Input: Learning and memory deficits in ecstasy users and their neural correlates during a face - learning task. It has been consistently shown that ecstasy users display impairments in learning and memory performance. In addition, working memory processing in ecstasy users has been shown to be associated with neural alterations in hippocampal and / or cortical regions as measured by functional magnetic resonance imaging (fMRI). Using functional imaging and a face - learning task, we investigated neural correlates of encoding and recalling face - name associations in 20 recreational drug users whose predominant drug use was ecstasy and 20 controls. To address the potential confounding effects of the cannabis use of the ecstasy using group, a second analysis included 14 previously tested cannabis users (Nestor, L., Roberts, G., Garavan, H., Hester, R., 2008. Deficits in learning and memory: parahippocampal hyperactivity and frontocortical hypoactivity in cannabis users. Neuroimage 40, 1328 - 1339). Ecstasy users performed significantly worse in learning and memory compared to controls and cannabis users. A conjunction analysis of the encode and recall phases of the task revealed ecstasy - specific hyperactivity in bilateral frontal regions, left temporal, right parietal, bilateral temporal, and bilateral occipital brain regions. Ecstasy - specific hypoactivity was evident in the right dorsal anterior cingulated cortex (ACC) and left posterior cingulated cortex. In both ecstasy and cannabis groups brain activation was decreased in the right medial frontal gyrus, left parahippocampal gyrus, left dorsal cingulate gyrus, and left caudate. These results elucidated ecstasy - related deficits, only some of which might be attributed to cannabis use. These ecstasy - specific effects may be related to the vulnerability of isocortical and allocortical regions to the neurotoxic effects of ecstasy.

Learning and memory deficits

Learning and memory deficits

memory deficits

impairments in learning and memory

impairments in learning

impairments in learning and memory

Deficits in learning and memory

Deficits in learning

Deficits in learning and memory

hyperactivity

hyperactivity

neurotoxic

ecstasy

ecstasy

ecstasy

ecstasy

cannabis

ecstasy

cannabis

cannabis

Ecstasy

cannabis

ecstasy

Ecstasy

ecstasy

cannabis

ecstasy

cannabis

ecstasy

ecstasy

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

Ecstasy

Learning and memory deficits

Ecstasy

memory deficits

Ecstasy

impairments in learning and memory

Ecstasy

impairments in learning and memory

Ecstasy

Deficits in learning and memory

Ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

Ecstasy

Learning and memory deficits

Ecstasy

memory deficits

Ecstasy

impairments in learning and memory

Ecstasy

impairments in learning and memory

Ecstasy

Deficits in learning and memory

Ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

memory deficits

ecstasy

impairments in learning and memory

ecstasy

impairments in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Deficits in learning and memory

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

Ecstasy

Learning and memory deficits

Ecstasy

impairments in learning

Ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

Ecstasy

Learning and memory deficits

Ecstasy

impairments in learning

Ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning

ecstasy

Learning and memory deficits

ecstasy

impairments in learning

ecstasy

Deficits in learning


Input: Prolonged elevation of plasma argatroban in a cardiac transplant patient with a suspected history of heparin - induced thrombocytopenia with thrombosis. BACKGROUND: Direct thrombin inhibitors (DTIs) provide an alternative method of anticoagulation for patients with a history of heparin - induced thrombocytopenia (HIT) or HIT with thrombosis (HITT) undergoing cardiopulmonary bypass (CPB). In the following report, a 65 - year - old critically ill patient with a suspected history of HITT was administered argatroban for anticoagulation on bypass during heart transplantation. The patient required massive transfusion support (55 units of red blood cells, 42 units of fresh - frozen plasma, 40 units of cryoprecipitate, 40 units of platelets, and three doses of recombinant Factor VIIa) for severe intraoperative and postoperative bleeding. STUDY DESIGN AND METHODS: Plasma samples from before and after CPB were analyzed postoperatively for argatroban concentration using a modified ecarin clotting time (ECT) assay. RESULTS: Unexpectedly high concentrations of argatroban were measured in these samples (range, 0 - 32 microg / mL), and a prolonged plasma argatroban half life (t (1 / 2)) of 514 minutes was observed (published elimination t (1 / 2) is 39 - 51 minutes [< or = 181 minutes with hepatic impairment]). CONCLUSIONS: Correlation of plasma argatroban concentration versus the patient' s coagulation variables and clinical course suggest that prolonged elevated levels of plasma argatroban may have contributed to the patient' s extended coagulopathy. Because DTIs do not have reversal agents, surgical teams and transfusion services should remain aware of the possibility of massive transfusion events during anticoagulation with these agents. This is the first report to measure plasma argatroban concentration in the context of CPB and extended coagulopathy.

argatroban

heparin

heparin

argatroban

argatroban

argatroban

argatroban

argatroban

argatroban

argatroban

thrombocytopenia

thrombosis

thrombocytopenia

HIT

HIT

thrombosis

HITT

critically ill

HITT

intraoperative and postoperative bleeding

intraoperative and postoperative bleeding

postoperative bleeding

hepatic impairment

coagulopathy

coagulopathy

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

intraoperative and postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding

argatroban

postoperative bleeding


Input: Antituberculosis therapy - induced acute liver failure: magnitude, profile, prognosis, and predictors of outcome. Antituberculosis therapy (ATT) - associated acute liver failure (ATT - ALF) is the commonest drug - induced ALF in South Asia. Prospective studies on ATT - ALF are lacking. The current study prospectively evaluated the magnitude, clinical course, outcome, and prognostic factors in ATT - ALF. From January 1986 to January 2009, 1223 consecutive ALF patients were evaluated: ATT alone was the cause in 70 (5. 7%) patients. Another 15 (1. 2%) had ATT and simultaneous hepatitis virus infection. In 44 (62. 8%) patients, ATT was prescribed empirically without definitive evidence of tuberculosis. ATT - ALF patients were younger (32. 87 [+ / - 15. 8] years), and 49 (70%) of them were women. Most had hyperacute presentation; the median icterus encephalopathy interval was 4. 5 (0 - 30) days. The median duration of ATT before ALF was 30 (7 - 350) days. At presentation, advanced encephalopathy and cerebral edema were present in 51 (76%) and 29 (41. 4%) patients, respectively. Gastrointestinal bleed, seizures, infection, and acute renal failure were documented in seven (10%), five (7. 1%), 26 (37. 1%), and seven (10%) patients, respectively. Compared with hepatitis E virus (HEV) and non - A non - E - induced ALF, ATT - ALF patients had nearly similar presentations except for older age and less elevation of liver enzymes. The mortality rate among patients with ATT - ALF was high (67. 1%, n = 47), and only 23 (32. 9%) patients recovered with medical treatment. In multivariate analysis, three factors independently predicted mortality: serum bilirubin (> or = 10. 8 mg / dL), prothrombin time (PT) prolongation (> or = 26 seconds), and grade III / IV encephalopathy at presentation. CONCLUSION: ATT - ALF constituted 5. 7% of ALF at our center and had a high mortality rate. Because the mortality rate is so high, determining which factors are predictors is less important. A high proportion of patients had consumed ATT empirically, which could have been prevented.

Antituberculosis

Antituberculosis

bilirubin

acute liver failure

acute liver failure

ALF

ALF

ALF

ALF

ALF

hepatitis virus infection

tuberculosis

ALF

icterus

encephalopathy

ALF

encephalopathy

cerebral edema

Gastrointestinal bleed

seizures

infection

acute renal failure

hepatitis E

ALF

ALF

ALF

encephalopathy

ALF

ALF

Antituberculosis

acute liver failure

Antituberculosis

acute liver failure

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

acute liver failure

Antituberculosis

acute liver failure

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF

Antituberculosis

ALF


Input: Central nervous system complications during treatment of acute lymphoblastic leukemia in a single pediatric institution. Central nervous system (CNS) complications during treatment of childhood acute lymphoblastic leukemia (ALL) remain a challenging clinical problem. Outcome improvement with more intensive chemotherapy has significantly increased the incidence and severity of adverse events. This study analyzed the incidence of neurological complications during ALL treatment in a single pediatric institution, focusing on clinical, radiological, and electrophysiological findings. Exclusion criteria included CNS leukemic infiltration at diagnosis, therapy - related peripheral neuropathy, late - onset encephalopathy, or long - term neurocognitive defects. During a 9 - year period, we retrospectively collected 27 neurological events (11%) in as many patients, from 253 children enrolled in the ALL front - line protocol. CNS complications included posterior reversible leukoencephalopathy syndrome (n = 10), stroke (n = 5), temporal lobe epilepsy (n = 2), high - dose methotrexate toxicity (n = 2), syndrome of inappropriate antidiuretic hormone secretion (n = 1), and other unclassified events (n = 7). In conclusion, CNS complications are frequent events during ALL therapy, and require rapid detection and prompt treatment to limit permanent damage.

