ventricular tachycardia.

Darob Knoll Pharmaceutical Brand of Sotalol MJ 1999 MJ-1999 MJ1999 Hydrochloride Monohydrochloride

An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.


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


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.


An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).


A 54-year-old man with severe left ventricular dysfunction due to dilated cardiomyopathy was referred to our hospital for symptomatic incessant sustained ventricular tachycardia (VT). After the administration of nifekalant hydrochloride, sustained VT was terminated. An alternate class III agent, sotalol, was also effective for the prevention of VT. However, one month after switching over nifekalant to sotalol, a short duration of ST elevation was documented in ECG monitoring at almost the same time for three consecutive days. ST elevation with chest discomfort disappeared since he began taking long-acting diltiazem. Coronary vasospasm may be induced by the non-selective beta-blocking properties of sotalol.

A condition in which HEART VENTRICLES exhibit impaired function.


1,3-dimethyl-6-((2-(N-(2-hydroxyethyl)-3-(4-nitrophenyl)propylamino)ethylamino)-2,4(1H),3H)-pyrimidinedione hydrochloride MS 551 MS-551 nifekalant


Aldizem Biovail Brand of Diltiazem Hydrochloride CRD 401 CRD-401 CRD401 Cardil Cardizem Dilacor XR Dilren Malate Dilzem Tiazac Watson Pharmaceuticals Diltazem

A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.


Effects of the antidepressant trazodone, a 5-HT 2A/2C receptor antagonist, on dopamine-dependent behaviors in rats.

AF 1161 AF-1161 AF1161 Apo Trazodone Apo-Trazodone Apotex Brand of Hydrochloride Apothecon Aventis Pharma Boehringer Ingelheim Bristol Myers Squibb Bristol-Myers Deprax Desyrel Farma Lepori Gen Gen-Trazodone Genpharm Hexal Molipaxin Novo Novo-Trazodone Novopharm Nu Pharm Nu-Pharm Nu-Trazodone PMS PMS-Trazodone Pharmascience Ratiopharm Searle Sidmark Thombran Tradozone Trazodon neuraxpharm Trazodon-neuraxpharm Trazon Trittico ratio ratio-Trazodone

A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309)


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.


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.


RATIONALE: 5-Hydroxytryptamine, via stimulation of 5-HT 2C receptors, exerts a tonic inhibitory influence on dopaminergic neurotransmission, whereas activation of 5-HT 2A receptors enhances stimulated DAergic neurotransmission. The antidepressant trazodone is a 5-HT 2A/2C receptor antagonist. OBJECTIVES: To evaluate the effect of trazodone treatment on behaviors dependent on the functional status of the nigrostriatal DAergic system. METHODS: The effect of pretreatment with trazodone on dexamphetamine- and apomorphine-induced oral stereotypies, on catalepsy induced by haloperidol and apomorphine (0.05 mg/kg, i.p.), on ergometrine-induced wet dog shake (WDS) behavior and fluoxetine-induced penile erections was studied in rats. We also investigated whether trazodone induces catalepsy in rats. RESULTS: Trazodone at 2.5-20 mg/kg i.p. did not induce catalepsy, and did not antagonize apomorphine (1.5 and 3 mg/kg) stereotypy and apomorphine (0.05 mg/kg)-induced catalepsy. However, pretreatment with 5, 10 and 20 mg/kg i.p. trazodone enhanced dexamphetamine stereotypy, and antagonized haloperidol catalepsy, ergometrine-induced WDS behavior and fluoxetine-induced penile erections. Trazodone at 30, 40 and 50 mg/kg i.p. induced catalepsy and antagonized apomorphine and dexamphetamine stereotypies. CONCLUSIONS: Our results indicate that trazodone at 2.5-20 mg/kg does not block pre- and postsynaptic striatal D2 DA receptors, while at 30, 40 and 50 mg/kg it blocks postsynaptic striatal D2 DA receptors. Furthermore, at 5, 10 and 20 mg/kg, trazodone blocks 5-HT 2A and 5-HT 2C receptors. We suggest that trazodone (5, 10 and 20 mg/kg), by blocking the 5-HT 2C receptors, releases the nigrostriatal DAergic neurons from tonic inhibition caused by 5-HT, and thereby potentiates dexamphetamine stereotypy and antagonizes haloperidol catalepsy.


Celltech Brand of Dextroamphetamine Sulfate Curban Dexamfetamine Dexamphetamine Dexedrine Dextro Amphetamine Dextro-Amphetamine DextroStat GlaxoSmithKline Mallinckrodt Oxydess Pasadena Shire Vortech d d-Amphetamine dextro dextro-Amphetamine

The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.


Aguettant Brand of Apomorphine Hydrochloride Anhydrous Apokinon Apomorphin Teclapharm Apomorphin-Teclapharm ApomorphinTeclapharm Chloride Hemihydrate Britaject Britannia

A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.


