Palpable purpura is a concerning clinical finding in pediatric patients and can have many causes, including infectious and autoimmune processes. A rare cause, drug-induced vasculitis, may result from the production of antineutrophil cytoplasmic antibodies (ANCAs) in response to a medication. We report a girl with Turner syndrome and Graves' disease who presented with palpable purpuric lesions. The diagnosis of propylthiouracil (PTU)-associated vasculitis was made by observation of consistent clinical features, the detection of elevated ANA and ANCA in the blood, and the observed clinical resolution of symptoms following withdrawal of PTU. Subsequent treatment of persistent hyperthyroidism with radioablation did not result in an exacerbation of the vasculitis, a complication described in prior case reports.

Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. When the size of the discolorization is >2-3 cm it is generally called Ecchymoses (ECCHYMOSIS).


Angiitides Angiitis Vasculitides Vasculitis

Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.


Bonnevie Ullrich Syndrome Bonnevie-Ullrich Gonadal Dysgenesis 45,X XO Monosomy X Status Ullrich-Turner Turner Turner's Turners

A syndrome of defective gonadal development in phenotypic females associated with the karyotype 45,X (or 45,XO). Patients generally are of short stature with undifferentiated GONADS (streak gonads), SEXUAL INFANTILISM, HYPOGONADISM, webbing of the neck, cubitus valgus, elevated GONADOTROPINS, decreased ESTRADIOL level in blood, and CONGENITAL HEART DEFECTS. NOONAN SYNDROME (also called Pseudo-Turner Syndrome and Male Turner Syndrome) resembles this disorder; however, it occurs in males and females with a normal karyotype and is inherited as an autosomal dominant.


Basedow Disease Basedow's Basedows Graves Graves' Exophthalmic Goiter Goiters Hyperthyroidism Autoimmune

A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).


6 Propyl 2 Thiouracil 6-Propyl-2-Thiouracil Propylthiouracil

A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534)


Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.


Succinylcholine-induced masseter muscle rigidity during bronchoscopic removal of a tracheal foreign body.

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.


Lock Jaw Lockjaw Masseter Muscle Spasm Spasms Trismus

Spasmodic contraction of the masseter muscle resulting in forceful jaw closure. This may be seen with a variety of diseases, including TETANUS, as a complication of radiation therapy, trauma, or in association with neoplastic conditions.


Masseter muscle rigidity during general anesthesia is considered an early warning sign of a possible episode of malignant hyperthermia. The decision whether to continue or discontinue the procedure depends on the urgency of the surgery and severity of masseter muscle rigidity. Here, we describe a case of severe masseter muscle rigidity (jaw of steel) after succinylcholine (Sch) administration during general anesthetic management for rigid bronchoscopic removal of a tracheal foreign body. Anesthesia was continued uneventfully with propofol infusion while all facilities were available to detect and treat malignant hyperthermia.


Anesthesia Hyperthermia Hyperthermias Related Hyperpyrexia Malignant Hyperpyrexias of

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


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.


Minor neurological dysfunction, cognitive development, and somatic development at the age of 3 to 7 years after dexamethasone treatment in very-low birth-weight infants.

Disease Nervous System Diseases Disorder Neurologic Neurological Disorders

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


Alcon Brand of Dexamethasone Decaject L.A. Decaject-L.A. Decameth Decaspray Dexasone Dexpak ECR Foy Hexadecadrol Hexadrol ICN Maxidex Merck Merz 1 2 Methylfluorprednisolone Millicorten Oradexon


The objective of this study was to assess minor neurological dysfunction, cognitive development, and somatic development after dexamethasone therapy in very-low-birthweight infants. Thirty-three children after dexamethasone treatment were matched to 33 children without dexamethasone treatment. Data were assessed at the age of 3-7 years. Dexamethasone was started between the 7th and the 28th day of life over 7 days with a total dose of 2.35 mg/kg/day. Exclusion criteria were asphyxia, malformations, major surgical interventions, small for gestational age, intraventricular haemorrhage grades III and IV, periventricular leukomalacia, and severe psychomotor retardation. Each child was examined by a neuropediatrician for minor neurological dysfunctions and tested by a psychologist for cognitive development with a Kaufman Assessment Battery for Children and a Draw-a-Man Test. There were no differences in demographic data, growth, and socio-economic status between the two groups. Fine motor skills and gross motor function were significantly better in the control group (p<0.01). In the Draw-a-Man Test, the control group showed better results (p<0.001). There were no differences in development of speech, social development, and the Kaufman Assessment Battery for Children. After dexamethasone treatment, children showed a higher rate of minor neurological dysfunctions. Neurological development was affected even without neurological diagnosis. Further long-term follow-up studies will be necessary to fully evaluate the impact of dexamethasone on neurological and cognitive development.


Asphyxia Asphyxias Suffocation Suffocations

A pathological condition caused by lack of oxygen, manifested in impending or actual cessation of life.


Abnormalities Drug Induced Drug-Induced Abnormality

Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.


Bleeding or escape of blood from a vessel.


Cerebral Leukomalacia Neonatal Leukomalacias Cystic Periventricular Encephalomalacia Encephalomalacias Leucomalacia Leucomalacias

Degeneration of white matter adjacent to the CEREBRAL VENTRICLES following cerebral hypoxia or BRAIN ISCHEMIA in neonates. The condition primarily affects white matter in the perfusion zone between superficial and deep branches of the MIDDLE CEREBRAL ARTERY. Clinical manifestations include VISION DISORDERS; CEREBRAL PALSY; PARAPLEGIA; SEIZURES; and cognitive disorders. (From Adams et al., Principles of Neurology, 6th ed, p1021; Joynt, Clinical Neurology, 1997, Ch4, pp30-1)


Developmental Psychomotor Disorder Disorders Impairment Impairments

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


Force overflow and levodopa-induced dyskinesias in Parkinson's disease.

