Input: Case report: Dexatrim (Phenylpropanolamine) as a cause of myocardial infarction. Phenylpropanolamine (PPA) is a sympathetic amine used in over - the - counter cold remedies and weight - control preparations worldwide. Its use has been associated with hypertensive episodes and hemorrhagic strokes in younger women. Several reports have linked the abuse of PPA with myocardial injury, especially when overdose is involved. We report here the first case of Dexatrim (PPA) - induced myocardial injury in a young woman who was using it at recommended doses for weight control. In addition, we review the 7 other cases of PPA related myocardial injury that have been reported so far. Physicians and patients should be alert to the potential cardiac risk associated with the use of PPA, even at doses generally considered to be safe.

Dexatrim

Phenylpropanolamine

Phenylpropanolamine

PPA

amine

PPA

Dexatrim

PPA

PPA

PPA

myocardial infarction

hypertensive

hemorrhagic strokes

hemorrhagic

strokes

myocardial injury

overdose

myocardial injury

myocardial injury

Dexatrim

myocardial infarction

Phenylpropanolamine

myocardial infarction

Phenylpropanolamine

myocardial infarction

PPA

myocardial infarction

PPA

myocardial infarction

Dexatrim

myocardial infarction

PPA

myocardial infarction

PPA

myocardial infarction

PPA

myocardial infarction


Input: Risperidone - associated, benign transient visual disturbances in schizophrenic patients with a past history of LSD abuse. Two schizophrenic patients, who had a prior history of LSD abuse and who had previously developed EPS with classic antipsychotics, were successfully treated with risperidone. They both reported short episodes of transient visual disturbances, which appeared immediately after starting treatment with risperidone. This imagery resembled visual disturbances previously experienced as " flashbacks " related to prior LSD consumption. Risperidone administration was continued and the visual disturbances gradually wore off. During a six - month follow - up period, there was no recurrence of visual disturbances. This phenomenon may be interpreted as a benign, short - term and self - limiting side effect which does not contraindicate the use of risperidone or interfere with treatment. Conclusions based on two case reports should be taken with appropriate caution.

Risperidone

LSD

LSD

risperidone

risperidone

LSD

Risperidone

risperidone

visual disturbances

schizophrenic

schizophrenic

EPS

visual disturbances

visual disturbances

visual disturbances

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

Risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances

risperidone

visual disturbances


Input: Activation of poly (ADP - ribose) polymerase contributes to development of doxorubicin - induced heart failure. Activation of the nuclear enzyme poly (ADP - ribose) polymerase (PARP) by oxidant - mediated DNA damage is an important pathway of cell dysfunction and tissue injury in conditions associated with oxidative stress. Increased oxidative stress is a major factor implicated in the cardiotoxicity of doxorubicin (DOX), a widely used antitumor anthracycline antibiotic. Thus, we hypothesized that the activation of PARP may contribute to the DOX - induced cardiotoxicity. Using a dual approach of PARP - 1 suppression, by genetic deletion or pharmacological inhibition with the phenanthridinone PARP inhibitor PJ34, we now demonstrate the role of PARP in the development of cardiac dysfunction induced by DOX. PARP - 1 + / + and PARP - 1 - / - mice received a single injection of DOX (25 mg / kg i. p). Five days after DOX administration, left ventricular performance was significantly depressed in PARP - 1 + / + mice, but only to a smaller extent in PARP - 1 - / - ones. Similar experiments were conducted in BALB / c mice treated with PJ34 or vehicle. Treatment with a PJ34 significantly improved cardiac dysfunction and increased the survival of the animals. In addition PJ34 significantly reduced the DOX - induced increase in the serum lactate dehydrogenase and creatine kinase activities but not metalloproteinase activation in the heart. Thus, PARP activation contributes to the cardiotoxicity of DOX. PARP inhibitors may exert protective effects against the development of severe cardiac complications associated with the DOX treatment.