Cancer of Mouth the Oral Cancers Neoplasm Neoplasms


Anochlesia Anochlesias Catalepsies Catalepsy Cerea Flexibilitas Flexibilities Waxy Flexibility

A condition characterized by inactivity, decreased responsiveness to stimuli, and a tendency to maintain an immobile posture. The limbs tend to remain in whatever position they are placed (waxy flexibility). Catalepsy may be associated with PSYCHOTIC DISORDERS (e.g., SCHIZOPHRENIA, CATATONIC), nervous system drug toxicity, and other conditions.


A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279)


Bedford Brand of Ergonovine Maleate Ergobasin Ergometrin Ergometrine Ergotrate

An ergot alkaloid (ERGOT ALKALOIDS) with uterine and VASCULAR SMOOTH MUSCLE contractile properties.


Fluoxetin Fluoxetine Hydrochloride Lilly 110140 Lilly-110140 Lilly110140 N-Methyl-gamma-(4-(trifluoromethyl)phenoxy)benzenepropanamine Prozac Sarafem

The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.


Swallowing abnormalities and dyskinesia in Parkinson's disease.

Benign Neonatal Sleep Myoclonus Drunkenness Drunkennesses Parasomnia Parasomnias Paroxysm Sensory Paroxysms Related Abnormal Swallowing Syndrome Sleep-Related

Movements or behaviors associated with sleep, sleep stages, or partial arousals from sleep that may impair sleep maintenance. Parasomnias are generally divided into four groups: arousal disorders, sleep-wake transition disorders, parasomnias of REM sleep, and nonspecific parasomnias. (From Thorpy, Sleep Disorders Medicine, 1994, p191)


Drug-Induced Dyskinesia Dyskinesias Drug Induced Medication Medication-Induced

Abnormal movements, including HYPERKINESIS; HYPOKINESIA; TREMOR; and DYSTONIA, associated with the use of certain medications or drugs. Muscles of the face, trunk, neck, and extremities are most commonly affected. Tardive dyskinesia refers to abnormal hyperkinetic movements of the muscles of the face, tongue, and neck associated with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS). (Adams et al., Principles of Neurology, 6th ed, p1199)


Idiopathic Parkinson Disease Parkinson's Lewy Body Paralysis Agitans Parkinsonism Primary

A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)


Gastrointestinal abnormalities in Parkinson's disease (PD) have been known for almost two centuries, but many aspects concerning their pathophysiology have not been completely clarified. The aim of this study was to characterize the oropharyngeal dynamics in PD patients with and without levodopa-induced dyskinesia. Fifteen dyskinetic, 12 nondyskinetic patients, and a control group were included. Patients were asked about dysphagia and evaluated with the Unified Parkinson's Disease Rating Scale Parts II and III and the Hoehn and Yahr scale. Deglutition was assessed using modified barium swallow with videofluoroscopy. Nondyskinetic patients, but not the dyskinetic ones, showed less oropharyngeal swallowing efficiency (OPSE) for liquid food than controls (Dunnett, P = 0.02). Dyskinetic patients tended to have a greater OPSE than nondyskinetic (Dunnett, P = 0.06). Patients who were using a higher dose of levodopa had a greater OPSE and a trend toward a smaller oral transit time (Pearson's correlation, P = 0.01 and 0.08, respectively). Neither the report of dysphagia nor any of the PD severity parameters correlated to the videofluoroscopic variables. In the current study, dyskinetic patients performed better in swallowing function, which could be explained on the basis of a greater levodopa dose. Our results suggest a role for levodopa in the oral phase of deglutition and confirm that dysphagia is not a good predictor of deglutition alterations in PD.

Cholera Infantum Disease Gastrointestinal Diseases Disorder Functional Disorders

Diseases in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.


3 Hydroxy L tyrosine 3-Hydroxy-L-tyrosine Dopaflex Dopar 3,4 Dihydroxyphenylalanine Dopa L-3,4-Dihydroxyphenylalanine L-Dopa Larodopa Levodopa Levopa Medphano Brand of Roberts Roche

The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.


Deglutition Disorder Disorders Dysphagia Esophageal Oropharyngeal Swallowing

Difficulty in SWALLOWING which may result from neuromuscular disorder or mechanical obstruction. Dysphagia is classified into two distinct types: oropharyngeal dysphagia due to malfunction of the PHARYNX and UPPER ESOPHAGEAL SPHINCTER; and esophageal dysphagia due to malfunction of the ESOPHAGUS.


An element of the alkaline earth group of metals. It has an atomic symbol Ba, atomic number 56, and atomic weight 138. All of its acid-soluble salts are poisonous.


Inhibition of nuclear factor-kappaB activation attenuates tubulointerstitial nephritis induced by gentamicin.

Interstitial Nephritides Nephritis Tubulointerstitial

Inflammation of the interstitial tissue of the kidney. This term is generally used for primary inflammation of KIDNEY TUBULES and/or surrounding interstitium. For primary inflammation of glomerular interstitium, see GLOMERULONEPHRITIS. Infiltration of the inflammatory cells into the interstitial compartment results in EDEMA, increased spaces between the tubules, and tubular renal dysfunction.


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.


