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


Primary dysmenorrhea is a syndrome characterized by painful uterine contractility caused by a hypersecretion of endometrial prostaglandins; non-steroidal anti-inflammatory drugs are the first choice for its treatment. However, in vivo and in vitro studies have demonstrated that myometrial cells are also targets of the relaxant effects of nitric oxide (NO). The aim of the present study was to determine the efficacy of glyceryl trinitrate (GTN), an NO donor, in the resolution of primary dysmenorrhea in comparison with diclofenac (DCF). A total of 24 patients with the diagnosis of severe primary dysmenorrhea were studied during two consecutive menstrual cycles. In an open, cross-over, controlled design, patients were randomized to receive either DCF per os or GTN patches the first days of menses, when menstrual cramps became unendurable. In the subsequent cycle the other treatment was used. Patients received up to 3 doses/day of 50 mg DCF or 2.5 mg/24 h transdermal GTN for the first 3 days of the cycle, according to their needs. The participants recorded menstrual symptoms and possible side-effects at different times (0, 30, 60, 120 minutes) after the first dose of medication on the first day of the cycle, with both drugs. The difference in pain intensity score (DPI) was the main outcome variable. Both treatments significantly reduced DPI by the 30th minute (GTN, -12.8 +/- 17.9; DCF, -18.9 +/- 16.6). However, DCF continued to be effective in reducing pelvic pain for two hours, whereas GTN scores remained more or less stable after 30 min and significantly higher than those for DFC (after one hour: GTN, -12.8 +/- 17.9; DFC, -18.9 +/- 16.6 and after two hours: GTN, -23.7 +/- 20.5; DFC, -59.7 +/- 17.9, p = 0.0001). Low back pain was also relieved by both drugs. Headache was significantly increased by GTN but not by DCF. Eight patients stopped using GTN because headache--attributed to its use--became intolerable. These findings indicate that GTN has a reduced efficacy and tolerability by comparison with DCF in the treatment of primary dysmenorrhea.

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

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


Anginine Dynamite Gilustenon Glyceryl Trinitrate Nitrangin Nitro Bid Dur Nitro-Bid Nitro-Dur NitroBid NitroDur Nitrocard Nitroderm TTS Nitroglycerin Nitroglyn Nitrol Nitrolan Nitrong Nitrospan Nitrostat Perlinganit Susadrin Sustac Sustak Sustonit Transderm Tridil Trinitrin Trinitrolong

A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.


Dichlofenal Diclofenac Potassium Sodium Diclonate P Diclophenac Dicrofenac Feloran GP 45,840 GP-45,840 GP45,840 Novapirina Orthofen Orthophen Ortofen SR 38 SR-38 SR38 Voltaren Voltarol

A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.


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

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


Pain in the pelvic region of genital and non-genital origin and of organic or psychogenic etiology. Frequent causes of pain are distension or contraction of hollow viscera, rapid stretching of the capsule of a solid organ, chemical irritation, tissue ischemia, and neuritis secondary to inflammatory, neoplastic, or fibrotic processes in adjacent organs. (Kase, Weingold & Gershenson: Principles and Practice of Clinical Gynecology, 2d ed, pp479-508)


Ache Low Back Aches Pain Lower Pains Backache Backaches Mechanical Posterior Compartment Postural Recurrent Lumbago

Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous SPRAINS AND STRAINS; INTERVERTEBRAL DISK DISPLACEMENT; and other conditions.


Bilateral Headache Headaches Cephalalgia Cephalalgias Cephalgia Cephalgias Cephalodynia Cephalodynias Cranial Pain Pains Generalized Head Ocular Orthostatic Periorbital Retro-Ocular Sharp Throbbing Unilateral Vertex Hemicrania Retro

The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.


Temocapril, a long-acting non-SH group angiotensin converting enzyme inhibitor, modulates glomerular injury in chronic puromycin aminonucleoside nephrosis.

CS 622 CS-622 CS622 alpha-((2S,6R)-6-((1S)-1-ethoxycarbonyl-3-phenylpropyl)amino-5-oxo-2-(2-thienyl)perhydro-1,4-thiazepin-4-yl)acetic acid.HCl temocapril hydrochloride


Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.


Pathological processes of the KIDNEY or its component tissues.


3' Amino 3' deoxy N,N dimethyladenosine 3'-Amino-3'-deoxy-N,N-dimethyladenosine Aminonucleoside Puromycin

PUROMYCIN derivative that lacks the methoxyphenylalanyl group on the amine of the sugar ring. It is an antibiotic with antineoplastic properties and can cause nephrosis.


Pathological processes of the KIDNEY without inflammatory or neoplastic components. Nephrosis may be a primary disorder or secondary complication of other diseases. It is characterized by the NEPHROTIC SYNDROME indicating the presence of PROTEINURIA and HYPOALBUMINEMIA with accompanying EDEMA.


The purpose of the present study was to determine whether chronic administration of temocapril, a long-acting non-SH group angiotensin converting enzyme (ACE) inhibitor, reduced proteinuria, inhibited glomerular hypertrophy and prevented glomerulosclerosis in chronic puromycin aminonucleoside (PAN) - induced nephrotic rats. Nephrosis was induced by injection of PAN (15mg/100g body weight) in male Sprague-Dawley (SD) rats. Four groups were used, i) the PAN group (14), ii) PAN/temocapril (13), iii) temocapril (14) and iv) untreated controls (15). Temocapril (8 mg/kg/day) was administered to the rats which were killed at weeks 4, 14 or 20. At each time point, systolic blood pressure (BP), urinary protein excretion and renal histopathological findings were evaluated, and morphometric image analysis was done. Systolic BP in the PAN group was significantly high at 4, 14 and 20 weeks, but was normal in the PAN/temocapril group. Urinary protein excretion in the PAN group increased significantly, peaking at 8 days, then decreased at 4 weeks, but rose again significantly at 14 and 20 weeks. Temocapril did not attenuate proteinuria at 8 days, but it did markedly lower it from weeks 4 to 20. The glomerulosclerosis index (GSI) was 6.21 % at 4 weeks and respectively 25.35 % and 30.49 % at 14 and 20 weeks in the PAN group. There was a significant correlation between urinary protein excretion and GSI (r = 0.808, p < 0.0001). The ratio of glomerular tuft area to the area of Bowman's capsules (GT/BC) in the PAN group was significantly increased, but it was significantly lower in the PAN/temocapril group. It appears that temocapril was effective in retarding renal progression and protected renal function in PAN neprotic rats.


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


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).


Bright Disease Glomerulonephritides Glomerulonephritis

Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.


A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.


Pulmonary hypertension after ibuprofen prophylaxis in very preterm infants.

Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.


Aluminum Salt Ibuprofen Brufen Calcium I.V. Solution IP 82 IP-82 IP82 Ibumetin Zinc (+-)-Isomer (R)-Isomer (S)-Isomer Copper (2+) Magnesium Potassium Sodium Ibuprofen-Zinc Motrin Nuprin Rufen Salprofen Trauma Dolgit Gel Trauma-Dolgit TraumaDolgit alpha-Methyl-4-(2-methylpropyl)benzeneacetic Acid

A nonsteroidal anti-inflammatory agent with analgesic properties used in the therapy of rheumatism and arthritis.


We report three cases of severe hypoxaemia after ibuprofen administration during a randomised controlled trial of prophylactic treatment of patent ductus arteriosus with ibuprofen in premature infants born at less than 28 weeks of gestation. Echocardiography showed severely decreased pulmonary blood flow. Hypoxaemia resolved quickly on inhaled nitric oxide therapy. We suggest that investigators involved in similar trials pay close attention to pulmonary pressure if hypoxaemia occurs after prophylactic administration of ibuprofen.