poly (ADP - ribose)

doxorubicin

poly (ADP - ribose)

doxorubicin

DOX

anthracycline

DOX

DOX

DOX

DOX

DOX

lactate

creatine

DOX

DOX

heart failure

cardiotoxicity

cardiotoxicity

cardiac dysfunction

cardiac dysfunction

cardiotoxicity

cardiac complications

doxorubicin

heart failure

doxorubicin

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure

DOX

heart failure


Input: Fluconazole - induced torsade de pointes. OBJECTIVE: To present a case of fluconazole - associated torsade de pointes (TDP) and discuss fluconazole' s role in causing TDP. CASE SUMMARY: A 68 - year - old white woman with Candida glabrata isolated from a presacral abscess developed TDP eight days after commencing oral fluconazole The patient had no other risk factors for TDP, including coronary artery disease, cardiomyopathy, congestive heart failure, and electrolyte abnormalities There was a temporal association between the initiation of fluconazole and TDP. The TDP resolved when fluconazole was discontinued; however, the patient continued to have premature ventricular contractions and nonsustained ventricular tachycardia (NSVT) until six days after drug cessation DISCUSSION: Use of the Naranjo probability scale indicates a probable relationship between the use of fluconazole and the development of TDP. The possible mechanism is depression of rapidly activating delayed rectifier potassium currents. In our patient, there was no other etiology identified that could explain QT prolongation or TDP The complete disappearance of NSVT and premature ventricular contractions followed by normalization of QT interval after the drug was stopped strongly suggests fluconazole as the etiology. CONCLUSIONS: Clinicians should be aware that fluconazole, even at low doses, may cause prolongation of the QT interval, leading to TDP. Serial electrocardiographic monitoring may be considered when fluconazole is administered in patients who are at risk for ventricular arrhythmias.

Fluconazole

fluconazole

fluconazole

fluconazole

fluconazole

fluconazole

fluconazole

potassium

fluconazole

fluconazole

fluconazole

torsade de pointes

torsade de pointes

TDP

TDP

TDP

TDP

coronary artery disease

cardiomyopathy

congestive heart failure

TDP

TDP

premature ventricular contractions

ventricular tachycardia

NSVT

TDP

depression

QT prolongation

TDP

NSVT

premature ventricular contractions

prolongation of the QT interval

TDP

ventricular arrhythmias

Fluconazole

torsade de pointes

Fluconazole

torsade de pointes

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

Fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

torsade de pointes

fluconazole

torsade de pointes

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP

fluconazole

TDP


Input: High - dose methylprednisolone may do more harm for spinal cord injury. Because of the National Acute Spinal Cord Injury Studies (NASCIS), high - dose methylprednisolone became the standard of care for the acute spinal cord injury. In the NASCIS, there was no mention regarding the possibility of acute corticosteroid myopathy that high - dose methylprednisolone may cause. The dosage of methylprednisolone recommended by the NASCIS 3 is the highest dose of steroids ever being used during a 2 - day period for any clinical condition. We hypothesize that it may cause some damage to the muscle of spinal cord injury patients. Further, steroid myopathy recovers naturally and the neurological improvement shown in the NASCIS may be just a recording of this natural motor recovery from the steroid myopathy, instead of any protection that methylprednisolone offers to the spinal cord injury. To our knowledge, this is the first discussion considering the possibility that the methylprednisolone recommended by NASCIS may cause acute corticosteroid myopathy.

methylprednisolone

methylprednisolone

corticosteroid

methylprednisolone

methylprednisolone

steroids

steroid

steroid

methylprednisolone

methylprednisolone

corticosteroid

spinal cord injury

Spinal Cord Injury

spinal cord injury

myopathy

damage to the muscle

spinal cord injury

myopathy

myopathy

spinal cord injury

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

damage to the muscle

methylprednisolone

myopathy

methylprednisolone

myopathy

methylprednisolone

myopathy


Input: Probing peripheral and central cholinergic system responses. OBJECTIVE: The pharmacological response to drugs that act on the cholinergic system of the iris has been used to predict deficits in central cholinergic functioning due to diseases such as Alzheimer' s disease, yet correlations between central and peripheral responses have not been properly studied. This study assessed the effect of normal aging on (1) the tropicamide - induced increase in pupil diameter, and (2) the reversal of this effect with pilocarpine. Scopolamine was used as a positive control to detect age - dependent changes in central cholinergic functioning in the elderly. DESIGN: Randomized double - blind controlled trial. PARTICIPANTS: Ten healthy elderly (mean age 70) and 9 young (mean age 33) volunteers. INTERVENTIONS: Pupil diameter was monitored using a computerized infrared pupillometer over 4 hours. The study involved 4 sessions. In 1 session, tropicamide (20 microL, 0. 01%) was administered to one eye and placebo to the other. In another session, tropicamide (20 microL, 0. 01%) was administered to both eyes, followed 23 minutes later by the application of pilocarpine (20 microL, 0. 1%) to one eye and placebo to the other. All eye drops were given in a randomized order. In 2 separate sessions, a single dose of scopolamine (0. 5 mg, intravenously) or placebo was administered, and the effects on word recall were measured using the Buschke Selective Reminding Test over 2 hours. OUTCOME MEASURES: Pupil size at time points after administration of tropicamide and pilocarpine; scopolamine - induced impairment in word recall. RESULTS: There was no significant difference between elderly and young volunteers in pupillary response to tropicamide at any time point (p > 0. 05). The elderly group had a significantly greater pilocarpine - induced net decrease in pupil size 85, 125, 165 and 215 minutes after administration, compared with the young group (p < 0. 05). Compared with the young group, the elderly group had greater scopolamine - induced impairment in word recall 60, 90 and 120 minutes after administration (p < 0. 05). CONCLUSION: There is an age - related pupillary response to pilocarpine that is not found with tropicamide. Thus, pilocarpine may be useful to assess variations in central cholinergic function in elderly patients.