BACKGROUND: Animals treated with gentamicin can show residual areas of interstitial fibrosis in the renal cortex. This study investigated the expression of nuclear factor-kappaB (NF-kappaB), mitogen-activated protein (MAP) kinases and macrophages in the renal cortex and structural and functional renal changes of rats treated with gentamicin or gentamicin + pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor. METHODS: 38 female Wistar rats were injected with gentamicin, 40 mg/kg, twice a day for 9 days, 38 with gentamicin + PDTC, and 28 with 0.15 M NaCl solution. The animals were killed 5 and 30 days after these injections and the kidneys were removed for histological and immunohistochemical studies. The results of the immunohistochemical studies were scored according to the extent of staining. The fractional interstitial area was determined by morphometry. RESULTS: Gentamicin-treated rats presented a transitory increase in plasma creatinine levels. Increased ED-1, MAP kinases and NF-kappaB staining were also observed in the renal cortex from all gentamicin-treated rats compared to control (p < 0.05). The animals killed on day 30 also presented fibrosis in the renal cortex despite the recovery of renal function. Treatment with PDTC reduced the functional and structural changes induced by gentamicin. CONCLUSIONS: These data show that inhibition of NF-kappaB activation attenuates tubulointerstitial nephritis induced by gentamicin.


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


Pyrrolidinedithiocarbamate ammonium pyrrolidine dithiocarbamate tetramethylene dithiocarbamic acid salt sodium


Saline Solution Sodium Chloride (22)Na (24)NaCl

A ubiquitous sodium salt that is commonly used to season food.


Glucose metabolism in patients with schizophrenia treated with atypical antipsychotic agents: a frequently sampled intravenous glucose tolerance test and minimal model analysis.

Anhydrous Dextrose D Glucose D-Glucose Monohydrate (DL)-Isomer (L)-Isomer (alpha-D)-Isomer (beta-D)-Isomer L L-Glucose

A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.


Dementia Praecox Disorder Schizophrenic Disorders Schizophrenia Schizophrenias

A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.


BACKGROUND: While the incidence of new-onset diabetes mellitus may be increasing in patients with schizophrenia treated with certain atypical antipsychotic agents, it remains unclear whether atypical agents are directly affecting glucose metabolism or simply increasing known risk factors for diabetes. OBJECTIVE: To study the 2 drugs most clearly implicated (clozapine and olanzapine) and risperidone using a frequently sampled intravenous glucose tolerance test. DESIGN: A cross-sectional design in stable, treated patients with schizophrenia evaluated using a frequently sampled intravenous glucose tolerance test and the Bergman minimal model analysis. SETTING: Subjects were recruited from an urban community mental health clinic and were studied at a general clinical research center. Patients Fifty subjects signed informed consent and 41 underwent the frequently sampled intravenous glucose tolerance test. Thirty-six nonobese subjects with schizophrenia or schizoaffective disorder, matched by body mass index and treated with either clozapine, olanzapine, or risperidone, were included in the analysis. MAIN OUTCOME MEASURES: Fasting plasma glucose and fasting serum insulin levels, insulin sensitivity index, homeostasis model assessment of insulin resistance, and glucose effectiveness. RESULTS: The mean +/- SD duration of treatment with the identified atypical antipsychotic agent was 68.3 +/- 28.9 months (clozapine), 29.5 +/- 17.5 months (olanzapine), and 40.9 +/- 33.7 (risperidone). Fasting serum insulin concentrations differed among groups (F(33) = 3.35; P = .047) (clozapine>olanzapine>risperidone) with significant differences between clozapine and risperidone (t(33) = 2.32; P = .03) and olanzapine and risperidone (t(33) = 2.15; P = .04). There was a significant difference in insulin sensitivity index among groups (F(33) = 10.66; P<.001) (clozapine<olanzapine<risperidone), with subjects who received clozapine and olanzapine exhibiting significant insulin resistance compared with subjects who were treated with risperidone (clozapine vs risperidone, t(33) = -4.29; P<.001; olanzapine vs risperidone, t(33) = -3.62; P = .001 [P<.001]). The homeostasis model assessment of insulin resistance also differed significantly among groups (F(33) = 4.92; P = .01) (clozapine>olanzapine>risperidone) (clozapine vs risperidone, t(33) = 2.94; P = .006; olanzapine vs risperidone, t(33) = 2.42; P = .02). There was a significant difference among groups in glucose effectiveness (F(30) = 4.18; P = .02) (clozapine<olanzapine<risperidone) with significant differences between clozapine and risperidone (t(30) = -2.59; P = .02) and olanzapine and risperidone (t(30) = -2.34, P = .03). CONCLUSIONS: Both nonobese clozapine- and olanzapine-treated groups displayed significant insulin resistance and impairment of glucose effectiveness compared with risperidone-treated subjects. Patients taking clozapine and olanzapine must be examined for insulin resistance and its consequences.

A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.


A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.


2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno(2,3-b)(1,5)benzodiazepine LY 170053 LY-170052 Zyprexa olanzapine pamoate


Consta Risperdal R 64,766 64766 R-64,766 R-64766 R64,766 R64766 Risperidal Risperidone

A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.


Brief Reactive Psychoses Psychosis Disorder Psychotic Schizoaffective Schizophreniform Disorders

Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)


Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.


Focal cerebral ischemia in rats: effect of phenylephrine-induced hypertension during reperfusion.