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)


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)


We assessed force coordination of the hand in Parkinson's disease and its relationship to motor complications of levodopa therapy, particularly to levodopa-induced dyskinesias (LID). We studied two groups of Parkinson's disease patients with (Parkinson's disease + LID, n = 23) and without levodopa-induced dyskinesias (Parkinson's disease - LID, n = 10), and age-matched healthy controls. The motor score of the Unified Parkinson's Disease Rating Scale, a dyskinesia score and force in a grip-lift paradigm were assessed ON and OFF levodopa. A pathological increase of forces was seen in ON-state in Parkinson's disease + LID only. In Parkinson's disease + LID, the force involved in pressing down the object before lifting was significantly increased by levodopa (by 61%, P < 0.05). An overshooting of peak grip force by 51% (P < 0.05) and of static grip force by 45% (P < 0.01) was observed in the ON- compared with the OFF-drug condition. In contrast, no excessive force was found in Parkinson's disease - LID. Peak grip force in ON-state was 140% (P < 0.05) higher in Parkinson's disease + LID than in Parkinson's disease - LID, while static grip force was increased by 138% (P < 0.01) between groups. Severity of peak-dose dyskinesias was strongly correlated with grip force in ON-state (r = 0.79 with peak force, P < 0.01). No correlation was observed between forces and the motor score as well as with the daily dose of dopaminergic medication. Force excess was only observed in patients with LID and motor fluctuations. A close relationship was seen between the overshooting of forces and dyskinesias in the ON-drug condition. We postulate that both LID and grip force excess share common pathophysiological mechanisms related to motor fluctuations.


Postinfarction ventricular septal defect associated with long-term steroid therapy.

Septal Rupture Ventricular Ruptures Perforation

Laceration or tearing of the VENTRICULAR SEPTUM, usually caused by MYOCARDIAL INFARCTION.


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


Two cases of postinfarction ventricular septal rupture in patients on long-term steroid therapy are presented and the favourable outcome in both cases described. A possible association between steroid therapy and subsequent postinfarction septal rupture is discussed.


Angioedema associated with droperidol administration.

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

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


Dehidrobenzperidol Dehydrobenzperidol Droleptan Droperidol Inapsine Janssen Brand of Kern Taylor

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


Angioedema, also known as angioneurotic edema or Quincke's disease, is a well-demarcated, localized edema involving the subcutaneous tissues that may cause upper-airway obstruction. We report the case of a previously healthy 19-year-old man with no known drug allergies in whom angioedema with significant tongue swelling and protrusion developed within 10 minutes of the administration of a single IV dose of droperidol.


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


Any hindrance to the passage of air into and out of the lungs.


Allergies Drug Allergy Hypersensitivities Hypersensitivity

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


Disease Tongue Diseases Microglossia Microglossias


Clarithromycin-associated visual hallucinations in a patient with chronic renal failure on continuous ambulatory peritoneal dialysis.

6-O-Methylerythromycin A 56268 A-56268 A56268 Biaxin Clarithromycin TE 031 TE-031 TE031

A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.


Auditory Hallucination Verbal Hallucinations Body Sensation Dissociative Elementary Gustatory of Hypnagogic Hypnapompic Kinesthetic Mood Congruent Incongruent Olfactory Organic Reflex Sensory Somatic Tactile Visual Formed People Internal Unformed

Subjectively experienced sensations in the absence of an appropriate stimulus, but which are regarded by the individual as real. They may be of organic origin or associated with MENTAL DISORDERS.


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.


Visual hallucinations are a rare event in chronic renal failure and not related to uremia per se. Unreported in the literature is visual hallucinations occurring in association with the new macrolide antibiotic, clarithromycin. We describe such a case in a patient with end-stage renal disease (ESRD) maintained on continuous ambulatory peritoneal dialysis (CAPD). The combination of a relatively high dose of clarithromycin in face of chronic renal failure in a functionally anephric patient, with underlying aluminum intoxication, may have facilitated the appearance of this neurotoxic side effect. It is important to understand the pharmacokinetics of medications in face of chronic renal failure, the possibility of drug interactions, and how these factors should help guide medication therapy in the ESRD patient.


A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.


A group of often glycosylated macrocyclic compounds formed by chain extension of multiple PROPIONATES cyclized into a large (typically 12, 14, or 16)-membered lactone. Macrolides belong to the POLYKETIDES class of natural products, and many members exhibit ANTIBIOTIC properties.


A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98.


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.


Acute renal toxicity of doxorubicin (adriamycin)-loaded cyanoacrylate nanoparticles.

Pathological processes of the KIDNEY or its component tissues.


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.


A group of compounds having the general formula CH2=C(CN)-COOR; it polymerizes on contact with moisture; used as tissue adhesive; higher homologs have hemostatic and antibacterial properties.


Acute doxorubicin-loaded nanoparticle (DXNP) renal toxicity was explored in both normal rats and rats with experimental glomerulonephritis. In normal rats, 2/6 rats given free doxorubicin (DX) (5 mg/kg) died within one week, whereas all control animals and all rats having received free NP or DXNP survived. A 3 times higher proteinuria appeared in animals treated with DXNP than in those treated with DX. Free NP did not provoke any proteinuria. Two hr post-injection, DXNP was 2.7 times more concentrated in kidneys than free DX (p < 0.025). In rats with immune experimental glomerulonephritis, 5/6 rats given DX died within 7 days, in contrast to animals treated by DXNP, NP, or untreated, which all survived. Proteinuria appeared in all series, but was 2-5 times more intense (p > 0.001) and prolonged after doxorubicin treatment (400-700 mg/day), without significant difference between DXNP and DX. Rats treated by unloaded NP behaved as controls. These results demonstrate that, in these experimental conditions, DXNP killed less animals than free DX, despite of an enhanced renal toxicity of the former. Both effects (better survival and nephrosis) are most probably related to an enhanced capture of DXNP by cells of the mononuclear phagocyte system, including mesangial cells.


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.


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


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.


Baxter Brand of Etoposide Oncology Bristol Myers Squibb Bristol-Myers Celltop Demethyl Epipodophyllotoxin Ethylidine Glucoside Eposide Eposin Eto GRY Eto-GRY Etomedac Etopos Pierre Fabre Teva (5S)-Isomer (5a alpha)-Isomer alpha,9 alpha D Glucopyranosyl Isomer alpha-D-Glucopyranosyl Etoposido Ferrer Farma Exitop Gry Lastet Lemery Medac NSC 141540 NSC-141540 NSC141540 Novartis Onkoposid Onkoworks Pharmachemie Prasfarma Riboposid Sanfer Tedec Meiji Toposar VP 16 213 16-213 16213 VP-16 VP16 Vepesid

A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.


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).


The occurrence of a myocardial infarction is reported after chemotherapy containing etoposide, in a man with no risk factors for coronary heart disease. Possible causal mechanisms are discussed.


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.


Subjective assessment of sexual dysfunction of patients on long-term administration of digoxin.