Alzheimer' s disease

impairment in word recall

impairment in word recall

tropicamide

pilocarpine

Scopolamine

tropicamide

tropicamide

pilocarpine

scopolamine

tropicamide

pilocarpine

scopolamine

tropicamide

pilocarpine

scopolamine

pilocarpine

tropicamide

pilocarpine

Scopolamine

impairment in word recall

Scopolamine

impairment in word recall

scopolamine

impairment in word recall

scopolamine

impairment in word recall

scopolamine

impairment in word recall

scopolamine

impairment in word recall

scopolamine

impairment in word recall

scopolamine

impairment in word recall


Input: Acetazolamide - induced Gerstmann syndrome. Acute confusion induced by acetazolamide is a well known adverse drug reaction in patients with renal impairment. We report a case of acetazolamide - induced Gerstmann syndrome in a patient with normal renal function, to highlight predisposing factors that are frequently overlooked.

Acetazolamide

acetazolamide

acetazolamide

Gerstmann syndrome

confusion

renal impairment

Gerstmann syndrome

Acetazolamide

Gerstmann syndrome

Acetazolamide

Gerstmann syndrome

acetazolamide

Gerstmann syndrome

acetazolamide

Gerstmann syndrome

acetazolamide

Gerstmann syndrome

acetazolamide

Gerstmann syndrome


Input: Hypomania - like syndrome induced by olanzapine. We report a female patient with a diagnosis of a not otherwise specified psychotic disorder (DSM - IV) who developed hypomania shortly after the introduction of olanzapine treatment.

Hypomania

psychotic disorder

hypomania

olanzapine

olanzapine

olanzapine

Hypomania

olanzapine

hypomania

olanzapine

Hypomania

olanzapine

hypomania


Input: Neutrophil superoxide and hydrogen peroxide production in patients with acute liver failure. Defects in superoxide and hydrogen peroxide production may be implicated in the high incidence of bacterial infections in patients with acute liver failure (ALF). In the present study, oxygen radical production in patients with ALF due to paracetamol overdose was compared with that of healthy volunteers. Neutrophils from 14 ALF patients were stimulated via the complement receptors using zymosan opsonized with ALF or control serum. Superoxide and hydrogen peroxide production by ALF neutrophils stimulated with zymosan opsonized with ALF serum was significantly reduced compared with the control subjects (P < 0. 01). This defect persisted when zymosan opsonized by control serum was used (P < 0. 05). Superoxide and hydrogen peroxide production in neutrophils stimulated with formyl - methionyl - leucyl - phenylalanine (fMLP) from a further 18 ALF patients was unaffected compared with control neutrophils. Serum C3 complement levels were significantly reduced in ALF patients compared with control subjects (P < 0. 0005). These results demonstrate a neutrophil defect in ALF due to paracetamol overdose, that is complement dependent but independent of serum complement, possibly connected to the complement receptor.