Anoxemia Anoxemias Anoxia Anoxias Deficiencies Oxygen Deficiency Hypoxemia Hypoxemias Hypoxia Hypoxias

Relatively complete absence of oxygen in one or more tissues.


Ductus Arteriosus Patent Patency of the Familial

A congenital heart defect characterized by the persistent opening of fetal DUCTUS ARTERIOSUS that connects the PULMONARY ARTERY to the descending aorta (AORTA, DESCENDING) allowing unoxygenated blood to bypass the lung and flow to the PLACENTA. Normally, the ductus is closed shortly after birth.


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


Hyponatremia and syndrome of inappropriate anti-diuretic hormone reported with the use of Vincristine: an over-representation of Asians?

Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)


syndrome of inappropriate anti-diuretic hormone

ADH Syndrome Inappropriate Antidiuretic Hormone Secretion Vasopressin SIADH Schwartz Bartter Schwartz-Bartter of (SIADH)

A condition of HYPONATREMIA and renal salt loss attributed to overexpansion of BODY FLUIDS resulting from sustained release of ANTIDIURETIC HORMONES which stimulates renal resorption of water. It is characterized by normal KIDNEY function, high urine OSMOLALITY, low serum osmolality, and neurological dysfunction. Etiologies include ADH-producing neoplasms, injuries or diseases involving the HYPOTHALAMUS, the PITUITARY GLAND, and the LUNG. This syndrome can also be drug-induced.


Bristol-Myers Squibb Brand of Vincristine Sulfate Citomid Columbia EG Labo Farmistin Irisfarma Lemery Leurocristine Lilly Oncovin Oncovine Onkocristin Onkoworks PFS Vincasar Pfizer Teva Vincristin Bristol Liquid medac Vincrisul Vintec cell pharm cellcristin

Antitumor alkaloid isolated from Vinca Rosea. (Merck, 11th ed.)


PURPOSE: This retrospective study used a pharmaceutical company's global safety database to determine the reporting rate of hyponatremia and/or syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) among vincristine-treated patients and to explore the possibility of at-risk population subgroups. METHOD: We searched the Eli Lilly and Company's computerized adverse event database for all reported cases of hyponatremia and/or SIADH as of 1 November 1999 that had been reported during the use of vincristine. RESULTS: A total of 76 cases of hyponatremia and/or SIADH associated with vincristine use were identified. The overall reporting rate was estimated to be 1.3/100,000 treated patients. The average age of patients was 35.6 +/- 28.3 years, and 62% were males. Approximately 75% of the patients were receiving treatment for leukemia or lymphoma. Among the 39 reports that included information on race, the racial distribution was: 1 Black, 3 Caucasian, and 35 Asian. CONCLUSION: Our data suggest that Asian patients may be at increased risk of hyponatremia and/or SIADH associated with vincristine use. Although the overall reported rate of SIADH associated with vincristine is very low, physicians caring for Asian oncology patients should be aware of this potential serious but reversible adverse event.


syndrome of inappropriate secretion of anti-diuretic hormone


Leucocythaemia Leucocythaemias Leucocythemia Leucocythemias Leukemia Leukemias

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


Germinoblastic Sarcoma Sarcomas Germinoblastoma Germinoblastomas Lymphoma Malignant Lymphomas Reticulolymphosarcoma Reticulolymphosarcomas

A general term for various neoplastic diseases of the lymphoid tissue.


Delayed toxicity of cyclophosphamide on the bladder of DBA/2 and C57BL/6 female mouse.

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.


Anhydrous Cyclophosphamide B 518 B-518 B518 Monohydrate (R)-Isomer (S)-Isomer Cyclophosphane Cytophosphan Cytophosphane Cytoxan Endoxan NSC 26271 NSC-26271 NSC26271 Neosar Procytox Sendoxan

Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.


The present study describes the delayed development of a severe bladder pathology in a susceptible strain of mice (DBA/2) but not in a resistant strain (C57BL/6) when both were treated with a single 300 mg/kg dose of cyclophosphamide (CY). Inbred DBA/2 and C57BL/6 female mice were injected with CY, and the effect of the drug on the bladder was assessed during 100 days by light microscopy using different staining procedures, and after 30 days by conventional electron microscopy. Early CY toxicity caused a typical haemorrhagic cystitis in both strains that was completely repaired in about 7-10 days. After 30 days of CY injection ulcerous and non-ulcerous forms of chronic cystitis appeared in 86% of DBA/2 mice but only in 4% of C57BL/6 mice. Delayed cystitis was characterized by infiltration and transepithelial passage into the lumen of inflammatory cells and by frequent exfoliation of the urothelium. Mast cells appeared in the connective and muscular layers of the bladder at a much higher number in DBA/2 mice than in C57BL/6 mice or untreated controls. Electron microscopy disclosed the absence of the typical discoidal vesicles normally present in the cytoplasm of surface cells. Instead, numerous abnormal vesicles containing one or several dark granules were observed in the cytoplasm of cells from all the epithelial layers. Delayed cystitis still persisted in DBA/2 mice 100 days after treatment. These results indicate that delayed toxicity of CY in female DBA/2 mice causes a bladder pathology that is not observed in C57BL/6 mice. This pathology resembles interstitial cystitis in humans and could perhaps be used as an animal model for studies on the disease.


Bleeding or escape of blood from a vessel.


Inflammation of the URINARY BLADDER, either from bacterial or non-bacterial causes. Cystitis is usually associated with painful urination (dysuria), increased frequency, urgency, and suprapubic pain.


Chronic Interstitial Cystitides Cystitis Painful Bladder Syndrome

A condition with recurring discomfort or pain in the URINARY BLADDER and the surrounding pelvic region without an identifiable disease. Severity of pain in interstitial cystitis varies greatly and often is accompanied by increased urination frequency and urgency.


High-dose 5-fluorouracil / folinic acid in combination with three-weekly mitomycin C in the treatment of advanced gastric cancer. A phase II study.

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.


5 Formyltetrahydrofolate Formyltetrahydropteroylglutamate 5-Formyltetrahydrofolate 5-Formyltetrahydropteroylglutamate Acid Folinic Calcium Folinate Leucovorin Citrovorum Factor SF Acid-SF (D)-Isomer (DL)-Isomer (R)-Isomer (1:1) Salt Pentahydrate Monosodium Leukovorin Leukovorum N(5)-Formyltetrahydrofolate Wellcovorin

The active metabolite of FOLIC ACID. Leucovorin is used principally as its calcium salt as an antidote to folic acid antagonists which block the conversion of folic acid to folinic acid.


Ametycine Mitocin C Mitocin-C MitocinC Mitomycin Mitomycin-C Mutamycin NSC 26980 NSC-26980 NSC26980

An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.