Brain Ischemia Ischemias Cerebral Encephalopathy Ischemic Encephalopathies

Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.


(R)-3-Hydroxy-alpha-((methylamino)methyl)benzenemethanol Metaoxedrin Metasympatol Mezaton Neo Synephrine Neo-Synephrine Neosynephrine Phenylephrine Hydrochloride Tannate

An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.


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.


After 180 min of temporary middle cerebral artery occlusion in spontaneously hypertensive rats, the effect of phenylephrine-induced hypertension on ischemic brain injury and blood-brain barrier permeability was determined. Blood pressure was manipulated by one of the following schedules during 120 min of reperfusion: Control, normotensive reperfusion; 90/hypertension (90/HTN), blood pressure was increased by 35 mm Hg during the initial 90 min of reperfusion only; 15/hypertension (15/HTN), normotensive reperfusion for 30 min followed by 15 min of hypertension and 75 min of normotension. Part A, for eight rats in each group brain injury was evaluated by staining tissue using 2,3,5-triphenyltetrazolium chloride and edema was evaluated by microgravimetry. Part B, for eight different rats in each group blood-brain barrier permeability was evaluated by measuring the amount and extent of extravasation of Evans Blue dye. Brain injury (percentage of the ischemic hemisphere) was less in the 15/HTN group (16 +/- 6, mean +/- SD) versus the 90/HTN group (30 +/- 6), which was in turn less than the control group (42 +/- 5). Specific gravity was greater in the 15/HTN group (1.043 +/- 0.002) versus the 90/HTN (1.036 +/- 0.003) and control (1.037 +/- 0.003) groups. Evans Blue (mug g-1 of brain tissue) was greater in the 90/HTN group (24.4 +/- 6.0) versus the control group (12.3 +/- 4.1), which was in turn greater than the 15/HTN group (7.3 +/- 3.2). This study supports a hypothesis that during reperfusion, a short interval of hypertension decreases brain injury and edema; and that sustained hypertension increases the risk of vasogenic edema.

Cerebral Infarction Middle Cerebral Artery Embolic Embolus Left MCA Circulation Occlusion Stroke Syndrome Thrombosis Thrombotic Right

NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.


Acute Brain Injuries Injury Contusion Contusions Diffuse Focal Traumatic Laceration Lacerations Trauma Traumas Cortical Encephalopathies Post-Concussive Post-Traumatic Encephalopathy Post Concussive Mild TBI (Traumatic Injury) TBIs

Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.


2,3,5-triphenyltetrazolium chloride triphenyltetrazolium bromide


Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.


Azovan Blue Evan's Evans C.I. 23860 Direct 53 Evan

An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.


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)


People aged over 75 in atrial fibrillation on warfarin: the rate of major hemorrhage and stroke in more than 500 patient-years of follow-up.

Atrial Fibrillation Fibrillations Auricular Familial

Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.


4-Hydroxy-3-(3-oxo-1-phenylbutyl)-2H-1-benzopyran-2-one Aldo Brand of Warfarin Sodium Aldocumar Antigen Apo-Warfarin Apotex Bailly Boots Bristol-Myers Squibb Coumadin Coumadine Estedi Gen-Warfarin Genpharm Goldshield Marevan Potassium Tedicumar Warfant

An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.


Bleeding or escape of blood from a vessel.


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)


OBJECTIVES: To determine the incidence of major hemorrhage and stroke in people aged 76 and older with atrial fibrillation on adjusted-dose warfarin who had been recently been admitted to hospital. DESIGN: A retrospective observational cohort study. SETTING: A major healthcare network involving four tertiary hospitals. PARTICIPANTS: Two hundred thirty-five patients aged 76 and older admitted to a major healthcare network between July 1, 2001, and June 30, 2002, with atrial fibrillation on warfarin were enrolled. MEASUREMENTS: Information regarding major bleeding episodes, strokes, and warfarin use was obtained from patients, relatives, primary physicians, and medical records. RESULTS: Two hundred twenty-eight patients (42% men) with a mean age of 81.1 (range 76-94) were included in the analysis. Total follow-up on warfarin was 530 years (mean 28 months). There were 53 major hemorrhages, for an annual rate of 10.0%, including 24 (45.3%) life-threatening and five (9.4%) fatal bleeds. The annual stroke rate after initiation of warfarin was 2.6%. CONCLUSION: The rate of major hemorrhage was high in this old, frail group, but excluding fatalities, resulted in no long-term sequelae, and the stroke rate on warfarin was low, demonstrating how effective warfarin treatment is.


Safety of celecoxib in patients with adverse skin reactions to acetaminophen (paracetamol) and nimesulide associated or not with common non-steroidal anti-inflammatory drugs.

4-(5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide Celebrex SC 58635 SC-58635 celecoxib


Dermatitis Medicamentosa Adverse Drug Reaction Eruption Maculopapular Eruptions Morbilliform Reactions Exanthem Exanthems

Adverse cutaneous reactions caused by ingestion, parenteral use, or local application of a drug. These may assume various morphologic patterns and produce various types of lesions.