superoxide

hydrogen peroxide

superoxide

hydrogen peroxide

oxygen

paracetamol

Superoxide

hydrogen peroxide

Superoxide

hydrogen peroxide

formyl - methionyl - leucyl - phenylalanine

fMLP

paracetamol

acute liver failure

bacterial infections

acute liver failure

ALF

ALF

overdose

ALF

ALF

ALF

ALF

ALF

ALF

ALF

overdose

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

acute liver failure

paracetamol

acute liver failure

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF

paracetamol

ALF


Input: Absence of effect of sertraline on time - based sensitization of cognitive impairment with haloperidol. This double - blind, randomized, placebo - controlled study evaluated the effects of haloperidol alone and haloperidol plus sertraline on cognitive and psychomotor function in 24 healthy male subjects. METHOD: All subjects received placebo on Day 1 and haloperidol 2 mg on Days 2 and 25. From Days 9 to 25, subjects were randomly assigned to either sertraline (12 subjects) or placebo (12 subjects); the sertraline dose was titrated from 50 to 200 mg / day from Days 9 to 16, and remained at 200 mg / day for the final 10 days of the drug administration period. Cognitive function testing was performed before dosing and over a 24 - hour period after dosing on Days 1, 2, and 25. RESULTS: Impairment of cognitive function was observed 6 to 8 hours after administration of haloperidol on Day 2 but was not evident 23 hours after dosing. When single - dose haloperidol was given again 25 days later, greater impairment with earlier onset was noted in several tests in both treatment groups, suggesting enhancement of this effect. There was no indication that sertraline exacerbated the impairment produced by haloperidol since an equivalent effect also occurred in the placebo group. Three subjects (2 on sertraline and 1 on placebo) withdrew from the study because of side effects. Ten subjects in each group reported side effects related to treatment. The side effect profiles of sertraline and of placebo were similar. CONCLUSION: Haloperidol produced a clear profile of cognitive impairment that was not worsened by concomitant sertraline administration.

sertraline

haloperidol

haloperidol

haloperidol

sertraline

haloperidol

sertraline

sertraline

haloperidol

haloperidol

sertraline

haloperidol

sertraline

sertraline

Haloperidol

sertraline

cognitive impairment

Impairment of cognitive function

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

haloperidol

cognitive impairment

haloperidol

Impairment of cognitive function

haloperidol

cognitive impairment

Haloperidol

cognitive impairment

Haloperidol

Impairment of cognitive function

Haloperidol

cognitive impairment


Input: Ciprofloxacin - induced nephrotoxicity in patients with cancer. Nephrotoxicity associated with ciprofloxacin is uncommon. Five patients with cancer who developed acute renal failure that followed treatment with ciprofloxacin are described and an additional 15 cases reported in the literature are reviewed. Other than elevation of serum creatinine levels, characteristic clinical manifestations and abnormal laboratory findings are not frequently present. Allergic interstitial nephritis is believed to be the underlying pathological - process. Definitive diagnosis requires performance of renal biopsy, although this is not always feasible. An improvement in renal function that followed the discontinuation of the offending antibiotic supports the presumptive diagnosis of ciprofloxacin - induced acute renal failure.

Ciprofloxacin

ciprofloxacin

ciprofloxacin

creatinine

ciprofloxacin

nephrotoxicity

cancer

Nephrotoxicity

cancer

acute renal failure

interstitial nephritis

acute renal failure

Ciprofloxacin

acute renal failure

Ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure

ciprofloxacin

acute renal failure


Input: Case report: pentamidine and polymorphic ventricular tachycardia revisited. Pentamidine isethionate has been associated with ventricular tachyarrhythmias, including torsade de pointes. This article reports two cases of this complication and reviews all reported cases to date. Pentamidine - induced torsade de pointes may be related to serum magnesium levels and hypomagnesemia may synergistically induce torsade. Torsade de pointes occurred after an average of 10 days of treatment with pentamidine. In these patients, no other acute side effects of pentamidine were observed. Torsade de pointes can be treated when recognized early, possibly without discontinuation of pentamidine. When QTc interval prolongation is observed, early magnesium supplementation is advocated.