Central nervous system complications

acute lymphoblastic leukemia

Central nervous system (CNS) complications

acute lymphoblastic leukemia

ALL

neurological complications

ALL

leukemic infiltration

peripheral neuropathy

encephalopathy

neurocognitive defects

ALL

leukoencephalopathy

stroke

temporal lobe epilepsy

toxicity

inappropriate antidiuretic hormone secretion

ALL

methotrexate

methotrexate

Central nervous system complications

methotrexate

Central nervous system (CNS) complications

methotrexate

neurological complications

methotrexate

neurocognitive defects


Input: Safety of capecitabine: a review. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5 - fluorouracil (5 - FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5 - FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety / efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand - foot syndrome. Capecitabine has a well - established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions.

capecitabine

Fluoropyrimidines

5 - fluorouracil

5 - FU

capecitabine

capecitabine

capecitabine

Capecitabine

5 - FU

capecitabine

Capecitabine

tumors

colorectal, breast and head and neck cancers

colorectal, breast and head and neck cancers

breast and head and neck cancers

head and neck cancers

renal and kidney disease

colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers

colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers

breast, pancreaticobiliary, gastric, renal cell and head and neck cancers

pancreaticobiliary, gastric, renal cell and head and neck cancers

gastric, renal cell and head and neck cancers

renal cell and head and neck cancers

head and neck cancers

diarrhea

nausea

vomiting

stomatitis

hand - foot syndrome

hepatic and renal dysfunctions

hepatic and renal dysfunctions

renal dysfunctions

capecitabine

hand - foot syndrome

capecitabine

hand - foot syndrome

capecitabine

hand - foot syndrome

capecitabine

hand - foot syndrome

Capecitabine

hand - foot syndrome

capecitabine

hand - foot syndrome

Capecitabine

hand - foot syndrome

capecitabine

stomatitis

capecitabine

stomatitis

capecitabine

stomatitis

capecitabine

stomatitis

Capecitabine

stomatitis

capecitabine

stomatitis

Capecitabine

stomatitis

capecitabine

vomiting

capecitabine

vomiting

capecitabine

vomiting

capecitabine

vomiting

Capecitabine

vomiting

capecitabine

vomiting

Capecitabine

vomiting

capecitabine

diarrhea

capecitabine

diarrhea

capecitabine

diarrhea

capecitabine

diarrhea

Capecitabine

diarrhea

capecitabine

diarrhea

Capecitabine

diarrhea

capecitabine

nausea

capecitabine

nausea

capecitabine

nausea

capecitabine

nausea

Capecitabine

nausea

capecitabine

nausea

Capecitabine

nausea


Input: Effects of pallidal neurotensin on haloperidol - induced parkinsonian catalepsy: behavioral and electrophysiological studies. OBJECTIVE: The globus pallidus plays a critical role in movement regulation. Previous studies have indicated that the globus pallidus receives neurotensinergic innervation from the striatum, and systemic administration of a neurotensin analog could produce antiparkinsonian effects. The present study aimed to investigate the effects of pallidal neurotensin on haloperidol - induced parkinsonian symptoms. METHODS: Behavioral experiments and electrophysiological recordings were performed in the present study. RESULTS: Bilateral infusions of neurotensin into the globus pallidus reversed haloperidol - induced parkinsonian catalepsy in rats. Electrophysiological recordings showed that microinjection of neurotensin induced excitation of pallidal neurons in the presence of systemic haloperidol administration. The neurotensin type - 1 receptor antagonist SR48692 blocked both the behavioral and the electrophysiological effects induced by neurotensin. CONCLUSION: Activation of pallidal neurotensin receptors may be involved in neurotensin - induced antiparkinsonian effects.

neurotensin

haloperidol

neurotensin

neurotensin

haloperidol

neurotensin

haloperidol

neurotensin

haloperidol

neurotensin type - 1 receptor antagonist

neurotensin

neurotensin

neurotensin

parkinsonian catalepsy

parkinsonian symptoms

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy

haloperidol

parkinsonian catalepsy


Input: Antihypertensive drugs and depression: a reappraisal. Eighty - nine new referral hypertensive out - patients and 46 new referral non - hypertensive chronically physically ill out - patients completed a mood rating scale at regular intervals for one year. The results showed a high prevalence of depression in both groups of patients, with no preponderance in the hypertensive group. Hypertensive patients with psychiatric histories had a higher prevalence of depression than the comparison patients. This was accounted for by a significant number of depressions occurring in methyl dopa treated patients with psychiatric histories.

depression

hypertensive

hypertensive

depression

hypertensive

Hypertensive

psychiatric

depression

depressions

psychiatric

methyl dopa

methyl dopa

depression

methyl dopa

depression

methyl dopa

depression

methyl dopa

depressions


Input: Pulmonary shunt and cardiovascular responses to CPAP during nitroprusside - induced hypotension. The effects of continuous positive airway pressure (CPAP) on cardiovascular dynamics and pulmonary shunt (QS / QT) were investigated in 12 dogs before and during sodium nitroprusside infusion that decreased mean arterial blood pressure 40 - 50 per cent. Before nitroprusside infusion, 5 cm H2O CPAP significantly, P less than. 05, decreased arterial blood pressure, but did not significantly alter heart rate, cardiac output, systemic vascular resistance, or QS / QT. Ten cm H2O CPAP before nitroprusside infusion produced a further decrease in arterial blood pressure and significantly increased heart rate and decreased cardiac output and QS / QT. Nitroprusside caused significant decreases in arterial blood pressure and systemic vascular resistance and increases in heart rate, but did not change cardiac output or QS / QT. Five cm H2O CPAP during nitroprusside did not further alter any of the above - mentioned variables. However, 10 cm H2O CPAP decreased arterial blood pressure, cardiac output, and QS / QT. These data indicate that nitroprusside infusion rates that decrease mean arterial blood pressure by 40 - 50 per cent do not change cardiac output or QS / QT. During nitroprusside infusion low levels of CPAP do not markedly alter cardiovascular dynamics, but high levels of CPAP (10 cm H2O), while decreasing QS / QT, produce marked decreases in arterial blood pressure and cardiac output.

nitroprusside

sodium nitroprusside

nitroprusside

nitroprusside

Nitroprusside

nitroprusside

nitroprusside

nitroprusside

hypotension

decrease in arterial blood pressure

decreased cardiac output

decreases in arterial blood pressure

decreases in arterial blood pressure and cardiac output

decreases in arterial blood pressure

decreases in arterial blood pressure and cardiac output

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure

sodium nitroprusside

hypotension

sodium nitroprusside

decrease in arterial blood pressure

sodium nitroprusside

decreases in arterial blood pressure

sodium nitroprusside

decreases in arterial blood pressure and cardiac output

sodium nitroprusside

decreases in arterial blood pressure

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure

Nitroprusside

hypotension

Nitroprusside

decrease in arterial blood pressure

Nitroprusside

decreases in arterial blood pressure

Nitroprusside

decreases in arterial blood pressure and cardiac output

Nitroprusside

decreases in arterial blood pressure

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure

nitroprusside

hypotension

nitroprusside

decrease in arterial blood pressure

nitroprusside

decreases in arterial blood pressure

nitroprusside

decreases in arterial blood pressure and cardiac output

nitroprusside

decreases in arterial blood pressure


Input: Mediation of enhanced reflex vagal bradycardia by L - dopa via central dopamine formation in dogs. L - Dopa (5 mg / kg i. v.) decreased blood pressure and heart rate after extracerebral decarboxylase inhibition with MK - 486 (25 mg / kg i. v.) in anesthetize MAO - inhibited dogs. In addition, reflex bradycardia caused by injected norepinephrine was significantly enhanced by L - dopa, DL - Threo - dihydroxyphenylserine had no effect on blood pressure, heart rate or reflex responses to norepinephrine. FLA - 63, a dopamine - beta - oxidase inhibitor, did not have any effect on the hypotension, bradycardia or reflex - enhancing effect of L - dopa. Pimozide did not affect the actions of L - dopa on blood pressure and heart rate but completely blocked the enhancement of reflexes. Removal of the carotid sinuses caused an elevation blood pressure and heart rate and abolished the negative chronotropic effect of norepinephrine. However, L - dopa restored the bradycardia caused by norepinephrine in addition to decreasing blood pressure and heart rate. 5 - HTP (5 mg / kg i. v.) decreased blood pressure and heart rate and decreased the reflex bradycardia to norepinephrine. It is concluded that L - dopa enhances reflex bradycardia through central alpha - receptor stimulation. Furthermore, the effects are mediated through dopamine rather than norepinephrine and do not require the carotid sinus baroreceptors.

bradycardia

bradycardia

hypotension

bradycardia

bradycardia

bradycardia

bradycardia

L - dopa

dopamine

L - Dopa

MK - 486

MAO

norepinephrine

L - dopa

DL - Threo - dihydroxyphenylserine

norepinephrine

FLA - 63

dopamine

L - dopa

Pimozide

L - dopa

norepinephrine

L - dopa

norepinephrine

5 - HTP

norepinephrine

L - dopa

dopamine

norepinephrine

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia

norepinephrine

bradycardia


Input: Cocaine - induced myocardial infarction: clinical observations and pathogenetic considerations. Clinical and experimental data published to date suggest several possible mechanisms by which cocaine may result in acute myocardial infarction. In individuals with preexisting, high - grade coronary arterial narrowing, acute myocardial infarction may result from an increase in myocardial oxygen demand associated with cocaine - induced increase in rate - pressure product. In other individuals with no underlying atherosclerotic obstruction, coronary occlusion may be due to spasm, thrombus, or both. With regard to spasm, the clinical findings are largely circumstantial, and the locus of cocaine - induced vasoconstriction remains speculative. Although certain clinical and experimental findings support the hypothesis that spasm involves the epicardial, medium - size vessels, other data suggest intramural vasoconstriction. Diffuse intramural vasoconstriction is not consistent with reports of segmental, discrete infarction. Whereas certain in vivo data suggest that these effects are alpha - mediated, other in vitro data suggest the opposite. The finding of cocaine - induced vasoconstriction in segments of (noninnervated) human umbilical artery suggests that the presence or absence of intact innervation is not sufficient to explain the discrepant data involving the possibility of alpha - mediated effects. Finally, the contribution of a primary, thrombotic effect of cocaine has not been excluded.