APAP Acamol Acephen Acetaco Acetamidophenol Acetaminophen Acetominophen Algotropyl Anacin 3 Anacin-3 Anacin3 Datril Hydroxyacetanilide N-(4-Hydroxyphenyl)acetanilide N-Acetyl-p-aminophenol Panadol Paracetamol Tylenol p-Acetamidophenol p-Hydroxyacetanilide

Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.


4-nitro-2-phenoxymethanesulfonanilide Antifloxil Aulin Eskaflam Guaxan Mesulid Nexen Nimesil R 805 R-805 Redaflam lizepat nimesulide


BACKGROUND: Acetaminophen (paracetamol--P) and Nimesulide (N) are widely used analgesic-antipyretic/anti-inflammatory drugs. The rate of adverse hypersensitivity reactions to these agents is generally low. On the contrary non-steroidal anti-inflammatory drugs (NSAIDs) are commonly involved in such reactions. Celecoxib (CE) is a novel drug, with high selectivity and affinity for COX-2 enzyme. OBJECTIVE: We evaluated the tolerability of CE in a group of patients with documented history of adverse cutaneous reactions to P and N associated or not to classic NSAIDs. METHODS: We studied 9 patients with hypersensitivity to P and N with or without associated reactions to classic NSAIDs. The diagnosis of P and N-induced skin reactions was based in vivo challenge. The placebo was blindly administered at the beginning of each challenge. After three days, a cumulative dosage of 200 mg of CE in refracted doses were given. After 2-3 days, a single dose of 200 mg was administered. All patients were observed for 6 hours after each challenge, and controlled again after 24 hours to exclude delayed reactions. The challenge was considered positive if one or more of the following appeared: erythema, rush or urticaria-angioedema. RESULTS: No reaction was observed with placebo and eight patients (88.8%) tolerated CE. Only one patient developed a moderate angioedema of the lips. CONCLUSION: Only one hypersensitivity reaction to CE was documented among 9 P and N-highly NSAIDs intolerant patients. Thus, we conclude that CE is a reasonably safe alternative to be used in subjects who do not tolerate P and N.


Allergies Drug Allergy Hypersensitivities Hypersensitivity

Immunologically mediated adverse reactions to medicinal substances used legally or illegally.


Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes.


A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress.


Angioedema Angioedemas Angioneurotic Edema Edemas Quincke's Giant Urticaria Urticarias Quincke Quinckes

Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.


Case-control study of regular analgesic and nonsteroidal anti-inflammatory use and end-stage renal disease.

Chronic Kidney Failure Renal Disease End-Stage ESRD End Stage

The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.


BACKGROUND: Studies on the association between the long-term use of aspirin and other analgesic and nonsteroidal anti-inflammatory drugs (NSAIDs) and end-stage renal disease (ESRD) have given conflicting results. In order to examine this association, a case-control study with incident cases of ESRD was carried out. METHODS: The cases were all patients entering the local dialysis program because of ESRD in the study area between June 1, 1995 and November 30, 1997. They were classified according to the underlying disease, which had presumably led them to ESRD. Controls were patients admitted to the same hospitals from where the cases arose, also matched by age and sex. Odds ratios were calculated using a conditional logistic model, including potential confounding factors, both for the whole study population and for the various underlying diseases. RESULTS: Five hundred and eighty-three cases and 1190 controls were included in the analysis. Long-term use of any analgesic was associated with an overall odds ratio of 1.22 (95% CI, 0.89-1.66). For specific groups of drugs, the risks were 1.56 (1.05-2.30) for aspirin, 1.03 (0.60-1.76) for pyrazolones, 0.80 (0.39-1.63) for paracetamol, and 0.94 (0.57-1.56) for nonaspirin NSAIDs. The risk of ESRD associated with aspirin was related to the cumulated dose and duration of use, and it was particularly high among the subset of patients with vascular nephropathy as underlying disease [2.35 (1.17-4.72)]. CONCLUSION: Our data indicate that long-term use of nonaspirin analgesic drugs and NSAIDs is not associated with an increased risk of ESRD. However, the chronic use of aspirin may increase the risk of ESRD.

2-(Acetyloxy)benzoic Acid Acetylsalicylic Acetysal Acylpyrin Aloxiprimum Aspirin Colfarit Dispril Easprin Ecotrin Endosprin Magnecyl Micristin Polopirin Polopiryna Solprin Solupsan Zorprin

The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)


Pyrazolin 5 Ones Pyrazolin-5-Ones Pyrazolones

Compounds with a five-membered heterocyclic ring with two nitrogens and a keto OXYGEN. Some are inhibitors of TNF-ALPHA production.


Pathological processes of the KIDNEY or its component tissues.


Two cases of amisulpride overdose: a cause for prolonged QT syndrome.

Barnetil DAN 2163 LIN 1418 N-(ethyl-1-pyrrolidinyl- 2-methyl)methoxy-2-ethylsulfonyl-5-benzamide Solian amisulpride sultopride hydrochloride


Accidental or deliberate use of a medication or street drug in excess of normal dosage.


A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.


Two cases of deliberate self-poisoning with 5 g and 3.6 g of amisulpride, respectively, are reported. In both cases, QT prolongation and hypocalcaemia were noted. The QT prolongation appeared to respond to administration of i.v. calcium gluconate.