Cancer of Stomach the Gastric Cancers Familial Diffuse Neoplasm Neoplasms


BACKGROUND: The 24-hour continuous infusion of 5-fluorouracil (5-FU) and folinic acid (FA) as part of several new multidrug chemotherapy regimens in advanced gastric cancer (AGC) has shown to be effective, with low toxicity. In a previous phase II study with 3-weekly bolus 5-FU, FA and mitomycin C (MMC) we found a low toxicity rate and response rates comparable to those of regimens such as ELF, FAM or FAMTX, and a promising median overall survival. In order to improve this MMC-dependent schedule we initiated a phase II study with high-dose 5-FU/FA and 3-weekly bolus MMC. PATIENTS AND METHODS: From February, 1998 to September, 2000 we recruited 33 patients with AGC to receive weekly 24-hour 5-FU 2,600 mg/m(2) preceded by 2-hour FA 500 mg/m(2) for 6 weeks, followed by a 2-week rest period. Bolus MMC 10 mg/m(2) was added in 3-weekly intervals. Treatment given on an outpatient basis, using portable pump systems, was repeated on day 57. Patients' characteristics were: male/female ratio 20/13; median age 57 (27-75) years; median WHO status 1 (0-2). 18 patients had a primary AGC, and 15 showed a relapsed AGC. Median follow-up was 11.8 months (range of those surviving: 2.7-11.8 months). RESULTS: 32 patients were evaluable for response - complete remission 9.1% (n = 3), partial remission 45.5% (n = 15), no change 27.3% (n = 9), progressive disease 15.1% (n = 5). Median overall survival time was 10.2 months [95% confidence interval (CI): 8.7-11.6], and median progression-free survival time was 7.6 months (95% CI: 4.4-10.9). The worst toxicities (%) observed were (CTC-NCI 1/2/3): leukopenia 45.5/18.2/6.1, thrombocytopenia 33.3/9.1/6.1, vomitus 24.2/9.1/0, diarrhea 36.4/6.1/3.0, stomatitis 18.2/9.1/0, hand-foot syndrome 12.1/0/0. Two patients developed hemolytic-uremic syndrome (HUS). CONCLUSIONS: High-dose 5-FU/FA/MMC is an effective and well-tolerated outpatient regimen for AGC (objective response rate 54.6%). It may serve as an alternative to cisplatin-containing regimens; however, it has to be considered that possibly HUS may occur.


Leukocytopenia Leukocytopenias Leukopenia Leukopenias


Thrombocytopenia Thrombocytopenias Thrombopenia Thrombopenias


The forcible expulsion of the contents of the STOMACH through the MOUTH.


An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.


Mucositides Oral Mucositis Oromucositides Oromucositis Stomatitides Stomatitis

INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.


Acral Erythema Chemotherapy-Induced Erythemas Chemotherapy Induced Palmoplantar Erythrodysesthesia Erythrodysesthesias Hand Foot Syndrome Hand-Foot Syndromes

Chemotherapy-induced dermal side effects that are associated with the use of various CYTOSTATIC AGENTS. Symptoms range from mild ERYTHEMA and/or PARESTHESIA to severe ulcerative dermatitis with debilitating pain involving typically palmoplantar and intertriginous areas. These cutaneous manifestations are sometimes accompanied by nail anomalies.


Gasser Syndrome Gasser's Gassers Hemolytic Uremic Hemolytic-Uremic

A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.


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

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


Persistent sterile leukocyturia is associated with impaired renal function in human immunodeficiency virus type 1-infected children treated with indinavir.

Pathological processes of the KIDNEY or its component tissues.


human immunodeficiency virus type 1-infected

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

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


A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.


BACKGROUND: Prolonged administration of indinavir is associated with the occurrence of a variety of renal complications in adults. These well-documented side effects have restricted the use of this potent protease inhibitor in children. DESIGN: A prospective study to monitor indinavir-related nephrotoxicity in a cohort of 30 human immunodeficiency virus type 1-infected children treated with indinavir. METHODS: Urinary pH, albumin, creatinine, the presence of erythrocytes, leukocytes, bacteria and crystals, and culture were analyzed every 3 months for 96 weeks. Serum creatinine levels were routinely determined at the same time points. Steady-state pharmacokinetics of indinavir were done at week 4 after the initiation of indinavir. RESULTS: The cumulative incidence of persistent sterile leukocyturia (> or =75 cells/ micro L in at least 2 consecutive visits) after 96 weeks was 53%. Persistent sterile leukocyturia was frequently associated with a mild increase in the urine albumin/creatinine ratio and by microscopic hematuria. The cumulative incidence of serum creatinine levels >50% above normal was 33% after 96 weeks. Children with persistent sterile leukocyturia more frequently had serum creatinine levels of 50% above normal than those children without persistent sterile leukocyturia. In children younger than 5.6 years, persistent sterile leukocyturia was significantly more frequent than in older children. A higher cumulative incidence of persistent leukocyturia was found in children with an area under the curve >19 mg/L x h or a peak serum level of indinavir >12 mg/L. In 4 children, indinavir was discontinued because of nephrotoxicity. Subsequently, the serum creatinine levels decreased, the urine albumin/creatinine ratios returned to zero, and the leukocyturia disappeared within 3 months. CONCLUSIONS: Children treated with indinavir have a high cumulative incidence of persistent sterile leukocyturia. Children with persistent sterile leukocyturia more frequently had an increase in serum creatinine levels of >50% above normal. Younger children have an additional risk for renal complications. The impairment of the renal function in these children occurred in the absence of clinical symptoms of nephrolithiasis. Indinavir-associated nephrotoxicity must be monitored closely, especially in children with risk factors such as persistent sterile leukocyturia, age <5.6 years, an area under the curve of indinavir >19 mg/L x h, and a C(max) >12 mg/L.


Utility of troponin I in patients with cocaine-associated chest pain.

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


Pressure, burning, or numbness in the chest.


Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. OBJECTIVE: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. METHODS: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). RESULTS: Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. CONCLUSIONS: Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.

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).


Cardiovascular Stroke Strokes Infarct Myocardial Infarction Infarctions Infarcts

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


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.


Cardiac Death Determination of Near-Death Experience

Irreversible cessation of all bodily functions, manifested by absence of spontaneous breathing and total loss of cardiovascular and cerebral functions.


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


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.


Acute interstitial nephritis due to nicergoline (Sermion).

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.


Aventis Brand of Nicergoline Circo Maren Circo-Maren Dexcel F.I. 6714 Fisifax Hexal Hormosan Kenfarma Krewel Lindopharm Nicergobeta Nicergolin Atid Lindo TEVA neuraxpharm ratiopharm Nicergolin-TEVA Nicergolin-neuraxpharm Nicergolin-ratiopharm Pfizer Teva Nicerium Nicotergoline Nimergoline Reig Jofre Sermion betapharm ct Arzneimittel ct-Arzneimittel ergobel nicergolin von

An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It has been suggested to ameliorate cognitive deficits in cerebrovascular disease.


We report a case of acute interstitial nephritis (AIN) due to nicergoline (Sermion). A 50-year-old patient admitted to our hospital for fever and acute renal failure. Before admission, he had been taking nicergoline and bendazac lysine due to retinal vein occlusion at ophthalmologic department. Thereafter, he experienced intermittent fever and skin rash. On admission, clinical symptoms (i.e. arthralgia and fever) and laboratory findings (i.e. eosinophilia and renal failure) suggested AIN, and which was confirmed by pathologic findings on renal biopsy. A lymphocyte transformation test demonstrated a positive result against nicergoline. Treatment was consisted of withdrawal of nicergoline and intravenous methylprednisolone, and his renal function was completely recovered. To our knowledge, this is the first report of nicergoline-associated AIN.


Fever Fevers Hyperthermia Hyperthermias Pyrexia Pyrexias

An abnormal elevation of body temperature, usually as a result of a pathologic process.


Acute Kidney Failure Failures Injuries Injury Insufficiencies Insufficiency Renal

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


AF 1934 AF-1934 Bendalina Bendaline bendazac lysine salt


Occlusion Retinal Vein Occlusions Thromboses Thrombosis

Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.


Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.


Arthralgia Arthralgias Joint Pain Pains Polyarthralgia Polyarthralgias


Abnormal increase of EOSINOPHILS in the blood, tissues or organs.


Failure Kidney Renal Failures Insufficiency Insufficiencies

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


6 Methylprednisolone 6-Methylprednisolone Medrol Metipred Urbason

A PREDNISOLONE derivative with similar anti-inflammatory action.


Neuroleptic malignant syndrome complicated by massive intestinal bleeding in a patient with chronic renal failure.