Cocaine

cocaine

oxygen

cocaine

cocaine

cocaine

cocaine

myocardial infarction

acute myocardial infarction

acute myocardial infarction

atherosclerotic obstruction

coronary occlusion

spasm

thrombus

spasm

spasm

infarction

thrombotic

Cocaine

myocardial infarction

Cocaine

acute myocardial infarction

Cocaine

acute myocardial infarction

cocaine

myocardial infarction

cocaine

acute myocardial infarction

cocaine

acute myocardial infarction

cocaine

myocardial infarction

cocaine

acute myocardial infarction

cocaine

acute myocardial infarction

cocaine

myocardial infarction

cocaine

acute myocardial infarction

cocaine

acute myocardial infarction

cocaine

myocardial infarction

cocaine

acute myocardial infarction

cocaine

acute myocardial infarction

cocaine

myocardial infarction

cocaine

acute myocardial infarction

cocaine

acute myocardial infarction


Input: Rabbit syndrome, antidepressant use, and cerebral perfusion SPECT scan findings. The rabbit syndrome is an extrapyramidal side effect associated with chronic neuroleptic therapy. Its occurrence in a patient being treated with imipramine is described, representing the first reported case of this syndrome in conjunction with antidepressants. Repeated cerebral perfusion SPECT scans revealed decreased basal ganglia perfusion while the movement disorder was present, and a return to normal perfusion when the rabbit syndrome resolved.

Rabbit syndrome

rabbit syndrome

decreased basal ganglia perfusion

movement disorder

rabbit syndrome

antidepressant

imipramine

antidepressants

imipramine

Rabbit syndrome

imipramine

rabbit syndrome

imipramine

decreased basal ganglia perfusion

imipramine

rabbit syndrome


Input: Acute bronchodilating effects of ipratropium bromide and theophylline in chronic obstructive pulmonary disease. The bronchodilator effects of a single dose of ipratropium bromide aerosol (36 micrograms) and short - acting theophylline tablets (dose titrated to produce serum levels of 10 - 20 micrograms / mL) were compared in a double - blind, placebo - controlled crossover study in 21 patients with stable, chronic obstructive pulmonary disease. Mean peak forced expiratory volume in 1 second (FEV1) increases over baseline and the proportion of patients attaining at least a 15% increase in the FEV1 (responders) were 31% and 90%, respectively, for ipratropium and 17% and 50%, respectively, for theophylline. The average FEV1 increases during the 6 - hour observation period were 18% for ipratropium and 8% for theophylline. The mean duration of action was 3. 8 hours with ipratropium and 2. 4 hours with theophylline. While side effects were rare, those experienced after theophylline use did involve the cardiovascular and gastrointestinal systems. These results show that ipratropium is a more potent bronchodilator than oral theophylline in patients with chronic airflow obstruction.

ipratropium bromide

theophylline

ipratropium bromide

theophylline

ipratropium

theophylline

ipratropium

theophylline

ipratropium

theophylline

theophylline

ipratropium

theophylline

chronic obstructive pulmonary disease

chronic obstructive pulmonary disease

cardiovascular and gastrointestinal systems

cardiovascular and gastrointestinal systems

gastrointestinal systems

chronic airflow obstruction

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

cardiovascular and gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems

theophylline

gastrointestinal systems


Input: Irreversible damage to the medullary interstitium in experimental analgesic nephropathy in F344 rats. Renal papillary necrosis (RPN) and a decreased urinary concentrating ability developed during continuous long - term treatment with aspirin and paracetamol in female Fischer 344 rats. Renal structure and concentrating ability were examined after a recovery period of up to 18 weeks, when no analgesics were given, to investigate whether the analgesic - induced changes were reversible. There was no evidence of repair to the damaged medullary interstitial matrix, or proliferation of remaining undamaged type 1 medullary interstitial cells after the recovery period following analgesic treatment. The recovery of urinary concentrating ability was related to the length of analgesic treatment and the extent of the resulting inner medullary structural damage. During the early stages of analgesic treatment, the changes in urinary concentrating ability were reversible, but after prolonged analgesic treatment, maximum urinary concentrating ability failed to recover. This study shows that prolonged analgesic treatment in Fischer 344 rats causes progressive and irreversible damage to the interstitial matrix and type 1 interstitial cells leading to RPN. The associated urinary concentrating defect is reversible only during the early stages of structural damage to the inner medulla.

nephropathy

Renal papillary necrosis

RPN

RPN

aspirin

paracetamol

paracetamol

Renal papillary necrosis

paracetamol

RPN

paracetamol

RPN

aspirin

Renal papillary necrosis

aspirin

RPN

aspirin

RPN


Input: Less frequent lithium administration and lower urine volume. OBJECTIVE: This study was designed to determine whether patients maintained on a regimen of lithium on a once - per - day schedule have lower urine volumes than do patients receiving multiple doses per day. METHOD: This was a cross - sectional study of 85 patients from a lithium clinic who received different dose schedules. Patients were admitted to the hospital for measurement of lithium level, creatinine clearance, urine volume, and maximum osmolality. RESULTS: Multiple daily doses of lithium were associated with higher urine volumes. The dosing schedule, duration of lithium treatment, and daily dose of lithium did not affect maximum osmolality or creatinine clearance. CONCLUSIONS: Urine volume can be reduced by giving lithium once daily and / or by lowering the total daily dose. Lithium - induced polyuria seems to be related to extrarenal as well as to renal effects.

lithium

lithium

lithium

lithium

creatinine

lithium

lithium

lithium

creatinine

lithium

Lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

lithium

polyuria

Lithium

polyuria


Input: Effect of adriamycin combined with whole body hyperthermia on tumor and normal tissues. Thermal enhancement of Adriamycin - mediated antitumor activity and normal tissue toxicities by whole body hyperthermia were compared using a F344 rat model. Antitumor activity was studied using a tumor growth delay assay. Acute normal tissue toxicities (i. e., leukopenia and thrombocytopenia) and late normal tissue toxicities (i. e., myocardial and kidney injury) were evaluated by functional / physiological assays and by morphological techniques. Whole body hyperthermia (120 min at 41. 5 degrees C) enhanced both Adriamycin - mediated antitumor activity and toxic side effects. The thermal enhancement ratio calculated for antitumor activity was 1. 6. Thermal enhancement ratios estimated for " acute " hematological changes were 1. 3, whereas those estimated for " late " damage (based on morphological cardiac and renal lesions) varied between 2. 4 and 4. 3. Thus, while whole body hyperthermia enhances Adriamycin - mediated antitumor effect, normal tissue toxicity is also increased, and the potential therapeutic gain of the combined modality treatment is eroded.

adriamycin

Adriamycin

Adriamycin

Adriamycin

hyperthermia

tumor

toxicities

hyperthermia

tumor

toxicities

leukopenia

thrombocytopenia

toxicities

myocardial and kidney injury

myocardial and kidney injury

kidney injury

hyperthermia

cardiac and renal lesions

cardiac and renal lesions

renal lesions

hyperthermia

toxicity

adriamycin

myocardial and kidney injury

adriamycin

myocardial and kidney injury

adriamycin

cardiac and renal lesions

adriamycin

cardiac and renal lesions

Adriamycin

myocardial and kidney injury

Adriamycin

myocardial and kidney injury

Adriamycin

cardiac and renal lesions

Adriamycin

cardiac and renal lesions

Adriamycin

myocardial and kidney injury

Adriamycin

myocardial and kidney injury

Adriamycin

cardiac and renal lesions

Adriamycin

cardiac and renal lesions

Adriamycin

myocardial and kidney injury

Adriamycin

myocardial and kidney injury

Adriamycin

cardiac and renal lesions

Adriamycin

cardiac and renal lesions


Input: Prazosin - induced stress incontinence. A case of genuine stress incontinence due to prazosin, a common antihypertensive drug, is presented. Prazosin exerts its antihypertensive effects through vasodilatation caused by selective blockade of postsynaptic alpha - 1 adrenergic receptors. As an alpha - blocker, it also exerts a significant relaxant effect on the bladder neck and urethra. The patient' s clinical course is described and correlated with initial urodynamic studies while on prazosin and subsequent studies while taking verapamil. Her incontinence resolved with the change of medication. The restoration of continence was accompanied by a substantial rise in maximum urethral pressure, maximum urethral closure pressure, and functional urethral length. Patients who present with stress incontinence while taking prazosin should change their antihypertensive medication before considering surgery, because their incontinence may resolve spontaneously with a change in drug therapy.