Arousal Disorders Sexual Aversion Disorder Psychosexual Orgasmic Dysfunction Psychological Dysfunctions Frigidity Hypoactive Desire

Disturbances in sexual desire and the psychophysiologic changes that characterize the sexual response cycle and cause marked distress and interpersonal difficulty. (APA, DSM-IV, 1994)


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)


Various data suggest that male patients who have received digoxin on a longterm basis have increased levels of serum estrogen and decreased levels of plasma testosterone and luteinizing hormone (LH). This study was undertaken to investigate the links between the long-term administration of digoxin therapy and sexual behavior, and the effect of digoxin on plasma levels of estradiol, testosterone, and LH. The patients of the study and control group (without digoxin) were of similar cardiac functional capacity and age (25-40 years) and were randomly selected from the rheumatic heart disease patients. A subjective assessment of sexual behavior in the study and control groups was carried out, using parameters such as sexual desire, sexual excitement, and frequency of sexual relations. Personal interviews and a questionnaire were also used for the evaluation of sexual behavior. The findings support the reports concerning digoxin effect on plasma estradiol, testosterone, and LH. The differences in the means were significant. Tests used to evaluate the changes in sexual behavior showed a significant decrease in sexual desire, sexual excitement phase (erection), and frequency of sexual relations in the study group.


Agents Estrogenic Agonists Estrogen Receptor Compounds Effects Effect Estrogens

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


17 beta Hydroxy 4 Androsten 3 one 8 alpha 17-beta-Hydroxy-4-Androsten-3-one 17-beta-Hydroxy-8 alpha-4-Androsten-3-one Isotestosterone 8-Isotestosterone AndroGel Androderm Andropatch Androtop AstraZeneca Brand of Testosterone Auxilium Pharmaceuticals Inc. Bartor CEPA Dr. Kade Faulding Ferring GlaxoSmithKline Hauck Histerone Ortho Paladin Pasadena Schering SmithKline Beecham Solvay Sterotate Sustanon Testim Testoderm Testolin Testopel Sulfate Ulmer Unimed Watson

A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.


17 beta Estradiol Oestradiol beta-Estradiol beta-Oestradiol Aerodiol Estrace Estraderm TTS alpha 17beta Anhydrous Hemihydrate (17 alpha)-Isomer Monohydrate Orion Brand (+-)-Isomer (-)-Isomer (16 alpha,17 beta)-Isomer (17-alpha)-Isomer (8 beta)-(+-)-Isomer (9 beta,17 Monosodium Salt Sodium Estradiol-17 Estradiol-17beta Novartis Pharmaceuticals of Ovocyclin Vivelle

The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.


Bouillaud Disease Bouillaud's Bouillauds Rheumatic Heart Diseases

Cardiac manifestation of systemic rheumatological conditions, such as RHEUMATIC FEVER. Rheumatic heart disease can involve any part the heart, most often the HEART VALVES and the ENDOCARDIUM.


Fatal aplastic anemia due to indomethacin--lymphocyte transformation tests in vitro.

A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.


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.


Although indomethacin has been implicated as a possible cause of aplastic anemia on the basis of a few clinical observations, its role has not been definitely established. A case of fatal aplastic anemia is described in which no drugs other than allopurinol and indomethacin were given. Indomethacin was first given four weeks prior to the onset of symptoms. A positive lymphocyte transformation test with indomethacin in vitro further substantiates the potential role of this drug in causing aplastic anemia in a susceptible patient. Fortunately, this seems to be a very rare complication.


APS Brand of Allopurinol Allohexal Allohexan Alloprin Allopurin Alphapharm Amrad Ashbourne Azupharma BASF Bicther Boots Clonmel Dorsch Douglas Hennig Hexal Horner ICN Jenapharm Merckle Merz Multipharma Nicholas Novopharm Pharmafarm Pinewood Protea R.A.N. Rima Roche Rosen Rougier TAD Thiemann Wellcome gepepharm Allorin Allpargin Allural Apulonga Apurin Atisuril Bleminol Boehringer Mannheim Byk Gulden Caplenal Capurate Cellidrin Embarin Fawns & McAllan Foligan Glaxo Hamarin Henning Berlin Jenapuri

A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.


Plasma and urinary lipids and lipoproteins during the development of nephrotic syndrome induced in the rat by puromycin aminonucleoside.

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.


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.


This study was undertaken to ascertain whether the alterations of plasma lipoproteins found in nephrotic syndrome induced by puromycin aminonucleoside were due to nephrotic syndrome per se, or, at least in part, to the aminonucleoside. The purpose of the present study was to investigate the changes in plasma and urinary lipoproteins during the administration of puromycin aminonucleoside (20 mg/kg for 7 days) and the subsequent development of nephrotic syndrome. Since massive albuminuria occurred after 6 days of treatment, the time-course study was divided into two stages: pre-nephrotic stage (day 1-5) and nephrotic stage (day 6-11). In pre-nephrotic stage the plasma level of fatty acids, triacylglycerol and VLDL decreased while that of phospholipid, cholesteryl esters and HDL remained constant. Plasma apolipoprotein A-I tended to increase (40% increase at day 5). At the beginning of nephrotic stage (day 6) the concentration of plasma albumin dropped to a very low level, while that of apolipoprotein A-I increased abruptly (4-fold increase) and continued to rise, although less steeply, in the following days. The plasma concentration of HDL followed the same pattern. Plasma VLDL and LDL increased at a later stage (day 9). Plasma apolipoprotein A-I was found not only in HDL (1.063-1.210 g/ml) but also in the LDL density class (1.025-1.050 g/ml). In the pre-nephrotic stage lipoproteinuria was negligible, while in the early nephrotic stage the urinary loss of plasma lipoproteins consisted mainly of HDL. These observations indicate that puromycin aminonucleoside alters plasma lipoproteins by lowering VLDL and increasing HDL. It is likely that the early and striking increase of plasma HDL found in nephrotic rats is related to a direct effect of the drug on HDL metabolism.


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


Acids Aliphatic Esterified Fatty Saturated

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


Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.


Circulating lysosomal enzymes and acute hepatic necrosis.

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.


The activities of the lysosomal enzymes acid and neutral protease, N-acetylglucosaminidase, and acid phosphatase were measured in the serum of patients with fulminant hepatic failure. Acid protease (cathepsin D) activity was increased about tenfold in patients who died and nearly fourfold in those who survived fulminant hepatic failure after paracetamol overdose, whereas activities were increased equally in patients with fulminant hepatic failure due to viral hepatitis whether or not they survived. A correlation was found between serum acid protease activity and prothrombin time, and the increase in cathepsin D activity was sustained over several days compared with aspartate aminotransferase, which showed a sharp early peak and then a fall. Circulating lysosomal proteases can damage other organs, and measurement of their activity may therefore be of added value in assessing prognosis in this condition.


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.