NMS (Neuroleptic Malignant Syndrome) NMSs Neuroleptic Induced Neuroleptic Syndrome Syndromes Neuroleptic-Induced Neuroleptic-Malignant

A potentially fatal syndrome associated primarily with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS) which are in turn associated with dopaminergic receptor blockade (see RECEPTORS, DOPAMINE) in the BASAL GANGLIA and HYPOTHALAMUS, and sympathetic dysregulation. Clinical features include diffuse MUSCLE RIGIDITY; TREMOR; high FEVER; diaphoresis; labile blood pressure; cognitive dysfunction; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present. (From Adams et al., Principles of Neurology, 6th ed, p1199; Psychiatr Serv 1998 Sep;49(9):1163-72)


Bleeding or escape of blood from a vessel.


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.


A patient with chronic renal failure (CRF) developed neuroleptic malignant syndrome (NMS) after administration of risperidone and levomepromazine. In addition to the typical symptoms of NMS, massive intestinal bleeding was observed during the episode. This report suggests that NMS in a patient with CRF may be complicated by intestinal bleeding and needs special caution for this complication.


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.


Levomeprazin Levomepromazine Levopromazine Methotrimeprazine Tisercin Tizercine Tizertsin

A phenothiazine with pharmacological activity similar to that of both CHLORPROMAZINE and PROMETHAZINE. It has the histamine-antagonist properties of the antihistamines together with CENTRAL NERVOUS SYSTEM effects resembling those of chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604)


The asymmetrical breakdown of the blood-brain barrier (BBB) was studied in female rats. Paw preference was assessed by a food reaching test. Adrenaline-induced hypertension was used to destroy the BBB, which was evaluated using triphenyltetrazolium (TTC) staining of the brain slices just after giving adrenaline for 30 s. In normal rats, the whole brain sections exhibited complete staining with TTC. After adrenaline infusion for 30 s, there were large unstained areas in the left brain in right-pawed animals, and vice versa in left-pawed animals. Similar results were obtained in seizure-induced breakdown of BBB. These results were explained by an asymmetric cerebral blood flow depending upon the paw preference in rats. It was suggested that this new method and the results are consistent with contralateral motor control that may be important in determining the dominant cerebral hemisphere in animals.

4-(1-Hydroxy-2-(methylamino)ethyl)-1,2-benzenediol Acetate Epinephrine Adrenaline Acid Tartrate Bitartrate Hydrochloride Allergan Brand of Epifrin Hydrogen Epitrate Lyophrin Medihaler-Epi

The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.


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.


2,3,5-triphenyltetrazolium chloride triphenyltetrazolium bromide


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."


Carvedilol protects against doxorubicin-induced mitochondrial cardiomyopathy.

BM 14190 BM-14190 Coreg Coropres Dilatrend Eucardic Kredex Querto carvedilol hydrochloride (+-)-isomer (R)-isomer (S)-isomer 14C-labeled


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.


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).


Several cytopathic mechanisms have been suggested to mediate the dose-limiting cumulative and irreversible cardiomyopathy caused by doxorubicin. Recent evidence indicates that oxidative stress and mitochondrial dysfunction are key factors in the pathogenic process. The objective of this investigation was to test the hypothesis that carvedilol, a nonselective beta-adrenergic receptor antagonist with potent antioxidant properties, protects against the cardiac and hepatic mitochondrial bioenergetic dysfunction associated with subchronic doxorubicin toxicity. Heart and liver mitochondria were isolated from rats treated for 7 weeks with doxorubicin (2 mg/kg sc/week), carvedilol (1 mg/kg ip/week), or the combination of the two drugs. Heart mitochondria isolated from doxorubicin-treated rats exhibited depressed rates for state 3 respiration (336 +/- 26 versus 425 +/- 53 natom O/min/mg protein) and a lower respiratory control ratio (RCR) (4.3 +/- 0.6 versus 5.8 +/- 0.4) compared with cardiac mitochondria isolated from saline-treated rats. Mitochondrial calcium-loading capacity and the activity of NADH-dehydrogenase were also suppressed in cardiac mitochondria from doxorubicin-treated rats. Doxorubicin treatment also caused a decrease in RCR for liver mitochondria (3.9 +/- 0.9 versus 5.6 +/- 0.7 for control rats) and inhibition of hepatic cytochrome oxidase activity. Coadministration of carvedilol decreased the extent of cellular vacuolization in cardiac myocytes and prevented the inhibitory effect of doxorubicin on mitochondrial respiration in both heart and liver. Carvedilol also prevented the decrease in mitochondrial Ca(2+) loading capacity and the inhibition of the respiratory complexes of heart mitochondria caused by doxorubicin. Carvedilol by itself did not affect any of the parameters measured for heart or liver mitochondria. It is concluded that this protection by carvedilol against both the structural and functional cardiac tissue damage may afford significant clinical advantage in minimizing the dose-limiting mitochondrial dysfunction and cardiomyopathy that accompanies long-term doxorubicin therapy in cancer patients.


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.


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.


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


Benign Neoplasm Neoplasms Cancer Cancers Neoplasia Tumor Tumors

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


Cocaine-induced hyperactivity is more influenced by adenosine receptor agonists than amphetamine-induced hyperactivity.

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


Generalized Hyperkinesia Hyperkinesias Hyperactivity Motor Hyperkinesis Hyperkinetic Movement Movements

Excessive movement of muscles of the body as a whole, which may be associated with organic or psychological disorders.


A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.


Amfetamine Amphetamine Sulfate (2:1) Centramina Desoxynorephedrin Fenamine Levoamphetamine Miquel Brand of Mydrial Phenamine Phenopromin Thyramine l l-Amphetamine levo levo-Amphetamine

A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.


The influence of adenosine receptor agonists and antagonists on cocaine-and amphetamine-induced hyperactivity was examined in mice. All adenosine receptor agonists significantly decreased the locomotor activity in mice, and the effects were dose-dependent. It seems that adenosine A1 and A2 receptors might be involved in this reaction. Moreover, all adenosine receptor agonists: 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680), A2A receptor agonist, N6-cyclopentyladenosine (CPA), A1 receptor agonist, and 5'-N-ethylcarboxamidoadenosine (NECA), A2/A1 receptor agonist significantly and dose-dependently decreased cocaine-induced locomotor activity. CPA reduced cocaine action at the doses which, given alone, did not influence motility, while CGS 21680 and NECA decreased the action of cocaine at the doses which, given alone, decreased locomotor activity in animals. These results suggest the involvement of both adenosine receptors in the action of cocaine although agonists of A1 receptors seem to have stronger influence on it. The selective blockade of A2 adenosine receptor by DMPX (3,7-dimethyl-1-propargylxanthine) significantly enhanced cocaine-induced locomotor activity of animals. Caffeine had similar action but the effect was not significant. CPT (8-cyclopentyltheophylline)--A1 receptor antagonist, did not show any influence in this test. Similarly, all adenosine receptor agonists decreased amphetamine-induced hyperactivity, but at the higher doses than those which were active in cocaine-induced hyperactivity. The selective blockade of A2 adenosine receptors (DMPX) and non-selective blockade of adenosine receptors (caffeine) significantly increased the action of amphetamine in the locomotor activity test. Our results have shown that all adenosine receptor agonists (A1 and A2) reduce cocaine- and amphetamine-induced locomotor activity and indicate that cocaine-induced hyperactivity is more influenced by adenosine receptor agonists (particularly A1 receptors) than amphetamine-induced hyperactivity.


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)


2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride Benzenepropanoic acid 4-(2-((6-amino-9-(N-ethyl-beta-D-ribofuranuronamidosyl)-9H-purin-2-yl)amino)ethyl)- CGS 21680 21680A CGS-21680C CGS21680


5' N Ethylcarboxamidoadenosine 5'-N-Ethylcarboxamidoadenosine Adenosine ethyluronamide N6-Ethyl-carboxamido Adenosine-5'-(N-ethylcarboxamide) Adenosine-5'-N-ethyluronamide N-Ethylcarboxamidoadenosine N6 Ethyl carboxamido NECA

A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.