Prazosin

prazosin

Prazosin

prazosin

verapamil

prazosin

stress incontinence

stress incontinence

incontinence

stress incontinence

incontinence

Prazosin

stress incontinence

Prazosin

stress incontinence

Prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

Prazosin

stress incontinence

Prazosin

stress incontinence

Prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence

prazosin

stress incontinence


Input: Myocardial infarction following sublingual administration of isosorbide dinitrate. A 78 - year - old with healed septal necrosis suffered a recurrent myocardial infarction of the anterior wall following the administration of isosorbide dinitrate 5 mg sublingually. After detailing the course of events, we discuss the role of paradoxical coronary spasm and hypotension - mediated myocardial ischemia occurring downstream to significant coronary arterial stenosis in the pathophysiology of acute coronary insufficiency.

Myocardial infarction

necrosis

myocardial infarction

spasm

hypotension

myocardial ischemia

coronary arterial stenosis

acute coronary insufficiency

isosorbide dinitrate

isosorbide dinitrate

isosorbide dinitrate

Myocardial infarction

isosorbide dinitrate

myocardial infarction

isosorbide dinitrate

Myocardial infarction

isosorbide dinitrate

myocardial infarction


Input: Fluoxetine - induced akathisia: clinical and theoretical implications. Five patients receiving fluoxetine for the treatment of obsessive compulsive disorder or major depression developed akathisia. The typical fluoxetine - induced symptoms of restlessness, constant pacing, purposeless movements of the feet and legs, and marked anxiety were indistinguishable from those of neuroleptic - induced akathisia. Three patients who had experienced neuroleptic - induced akathisia in the past reported that the symptoms of fluoxetine - induced akathisia were identical, although somewhat milder. Akathisia appeared to be a common side effect of fluoxetine and generally responded well to treatment with the beta - adrenergic antagonist propranolol, dose reduction, or both. The authors suggest that fluoxetine - induced akathisia may be caused by serotonergically mediated inhibition of dopaminergic neurotransmission and that the pathophysiology of fluoxetine - induced akathisia and tricyclic antidepressant - induced " jitteriness " may be identical.

Fluoxetine

fluoxetine

fluoxetine

fluoxetine

fluoxetine

propranolol

fluoxetine

fluoxetine

antidepressant

akathisia

obsessive compulsive disorder

major depression

akathisia

anxiety

akathisia

akathisia

akathisia

Akathisia

akathisia

akathisia

Fluoxetine

akathisia

Fluoxetine

akathisia

Fluoxetine

akathisia

Fluoxetine

akathisia

Fluoxetine

akathisia

Fluoxetine

Akathisia

Fluoxetine

akathisia

Fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

akathisia

fluoxetine

Akathisia

fluoxetine

akathisia

fluoxetine

akathisia


Input: Chronic active hepatitis associated with diclofenac sodium therapy. Diclofenac sodium (Voltarol, Geigy Pharmaceuticals) is a non - steroidal anti - inflammatory derivative of phenylacetic acid. Although generally well - tolerated, asymptomatic abnormalities of liver function have been recorded and, less commonly, severe hepatitis induced by diclofenac. The patient described developed chronic active hepatitis after six months therapy with diclofenac sodium which progressed despite the withdrawal of the drug, a finding not previously reported.

Chronic active hepatitis

abnormalities of liver function

hepatitis

chronic active hepatitis

diclofenac sodium

Diclofenac sodium

Voltarol

phenylacetic acid

diclofenac

diclofenac sodium

diclofenac sodium

abnormalities of liver function

diclofenac sodium

hepatitis

Diclofenac sodium

abnormalities of liver function

Diclofenac sodium

hepatitis

Voltarol

abnormalities of liver function

Voltarol

hepatitis

diclofenac

abnormalities of liver function

diclofenac

hepatitis

diclofenac sodium

abnormalities of liver function

diclofenac sodium

hepatitis


Input: Stroke associated with cocaine use. We describe eight patients in whom cocaine use was related to stroke and review 39 cases from the literature. Among these 47 patients the mean (+ / - SD) age was 32. 5 + / - 12. 1 years; 76% (34 / 45) were men. Stroke followed cocaine use by inhalation, intranasal, intravenous, and intramuscular routes. Intracranial aneurysms or arteriovenous malformations were present in 17 of 32 patients studied angiographically or at autopsy; cerebral vasculitis was present in two patients. Cerebral infarction occurred in 10 patients (22%), intracerebral hemorrhage in 22 (49%), and subarachnoid hemorrhage in 13 (29%). These data indicate that (1) the apparent incidence of stroke related to cocaine use is increasing; (2) cocaine - associated stroke occurs primarily in young adults; (3) stroke may follow any route of cocaine administration; (4) stroke after cocaine use is frequently associated with intracranial aneurysms and arteriovenous malformations; and (5) in cocaine - associated stroke, the frequency of intracranial hemorrhage exceeds that of cerebral infarction.

Stroke

stroke

Stroke

Intracranial aneurysms

arteriovenous malformations

cerebral vasculitis

Cerebral infarction

intracerebral hemorrhage

subarachnoid hemorrhage

stroke

stroke

stroke

stroke

intracranial aneurysms

arteriovenous malformations

stroke

intracranial hemorrhage

cerebral infarction

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

intracerebral hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

subarachnoid hemorrhage

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction

cocaine

Cerebral infarction

cocaine

cerebral infarction


Input: Glyburide - induced hepatitis. Drug - induced hepatotoxicity, although common, has been reported only infrequently with sulfonylureas. For glyburide, a second - generation sulfonylurea, only two brief reports of hepatotoxicity exist. Two patients with type II diabetes mellitus developed an acute hepatitis - like syndrome soon after initiation of glyburide therapy. There was no serologic evidence of viral infection, and a liver biopsy sample showed a histologic pattern consistent with drug - induced hepatitis. Both patients recovered quickly after stopping glyburide therapy and have remained well for a follow - up period of 1 year. Glyburide can produce an acute hepatitis - like illness in some persons.

Glyburide

sulfonylureas

glyburide

sulfonylurea

glyburide

glyburide

Glyburide

hepatitis

hepatotoxicity

hepatotoxicity

type II diabetes mellitus

acute hepatitis - like syndrome

viral infection

drug - induced hepatitis

acute hepatitis - like illness

Glyburide

hepatitis

Glyburide

hepatotoxicity

Glyburide

hepatotoxicity

Glyburide

acute hepatitis - like syndrome

Glyburide

drug - induced hepatitis

Glyburide

acute hepatitis - like illness

glyburide

hepatitis

glyburide

hepatotoxicity

glyburide

hepatotoxicity

glyburide

acute hepatitis - like syndrome

glyburide

drug - induced hepatitis

glyburide

acute hepatitis - like illness

glyburide

hepatitis

glyburide

hepatotoxicity

glyburide

hepatotoxicity

glyburide

acute hepatitis - like syndrome

glyburide

drug - induced hepatitis

glyburide

acute hepatitis - like illness

glyburide

hepatitis

glyburide

hepatotoxicity

glyburide

hepatotoxicity

glyburide

acute hepatitis - like syndrome

glyburide

drug - induced hepatitis

glyburide

acute hepatitis - like illness

Glyburide

hepatitis

Glyburide

hepatotoxicity

Glyburide

hepatotoxicity

Glyburide

acute hepatitis - like syndrome

Glyburide

drug - induced hepatitis

Glyburide

acute hepatitis - like illness


Input: Systolic pressure variation is greater during hemorrhage than during sodium nitroprusside - induced hypotension in ventilated dogs. The systolic pressure variation (SPV), which is the difference between the maximal and minimal values of the systolic blood pressure (SBP) after one positive - pressure breath, was studied in ventilated dogs subjected to hypotension. Mean arterial pressure was decreased to 50 mm Hg for 30 minutes either by hemorrhage (HEM, n = 7) or by continuous infusion of sodium nitroprusside (SNP, n = 7). During HEM - induced hypotension the cardiac output was significantly lower and systemic vascular resistance higher compared with that in the SNP group. The systemic, central venous, pulmonary capillary wedge pressures, and heart rates, were similar in the two groups. Analysis of the respiratory changes in the arterial pressure waveform enabled differentiation between the two groups. The SPV during hypotension was 15. 7 + / - 6. 7 mm Hg in the HEM group, compared with 9. 1 + / - 2. 0 mm Hg in the SNP group (P less than 0. 02). The delta down, which is the measure of decrease of SBP after a mechanical breath, was 20. 3 + / - 8. 4 and 10. 1 + / - 3. 8 mm Hg in the HEM and SNP groups, respectively, during hypotension (P less than 0. 02). It is concluded that increases in the SPV and the delta down are characteristic of a hypotensive state due to a predominant decrease in preload. They are thus more important during absolute hypovolemia than during deliberate hypotension.