A condition or physical state produced by the ingestion, injection, inhalation of or exposure to a deleterious agent.


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)


3M Brand of Calcium Gluconate Monohydrate Braun CBG Calciofon Calcipot Calcivitol Calglucon Chaix et du Marais Coophavet Ebucin Flopak Plain Fresenius Kabi Glucal Glucobiogen de Lavoisier Gluconato Calc Merial Pharmtech

The calcium salt of gluconic acid. The compound has a variety of uses, including its use as a calcium replenisher in hypocalcemic states.


Growth-associated protein 43 expression in hippocampal molecular layer of chronic epileptic rats treated with cycloheximide.

Aura Auras Awakening Epilepsy Cryptogenic Epilepsies Epileptic Seizure Seizures Disorder Disorders Single

A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)


Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.


PURPOSE: GAP43 has been thought to be linked with mossy fiber sprouting (MFS) in various experimental models of epilepsy. To investigate how GAP43 expression (GAP43-ir) correlates with MFS, we assessed the intensity (densitometry) and extension (width) of GAP43-ir in the inner molecular layer of the dentate gyrus (IML) of rats subject to status epilepticus induced by pilocarpine (Pilo), previously injected or not with cycloheximide (CHX), which has been shown to inhibit MFS. METHODS: CHX was injected before the Pilo injection in adult Wistar rats. The Pilo group was injected with the same drugs, except for CHX. Animals were killed between 30 and 60 days later, and brain sections were processed for GAP43 immunohistochemistry. RESULTS: Densitometry showed no significant difference regarding GAP43-ir in the IML between Pilo, CHX+Pilo, and control groups. However, the results of the width of the GAP43-ir band in the IML showed that CHX+Pilo and control animals had a significantly larger band (p = 0.03) as compared with that in the Pilo group. CONCLUSIONS: Our current finding that animals in the CHX+Pilo group have a GAP43-ir band in the IML, similar to that of controls, reinforces prior data on the blockade of MFS in these animals. The change in GAP43-ir present in Pilo-treated animals was a thinning of the band to a very narrow layer just above the granule cell layer that is likely to be associated with the loss of hilar cell projections that express GAP-43.


Absence Status Complex Partial Epilepticus Electrographic Generalized Convulsive Grand Mal Non Non-Convulsive Petit Simple Subclinical

A prolonged seizure or seizures repeated frequently enough to prevent recovery between episodes occurring over a period of 20-30 minutes. The most common subtype is generalized tonic-clonic status epilepticus, a potentially fatal condition associated with neuronal injury and respiratory and metabolic dysfunction. Nonconvulsive forms include petit mal status and complex partial status, which may manifest as behavioral disturbances. Simple partial status epilepticus consists of persistent motor, sensory, or autonomic seizures that do not impair cognition (see also EPILEPSIA PARTIALIS CONTINUA). Subclinical status epilepticus generally refers to seizures occurring in an unresponsive or comatose individual in the absence of overt signs of seizure activity. (From N Engl J Med 1998 Apr 2;338(14):970-6; Neurologia 1997 Dec;12 Suppl 6:25-30)


Hydrochloride Pilocarpine Isopilocarpine Isoptocarpine Nitrate Ocusert Mononitrate (3S-cis)-Isomer Monohydrochloride Salagen

A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.


Nicotine antagonizes caffeine- but not pentylenetetrazole-induced anxiogenic effect in mice.

Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.


1,3,7-Trimethylxanthine Berlin-Chemie Brand of Caffeine Bristol-Myers Squibb Caffedrine Coffeinum N Purrum Dexitac Durvitan GlaxoSmithKline Merck dura No Doz Passauer Percoffedrinol Percutaféine Pierre Fabre Quick-Pep Republic Drug Seid Thompson 1 2 Vivarin

A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.


Cardiazol Corasol Corazol Corazole Korazol Korazole Leptazole Metrazol Metrazole Pentamethylenetetrazole Pentazol Pentetrazole Pentylenetetrazol Pentylenetetrazole

A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.


RATIONALE: Nicotine and caffeine are widely consumed licit psychoactive drugs worldwide. Epidemiological studies showed that they were generally used concurrently. Although some studies in experimental animals indicate clear pharmacological interactions between them, no studies have shown a specific interaction on anxiety responses. OBJECTIVES: The present study investigates the effects of nicotine on anxiety induced by caffeine and another anxiogenic drug, pentylenetetrazole, in mice. The elevated plus-maze (EPM) test was used to evaluate the effects of drugs on anxiety. METHODS: Adult male Swiss Webster mice (25-32 g) were given nicotine (0.05-0.25 mg/kg s.c.) or saline 10 min before caffeine (70 mg/kg i.p.) or pentylenetetrazole (15 and 30 mg/kg i.p.) injections. After 15 min, mice were evaluated for their open- and closed-arm time and entries on the EPM for a 10-min session. Locomotor activity was recorded for individual groups by using the same treatment protocol with the EPM test. RESULTS: Nicotine (0.05-0.25 mg/kg) itself did not produce any significant effect in the EPM test, whereas caffeine (70 mg/kg) and pentylenetetrazole (30 mg/kg) produced an anxiogenic effect, apparent with decreases in open-arm time and entry. Nicotine (0.25 mg/kg) pretreatment blocked the caffeine- but not pentylenetetrazole-induced anxiety. Administration of each drug and their combinations did not produce any effect on locomotor activity. CONCLUSIONS: Our results suggest that the antagonistic effect of nicotine on caffeine-induced anxiety is specific to caffeine, instead of a non-specific anxiolytic effect. Thus, it may extend the current findings on the interaction between nicotine and caffeine.