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.


8-CPDMX 8-cyclopentyl-1,3-dimethylxanthine 8-cyclopentyltheophylline PD 116,600 116600 PD-116,600 PD-116600


Amiodarone and the risk of bradyarrhythmia requiring permanent pacemaker in elderly patients with atrial fibrillation and prior myocardial infarction.

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.


Bradyarrhythmia Bradyarrhythmias Bradycardia Bradycardias

Cardiac arrhythmias that are characterized by excessively slow HEART RATE, usually below 50 beats per minute in human adults. They can be classified broadly into SINOATRIAL NODE dysfunction and ATRIOVENTRICULAR BLOCK.


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.


Cardiovascular Stroke Strokes Infarct Myocardial Infarction Infarctions Infarcts

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


OBJECTIVES: The aim of this study was to determine whether the use of amiodarone in patients with atrial fibrillation (AF) increases the risk of bradyarrhythmia requiring a permanent pacemaker. BACKGROUND: Reports of severe bradyarrhythmia during amiodarone therapy are infrequent and limited to studies assessing the therapy's use in the management of patients with ventricular arrhythmias. METHODS: A study cohort of 8,770 patients age > or =65 years with a new diagnosis of AF was identified from a provincewide database of Quebec residents with a myocardial infarction (MI) between 1991 and 1999. Using a nested case-control design, 477 cases of bradyarrhythmia requiring a permanent pacemaker were matched (1:4) to 1,908 controls. Multivariable logistic regression was used to estimate the odds ratio (OR) of pacemaker insertion associated with amiodarone use, controlling for baseline risk factors and exposure to sotalol, Class I antiarrhythmic agents, beta-blockers, calcium channel blockers, and digoxin. RESULTS: amiodarone use was associated with an increased risk of pacemaker insertion (OR: 2.14, 95% confidence interval [CI]: 1.30 to 3.54). This effect was modified by gender, with a greater risk in women versus men (OR: 3.86, 95% CI: 1.70 to 8.75 vs. OR: 1.52, 95% CI: 0.80 to 2.89). Digoxin was the only other medication associated with an increased risk of pacemaker insertion (OR: 1.78, 95% CI: 1.37 to 2.31). CONCLUSIONS: This study suggests that the use of amiodarone in elderly patients with AF and a previous MI increases the risk of bradyarrhythmia requiring a permanent pacemaker. The finding of an augmented risk of pacemaker insertion in elderly women receiving amiodarone requires further investigation.


Arrhythmia Cardiac Arrhythmias Arrythmia Dysrhythmia

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


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.


AWD.pharma Brand of Digoxin Bertek Boehringer Digoxina Digacin Digitek Digoregen Digoxine Nativelle Dilanacin Glaxo Wellcome GlaxoSmithKline 1 2 Hemigoxine Kern Lanacordin Lanicor Lanoxicaps Lanoxin PG Lanoxin-PG Lenoxin Lilly Mapluxin Novartis Proctor & Gamble R.A.N. Roche Teofarma UDL Virco

A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666)


Indomethacin-induced morphologic changes in the rat urinary bladder epithelium.

Amuno Hydrochloride Indomethacin Indocid Indocin Indomet 140 Indometacin Metindol Osmosin

A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.


OBJECTIVES: To evaluate the morphologic changes in rat urothelium induced by indomethacin. Nonsteroidal anti-inflammatory drug-induced cystitis is a poorly recognized and under-reported condition. In addition to tiaprofenic acid, indomethacin has been reported to be associated with this condition. METHODS: Three groups were established: a control group (n = 10), a high-dose group (n = 10), treated with one intraperitoneal injection of indomethacin 20 mg/kg, and a therapeutic dose group (n = 10) in which oral indomethacin was administered 3.25 mg/kg body weight daily for 3 weeks. The animals were then killed and the bladders removed for light and electron microscopic studies. RESULTS: The light microscopic findings showed some focal epithelial degeneration that was more prominent in the high-dose group. When compared with the control group, both indomethacin groups revealed statistically increased numbers of mast cells in the mucosa (P <0.0001) and penetration of lanthanum nitrate through intercellular areas of the epithelium. Furthermore, the difference in mast cell counts between the high and therapeutic dose groups was also statistically significant (P <0.0001). CONCLUSIONS: Indomethacin resulted in histopathologic findings typical of interstitial cystitis, such as leaky bladder epithelium and mucosal mastocytosis. The true incidence of nonsteroidal anti-inflammatory drug-induced cystitis in humans must be clarified by prospective clinical trials.


Inflammation of the URINARY BLADDER, either from bacterial or non-bacterial causes. Cystitis is usually associated with painful urination (dysuria), increased frequency, urgency, and suprapubic pain.


Apo-Tiaprofenic Apotex brand of tiaprofenic acid Aventis FC 3001 Flanid Florizel Grünenthal Hoechst Novo-Tiaprofenic Novopharm Nu-Pharm Nu-Tiaprofenic PMS-Tiaprofenic Pharmascience Pierre Fabre RU 15060 Surgam SA calcium salt


lanthanide nitrate hexahydrate lanthanum


Chronic Interstitial Cystitides Cystitis Painful Bladder Syndrome

A condition with recurring discomfort or pain in the URINARY BLADDER and the surrounding pelvic region without an identifiable disease. Severity of pain in interstitial cystitis varies greatly and often is accompanied by increased urination frequency and urgency.


Disease Mast-Cell Diseases Mast Cell Mastocytoses Mastocytosis

A heterogenous group of disorders characterized by the abnormal increase of MAST CELLS in only the skin (MASTOCYTOSIS, CUTANEOUS), in extracutaneous tissues involving multiple organs (MASTOCYTOSIS, SYSTEMIC), or in solid tumors (MASTOCYTOMA).


An open-label phase II study of low-dose thalidomide in androgen-independent prostate cancer.

Celgene Brand of Thalidomide Sedoval Thalomid

A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.


Agents Androgenic Agonists Androgen Receptor Effect Effects Compounds Androgens

Compounds that interact with ANDROGEN RECEPTORS in target tissues to bring about the effects similar to those of TESTOSTERONE. Depending on the target tissues, androgenic effects can be on SEX DIFFERENTIATION; male reproductive organs, SPERMATOGENESIS; secondary male SEX CHARACTERISTICS; LIBIDO; development of muscle mass, strength, and power.


Cancer of Prostate the Prostatic Cancers Neoplasm Neoplasms


The antiangiogenic effects of thalidomide have been assessed in clinical trials in patients with various solid and haematological malignancies. Thalidomide blocks the activity of angiogenic agents including bFGF, VEGF and IL-6. We undertook an open-label study using thalidomide 100 mg once daily for up to 6 months in 20 men with androgen-independent prostate cancer. The mean time of study was 109 days (median 107, range 4-184 days). Patients underwent regular measurement of prostate-specific antigen (PSA), urea and electrolytes, serum bFGF and VEGF. Three men (15%) showed a decline in serum PSA of at least 50%, sustained throughout treatment. Of 16 men treated for at least 2 months, six (37.5%) showed a fall in absolute PSA by a median of 48%. Increasing levels of serum bFGF and VEGF were associated with progressive disease; five of six men who demonstrated a fall in PSA also showed a decline in bFGF and VEGF levels, and three of four men with a rising PSA showed an increase in both growth factors. Adverse effects included constipation, morning drowsiness, dizziness and rash, and resulted in withdrawal from the study by three men. Evidence of peripheral sensory neuropathy was found in nine of 13 men before treatment. In the seven men who completed six months on thalidomide, subclinical evidence of peripheral neuropathy was found in four before treatment, but in all seven at repeat testing. The findings indicate that thalidomide may be an option for patients who have failed other forms of therapy, provided close follow-up is maintained for development of peripheral neuropathy.