hemorrhage

hypotension

hypotension

hemorrhage

HEM

HEM

hypotension

hypotension

HEM

HEM

hypotension

hypotensive

hypovolemia

hypotension

sodium nitroprusside

sodium nitroprusside

SNP

SNP

SNP

SNP

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotensive

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotension

sodium nitroprusside

hypotensive

sodium nitroprusside

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotension

SNP

hypotensive

SNP

hypotension


Input: Drug - induced arterial spasm relieved by lidocaine. Case report. Following major intracranial surgery in a 35 - year - old man, sodium pentothal was intravenously infused to minimize cerebral ischaemia. Intense vasospasm with threatened gangrene arose in the arm used for the infusion. Since the cranial condition precluded use of more usual methods, lidocaine was given intra - arterially, with careful cardiovascular monitoring, to counteract the vasospasm. The treatment was rapidly successful.

spasm

cerebral ischaemia

vasospasm

gangrene

vasospasm

lidocaine

sodium pentothal

lidocaine

sodium pentothal

spasm


Input: Cerebral blood flow and metabolism during isoflurane - induced hypotension in patients subjected to surgery for cerebral aneurysms. Cerebral blood flow and cerebral metabolic rate for oxygen were measured during isoflurane - induced hypotension in 10 patients subjected to craniotomy for clipping of a cerebral aneurysm. Flow and metabolism were measured 5 - 13 days after the subarachnoid haemorrhage by a modification of the classical Kety - Schmidt technique using xenon - 133 i. v. Anaesthesia was maintained with an inspired isoflurane concentration of 0. 75% (plus 67% nitrous oxide in oxygen), during which CBF and CMRO2 were 34. 3 + / - 2. 1 ml / 100 g min - 1 and 2. 32 + / - 0. 16 ml / 100 g min - 1 at PaCO2 4. 1 + / - 0. 1 kPa (mean + / - SEM). Controlled hypotension to an average MAP of 50 - 55 mm Hg was induced by increasing the dose of isoflurane, and maintained at an inspired concentration of 2. 2 + / - 0. 2%. This resulted in a significant decrease in CMRO2 (to 1. 73 + / - 0. 16 ml / 100 g min - 1), while CBF was unchanged. After the clipping of the aneurysm the isoflurane concentration was reduced to 0. 75%. There was a significant increase in CBF, although CMRO2 was unchanged, compared with pre - hypotensive values. These changes might offer protection to brain tissue during periods of induced hypotension.

isoflurane

oxygen

isoflurane

xenon

isoflurane

nitrous oxide

oxygen

Hg

isoflurane

isoflurane

hypotension

cerebral aneurysms

hypotension

cerebral aneurysm

subarachnoid haemorrhage

hypotension

aneurysm

hypotensive

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension


Input: Allergic reaction to 5 - fluorouracil infusion. An allergic reaction consisting of angioneurotic edema secondary to continuous infusion 5 - fluorouracil occurred in a patient with recurrent carcinoma of the oral cavity, cirrhosis, and cisplatin - induced impaired renal function. This reaction occurred during the sixth and seventh courses of infusional chemotherapy. Oral diphenhydramine and prednisone were ineffective in preventing the recurrence of the allergic reaction. Discontinuance of effective chemotherapy in this patient during partial remission resulted in fatal disease progression.

Allergic reaction

allergic reaction

angioneurotic edema

carcinoma of the oral cavity

cirrhosis

impaired renal function

allergic reaction

5 - fluorouracil

5 - fluorouracil

cisplatin

diphenhydramine

prednisone

5 - fluorouracil

angioneurotic edema

5 - fluorouracil

angioneurotic edema


Input: Amiodarone - induced sinoatrial block. We observed sinoatrial block due to chronic amiodarone administration in a 5 - year - old boy with primary cardiomyopathy, Wolff - Parkinson - White syndrome and supraventricular tachycardia. Reduction in the dosage of amiodarone resulted in the disappearance of the sinoatrial block and the persistence of asymptomatic sinus bradycardia.

Amiodarone

amiodarone

amiodarone

sinoatrial block

sinoatrial block

primary cardiomyopathy

Wolff - Parkinson - White syndrome

supraventricular tachycardia

sinoatrial block

sinus bradycardia

Amiodarone

sinoatrial block

Amiodarone

sinoatrial block

Amiodarone

sinoatrial block

amiodarone

sinoatrial block

amiodarone

sinoatrial block

amiodarone

sinoatrial block

amiodarone

sinoatrial block

amiodarone

sinoatrial block

amiodarone

sinoatrial block


Input: Possible teratogenicity of sulphasalazine. Three infants, born of two mothers with inflammatory bowel disease who received treatment with sulphasalazine throughout pregnancy, were found to have major congenital anomalies. In the singleton pregnancy, the mother had ulcerative colitis, and the infant, a male, had coarctation of the aorta and a ventricular septal defect. In the twin pregnancy, the mother had Crohn' s disease. The first twin, a female, had a left Potter - type IIa polycystic kidney and a rudimentary left uterine cornu. The second twin, a male, had some features of Potter' s facies, hypoplastic lungs, absent kidneys and ureters, and talipes equinovarus. Despite reports to the contrary, it is suggested that sulphasalazine may be teratogenic.

sulphasalazine

sulphasalazine

sulphasalazine

inflammatory bowel disease

congenital anomalies

ulcerative colitis

coarctation of the aorta

ventricular septal defect

Crohn' s disease

Potter - type IIa polycystic kidney

rudimentary left uterine cornu

Potter' s facies

hypoplastic lungs

absent kidneys and ureters

talipes equinovarus

sulphasalazine

talipes equinovarus

sulphasalazine

talipes equinovarus

sulphasalazine

talipes equinovarus

sulphasalazine

coarctation of the aorta

sulphasalazine

coarctation of the aorta

sulphasalazine

coarctation of the aorta

sulphasalazine

ventricular septal defect

sulphasalazine

ventricular septal defect

sulphasalazine

ventricular septal defect

sulphasalazine

Potter - type IIa polycystic kidney

sulphasalazine

Potter - type IIa polycystic kidney

sulphasalazine

Potter - type IIa polycystic kidney


Input: Veno - occlusive liver disease after dacarbazine therapy (DTIC) for melanoma. A case of veno - occlusive disease of the liver with fatal outcome after dacarbazine (DTIC) therapy for melanoma is reported. There was a fulminant clinical course from start of symptoms until death. At autopsy the liver was enlarged and firm with signs of venous congestion. Small - and medium - sized hepatic veins were blocked by thrombosis. Eosinophilic infiltrations were found around the vessels. Published cases from the literature are reviewed and pertinent features discussed.

Veno - occlusive liver disease

melanoma

veno - occlusive disease of the liver

melanoma

death

venous congestion

thrombosis

dacarbazine

DTIC

dacarbazine

DTIC

dacarbazine

Veno - occlusive liver disease

dacarbazine

veno - occlusive disease of the liver

DTIC

Veno - occlusive liver disease

DTIC

veno - occlusive disease of the liver

dacarbazine

Veno - occlusive liver disease

dacarbazine

veno - occlusive disease of the liver

DTIC

Veno - occlusive liver disease

DTIC

veno - occlusive disease of the liver


Input: A case of tardive dyskinesia caused by metoclopramide. Abnormal involuntary movements appeared in the mouth, tongue, neck and abdomen of a 64 - year - old male patient after he took metoclopramide for gastrointestinal disorder in a regimen of 30 mg per day for a total of about 260 days. The symptoms exacerbated to a maximum in a month. When the metoclopramide administration was discontinued, the abnormal movements gradually improved to a considerable extent. Attention to the possible induction of specific tardive dyskinesia is called for in the use of this drug.

tardive dyskinesia

Abnormal involuntary movements

gastrointestinal disorder

abnormal movements

tardive dyskinesia

metoclopramide

metoclopramide

metoclopramide

metoclopramide

tardive dyskinesia

metoclopramide

Abnormal involuntary movements

metoclopramide

abnormal movements

metoclopramide

tardive dyskinesia

metoclopramide

tardive dyskinesia

metoclopramide

Abnormal involuntary movements

metoclopramide

abnormal movements

metoclopramide

tardive dyskinesia

metoclopramide

tardive dyskinesia

metoclopramide

Abnormal involuntary movements

metoclopramide

abnormal movements

metoclopramide

tardive dyskinesia


Input: Further observations on the electrophysiologic effects of oral amiodarone therapy. A case is presented of a reversible intra - Hisian block occurring under amiodarone treatment for atrial tachycardia in a patient without clear intraventricular conduction abnormalities. His bundle recordings showed an atrial tachycardia with intermittent exit block and greatly prolonged BH and HV intervals (40 and 100 msec, respectively). Thirty days after amiodarone discontinuation, His bundle electrograms showed atrial flutter without intra - Hisian or infra - Hisian delay. Amiodarone should be used with caution during long - term oral therapy in patients with or without clear intraventricular conduction defects.

amiodarone

amiodarone

amiodarone

Amiodarone

intra - Hisian block

atrial tachycardia

intraventricular conduction abnormalities

atrial tachycardia

atrial flutter

amiodarone

intra - Hisian block

amiodarone

intra - Hisian block

amiodarone

intra - Hisian block

Amiodarone

intra - Hisian block


Input: Busulfan - induced hemorrhagic cystitis. A case of a busulfan - induced hemorrhage cystitis is reported. Spontaneous resolution occurred following cessation of the drug. The similarity between the histologic appearances of busulfan cystitis and both radiation and cyclophosphamide - induced cystitis is discussed and the world literature reviewed. In view of the known tendency of busulfan to induce cellular atypia and carcinoma in other sites, periodic urinary cytology is suggested in patients on long - term therapy.