INFLAMMATION of the LIVER in humans due to infection by VIRUSES. There are several significant types of human viral hepatitis with infection caused by enteric-transmission (HEPATITIS A; HEPATITIS E) or blood transfusion (HEPATITIS B; HEPATITIS C; and HEPATITIS D).


(+-)-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.


Transketolase abnormality in tolazamide-induced Wernicke's encephalopathy.

A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE.


Beriberi Cerebral Encephalopathies Wernicke Encephalopathy Gayet Gayet-Wernicke Wernicke's Wernickes Disease Polioencephalitis Superior Hemorrhagic Syndrome

An acute neurological disorder characterized by the triad of ophthalmoplegia, ataxia, and disturbances of mental activity or consciousness. Eye movement abnormalities include nystagmus, external rectus palsies, and reduced conjugate gaze. THIAMINE DEFICIENCY and chronic ALCOHOLISM are associated conditions. Pathologic features include periventricular petechial hemorrhages and neuropil breakdown in the diencephalon and brainstem. Chronic thiamine deficiency may lead to KORSAKOFF SYNDROME. (Adams et al., Principles of Neurology, 6th ed, pp1139-42; Davis & Robertson, Textbook of Neuropathology, 2nd ed, pp452-3)


We studied a thiamine-dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke's encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke-Korsakoff syndrome. In addition to this patient, we also studied this enzyme from three diabetic kindreds without any history of Wernicke's encephalopathy and from four normal controls. We found that the above-mentioned patient and one of the diabetic kindreds with no history of Wernicke's encephalopathy had abnormal transketolase as determined by its Km for TPP. These data suggest a similarity between postalcoholic Wernicke-Korsakoff syndrome and the patient with tolazamide-induced Wernicke's encephalopathy from the standpoint of transketolase abnormality.

Aneurin Mononitrate Thiamine Vitamin B 1 B1


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


Berolase Cocarboxylase Pyrophosphate Thiamine Diphosphate

The coenzyme form of Vitamin B1 present in many animal tissues. It is a required intermediate in the PYRUVATE DEHYDROGENASE COMPLEX and the KETOGLUTARATE DEHYDROGENASE COMPLEX.


Korsakoff Psychoses Psychosis Syndrome Wernicke-Korsakoff Syndromes Wernicke

An acquired cognitive disorder characterized by inattentiveness and the inability to form short term memories. This disorder is frequently associated with chronic ALCOHOLISM; but it may also result from dietary deficiencies; CRANIOCEREBRAL TRAUMA; NEOPLASMS; CEREBROVASCULAR DISORDERS; ENCEPHALITIS; EPILEPSY; and other conditions. (Adams et al., Principles of Neurology, 6th ed, p1139)


Mechanisms of myocardial ischemia induced by epinephrine: comparison with exercise-induced ischemia.

Disease Ischemic Heart Diseases Ischemia Myocardial Ischemias

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


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.


A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.


The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise-induced myocardial ischemia was marked predominantly by increased heart rate and rate-pressure product with a minor contribution of end-diastolic volume, while epinephrine-induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate-pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.


Arterioscleroses Coronary Arteriosclerosis Artery Disease Diseases Atheroscleroses Atherosclerosis

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


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


Depression Endogenous Neurotic Unipolar Depressions Depressive Disorder Disorders Neuroses Neurosis Syndrome Syndromes Melancholia Melancholias

An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent.


Angina Pectoris Angor Stenocardia Stenocardias

The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.


Transient contralateral rotation following unilateral substantia nigra lesion reflects susceptibility of the nigrostriatal system to exhaustion by amphetamine.

Dyskinesia Syndrome Syndromes Lingual-Facial-Buccal Linguofacial Oral Oral-facial Orofacial Tardive Dyskinesias Dystonia Dystonias Etat Marbre Lingual Facial Buccal Movement Disorder Disorders facial Status Marmoratus

Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.


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.


Following unilateral 6-OHDA induced SN lesion, a transient period of contralateral rotation has been reported to precede the predominant ipsilateral circling. In order to clarify the nature of this initial contralateral rotation we examined the effect of the duration of recovery period after the lesion, on amphetamine-induced rotational behavior. Three days post lesion, most rats circled predominantly contralaterally to the lesion. Such contralateral rotation may result from either degeneration-induced breakdown of the DA pool, or lesion-induced increase of DA turnover in the spared neurons. A substantial degree of contralateral preference was still evident when amphetamine was administered for the first time 24 days after lesioning, indicating involvement of spared cells in the contralateral rotation. However, regardless of the duration of recovery (and irrespective of either lesion volume, amphetamine dose, or post-lesion motor exercise), amphetamine-induced rotation tended to become gradually more ipsilateral as the observation session progressed, and all rats circled ipsilaterally to the lesion in response to further amphetamine injections. These findings suggest that amphetamine has an irreversible effect on the post-lesion DA pool contributing to contralateral rotation.

6 Hydroxydopamine 6-Hydroxydopamine 6-OHDA Hydrobromide Oxidopamine Hydrochloride

A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.


Thyroid function and urine-concentrating ability during lithium treatment.

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


It has been suggested that adenylate cyclase inhibition may be important in the development of both nephrogenic diabetes insipidus and hypothyroidism during lithium treatment. We measured serum thyroxine and urine-concentrating ability (Umax) in response to desmopressin (DDAVP) in 85 patients receiving lithium. Hypothyroidism developed in eight patients while they were taking lithium. Impaired Umax was found in both euthyroid and hypothyroid patients while some hypothyroid patients concentrated their urine well. It is concluded that the dominant mechanisms by which lithium exerts these two effects are different.

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

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


A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.


3,5,3',5'-Tetraiodothyronine Abbot Brand of Levothyroxine Sodium Allphar Aventis Berlin Chemie Berlin-Chemie Berlthyrox Byk Deladande Levothyroxin Delalande Dexnon Eferox Eltroxin Eltroxine Euthyrox Eutirox Forest Genpharm GlaxoSmithKline GlaxoWellcome Goldshield Henning Hexal 1 2 Kern L Thyrox Thyroxin beta Thyroxine Roche L-3,5,3',5'-Tetraiodothyronine L-Thyrox L-Thyroxin L-Thyroxine LThyroxin Leo Tiroxina Levo T Levo-T LevoT Levothroid Levothyroid Levoxine Levoxyl Lévothyrox Merck Lipha Santé

The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.


Sensitivity of erythroid progenitor colonies to erythropoietin in azidothymidine treated immunodeficient mice.