Hematologic Malignancies Malignancy Neoplasm Neoplasms Hematological Hematopoietic

Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.


A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids.


Infrequent or difficult evacuation of FECES. These symptoms are associated with a variety of causes, including low DIETARY FIBER intake, emotional or nervous disturbances, systemic and structural disorders, drug-induced aggravation, and infections.


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

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


Dizziness Dizzyness Light Headedness Light-Headedness Lightheadedness Orthostasis

An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness.


Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.


Nerve Disease Peripheral Diseases Neuropathy PNS (Peripheral Nervous System) System Disorders Neuropathies

Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.


Central nervous system toxicity following the administration of levobupivacaine for lumbar plexus block: A report of two cases.

Encephalitides Toxic Encephalitis Encephalopathies Encephalopathy Nervous System Poisoning Poisonings Neurotoxic Disorder Disorders Neurotoxicity Syndrome Syndromes Neurotoxin Disease Diseases

Neurologic disorders caused by exposure to toxic substances through ingestion, injection, cutaneous application, or other method. This includes conditions caused by biologic, chemical, and pharmaceutical agents.


BACKGROUND AND OBJECTIVES: Central nervous system and cardiac toxicity following the administration of local anesthetics is a recognized complication of regional anesthesia. Levobupivacaine, the pure S(-) enantiomer of bupivacaine, was developed to improve the cardiac safety profile of bupivacaine. We describe 2 cases of grand mal seizures following accidental intravascular injection of levobupivacaine. CASE REPORT: Two patients presenting for elective orthopedic surgery of the lower limb underwent blockade of the lumbar plexus via the posterior approach. Immediately after the administration of levobupivacaine 0.5% with epinephrine 2.5 microgram/mL, the patients developed grand mal seizures, despite negative aspiration for blood and no clinical signs of intravenous epinephrine administration. The seizures were successfully treated with sodium thiopental in addition to succinylcholine in 1 patient. Neither patient developed signs of cardiovascular toxicity. Both patients were treated preoperatively with beta-adrenergic antagonist medications, which may have masked the cardiovascular signs of the unintentional intravascular administration of levobupivacaine with epinephrine. CONCLUSIONS: Although levobupivacaine may have a safer cardiac toxicity profile than racemic bupivacaine, if adequate amounts of levobupivacaine reach the circulation, it will result in convulsions. Plasma concentrations sufficient to result in central nervous system toxicity did not produce manifestations of cardiac toxicity in these 2 patients.

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.


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


Convulsion Disorder Tonic-Clonic Disorders Syndrome Syndromes Grand Mal Tonic Clonic Convulsions Cryptogenic Epilepsy Epilepsies Seizure Familial Symptomatic Major Motor

A generalized seizure disorder characterized by recurrent major motor seizures. The initial brief tonic phase is marked by trunk flexion followed by diffuse extension of the trunk and extremities. The clonic phase features rhythmic flexor contractions of the trunk and limbs, pupillary dilation, elevations of blood pressure and pulse, urinary incontinence, and tongue biting. This is followed by a profound state of depressed consciousness (post-ictal state) which gradually improves over minutes to hours. The disorder may be cryptogenic, familial, or symptomatic (caused by an identified disease process). (From Adams et al., Principles of Neurology, 6th ed, p329)


4-(1-Hydroxy-2-(methylamino)ethyl)-1,2-benzenediol Acetate Epinephrine Adrenaline Acid Tartrate Bitartrate Hydrochloride Allergan Brand of Epifrin Hydrogen Epitrate Lyophrin Medihaler-Epi

The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.


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."


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

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


Anectine Bromide Suxamethonium Celocurine Dibromide Succinylcholine Dichloride Diiodide Diperchlorate Ditilin Listenon Lysthenon Myorelaxin Quelicin Succicuran Chloride Di H2O Di-H2O Iodide Succinyldicholine

A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.


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


Anaesthetic complications associated with myotonia congenita: case study and comparison with other myotonic disorders.

Batten Turner Congenital Myopathy Batten-Turner Becker Disease Generalized Myotonia Thomsen Thomsen's Thomsens of Myotonias Congenita Autosomal Dominant Recessive Levior

Inherited myotonic disorders with early childhood onset MYOTONIA. Muscular hypertrophy is common and myotonia may impair ambulation and other movements. It is classified as Thomsen (autosomal dominant) or Becker (autosomal recessive) generalized myotonia mainly based on the inheritance pattern. Becker type is also clinically more severe. An autosomal dominant variant with milder symptoms and later onset is known as myotonia levior. Mutations in the voltage-dependent skeletal muscle chloride channel are associated with the disorders.


Congenita Paramyotonia Disease Eulenburg Eulenburg's Disorder Myotonic Disorders Eulenburgs Fluctuans Myotonia Myopathies Myopathy Congenitas

Diseases characterized by MYOTONIA, which may be inherited or acquired. Myotonia may be restricted to certain muscles (e.g., intrinsic hand muscles) or occur as a generalized condition.


Myotonia congenita (MC) is caused by a defect in the skeletal muscle chloride channel function, which may cause sustained membrane depolarisation. We describe a previously healthy 32-year-old woman who developed a life-threatening muscle spasm and secondary ventilation difficulties following a preoperative injection of suxamethonium. The muscle spasms disappeared spontaneously and the surgery proceeded without further problems. When subsequently questioned, she reported minor symptoms suggesting a myotonic condition. Myotonia was found on clinical examination and EMG. The diagnosis MC was confirmed genetically. Neither the patient nor the anaesthetist were aware of the diagnosis before this potentially lethal complication occurred. We give a brief overview of ion channel disorders including malignant hyperthermia and their anaesthetic considerations.


Inorganic compounds derived from hydrochloric acid that contain the Cl- ion.


Ciliary Body Spasm Spasms Generalized Muscle Muscular

An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.


Myotonia Percussion Myotonias Myotonic Phenomenon Phenomenons

Prolonged failure of muscle relaxation after contraction. This may occur after voluntary contractions, muscle percussion, or electrical stimulation of the muscle. Myotonia is a characteristic feature of MYOTONIC DISORDERS.


Anesthesia Hyperthermia Hyperthermias Related Hyperpyrexia Malignant Hyperpyrexias of

Rapid and excessive rise of temperature accompanied by muscular rigidity following general anesthesia.


Respiratory pattern in a rat model of epilepsy.

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)


PURPOSE: Apnea is known to occur during seizures, but systematic studies of ictal respiratory changes in adults are few. Data regarding respiratory pattern defects during interictal periods also are scarce. Here we sought to generate information with regard to the interictal period in animals with pilocarpine-induced epilepsy. METHODS: Twelve rats (six chronically epileptic animals and six controls) were anesthetized, given tracheotomies, and subjected to hyperventilation or hypoventilation conditions. Breathing movements caused changes in thoracic volume and forced air to flow tidally through a pneumotachograph. This flow was measured by using a differential pressure transducer, passed through a polygraph, and from this to a computer with custom software that derived ventilation (VE), tidal volume (VT), inspiratory time (TI), expiratory time (TE), breathing frequency (f), and mean inspiratory flow (VT/TI) on a breath-by-breath basis. RESULTS: The hyperventilation maneuver caused a decrease in spontaneous ventilation in pilocarpine-treated and control rats. Although VE had a similar decrease in both groups, in the epileptic group, the decrease in VE was due to a significant (p < 0.05) increase in TE peak in relation to that of the control animals. The hypoventilation maneuver led to an increase in the arterial Paco2, followed by an increase in VE. In the epileptic group, the increase in VE was mediated by a significant (p < 0.05) decrease in TE peak compared with the control group. Systemic application of KCN, to evaluate the effects of peripheral chemoreception activation on ventilation, led to a similar increase in VE for both groups. CONCLUSIONS: The data indicate that pilocarpine-treated animals have an altered ability to react to (or compensate for) blood gas changes with changes in ventilation and suggest that it is centrally determined. We speculate on the possible relation of the current findings on treating different epilepsy-associated conditions.