Busulfan

busulfan

busulfan

cyclophosphamide

busulfan

hemorrhagic cystitis

hemorrhagic

cystitis

hemorrhage cystitis

hemorrhage

cystitis

cystitis

cystitis

carcinoma

Busulfan

hemorrhagic cystitis

Busulfan

cystitis

Busulfan

hemorrhage cystitis

Busulfan

cystitis

Busulfan

cystitis

Busulfan

cystitis

busulfan

hemorrhagic cystitis

busulfan

cystitis

busulfan

hemorrhage cystitis

busulfan

cystitis

busulfan

cystitis

busulfan

cystitis

busulfan

hemorrhagic cystitis

busulfan

cystitis

busulfan

hemorrhage cystitis

busulfan

cystitis

busulfan

cystitis

busulfan

cystitis

busulfan

hemorrhagic cystitis

busulfan

cystitis

busulfan

hemorrhage cystitis

busulfan

cystitis

busulfan

cystitis

busulfan

cystitis

Busulfan

hemorrhagic

Busulfan

hemorrhage

busulfan

hemorrhagic

busulfan

hemorrhage

busulfan

hemorrhagic

busulfan

hemorrhage

busulfan

hemorrhagic

busulfan

hemorrhage


Input: Rebound hypertensive after sodium nitroprusside prevented by saralasin in rats. The role of the renin - - angiotensin system in the maintenance of blood pressure during halothane anesthesia and sodium nitroprusside (SNP) - induced hypotension was evaluated. Control rats received halothane anesthesia (1 MAC) for one hour, followed by SNP infusion, 40 microgram / kg / min, for 30 min, followed by a 30 - min recovery period. A second group of rats was treated identically and, in addition, received an infusion of saralasin (a competitive inhibitor of angiotensin II) throughout the experimental period. In each group, SNP infusion resulted in an initial decrease in blood pressure from 86 torr and 83 torr, respectively, to 48 torr. During the SNP infusion the control animals demonstrated a progressive increase in blood pressure to 61 torr, whereas the saralasin - treated animals showed no change. Following discontinuation of SNP, blood pressure in the control animals rebounded to 94 torr, as compared with 78 torr in the saralasin - treated rats. This study indicates that with stable halothane anesthesia, the partial recovery of blood pressure during SNP infusion and the post - SNP rebound of blood pressure can be completely blocked by saralasin. This demonstrates the participation of the renin - - angiotensin system in antagonizing the combined hypotensive effects of halothane and SNP.

hypertensive

hypotension

increase in blood pressure

hypotensive

sodium nitroprusside

saralasin

angiotensin

halothane

sodium nitroprusside

SNP

halothane

SNP

saralasin

angiotensin II

SNP

SNP

saralasin

SNP

saralasin

halothane

SNP

SNP

saralasin

angiotensin

halothane

SNP

sodium nitroprusside

hypotension

sodium nitroprusside

hypotensive

sodium nitroprusside

hypotension

sodium nitroprusside

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

SNP

hypotension

SNP

hypotensive

halothane

hypotension

halothane

hypotensive

halothane

hypotension

halothane

hypotensive

halothane

hypotension

halothane

hypotensive

halothane

hypotension

halothane

hypotensive


Input: Toxic hepatitis induced by antithyroid drugs: four cases including one with cross - reactivity between carbimazole and benzylthiouracil. OBJECTIVE: This study was conducted to assess the occurrence of hepatic adverse effects encountered with antithyroid drugs. METHODS: Retrospective review of medical records of 236 patients with hyperthyroidism admitted in our department (in - or out - patients) from 1986 to 1992. RESULTS: Four patients (1. 7%) were identified with toxic hepatitis which could reasonably be attributed to the use of antithyroid agent. Two patients had a cholestatic hepatitis induced by carbimazole (N omercazole). Two others had a mixed (cholestatic and cytolytic) hepatitis following carbimazole. One of the latter two patients further experienced a cytolytic hepatitis which appeared after Benzylthiouracil (Basd ne) had replaced carbimazole. Biological features of hepatitis disappeared in all cases after cessation of the incriminated drug, while biliary, viral and immunological searches were negative. Only 2 patients of our retrospective study experienced a mild or severe neutropenia. CONCLUSION: Toxic hepatitis is a potential adverse effect of antithyroid drugs which warrants, as for haematological disturbances, a pre - therapeutic determination and a careful follow - up of relevant biological markers. Moreover, hepatotoxicity may not be restricted to one class of antithyroid agents.

Toxic hepatitis

hepatic adverse effects

hyperthyroidism

toxic hepatitis

cholestatic hepatitis

cholestatic

hepatitis

cholestatic

hepatitis

hepatitis

hepatitis

neutropenia

Toxic hepatitis

hepatotoxicity

carbimazole

benzylthiouracil

carbimazole

N omercazole

carbimazole

Benzylthiouracil

Basd ne

carbimazole

carbimazole

Toxic hepatitis

carbimazole

hepatic adverse effects

carbimazole

toxic hepatitis

carbimazole

cholestatic hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

Toxic hepatitis

carbimazole

hepatotoxicity

carbimazole

Toxic hepatitis

carbimazole

hepatic adverse effects

carbimazole

toxic hepatitis

carbimazole

cholestatic hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

Toxic hepatitis

carbimazole

hepatotoxicity

N omercazole

Toxic hepatitis

N omercazole

hepatic adverse effects

N omercazole

toxic hepatitis

N omercazole

cholestatic hepatitis

N omercazole

hepatitis

N omercazole

hepatitis

N omercazole

hepatitis

N omercazole

hepatitis

N omercazole

Toxic hepatitis

N omercazole

hepatotoxicity

carbimazole

Toxic hepatitis

carbimazole

hepatic adverse effects

carbimazole

toxic hepatitis

carbimazole

cholestatic hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

Toxic hepatitis

carbimazole

hepatotoxicity

carbimazole

Toxic hepatitis

carbimazole

hepatic adverse effects

carbimazole

toxic hepatitis

carbimazole

cholestatic hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

hepatitis

carbimazole

Toxic hepatitis

carbimazole

hepatotoxicity

carbimazole

cholestatic

carbimazole

cholestatic

carbimazole

cholestatic

carbimazole

cholestatic

N omercazole

cholestatic

N omercazole

cholestatic

carbimazole

cholestatic

carbimazole

cholestatic

carbimazole

cholestatic

carbimazole

cholestatic


Input: Study of the role of vitamin B12 and folinic acid supplementation in preventing hematologic toxicity of zidovudine. A prospective, randomized study was conducted to evaluate the role of vitamin B12 and folinic acid supplementation in preventing zidovudine (ZDV) - induced bone marrow suppression. Seventy - five human immunodeficiency virus (HIV) - infected patients with CD4 + cell counts < 500 / mm3 were randomized to receive either ZDV (500 mg daily) alone (group I, n = 38) or in combination with folinic acid (15 mg daily) and intramascular vitamin B12 (1000 micrograms monthly) (group II, n = 37). Finally, 15 patients were excluded from the study (noncompliance 14, death 1); thus, 60 patients (31 in group I and 29 in group II) were eligible for analysis. No significant differences between groups were found at enrollment. During the study, vitamin B12 and folate levels were significantly higher in group II patients; however, no differences in hemoglobin, hematocrit, mean corpuscular volume, and white - cell, neutrophil and platelet counts were observed between groups at 3, 6, 9 and 12 months. Severe hematologic toxicity (neutrophil count < 1000 / mm3 and / or hemoglobin < 8 g / dl) occurred in 4 patients assigned to group I and 7 assigned to group II. There was no correlation between vitamin B12 or folate levels and development of myelosuppression. Vitamin B12 and folinic acid supplementation of ZDV therapy does not seem useful in preventing or reducing ZDV - induced myelotoxicity in the overall treated population, although a beneficial effect in certain subgroups of patients cannot be excluded.