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

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


The anaemia induced by 3'-azido-3'dideoxythymidine (AZT) is poorly understood. We have used a murine model of AIDS, infection of female C57BL/6 mice with LP-BM5 murine leukaemia (MuLV) virus, to determine if AZT-induced anaemia is due, in part, to decreased responsiveness of erythropoietic precursors (BFU-e) to erythropoietin (EPO). Mice in the early stage of LP-BM5 MuLV disease were given AZT in their drinking water at 1.0 and 2.5 mg/ml. AZT produced anaemia in both groups, in a dose-dependent fashion. Despite the anaemia, the number of splenic and bone marrow BFU-e in AZT treated mice increased up to five-fold over levels observed in infected untreated animals after 15 d of treatment. Colony formation by splenic and bone marrow BFUe was stimulated at lower concentrations of EPO in mice receiving AZT for 15 d than for infected, untreated mice. By day 30, sensitivity of both splenic and bone marrow BFU-e of treated animals returned to that observed from cells of infected untreated animals. The mean plasma levels of EPO observed in AZT treated mice were appropriate for the degree of anaemia observed when compared with phenylhydrazine (PHZ) treated mice. The numbers of BFU-e and the percentage of bone marrow erythroblasts observed were comparable in AZT and PHZ treated mice with similar degrees of anaemia. However, reticulocytosis was inappropriate for the degree of anaemia observed in AZT treated infected mice. AZT-induced peripheral anaemia in the face of increased numbers of BFU-e and increased levels of plasma EPO suggest a lesion in terminal differentiation.

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


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

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


Invasion of the host organism by microorganisms that can cause pathological conditions or diseases.


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)


phenylhydrazide phenylhydrazine hydrochloride monohydrochloride monosulfate


An increase in circulating RETICULOCYTES, which is among the simplest and most reliable signs of accelerated ERYTHROCYTE production. Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, particularly CONGENITAL HEMOLYTIC ANEMIA.


Detection of abnormal cardiac adrenergic neuron activity in adriamycin-induced cardiomyopathy with iodine-125-metaiodobenzylguanidine.

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).


(3-Iodo-(131I)benzyl)guanidine 123I Labeled 3-Iodobenzylguanidine 125I 3 Iodobenzylguanidine Iobenguane (131I) MIBG m m-Iodobenzylguanidine meta meta-Iodobenzylguanidine

A guanidine analog with specific affinity for tissues of the sympathetic nervous system and related tumors. The radiolabeled forms are used as antineoplastic agents and radioactive imaging agents. (Merck Index, 12th ed) MIBG serves as a neuron-blocking agent which has a strong affinity for, and retention in, the adrenal medulla and also inhibits ADP-ribosyltransferase.


Radiolabeled metaiodobenzylguanidine (MIBG), an analog of norepinephrine (NE), serves as an index of adrenergic neuron integrity and function. Using a rat model of adriamycin-induced cardiomyopathy, we tested the hypothesis that abnormal cardiac adrenergic neuron activity may appear and be exacerbated dose-dependently in adriamycin cardiomyopathy. The degree of vacuolar degeneration of myocardial cells was analyzed in relation to the duration of adriamycin treatment (2 mg/kg, once a week). There were no abnormalities or only isolated degeneration in the 1- or 2-wk treatment groups, isolated or scattered degeneration in half of the 3-wk group, frequent scattered degeneration in the 4-wk group, scattered or focal degeneration in the 5-wk group, and extensive degeneration in the 8-wk group. Myocardial accumulation of [125I]MIBG 4 hr after intravenous injection did not differ between the controls and the groups treated 3 wk or less. However, the 4-wk group had a slightly lower accumulation in the right ventricular wall (82% of the control) and significantly lower accumulation in the left ventricular wall (about 66% of the control: p less than 0.05). In the 5-wk group, MIBG accumulation in the right and left ventricular wall was 35% and 27% of that in controls, respectively (p less than 0.001). In the 8-wk group, MIBG accumulation in the right and left ventricular wall was 18% and 14% of that in controls, respectively (p less than 0.001). Thus, MIBG accumulation in the myocardium decreased in an adriamycin dose-dependent manner. The appearance of impaired cardiac adrenergic neuron activity in the presence of slight myocardial impairment (scattered or focal vacuolar degeneration) indicates that MIBG scintigraphy may be a useful method for detection of adriamycin-induced cardiomyopathy.


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

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


vacuolar degeneration of myocardial cells

Autophagic vacuolar myopathy Myopathy Vacuolar Infantile-Onset


Amnestic syndrome associated with propranolol toxicity: a case report.

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

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


AY 20694 AY-20694 AY20694 Anaprilin Anapriline Avlocardyl Betadren Dexpropranolol Dociton Hydrochloride Propranolol Inderal Obsidan Obzidan Propanolol Rexigen

A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.


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.


An elderly woman developed an Alzheimer-like subacute dementia as a result of propranolol toxicity. Analysis of the manifestations showed that severe impairment of memory accounted for virtually all of the abnormalities. There is evidence that cerebral reactions to drug toxicity can exhibit patterns that suggest highly selective involvement of functional subdivisions of the brain.

Acute Confusional Senile Dementia Alzheimer (AD) Disease Early Onset Late Sclerosis Syndrome Type (ATD) Alzheimer's Focal Alzheimer-Type Presenile Primary Degenerative Familial (FAD)

A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)


Amentia Amentias Dementia Familial Dementias Senile Paranoid

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


Biphasic response of the SA node of the dog heart in vivo to selective administration of ketamine.

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

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


Effect of ketamine on the SA node of the dog heart was studied in vivo using a selective perfusion technique of the SA node artery. Injections of ketamine in doses from 100 microgram to 3 mg into the artery produced a depression of the SA nodal activity by a direct action. This depression was followed by the sudden appearance of a stimulatory phase. Bilateral vagotomy and sympathectomy or prior administration of a ganglion blocker failed to inhibit the occurrence of the ketamine-induced tachycardia, while it was completely abolished in the reserpinized dogs or by a prior injection of a beta-blocking agent into the SA node artery. This may indicate that an activation of the peripheral adrenergic mechanism plays an important role in the induction of the excitatory effect of ketamine injected in the SA node artery.


Depression Endogenous Neurotic Unipolar Depressions Depressive Disorder Disorders Neuroses Neurosis Syndrome Syndromes Melancholia Melancholias

An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent.


Tachyarrhythmia Tachyarrhythmias Tachycardia Tachycardias

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


The use of serum cholinesterase in succinylcholine apnoea.

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.


A transient absence of spontaneous respiration.