A transient absence of spontaneous respiration.


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.


A pulmonary ventilation rate faster than is metabolically necessary for the exchange of gases. It is the result of an increased frequency of breathing, an increased tidal volume, or a combination of both. It causes an excess intake of oxygen and the blowing off of carbon dioxide.


Increased serum soluble Fas in patients with acute liver failure due to paracetamol overdose.

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.


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.


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


BACKGROUND/AIMS: Experimental studies have suggested that apoptosis via the Fas/Fas Ligand signaling system may play an important role in the development of acute liver failure. The aim of the study was to investigate the soluble form of Fas in patients with acute liver failure. METHODOLOGY: Serum levels of sFas (soluble Fas) were measured by ELISA in 24 patients with acute liver failure and 10 normal control subjects. Serum levels of tumor necrosis factor-alpha and interferon-gamma were also determined by ELISA. RESULTS: Serum sFas was significantly increased in patients with acute liver failure (median, 26.8 U/mL; range, 6.9-52.7 U/mL) compared to the normal controls (median, 8.6 U/mL; range, 6.5-12.0 U/mL, P < 0.0001). Levels were significantly greater in patients with acute liver failure due to paracetamol overdose (median, 28.7 U/mL; range, 12.8-52.7 U/mL, n = 17) than those due to non-A to E hepatitis (median, 12.5 U/mL; range, 6.9-46.0 U/mL, n = 7, P < 0.01). There was no relationship of sFas to eventual outcome in the patients. A significant correlation was observed between serum sFas levels and aspartate aminotransferase (r = 0.613, P < 0.01). CONCLUSIONS: The increased concentration of sFas in serum of patients with acute liver failure may reflect activation of Fas-mediated apoptosis in the liver and this together with increased tumor necrosis factor-alpha may be an important factor in liver cell loss.


Benign Neoplasm Neoplasms Cancer Cancers Neoplasia Tumor Tumors

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


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


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.


(+-)-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.


Bilateral subthalamic nucleus stimulation for Parkinson's disease.

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)


High frequency stimulation of the subthalamic nucleus (STN) is known to ameliorate the signs and symptoms of advanced Parkinson's disease. AIM: We studied the effect of high frequency STN stimulation in 23 patients. METHOD: Twenty-three patients suffering from severe Parkinson's disease (Stages III-V on Hoehn and Yahr scale) and, particularly bradykinesia, rigidity, and levodopa-induced dyskinesias underwent bilateral implantation of electrodes in the STN. Preoperative and postoperative assessments of these patients at 1, 3, 6 and 12 months follow-up, in "on" and "off" drug conditions, was carried out using Unified Parkinson's Disease Rating Scale, Hoehn and Yahr staging, England activities of daily living score and video recordings. RESULTS: After one year of electrical stimulation of the STN, the patients' scores for activities of daily living and motor examination scores (Unified Parkinson's Disease Rating Scale parts II and III) off medication improved by 62% and 61% respectively (p<0.0005). The subscores for the akinesia, rigidity, tremor and gait also improved. (p<0.0005). The average levodopa dose decreased from 813 mg to 359 mg. The cognitive functions remained unchanged. Two patients developed device-related complications and two patients experienced abnormal weight gain. CONCLUSION: Bilateral subthalamic nucleus stimulation is an effective treatment for advanced Parkinson's disease. It reduces the severity of "off" phase symptoms, improves the axial symptoms and reduces levodopa requirements. The reduction in the levodopa dose is useful in controlling drug-induced dyskinesias.


Antiorthostatic Hypokinesia Hypokinesias Bradykinesia Bradykinesias Hypodynamia

Slow or diminished movement of body musculature. It may be associated with BASAL GANGLIA DISEASES; MENTAL DISORDERS; prolonged inactivity due to illness; and other conditions.


Catatonic Rigidity Cogwheel Rigidities Extensor Extrapyramidal Gegenhalten Gegenhaltens Muscle Muscular Nuchal

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


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.


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)


Action Tremor Tremors Coarse Continuous Darkness Fine Intention Intermittent Involuntary Quiver Quivers Limb Massive Muscle Neonatal Nerve Passive Perioral Persistent Pill Rolling Rest Resting Saturnine Semirhythmic Senile Static

Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of CEREBELLAR DISEASES, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of PARKINSON DISEASE.


Ocular motility changes after subtenon carboplatin chemotherapy for retinoblastoma.

Almirall Brand of Carboplatin Blastocarb Bristol-Myers Squibb CBDCA Carboplat Carbosin Carbotec Chiesi Columbia Ercar JM 8 JM-8 JM8 Lemery NSC 241240 NSC-241240 NSC241240 Nealorin Neocarbo Neocorp Paraplatin Paraplatine Pharmachemie Platinwas Prasfarma Ribocarbo cis-Diammine(cyclobutanedicarboxylato)platinum II ribosepharm

An organoplatinum compound that possesses antineoplastic activity.


Eye Cancer Retinoblastoma Familial Retinoblastomas Glioblastoma Retinal Glioblastomas Glioma Gliomas Hereditary Neuroblastoma Neuroblastomas Sporadic

A malignant tumor arising from the nuclear layer of the retina that is the most common primary tumor of the eye in children. The tumor tends to occur in early childhood or infancy and may be present at birth. The majority are sporadic, but the condition may be transmitted as an autosomal dominant trait. Histologic features include dense cellularity, small round polygonal cells, and areas of calcification and necrosis. An abnormal pupil reflex (leukokoria); NYSTAGMUS, PATHOLOGIC; STRABISMUS; and visual loss represent common clinical characteristics of this condition. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2104)


BACKGROUND: Focal subtenon carboplatin injections have recently been used as a presumably toxicity-free adjunct to systemic chemotherapy for intraocular retinoblastoma. OBJECTIVE: To report our clinical experience with abnormal ocular motility in patients treated with subtenon carboplatin chemotherapy. METHODS: We noted abnormal ocular motility in 10 consecutive patients with retinoblastoma who had received subtenon carboplatin. During ocular manipulation under general anesthesia, we assessed their eyes by forced duction testing, comparing ocular motility after tumor control with ocular motility at diagnosis. Eyes subsequently enucleated because of treatment failure (n = 4) were examined histologically. RESULTS: Limitation of ocular motility was detected in all 12 eyes of 10 patients treated for intraocular retinoblastoma with 1 to 6 injections of subtenon carboplatin as part of multimodality therapy. Histopathological examination revealed many lipophages in the periorbital fat surrounding the optic nerve in 1 eye, indicative of phagocytosis of previously existing fat cells and suggesting prior fat necrosis. The enucleations were technically difficult and hazardous for globe rupture because of extensive orbital soft tissue adhesions. CONCLUSIONS: Subtenon carboplatin chemotherapy is associated with significant fibrosis of orbital soft tissues, leading to mechanical restriction of eye movements and making subsequent enucleation difficult. Subtenon carboplatin is not free of toxicity, and its use is best restricted to specific indications.


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.