pentamidine

Pentamidine isethionate

Pentamidine

magnesium

pentamidine

pentamidine

pentamidine

magnesium

ventricular tachycardia

ventricular tachyarrhythmias

torsade de pointes

torsade de pointes

hypomagnesemia

Torsade de pointes

Torsade de pointes

QTc interval prolongation

pentamidine

torsade de pointes

pentamidine

torsade de pointes

pentamidine

Torsade de pointes

pentamidine

Torsade de pointes

Pentamidine isethionate

torsade de pointes

Pentamidine isethionate

torsade de pointes

Pentamidine isethionate

Torsade de pointes

Pentamidine isethionate

Torsade de pointes

Pentamidine

torsade de pointes

Pentamidine

torsade de pointes

Pentamidine

Torsade de pointes

Pentamidine

Torsade de pointes

pentamidine

torsade de pointes

pentamidine

torsade de pointes

pentamidine

Torsade de pointes

pentamidine

Torsade de pointes

pentamidine

torsade de pointes

pentamidine

torsade de pointes

pentamidine

Torsade de pointes

pentamidine

Torsade de pointes

pentamidine

torsade de pointes

pentamidine

torsade de pointes

pentamidine

Torsade de pointes

pentamidine

Torsade de pointes


Input: Time dependence of plasma malondialdehyde, oxypurines, and nucleosides during incomplete cerebral ischemia in the rat. Incomplete cerebral ischemia (30 min) was induced in the rat by bilaterally clamping the common carotid arteries. Peripheral venous blood samples were withdrawn from the femoral vein four times (once every 5 min) before ischemia (0 time) and 5, 15, and 30 min after ischemia. Plasma extracts were analyzed by a highly sensitive high - performance liquid chromatographic method for the direct determination of malondialdehyde, oxypurines, and nucleosides. During ischemia, a time - dependent increase of plasma oxypurines and nucleosides was observed. Plasma malondialdehyde, which was present in minimal amount at zero time (0. 058 mumol / liter plasma; SD 0. 015), increased after 5 min of ischemia, resulting in a fivefold increase after 30 min of carotid occlusion (0. 298 mumol / liter plasma; SD 0. 078). Increased plasma malondialdehyde was also recorded in two other groups of animals subjected to the same experimental model, one receiving 20 mg / kg b. w. of the cyclooxygenase inhibitor acetylsalicylate intravenously immediately before ischemia, the other receiving 650 micrograms / kg b. w. of the hypotensive drug nitroprusside at a flow rate of 103 microliters / min intravenously during ischemia, although in this latter group malondialdehyde was significantly higher. The present data indicate that the determination of malondialdehyde, oxypurines, and nucleosides in peripheral blood, may be used to monitor the metabolic alterations of tissues occurring during ischemic phenomena. (ABSTRACT TRUNCATED AT 250 WORDS)

malondialdehyde

oxypurines

nucleosides

malondialdehyde

oxypurines

nucleosides

oxypurines

nucleosides

malondialdehyde

malondialdehyde

acetylsalicylate

nitroprusside

malondialdehyde

malondialdehyde

oxypurines

nucleosides

cerebral ischemia

cerebral ischemia

ischemia

ischemia

ischemia

ischemia

ischemia

hypotensive

ischemia

ischemic

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia

malondialdehyde

cerebral ischemia


Input: Cholinergic toxicity resulting from ocular instillation of echothiophate iodide eye drops. A patient developed a severe cholinergic syndrome from the use of echothiophate iodide ophthalmic drops, presented with profound muscle weakness and was initially given the diagnosis of myasthenia gravis. Red blood cell and serum cholinesterase levels were severely depressed and symptoms resolved spontaneously following discontinuation of the eye drops.

toxicity

muscle weakness

myasthenia gravis

echothiophate iodide

echothiophate iodide

echothiophate iodide

muscle weakness

echothiophate iodide

muscle weakness


Input: Acute renal failure in high dose carboplatin chemotherapy. Carboplatin has been reported to cause acute renal failure when administered in high doses to adult patients. We report a 4 1 / 2 - year - old girl who was treated with high - dose carboplatin for metastatic parameningeal embryonal rhabdomyosarcoma. Acute renal failure developed followed by a slow partial recovery of renal function. Possible contributing factors are discussed.

Acute renal failure

acute renal failure

embryonal rhabdomyosarcoma

Acute renal failure

carboplatin

Carboplatin

carboplatin

carboplatin

Acute renal failure

carboplatin

acute renal failure

carboplatin

Acute renal failure

Carboplatin

Acute renal failure

Carboplatin

acute renal failure

Carboplatin

Acute renal failure

carboplatin

Acute renal failure

carboplatin

acute renal failure

carboplatin

Acute renal failure


Input: Endometrial carcinoma after Hodgkin disease in childhood. A 34 - year - old patient developed metastic endometrial carcinoma after Hodgkin disease in childhood. She had ovarian failure after abdominal irradiation and chemotherapy for Hodgkin disease, and received exogenous estrogens, a treatment implicated in the development of endometrial cancer in menopausal women. Young women on replacement estrogens for ovarian failure after cancer therapy may also have increased risk of endometrial carcinoma and should be examined periodically.