Fifteen patients demonstrating unexpected prolonged apnoea lasting several hours after succinylcholine have been treated by a new preparation of human serum cholinesterase. Adequate spontaneous respiration was re-established in an average period of ten minutes after the injection. In 12 patients biochemical genetic examinations confirmed the presence of an atypical serum cholinesterase. In three patients none of the usual variants were found. It is therefore supposed that other unknown variants of serum cholinesterase exist which cannot hydrolyze succinylcholine. The use of serum cholinesterase in succinylcholine apnoea provided considerable relief to both patient and anaesthetist.


Orthostatic hypotension occurs following alpha 2-adrenoceptor blockade in chronic prazosin-pretreated conscious spontaneously hypertensive rats.

A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.


Douglas Brand of Prazosin Hydrochloride Furazosin HCL Minipress Pfizer Pratsiol

A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.


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.


1. Studies were performed to evaluate whether chronic prazosin treatment alters the alpha 2-adrenoceptor function for orthostatic control of arterial blood pressure in conscious spontaneously hypertensive rats (SHR). 2. Conscious SHR (male 300-350 g) were subjected to 90 degrees head-up tilts for 60 s following acute administration of prazosin (0.1 mg kg-1 i.p.) or rauwolscine (3 mg kg-1 i.v.). Orthostatic hypotension was determined by the average decrease (%) in mean arterial pressure (MAP femoral) over the 60-s tilt period. The basal MAP of conscious SHR was reduced to a similar extent by prazosin (-23%(-)-26% MAP) and rauwolscine (-16%(-)-33% MAP). However, the head-up tilt induced orthostatic hypotension in the SHR treated with prazosin (-16% MAP, n = 6), but not in the SHR treated with rauwolscine (less than +2% MAP, n = 6). 3. Conscious SHR were treated for 4 days with prazosin at 2 mg kg-1 day-1 i.p. for chronic alpha 1-adrenoceptor blockade. MAP in conscious SHR after chronic prazosin treatment was 14% lower than in the untreated SHR (n = 8). Head-up tilts in these rats did not produce orthostatic hypotension when performed either prior to or after acute dosing of prazosin (0.1 mg kg-1 i.p.). Conversely, administration of rauwolscine (3 mg kg-1 i.v.) in chronic prazosin treated SHR decreased the basal MAP by 12-31% (n = 4), and subsequent tilts induced further drops of MAP by 19-23% in these rats. 4. The pressor responses and bradycardia to the alpha 1-agonist cirazoline (0.6 and 2 micrograms kg-1 i.v.), the alpha 2-agonist Abbott-53693 (1 and 3 micrograms kg-1 i.v.), and noradrenaline (0.1 and 1.0 micrograms kg-1 i.v.) were determined in conscious SHR with and without chronic prazosin pretreatment. Both the pressor and bradycardia effects of cirazoline were abolished in chronic prazosin treated SHR (n = 4) as compared to the untreated SHR (n = 4). On the other hand, the pressor effects of Abbott-53693 were similar in both groups of SHR, but the accompanying bradycardia was greater in SHR with chronic prazosin treatment than without such treatment. Furthermore, the bradycardia that accompanied the noradrenaline-induced pressor effect in SHR was similar with and without chronic prazosin treatment despite a 47-71% reduction of the pressor effect in chronic alpha 1-receptor blocked SHR.(ABSTRACT TRUNCATED AT 400 WORDS)


Aphrodine Hydrochloride Aphrodyne Aventis Brand of Yohimbine Corynanthine Tartrate Glenwood Kramer Palisades Pluriviron Rauhimbine Rauwolscine Solvay Star StegroPharm Yocon Yohimbin Spiegel Houdé Yohimex

A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.


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.


2-(2'-cyclopropylphenoxymethyl)imidazoline hydrochloride LD 3098 LD-3098 cirazoline monohydrochloride


2-methyl-2,3,3a,4,5,9b-hexahydro-6,7-dihydroxy-1H-benz(e)isoindole A 53693 A-53693


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


Coexistence of cerebral venous sinus and internal carotid artery thrombosis associated with exogenous sex hormones. A case report.

Carotid Artery Thromboses Thrombosis Common External Internal

Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.


A forty-six year-old premenopausal woman developed headache, nausea and vomiting, left hemiparesis and seizure two days after parenteral use of progesterone and estradiol. Diabetes mellitus (DM) was found during admission. Computed tomography showed a hemorrhagic infarct in the right frontal lobe and increased density in the superior sagittal sinus (SSS). Left carotid angiography found occlusion of the left internal carotid artery (ICA). Right carotid angiograms failed to show the SSS and inferior sagittal sinus, suggestive of venous sinus thrombosis. Coexistence of the cerebral artery and the venous sinus occlusion has been described infrequently. In this case, the authors postulate that the use of estradiol and progesterone and the underlying DM increased vascular thrombogenicity, which provided a common denominator for thrombosis of both the ICA and the venous sinus.

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.


An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.


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


Brachial Pareses Paresis Crural Extremity Lower Upper Hemipareses Hemiparesis Monopareses Monoparesis Muscle Muscular

A general term referring to a mild to moderate degree of muscular weakness, occasionally used as a synonym for PARALYSIS (severe or complete loss of motor function). In the older literature, paresis often referred specifically to paretic neurosyphilis (see NEUROSYPHILIS). "General paresis" and "general paralysis" may still carry that connotation. Bilateral lower extremity paresis is referred to as PARAPARESIS.


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."


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

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


17 beta Estradiol Oestradiol beta-Estradiol beta-Oestradiol Aerodiol Estrace Estraderm TTS alpha 17beta Anhydrous Hemihydrate (17 alpha)-Isomer Monohydrate Orion Brand (+-)-Isomer (-)-Isomer (16 alpha,17 beta)-Isomer (17-alpha)-Isomer (8 beta)-(+-)-Isomer (9 beta,17 Monosodium Salt Sodium Estradiol-17 Estradiol-17beta Novartis Pharmaceuticals of Ovocyclin Vivelle

The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.


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


Brain Hemorrhage Cerebral Hemorrhages Parenchymal Cerebrum Intracerebral

Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.


Anterior Choroidal Artery Infarction Cerebral Left Hemisphere Right Infarctions Subcortical Posterior

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


occlusion of the left internal carotid artery

Arterial Obstructive Disease Diseases Occlusive

Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.


Cranial Sinus Thromboses Thrombosis Intracranial Thrombophlebitides Thrombophlebitis Petrous Venous

Formation or presence of a blood clot (THROMBUS) in the CRANIAL SINUSES, large endothelium-lined venous channels situated within the SKULL. Intracranial sinuses, also called cranial venous sinuses, include the superior sagittal, cavernous, lateral, petrous sinuses, and many others. Cranial sinus thrombosis can lead to severe HEADACHE; SEIZURE; and other neurological defects.