Anxiety Disorder Disorders Neuroses State Neurotic States


BACKGROUND: Hormone therapy (HT) is widely used for controlling menopausal symptoms. It has also been used for the management and prevention of cardiovascular disease, osteoporosis and dementia in older women but the evidence supporting its use for these indications is largely observational. OBJECTIVES: To assess the effect of long-term HT on mortality, heart disease, venous thromboembolism, stroke, transient ischaemic attacks, breast cancer, colorectal cancer, ovarian cancer, endometrial cancer, gallbladder disease, cognitive function, dementia, fractures and quality of life. SEARCH STRATEGY: We searched the following databases up to November 2004: the Cochrane Menstrual Disorders and Subfertility Group Trials Register, Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Biological Abstracts. Relevant non-indexed journals and conference abstracts were also searched. SELECTION CRITERIA: Randomised double-blind trials of HT (oestrogens with or without progestogens) versus placebo, taken for at least one year by perimenopausal or postmenopausal women. DATA COLLECTION AND ANALYSIS: Fifteen RCTs were included. Trials were assessed for quality and two review authors extracted data independently. They calculated risk ratios for dichotomous outcomes and weighted mean differences for continuous outcomes. Clinical heterogeneity precluded meta-analysis for most outcomes. MAIN RESULTS: All the statistically significant results were derived from the two biggest trials. In relatively healthy women, combined continuous HT significantly increased the risk of venous thromboembolism or coronary event (after one year's use), stroke (after 3 years), breast cancer (after 5 years) and gallbladder disease. Long-term oestrogen-only HT also significantly increased the risk of stroke and gallbladder disease. Overall, the only statistically significant benefits of HT were a decreased incidence of fractures and colon cancer with long-term use. Among relatively healthy women over 65 years taking continuous combined HT, there was a statistically significant increase in the incidence of dementia. Among women with cardiovascular disease, long-term use of combined continuous HT significantly increased the risk of venous thromboembolism. No trials focussed specifically on younger women. However, one trial analysed subgroups of 2839 relatively healthy 50 to 59 year-old women taking combined continuous HT and 1637 taking oestrogen-only HT, versus similar-sized placebo groups. The only significantly increased risk reported was for venous thromboembolism in women taking combined continuous HT; their absolute risk remained very low. AUTHORS' CONCLUSIONS: HT is not indicated for the routine management of chronic disease. We need more evidence on the safety of HT for menopausal symptom control, though short-term use appears to be relatively safe for healthy younger women.

The premature cessation of menses (MENSTRUATION) when the last menstrual period occurs in a woman under the age of 40. It is due to the depletion of OVARIAN FOLLICLES. Premature MENOPAUSE can be caused by diseases; OVARIECTOMY; RADIATION; chemicals; and chromosomal abnormalities.


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


Age Related Osteoporosis Age-Related Bone Loss Losses Osteoporoses Senile Involutional Post Traumatic Post-Traumatic

Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.


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.


Pathological conditions involving the HEART including its structural and functional abnormalities.


Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.


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)


Anterior Circulation Transient Ischemic Attack Attacks Brain Stem Ischemia TIA Brainstem Ischemias Carotid Cerebral Crescendo Posterior (Transient Attack) TIAs Vertebrobasilar

Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)


Breast Cancer Carcinoma Neoplasm Neoplasms Tumor Tumors of the Human Mammary Carcinomas Malignant


Cancer Colorectal Cancers Carcinoma Carcinomas Neoplasm Neoplasms Tumor Tumors

Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.


Cancer of Ovary the Ovarian Cancers Neoplasm Neoplasms

Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.


Cancer of Endometrium the Endometrial Cancers Carcinoma Carcinomas Neoplasm Neoplasms

Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.


Bladder Disease Gall Diseases Gallbladder

Diseases of the GALLBLADDER. They generally involve the impairment of BILE flow, GALLSTONES in the BILIARY TRACT, infections, neoplasms, or other diseases.


Agents Estrogenic Agonists Estrogen Receptor Compounds Effects Effect Estrogens

Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.


Pregnenedione Progesterone (13 alpha,17 alpha)-(+-)-Isomer (17 alpha)-Isomer (9 beta,10

The major progestational steroid that is secreted primarily by the CORPUS LUTEUM and the PLACENTA. Progesterone acts on the UTERUS, the MAMMARY GLANDS and the BRAIN. It is required in EMBRYO IMPLANTATION; PREGNANCY maintenance, and the development of mammary tissue for MILK production. Progesterone, converted from PREGNENOLONE, also serves as an intermediate in the biosynthesis of GONADAL STEROID HORMONES and adrenal CORTICOSTEROIDS.