vitamin B12

folinic acid

zidovudine

vitamin B12

folinic acid

zidovudine

ZDV

ZDV

folinic acid

vitamin B12

vitamin B12

folate

vitamin B12

folate

Vitamin B12

folinic acid

ZDV

ZDV

toxicity

bone marrow suppression

human immunodeficiency virus (HIV) - infected

death

toxicity

myelosuppression

myelotoxicity

zidovudine

bone marrow suppression

zidovudine

myelosuppression

zidovudine

myelotoxicity

zidovudine

bone marrow suppression

zidovudine

myelosuppression

zidovudine

myelotoxicity

ZDV

bone marrow suppression

ZDV

myelosuppression

ZDV

myelotoxicity

ZDV

bone marrow suppression

ZDV

myelosuppression

ZDV

myelotoxicity

ZDV

bone marrow suppression

ZDV

myelosuppression

ZDV

myelotoxicity

ZDV

bone marrow suppression

ZDV

myelosuppression

ZDV

myelotoxicity


Input: Acute confusion induced by a high - dose infusion of 5 - fluorouracil and folinic acid. A 61 - year - old man was treated with combination chemotherapy incorporating cisplatinum, etoposide, high - dose 5 - fluorouracil (2, 250 mg / m2 / 24 hours) and folinic acid for an inoperable gastric adenocarcinoma. He developed acute neurologic symptoms of mental confusion, disorientation and irritability, and then lapsed into a deep coma, lasting for approximately 40 hours during the first dose (day 2) of 5 - fluorouracil and folinic acid infusion. This complication reappeared on day 25 during the second dose of 5 - fluorouracil and folinic acid, which were then the only drugs given. Because folinic acid was unlikely to be associated with this condition, neurotoxicity due to high - dose 5 - fluorouracil was highly suspected. The pathogenesis of 5 - fluorouracil neurotoxicity may be due to a Krebs cycle blockade by fluoroacetate and fluorocitrate, thiamine deficiency, or dihydrouracil dehydrogenase deficiency. High - dose 5 - fluorouracil / folinic acid infusion therapy has recently become a popular regimen for various cancers. It is necessary that both oncologists and neurologists be fully aware of this unusual complication.

confusion

gastric adenocarcinoma

confusion

disorientation

irritability

coma

neurotoxicity

neurotoxicity

cancers

5 - fluorouracil

folinic acid

cisplatinum

etoposide

5 - fluorouracil

folinic acid

5 - fluorouracil

folinic acid

5 - fluorouracil

folinic acid

folinic acid

5 - fluorouracil

5 - fluorouracil

fluoroacetate

fluorocitrate

thiamine

dihydrouracil

5 - fluorouracil

folinic acid

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

folinic acid

confusion

folinic acid

confusion

folinic acid

disorientation

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

coma

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

5 - fluorouracil

confusion

5 - fluorouracil

confusion

5 - fluorouracil

disorientation

folinic acid

coma

folinic acid

coma

folinic acid

coma

folinic acid

coma

folinic acid

coma

folinic acid

coma


Input: Effect of switching carbamazepine to oxcarbazepine on the plasma levels of neuroleptics. A case report. Carbamazepine was switched to its 10 - keto analogue oxcarbazepine among six difficult - to - treat schizophrenic or organic psychotic patients using concomitantly haloperidol, chlorpromazine or clozapine. This change resulted within 2 - 4 weeks in the 50 - 200% increase in the plasma levels of these neuroleptics and the appearance of extrapyramidal symptoms. None of the patients showed any clinical deteriotation during the following 3 - 6 months. The results of this case report support the idea that in contrast with carbamazepine oxcarbazepine does not induce the hepatic microsomal enzyme systems regulating the inactivation of antipsychotic drugs.

carbamazepine

oxcarbazepine

Carbamazepine

oxcarbazepine

haloperidol

chlorpromazine

clozapine

carbamazepine

oxcarbazepine

schizophrenic

organic psychotic

extrapyramidal symptoms

haloperidol

extrapyramidal symptoms

chlorpromazine

extrapyramidal symptoms

clozapine

extrapyramidal symptoms

oxcarbazepine

extrapyramidal symptoms

oxcarbazepine

extrapyramidal symptoms

oxcarbazepine

extrapyramidal symptoms


Input: Erythema multiforme and hypersensitivity myocarditis caused by ampicillin. OBJECTIVE: To report a case of erythema multiforme and hypersensitivity myocarditis caused by ampicillin. CASE SUMMARY: A 13 - year - old boy was treated with ampicillin and gentamicin because of suspected septicemia. Medications were discontinued when erythema multiforme and congestive heart failure caused by myocarditis occurred. The patient was treated with methylprednisolone and gradually improved. Macrophage - migration inhibition (MIF) test with ampicillin was positive. DISCUSSION: After most infections causing erythema multiforme and myocarditis were ruled out, a drug - induced allergic reaction was suspected. Positive MIF test for ampicillin showed sensitization of the patient' s lymphocytes to ampicillin. CONCLUSIONS: Hypersensitivity myocarditis is a rare and dangerous manifestation of allergy to penicillins.

Erythema multiforme

hypersensitivity myocarditis

erythema multiforme

hypersensitivity myocarditis

septicemia

erythema multiforme

congestive heart failure

myocarditis

infections

erythema multiforme

myocarditis

drug - induced allergic reaction

Hypersensitivity myocarditis

allergy

ampicillin

ampicillin

ampicillin

gentamicin

methylprednisolone

ampicillin

ampicillin

ampicillin

penicillins

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

Erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

erythema multiforme

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

drug - induced allergic reaction

ampicillin

allergy

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

hypersensitivity myocarditis

ampicillin

myocarditis

ampicillin

myocarditis

ampicillin

Hypersensitivity myocarditis


Input: Immediate allergic reactions to amoxicillin. A large group of patients with suspected allergic reactions to beta - lactam antibiotics was evaluated. A detailed clinical history, together with skin tests, RAST (radioallergosorbent test), and controlled challenge tests, was used to establish whether patients allergic to beta - lactam antibiotics had selective immediate allergic responses to amoxicillin (AX) or were cross - reacting with other penicillin derivatives. Skin tests were performed with benzylpenicilloyl - poly - L - lysine (BPO - PLL), benzylpenicilloate, benzylpenicillin (PG), ampicillin (AMP), and AX. RAST for BPO - PLL and AX - PLL was done. When both skin test and RAST for BPO were negative, single - blind, placebo - controlled challenge tests were done to ensure tolerance of PG or sensitivity to AX. A total of 177 patients were diagnosed as allergic to beta - lactam antibiotics. We selected the 54 (30. 5%) cases of immediate AX allergy with good tolerance of PG. Anaphylaxis was seen in 37 patients (69%), the other 17 (31%) having urticaria and / or angioedema. All the patients were skin test negative to BPO; 49 of 51 (96%) were also negative to MDM, and 44 of 46 (96%) to PG. Skin tests with AX were positive in 34 (63%) patients. RAST was positive for AX in 22 patients (41%) and to BPO in just 5 (9%). None of the sera with negative RAST for AX were positive to BPO. Challenge tests with AX were performed in 23 subjects (43%) to establish the diagnosis of immediate allergic reaction to AX, and in 15 cases (28%) both skin test and RAST for AX were negative. PG was well tolerated by all 54 patients. We describe the largest group of AX - allergic patients who have tolerated PG reported so far. Diagnosis of these patients can be achieved only if specific AX - related reagents are employed. Further studies are necessary to determine the exact extent of this problem and to improve the efficacy of diagnostic methods.

allergic reactions

allergic reactions

allergic

allergic

allergic

allergy

Anaphylaxis

urticaria

angioedema

MDM

allergic reaction

allergic

amoxicillin

beta - lactam

beta - lactam

amoxicillin

AX

penicillin

benzylpenicilloyl - poly - L - lysine

BPO - PLL

benzylpenicilloate

benzylpenicillin

PG

ampicillin

AMP

AX

BPO - PLL

AX

BPO

PG

AX

beta - lactam

AX

PG

BPO

PG

AX

AX

BPO

AX

BPO

AX

AX

AX

PG

AX

PG

AX

amoxicillin

Anaphylaxis

amoxicillin

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

AX

Anaphylaxis

amoxicillin

allergic reactions

amoxicillin

allergic reactions

amoxicillin

allergic

amoxicillin

allergic

amoxicillin

allergic

amoxicillin

allergy

amoxicillin

allergic reaction

amoxicillin

allergic

amoxicillin

allergic reactions

amoxicillin

allergic reactions

amoxicillin

allergic

amoxicillin

allergic

amoxicillin

allergic

amoxicillin

allergy

amoxicillin

allergic reaction

amoxicillin

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

AX

allergic reactions

AX

allergic reactions

AX

allergic

AX

allergic

AX

allergic

AX

allergy

AX

allergic reaction

AX

allergic

amoxicillin

angioedema

amoxicillin

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema

AX

angioedema


Input: Persistent paralysis after prolonged use of atracurium in the absence of corticosteroids. Neuromuscular blocking agents (NMBAs) are often used for patients requiring prolonged mechanical ventilation. Reports of persistent paralysis after the discontinuance of these drugs have most often involved aminosteroid - based NMBAs such as vecuronium bromide, especially when used in conjunction with corticosteroids. Atracurium besylate, a short - acting benzylisoquinolinium NMBA that is eliminated independently of renal or hepatic function, has also been associated with persistent paralysis, but only when used with corticosteroids. We report a case of atracurium - related paralysis persisting for approximately 50 hours in a patient who was not treated with corticosteroids.