Chloroquine related complete heart block with blindness: case report.

Aralen Arechine Arequin Chingamin Chlorochin Chloroquine Sulfate Sulphate Khingamin Nivaquine

The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.


A V Dissociation A-V Dissociations Atrioventricular Auriculo Ventricular Auriculo-Ventricular Block Heart Blocks

Impaired conduction of cardiac impulse that can occur anywhere along the conduction pathway, such as between the SINOATRIAL NODE and the right atrium (SA block) or between atria and ventricles (AV block). Heart blocks can be classified by the duration, frequency, or completeness of conduction block. Reversibility depends on the degree of structural or functional defects.


Acquired Blindness Amauroses Amaurosis Complete Hysterical Legal Monocular Transient

The inability to see or the loss or absence of perception of visual stimuli. This condition may be the result of EYE DISEASES; OPTIC NERVE DISEASES; OPTIC CHIASM diseases; or BRAIN DISEASES affecting the VISUAL PATHWAYS or OCCIPITAL LOBE.


A 27-year old African woman with history of regular chloroquine ingestion presented with progressive deterioration of vision, easy fatiguability, dyspnoea, dizziness progressing to syncopal attacks. Ophthalmological assessment revealed features of chloroquine retinopathy, cardiac assessment revealed features of heart failure and a complete heart block with right bundle branch block pattern. The heart block was treated by pacemaker insertion and the heart failure resolved spontaneously following chloroquine discontinuation. She however remains blind.


Vision considered to be inferior to normal vision as represented by accepted standards of acuity, field of vision, or motility. Low vision generally refers to visual disorders that are caused by diseases that cannot be corrected by refraction (e.g., MACULAR DEGENERATION; RETINITIS PIGMENTOSA; DIABETIC RETINOPATHY, etc.).


The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.


Breath Shortness Shortnesses Breathlessness Breathlessnesses Dyspnea Dyspneas of


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.


Attack Drop Cardiogenic Syncope Syncopes Carotid Sinus Convulsive Deglutitional Attacks Effort Episode Syncopal Fainting Hyperventilation Micturition Postural Presyncope Presyncopes Situational Stokes-Adams Episodes Vertigo Stokes Adams Tussive Vertigos

A transient loss of consciousness and postural tone caused by diminished blood flow to the brain (i.e., BRAIN ISCHEMIA). Presyncope refers to the sensation of lightheadedness and loss of strength that precedes a syncopal event or accompanies an incomplete syncope. (From Adams et al., Principles of Neurology, 6th ed, pp367-9)


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

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


Anterior Fascicular Block Blocks Bundle Branch Bundle-Branch Left Posterior Right

A form of heart block in which the electrical stimulation of HEART VENTRICLES is interrupted at either one of the branches of BUNDLE OF HIS thus preventing the simultaneous depolarization of the two ventricles.


Systemic toxicity and resuscitation in bupivacaine-, levobupivacaine-, or ropivacaine-infused rats.

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.


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


1-propyl-2',6'-pipecoloxylidide AL 381 AL-381 LEA 103 LEA-103 Naropeine Naropin ropivacaine hydrochloride monohydrochloride (S)-isomer


We compared the systemic toxicity of bupivacaine, levobupivacaine, and ropivacaine in anesthetized rats. We also compared the ability to resuscitate rats after lethal doses of these local anesthetics. Bupivacaine, levobupivacaine, or ropivacaine was infused at a rate of 2 mg. kg(-1). min(-1) while electrocardiogram, electroencephalogram, and arterial pressure were continuously monitored. When asystole was recorded, drug infusion was stopped and a resuscitation sequence was begun. Epinephrine 0.01 mg/kg was administered at 1-min intervals while external cardiac compressions were applied. Resuscitation was considered successful when a systolic arterial pressure > or =100 mm Hg was achieved within 5 min. The cumulative doses of levobupivacaine and ropivacaine that produced seizures were similar and were larger than those of bupivacaine. The cumulative doses of levobupivacaine that produced dysrhythmias and asystole were smaller than the corresponding doses of ropivacaine, but they were larger than those of bupivacaine. The number of successful resuscitations did not differ among groups. However, a smaller dose of epinephrine was required in the Ropivacaine group than in the other groups. We conclude that the systemic toxicity of levobupivacaine is intermediate between that of ropivacaine and bupivacaine when administered at the same rate and that ropivacaine-induced cardiac arrest appears to be more susceptible to treatment than that induced by bupivacaine or levobupivacaine.


Arrest Cardiac Cardiopulmonary Heart Asystole Asystoles

Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.


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."


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.


22-oxacalcitriol suppresses secondary hyperparathyroidism without inducing low bone turnover in dogs with renal failure.

1,25-dihydroxy-22-oxavitamin D3 22-oxa-1,25-dihydroxyvitamin 22-oxa-calcitriol 22-oxacalcitriol Oxarol maxacalcitol maxacalcitriol


Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.


Bone Disease Metabolic Diseases Osteopenia Osteopenias


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.


BACKGROUND: Calcitriol therapy suppresses serum levels of parathyroid hormone (PTH) in patients with renal failure but has several drawbacks, including hypercalcemia and/or marked suppression of bone turnover, which may lead to adynamic bone disease. A new vitamin D analogue, 22-oxacalcitriol (OCT), has been shown to have promising characteristics. This study was undertaken to determine the effects of OCT on serum PTH levels and bone turnover in states of normal or impaired renal function. METHODS: Sixty dogs were either nephrectomized (Nx, N = 38) or sham-operated (Sham, N = 22). The animals received supplemental phosphate to enhance PTH secretion. Fourteen weeks after the start of phosphate supplementation, half of the Nx and Sham dogs received doses of OCT (three times per week); the other half were given vehicle for 60 weeks. Thereafter, the treatment modalities for a subset of animals were crossed over for an additional eight months. Biochemical and hormonal indices of calcium and bone metabolism were measured throughout the study, and bone biopsies were done at baseline, 60 weeks after OCT or vehicle treatment, and at the end of the crossover period. RESULTS: In Nx dogs, OCT significantly decreased serum PTH levels soon after the induction of renal insufficiency. In long-standing secondary hyperparathyroidism, OCT (0.03 microg/kg) stabilized serum PTH levels during the first months. Serum PTH levels rose thereafter, but the rise was less pronounced compared with baseline than the rise seen in Nx control. These effects were accompanied by episodes of hypercalcemia and hyperphosphatemia. In animals with normal renal function, OCT induced a transient decrease in serum PTH levels at a dose of 0.1 microg/kg, which was not sustained with lowering of the doses. In Nx dogs, OCT reversed abnormal bone formation, such as woven osteoid and fibrosis, but did not significantly alter the level of bone turnover. In addition, OCT improved mineralization lag time, (that is, the rate at which osteoid mineralizes) in both Nx and Sham dogs. CONCLUSIONS: These results indicate that even though OCT does not completely prevent the occurrence of hypercalcemia in experimental dogs with renal insufficiency, it may be of use in the management of secondary hyperparathyroidism because it does not induce low bone turnover and, therefore, does not increase the risk of adynamic bone disease.