Cancer of Colon the Colonic Cancers Neoplasm Neoplasms


Chronic Disease Diseases Illness Illnesses Chronically Ill

Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)


Drug-induced liver injury: an analysis of 461 incidences submitted to the Spanish registry over a 10-year period.

Acute Liver Injury Drug Induced Drug-Induced Disease Diseases Hepatitides Hepatitis Injuries Toxic

A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.


BACKGROUND & AIMS: Progress in the understanding of susceptibility factors to drug-induced liver injury (DILI) and outcome predictability are hampered by the lack of systematic programs to detect bona fide cases. METHODS: A cooperative network was created in 1994 in Spain to identify all suspicions of DILI following a prospective structured report form. The liver damage was characterized according to hepatocellular, cholestatic, and mixed laboratory criteria and to histologic criteria when available. Further evaluation of causality assessment was centrally performed. RESULTS: Since April 1994 to August 2004, 461 out of 570 submitted cases, involving 505 drugs, were deemed to be related to DILI. The antiinfective group of drugs was the more frequently incriminated, amoxicillin-clavulanate accounting for the 12.8% of the whole series. The hepatocellular pattern of damage was the most common (58%), was inversely correlated with age (P < .0001), and had the worst outcome (Cox regression, P < .034). Indeed, the incidence of liver transplantation and death in this group was 11.7% if patients had jaundice at presentation, whereas the corresponding figure was 3.8% in nonjaundiced patients (P < .04). Factors associated with the development of fulminant hepatic failure were female sex (OR = 25; 95% CI: 4.1-151; P < .0001), hepatocellular damage (OR = 7.9; 95% CI: 1.6-37; P < .009), and higher baseline plasma bilirubin value (OR = 1.15; 95% CI: 1.09-1.22; P < .0001). CONCLUSIONS: Patients with drug-induced hepatocellular jaundice have 11.7% chance of progressing to death or transplantation. Amoxicillin-clavulanate stands out as the most common drug related to DILI.


Bile Duct Obstruction Obstructions Biliary Stases Stasis Cholestases Cholestasis

Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).


Amox clav Amox-clav Amoxi Clavulanate Amoxi-Clavulanate Amoxicillin Clavulanic Acid Potassium Combination Amoxicillin-Clavulanic Amoxicillin-Potassium Amoxycillin Potentiated Amoxycillin-Clavulanic Augmentin BRL 25000 BRL-25000 BRL25000 Clavulanate-Amoxicillin Clavulin Co amoxiclav Co-amoxiclav Coamoxiclav Spektramox Synulox

A fixed-ratio combination of amoxicillin trihydrate and potassium clavulanate.


A clinical manifestation of HYPERBILIRUBINEMIA, characterized by the yellowish staining of the SKIN; MUCOUS MEMBRANE; and SCLERA. Clinical jaundice usually is a sign of LIVER dysfunction.


Acute Hepatic Failure Liver Fulminant Failures Fulminating

A form of rapid-onset LIVER FAILURE, also known as fulminant hepatic failure, caused by severe liver injury or massive loss of HEPATOCYTES. It is characterized by sudden development of liver dysfunction and JAUNDICE. Acute liver failure may progress to exhibit cerebral dysfunction even HEPATIC COMA depending on the etiology that includes hepatic ISCHEMIA, drug toxicity, malignant infiltration, and viral hepatitis such as post-transfusion HEPATITIS B and HEPATITIS C.


Bilirubin IX alpha (15E)-Isomer (4E)-Isomer (4E,15E)-Isomer Calcium Salt Disodium Monosodium Bilirubinate Hematoidin delta delta-Bilirubin

A bile pigment that is a degradation product of HEME.


Morphological evaluation of the effect of d-ribose on adriamycin-evoked cardiotoxicity in rats.

A pentose active in biological systems usually in its D-form.


Adriablastin Adriablastine Adriamycin Adriblastin Adriblastina Adriblastine Adrimedac Baxter Brand of Doxorubicin Hydrochloride Bedford Bristol-Myers Squibb Columbia DOXO cell DOXO-cell Doxolem Hexal NC Doxorubicina Ferrer Farm Funk Tedec Doxorubicine Doxotec Elan Farmiblastina Kenfarma Lemery Myocet Neocorp Onkodox Onkoworks Pfizer Prasfarma Ribodoxo Rubex Meiji Urokit Doxo Doxo-cell pharm medac ribosepharm

Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.


Cardiac Toxicities Toxicity Cardiotoxicities Cardiotoxicity

Damage to the heart or its function secondary to exposure to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.


The influence of d-ribose on adriamycin-induced myocardiopathy in rats was studied. Adriamycin in the cumulative dose of 25 mg/kg evoked fully developed cardiac toxicity. D-ribose in the multiple doses of 200 mg/kg did not influence ADR cardiotoxicity.


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).


In vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin-induced nephrotoxicity: protection by erdosteine.

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.


Pathological processes of the KIDNEY or its component tissues.


Dostein Edirel Esteclin RV 144 RV-144 S-(2-(N-3-(2-oxo-tetrahydrothienyl)acetamido))thioglycolic acid Vectrine erdosteine