paralysis

paralysis

paralysis

paralysis

atracurium

vecuronium bromide

Atracurium besylate

benzylisoquinolinium

atracurium

atracurium

paralysis

atracurium

paralysis

atracurium

paralysis

atracurium

paralysis

Atracurium besylate

paralysis

Atracurium besylate

paralysis

Atracurium besylate

paralysis

Atracurium besylate

paralysis

atracurium

paralysis

atracurium

paralysis

atracurium

paralysis

atracurium

paralysis

vecuronium bromide

paralysis

vecuronium bromide

paralysis

vecuronium bromide

paralysis

vecuronium bromide

paralysis


Input: Habitual use of acetaminophen as a risk factor for chronic renal failure: a comparison with phenacetin. Six epidemiologic studies in the United States and Europe indicate that habitual use of phenacetin is associated with the development of chronic renal failure and end - stage renal disease (ESRD), with a relative risk in the range of 4 to 19. As a result of these and other studies, phenacetin has now been withdrawn from the market in most countries. However, three case control studies, one each in North Carolina, northern Maryland, and West Berlin, Germany, showed that habitual use of acetaminophen is also associated with chronic renal failure and ESRD, with a relative risk in the range of 2 to 4. These studies suggest that both phenacetin and acetaminophen may contribute to the burden of ESRD, with the risk of the latter being somewhat less than that of the former. This apparent difference in risk may not be due to differences in nephrotoxic potential of the drugs themselves. A lower relative risk would be expected for acetaminophen if the risk of both drugs in combination with other analgesics was higher than the risk of either agent alone. Thus, acetaminophen has been used both as a single agent and in combination with other analgesics, whereas phenacetin was available only in combinations. The possibility that habitual use of acetaminophen alone increases the risk of ESRD has not been clearly demonstrated, but cannot be dismissed.

acetaminophen

phenacetin

phenacetin

phenacetin

acetaminophen

phenacetin

acetaminophen

acetaminophen

acetaminophen

phenacetin

acetaminophen

chronic renal failure

chronic renal failure

end - stage renal disease

ESRD

chronic renal failure

ESRD

ESRD

nephrotoxic

ESRD

phenacetin

chronic renal failure

phenacetin

chronic renal failure

phenacetin

end - stage renal disease

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

ESRD

phenacetin

ESRD

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

chronic renal failure

phenacetin

end - stage renal disease

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

ESRD

phenacetin

ESRD

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

chronic renal failure

phenacetin

end - stage renal disease

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

ESRD

phenacetin

ESRD

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

chronic renal failure

phenacetin

end - stage renal disease

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

ESRD

phenacetin

ESRD

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

chronic renal failure

phenacetin

end - stage renal disease

phenacetin

ESRD

phenacetin

chronic renal failure

phenacetin

ESRD

phenacetin

ESRD

phenacetin

ESRD


Input: Reduction of heparan sulphate - associated anionic sites in the glomerular basement membrane of rats with streptozotocin - induced diabetic nephropathy. Heparan sulphate - associated anionic sites in the glomerular basement membrane were studied in rats 8 months after induction of diabetes by streptozotocin and in age - adn sex - matched control rats, employing the cationic dye cuprolinic blue. Morphometric analysis at the ultrastructural level was performed using a computerized image processor. The heparan sulphate specificity of the cuprolinic blue staining was demonstrated by glycosaminoglycan - degrading enzymes, showing that pretreatment of the sections with heparitinase abolished all staining, whereas chondroitinase ABC had no effect. The majority of anionic sites (74% in diabetic and 81% in control rats) were found within the lamina rara externa of the glomerular basement membrane. A minority of anionic sites were scattered throughout the lamina densa and lamina rara interna, and were significantly smaller than those in the lamina rara externa of the glomerular basement membrane (p < 0. 001 and p < 0. 01 for diabetic and control rats, respectively). Diabetic rats progressively developed albuminuria reaching 40. 3 (32. 2 - 62. 0) mg / 24 h after 8 months in contrast to the control animals (0. 8 (0. 2 - 0. 9) mg / 24 h, p < 0. 002). At the same time, the number of heparan sulphate anionic sites and the total anionic site surface (number of anionic sites x mean anionic site surface) in the lamina rara externa of the glomerular basement membrane was reduced by 19% (p < 0. 021) and by 26% (p < 0. 02), respectively. Number and total anionic site surface in the remaining part of the glomerular basement membrane (lamina densa and lamina rara interna) were not significantly changed. We conclude that in streptozotocin - diabetic rats with an increased urinary albumin excretion, a reduced heparan sulphate charge barrier / density is found at the lamina rara externa of the glomerular basement membrane.

heparan sulphate

streptozotocin

Heparan sulphate

streptozotocin

cuprolinic blue

heparan sulphate

cuprolinic blue

glycosaminoglycan

heparan sulphate

streptozotocin

heparan sulphate

diabetic nephropathy

diabetes

diabetic

diabetic

Diabetic

albuminuria

diabetic

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy

streptozotocin

diabetic nephropathy


Input: Effect of some anticancer drugs and combined chemotherapy on renal toxicity. The nephrotoxic action of anticancer drugs such as nitrogranulogen (NG), methotrexate (MTX), 5 - fluorouracil (5 - FU) and cyclophosphamide (CY) administered alone or in combination [MTX + 5 - FU + CY (CMF)] was evaluated in experiments on Wistar rats. After drug administration, creatinine concentrations in the plasma and in the urine of the rats were determined, as well as creatinine clearance. Histopathologic evaluation of the kidneys was also performed. After MTX administration a significant increase (p = 0. 0228) in the plasma creatinine concentration and a significant (p = 0. 0001) decrease in creatinine clearance was noted compared to controls. After the administration of NG, 5 - FU and CY neither a statistically significant increase in creatinine concentration nor an increase in creatinine clearance was observed compared to the group receiving no cytostatics. Following polytherapy according to the CMF regimen, a statistically significant decrease (p = 0. 0343) in creatinine clearance was found, but creatinine concentration did not increase significantly compared to controls. CY caused hemorrhagic cystitis in 40% of rats, but it did not cause this complication when combined with 5 - FU and MTX. Histologic changes were found in rat kidneys after administration of MTX, CY and NG, while no such change was observed after 5 - FU and joint administration of MTX + 5 - FU + CY compared to controls. Our studies indicate that nephrotoxicity of MTX + 5 - FU + CY administered jointly is lower than in monotherapy.

renal toxicity

nephrotoxic

hemorrhagic cystitis

hemorrhagic

cystitis

nephrotoxicity

nitrogranulogen

NG

methotrexate

MTX

5 - fluorouracil

5 - FU

cyclophosphamide

CY

MTX

5 - FU

CY

creatinine

creatinine

MTX

creatinine

creatinine

NG

5 - FU

CY

creatinine

creatinine

creatinine

creatinine

CY

5 - FU

MTX

MTX

CY

NG

5 - FU

MTX

5 - FU

CY

MTX

5 - FU

CY

cyclophosphamide

hemorrhagic cystitis

cyclophosphamide

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

CY

hemorrhagic cystitis

CY

hemorrhagic

cyclophosphamide

cystitis

CY

cystitis

CY

cystitis

CY

cystitis

CY

cystitis

CY

cystitis

CY

cystitis

CY

cystitis


Input: Lithium - associated cognitive and functional deficits reduced by a switch to divalproex sodium: a case series. BACKGROUND: Lithium remains a first - line treatment for the acute and maintenance treatment of bipolar disorder. Although much has been written about the management of the more common adverse effects of lithium, such as polyuria and tremor, more subtle lithium side effects such as cognitive deficits, loss of creativity, and functional impairments remain understudied. This report summarizes our experience in switching bipolar patients from lithium to divalproex sodium to alleviate such cognitive and functional impairments. METHOD: Open, case series design. RESULTS: We report seven cases where substitution of lithium, either fully or partially, with divalproex sodium was extremely helpful in reducing the cognitive, motivational, or creative deficits attributed to lithium in our bipolar patients. CONCLUSION: In this preliminary report, divalproex sodium was a superior alternative to lithium in bipolar patients experiencing cognitive deficits, loss of creativity, and functional impairments.

Lithium

divalproex sodium

Lithium

lithium

lithium

lithium

divalproex sodium

lithium

divalproex sodium

lithium

divalproex sodium

lithium

cognitive and functional deficits

bipolar disorder

polyuria

tremor

cognitive deficits

loss of creativity

functional impairments

bipolar

cognitive and functional impairments

cognitive, motivational, or creative deficits

bipolar

bipolar

cognitive deficits

loss of creativity

functional impairments

Lithium

cognitive and functional deficits

Lithium

cognitive deficits

Lithium

loss of creativity

Lithium

functional impairments

Lithium

cognitive and functional impairments

Lithium

cognitive, motivational, or creative deficits

Lithium

cognitive deficits

Lithium

loss of creativity

Lithium

functional impairments

Lithium

cognitive and functional deficits

Lithium

cognitive deficits

Lithium

loss of creativity

Lithium

functional impairments

Lithium

cognitive and functional impairments

Lithium

cognitive, motivational, or creative deficits

Lithium

cognitive deficits

Lithium

loss of creativity

Lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments

lithium

cognitive and functional impairments

lithium

cognitive, motivational, or creative deficits

lithium

cognitive deficits

lithium

loss of creativity

lithium

functional impairments