1 alpha 25 dihydroxy 20 epi Vitamin D3 25-dihydroxy-20-epi-Vitamin alpha,25 Dihydroxycholecalciferol Dihydroxyvitamin alpha,25-Dihydroxycholecalciferol alpha,25-Dihydroxyvitamin 1,25 1,25(OH)2-20epi-D3 1,25-Dihydroxycholecalciferol 1,25-Dihydroxyvitamin 1,25-dihydroxy-20-epi-Vitamin 1alpha,25 dihydroxycholecaliferol 20-epi-1alpha,25-dihydroxycholecaliferol Abbott Brand of Calcitriol Alphapharm Bocatriol Calcijex Cryopharma Galderma Gry Jenapharm KyraMed Leo Medice Nefro RenaCare Roche Calcitriol

The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.


Hypercalcemia Hypercalcemias Milk Alkali Syndrome Milk-Alkali

Abnormally high level of calcium in the blood.


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


Pathological processes of the KIDNEY or its component tissues.


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.


A condition of abnormally high level of PHOSPHATES in the blood, usually significantly above the normal range of 0.84-1.58 mmol per liter of serum.


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


Chemotherapy of advanced inoperable non-small cell lung cancer with paclitaxel: a phase II trial.

Carcinoma Non Small Cell Lung Non-Small Non-Small-Cell Carcinomas Cancer Nonsmall

A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.


7 epi Taxol 7-epi-Taxol Anzatax Bris Bristol-Myers Brand of Paclitaxel Squibb Bull Ivax Lemery NSC 125973 NSC-125973 NSC125973 Onxol (4 alpha)-Isomer Paxene Praxel A

A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.


Paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) has demonstrated significant antineoplastic activity against different tumor types, notably ovarian and breast carcinoma. Two phase II trials of 24-hour paclitaxel infusions in chemotherapy-naive patients with stage IIIB or IV non-small cell lung cancer (NSCLC) reported response rates of 21% and 24%. Leukopenia was dose limiting: as many as 62.5% of patients experienced grade 4 leukopenia. We investigated the efficacy and toxicity of a 3-hour paclitaxel infusion in a phase II trial in patients with inoperable stage IIIB or IV NSCLC. The 58 patients treated (41 men and 17 women) had a median age of 59 years (age range, 25 to 75) and a performance status of 0 through 2. Most patients (72.4%) had stage IV NSCLC. Paclitaxel 225 mg/m2 was infused over 3 hours every 3 weeks with standard prophylactic premedication. Of 50 patients evaluable for response, 12 (24%) had partial remission, 26 (52%) had no change, and 12 had disease progression (24%). Hematologic toxicities were mild: only one patient (2%) developed grade 3 or 4 neutropenia, while 29% had grade 1 or 2. Grade 1 or 2 polyneuropathy affected 56% of patients while only one (2%) experienced severe polyneuropathy. Similarly, grade 1 or 2 myalgia/arthralgia was observed in 63.2% of patients, but only 14.3% experienced grade 3 or 4. Nausea and vomiting were infrequent, with 14% of patients experiencing grade 1 or 2 and only 2% experiencing grade 3 or 4. Paclitaxel is thus an active single agent in this patient population, with a 3-hour infusion proving comparably effective to a 24-hour infusion and superior in terms of the incidence of hematologic and nonhematologic toxicity. Further phase II studies with paclitaxel combined with other drugs active against NSCLC are indicated, and phase III studies comparing paclitaxel with standard chemotherapy remain to be completed.


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.


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


Leukocytopenia Leukocytopenias Leukopenia Leukopenias


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 decrease in the number of NEUTROPHILS found in the blood.


Acquired Polyneuropathies Polyneuropathy Critical Illness Familial Inherited Motor

Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.


Muscle Pain Soreness Sorenesses Tenderness Myalgia Pains


Arthralgia Arthralgias Joint Pain Pains Polyarthralgia Polyarthralgias


An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.


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


Cerebral hemorrhage associated with phenylpropanolamine in combination with caffeine.

Brain Hemorrhage Cerebral Hemorrhages Parenchymal Cerebrum Intracerebral

Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.


Dexatrim Hydrochloride Phenylpropanolamine Norephedrine Prolamine Propagest

A sympathomimetic that acts mainly by causing release of NOREPINEPHRINE but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant.


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.


Phenylpropanolamine (PPA) is a drug that has been associated with serious side effects including stroke. It is often combined with caffeine in diet preparations and "look-alike" pills. In order to determine if PPA/caffeine can lead to stroke in normotensive and/or hypertensive rats, we administered the combination in six times the allowed human dose calculated on a per weight basis for the rats two times per day for five days. Subarachnoid and cerebral hemorrhage was noted in 18% of the hypertensive rats. A single PPA/caffeine administration (same dose) lead to acute hypertension in both the normotensive and hypertensive animals. These results suggest that PPA/caffeine can lead to cerebral hemorrhage in previously hypertensive animals when administered in greater than the allowed dosage. An acute elevation in blood pressure may be a contributing factor.


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

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


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.


Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation.


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.


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


A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.


Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.


Arrest Cardiac Cardiopulmonary Heart Asystole Asystoles

Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.


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.


Appendicular Ataxia Ataxias Limb Motor Sensory Truncal Ataxy Coordination Impairment Impairments Lack Dyscoordination Dyssynergia Incoordination Incoordinations of Rubral Tremor Tremors

Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.


The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.


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).


Pathological processes involving the THYROID GLAND.


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.


Effect of calcium chloride and 4-aminopyridine therapy on desipramine toxicity in rats.

A salt used to replenish calcium levels, as an acid-producing diuretic, and as an antidote for magnesium poisoning.


4 Aminopyridine Sustained Release 4-Aminopyridine Fampridine SR Fampridine-SR Pymadine VMI 103 VMI-103 VMI103

One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.


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

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