Brown Tendon Sheath Syndrome Brown's Conjugate Gaze Spasm Spasms Convergence Excess Excesses Insufficiencies Insufficiency Cyclophoria Cyclophorias Deficiencies Smooth Pursuit Deficiency Deviation Skew Deviations Dyskinesia Paroxysmal Ocular Dyskinesias Eye Motility Disorder Disorders Movement Internuclear Ophthalmoplegia Ophthalmoplegias Torticollis Opsoclonus Parinaud Parinaud's Parinauds Pseudoophthalmoplegia Pseudoophthalmoplegias of

Disorders that feature impairment of eye movements as a primary manifestation of disease. These conditions may be divided into infranuclear, nuclear, and supranuclear disorders. Diseases of the eye muscles or oculomotor cranial nerves (III, IV, and VI) are considered infranuclear. Nuclear disorders are caused by disease of the oculomotor, trochlear, or abducens nuclei in the BRAIN STEM. Supranuclear disorders are produced by dysfunction of higher order sensory and motor systems that control eye movements, including neural networks in the CEREBRAL CORTEX; BASAL GANGLIA; CEREBELLUM; and BRAIN STEM. Ocular torticollis refers to a head tilt that is caused by an ocular misalignment. Opsoclonus refers to rapid, conjugate oscillations of the eyes in multiple directions, which may occur as a parainfectious or paraneoplastic condition (e.g., OPSOCLONUS-MYOCLONUS SYNDROME). (Adams et al., Principles of Neurology, 6th ed, p240)


Forcible or traumatic tear or break of an organ or other soft part of the body.


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


AHP Brand of Ethambutol Hydrochloride Dexambutol EMB Fatol Hefa EMB-Fatol EMB-Hefa Elan Etambutol Llorente Etibi Genopharm ICN Lederle Miambutol Myambutol Riemser SERB Sanavita Wernigerode Wyeth

An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863)


Cranial Nerve II Diseases Disorder Disk Optic Disorders Foster Kennedy Syndrome Foster-Kennedy Lesion Neural-Optical Lesions Neural Optical Neuropathies Neuropathy Disease Second

Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect.


PURPOSE: To demonstrate the association between ethambutol and optic neuropathy. METHOD: Thirteen patients who developed optic neuropathy after being treated with ethambutol for tuberculosis of the lung or lymph node at Siriraj Hospital between 1997 and 2001 were retrospectively reviewed. The clinical characteristics and initial and final visual acuity were analyzed to determine visual outcome. RESULTS: All patients had optic neuropathy between 1 to 6 months (mean = 2.9 months) after starting ethambutol therapy at a dosage ranging from 13 to 20 mg/kg/day (mean = 17 mg/kg/day). Seven (54%) of the 13 patients experienced visual recovery after stopping the drug. Of 6 patients with irreversible visual impairment, 4 patients had diabetes mellitus, glaucoma and a history of heavy smoking. CONCLUSION: Early recognition of optic neuropathy should be considered in patients with ethambutol therapy. A low dose and prompt discontinuation of the drug is recommended particularly in individuals with diabetes mellitus, glaucoma or who are heavy smokers.


Consumption Pulmonary Consumptions Phthises Phthisis Tuberculoses Tuberculosis


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).


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


An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)


Treatment of compensatory gustatory hyperhidrosis with topical glycopyrrolate.

Auriculotemporal Nerve Syndrome Baillarger Frey Frey's Gustatory Hyperhidroses Hyperhidrosis Sweating Salivosudoriparous Syndromes von Freys

An autonomic disorder characterized by excessive sweating of the forehead, upper lip, perioral region, or sternum subsequent to gustatory stimuli. The auriculotemporal syndrome features facial flushing or sweating limited to the distribution of the auriculotemporal nerve and may develop after trauma to the parotid gland, in association with PAROTID NEOPLASMS, or following their surgical removal. (From Ann Neurol 1997 Dec;42(6):973-5)


A muscarinic antagonist used as an antispasmodic, in some disorders of the gastrointestinal tract, and to reduce salivation with some anesthetics.


Gustatory hyperhidrosis is facial sweating usually associated with the eating of hot spicy food or even smelling this food. Current options of treatment include oral anticholinergic drugs, the topical application of anticholinergics or aluminum chloride, and the injection of botulinum toxin. Thirteen patients have been treated to date with 1.5% or 2% topical glycopyrrolate. All patients had gustatory hyperhidrosis, which interfered with their social activities, after transthroacic endoscopic sympathectomy, and which was associated with compensatory focal hyperhidrosis. After applying topical glycopyrrolate, the subjective effect was excellent (no sweating after eating hot spicy food) in 10 patients (77%), and fair (clearly reduced sweating) in 3 patients (23%). All had reported incidents of being very embarrassed whilst eating hot spicy foods. Adverse effects included a mildly dry mouth and a sore throat in 2 patients (2% glycopyrrolate), a light headache in 1 patient (1.5% glycopyrrolate). The topical application of a glycopyrrolate pad appeared to be safe, efficacious, well tolerated, and a convenient method of treatment for moderate to severe symptoms of gustatory hyperhidrosis in post transthoracic endoscopic sympathectomy or sympathicotomy patients, with few side effects.


AlCl3 Drysol aluminum chloride hexahydrate anhydrous trichloride


Excessive sweating. In the localized type, the most frequent sites are the palms, soles, axillae, inguinal folds, and the perineal area. Its chief cause is thought to be emotional. Generalized hyperhidrosis may be induced by a hot, humid environment, by fever, or by vigorous exercise.


Asialia Asialias Dryness Mouth Hyposalivation Hyposalivations Xerostomia Xerostomias


Pharyngitides Pharyngitis Sore Throat Throats


Bilateral Headache Headaches Cephalalgia Cephalalgias Cephalgia Cephalgias Cephalodynia Cephalodynias Cranial Pain Pains Generalized Head Ocular Orthostatic Periorbital Retro-Ocular Sharp Throbbing Unilateral Vertex Hemicrania Retro

The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.


Pharmacological characteristics and side effects of a new galenic formulation of propofol without soyabean oil.

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

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


We compared the pharmacokinetics, pharmacodynamics and safety profile of a new galenic formulation of propofol (AM149 1%), which does not contain soyabean oil, with a standard formulation of propofol (Disoprivan 1%). In a randomised, double-blind, cross-over study, 30 healthy volunteers received a single intravenous bolus injection of 2.5 mg.kg-1 propofol. Plasma propofol levels were measured for 48 h following drug administration and evaluated according to a three-compartment model. The pharmacodynamic parameters assessed included induction and emergence times, respiratory and cardiovascular effects, and pain on injection. Patients were monitored for side effects over 48 h. Owing to a high incidence of thrombophlebitis, the study was terminated prematurely and only the data of the two parallel treatment groups (15 patients in each group) were analysed. Plasma concentrations did not differ significantly between the two formulations. Anaesthesia induction and emergence times, respiratory and cardiovascular variables showed no significant differences between the two treatment groups. Pain on injection (80 vs. 20%, p < 0.01) and thrombophlebitis (93.3 vs. 6.6%, p < 0.001) occurred more frequently with AM149 than with Disoprivan. Although both formulations had similar pharmacokinetic and pharmacodynamic profiles the new formulation is not suitable for clinical use due to the high incidence of thrombophlebitis produced.


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

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


Dolens Phlegmasia Alba Thrombophlebitides Thrombophlebitis

Inflammation of a vein associated with a blood clot (THROMBUS).


Vinorelbine-related cardiac events: a meta-analysis of randomized clinical trials.

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


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.


Benign Neoplasm Neoplasms Cancer Cancers Neoplasia Tumor Tumors

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


Compound 112531 Desacetylvinblastine Amide EG Labo Brand of Vindesine Sulfate Eldisine Enison Lilly NSC 245467 NSC-245467 NSC245467 Vindesin

Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).


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.