Endometrial carcinoma

Hodgkin disease

endometrial carcinoma

Hodgkin disease

ovarian failure

Hodgkin disease

endometrial cancer

ovarian failure

cancer

endometrial carcinoma

estrogens

estrogens

estrogens

Endometrial carcinoma

estrogens

endometrial carcinoma

estrogens

endometrial cancer

estrogens

endometrial carcinoma

estrogens

Endometrial carcinoma

estrogens

endometrial carcinoma

estrogens

endometrial cancer

estrogens

endometrial carcinoma


Input: Induction of the obstructive sleep apnea syndrome in a woman by exogenous androgen administration. We documented airway occlusion during sleep and an abnormally high supraglottic resistance while awake in a 54 - yr - old woman who had developed physical changes and the syndrome of obstructive sleep apnea while being administered exogenous androgens. When the androgens were withdrawn, the patient' s physical changes, symptoms, sleep study, and supraglottic resistance all returned to normal. A rechallenge with androgen produced symptoms of obstructive sleep apnea that abated upon withdrawal of the hormone. Previous reports have favored a role of androgens in the pathogenesis of sleep apnea. Our report provides direct evidence for this role. Structural and functional measurements indicate that androgens exert a permissive or necessary action on the structural configuration of the oropharynx that predisposes to obstruction during sleep. Development of the obstructive sleep apnea syndrome must be considered a possible side effect of androgen therapy.

obstructive sleep apnea syndrome

syndrome of obstructive sleep apnea

obstructive sleep apnea

sleep apnea

obstructive sleep apnea syndrome

androgen

androgens

androgens

androgen

androgens

androgens

androgen

androgen

obstructive sleep apnea syndrome

androgen

syndrome of obstructive sleep apnea

androgen

obstructive sleep apnea

androgen

obstructive sleep apnea syndrome

androgens

obstructive sleep apnea syndrome

androgens

syndrome of obstructive sleep apnea

androgens

obstructive sleep apnea

androgens

obstructive sleep apnea syndrome

androgens

obstructive sleep apnea syndrome

androgens

syndrome of obstructive sleep apnea

androgens

obstructive sleep apnea

androgens

obstructive sleep apnea syndrome

androgen

obstructive sleep apnea syndrome

androgen

syndrome of obstructive sleep apnea

androgen

obstructive sleep apnea

androgen

obstructive sleep apnea syndrome

androgens

obstructive sleep apnea syndrome

androgens

syndrome of obstructive sleep apnea

androgens

obstructive sleep apnea

androgens

obstructive sleep apnea syndrome

androgens

obstructive sleep apnea syndrome

androgens

syndrome of obstructive sleep apnea

androgens

obstructive sleep apnea

androgens

obstructive sleep apnea syndrome

androgen

obstructive sleep apnea syndrome

androgen

syndrome of obstructive sleep apnea

androgen

obstructive sleep apnea

androgen

obstructive sleep apnea syndrome


Input: Effect of captopril on pre - existing and aminonucleoside - induced proteinuria in spontaneously hypertensive rats. Proteinuria is a side effect of captopril treatment in hypertensive patients. The possibility of reproducing the same renal abnormality with captopril was examined in SHR. Oral administration of captopril at 100 mg / kg for 14 days failed to aggravate proteinuria pre - existing in SHR. Also, captopril treatment failed to potentiate or facilitate development of massive proteinuria invoked by puromycin aminonucleoside in SHR. Captopril had little or no demonstrable effects on serum electrolyte concentrations, excretion of urine, sodium and potassium, endogenous creatinine clearance, body weight, and food and water consumption. However, ketone bodies were consistently present in urine and several lethalities occurred during multiple dosing of captopril in SHR.

captopril

aminonucleoside

captopril

captopril

captopril

captopril

puromycin aminonucleoside

Captopril

sodium

potassium

creatinine

ketone

captopril

proteinuria

hypertensive

Proteinuria

hypertensive

renal abnormality

proteinuria

proteinuria

aminonucleoside

proteinuria

aminonucleoside

Proteinuria

aminonucleoside

proteinuria

aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

Proteinuria

puromycin aminonucleoside

proteinuria

puromycin aminonucleoside

proteinuria


Input: Epileptogenic properties of enflurane and their clinical interpretation. Three cases of EEG changes induced by single exposure to enflurane anesthesia are reported. In one patient, enflurane administered during a donor nephrectomy resulted in unexpected partial motor seizures. Until the cause of the seizures was correctly identified, the patient was inappropriately treated with anticonvulsants. Two other patients suffered from partial, complex and generalized seizures uncontrolled by medication. Epileptic foci delineated and activated by enflurane were surgically ablated and the patients are now seizure - free. Previous exposures to enflurane have to be disclosed to avoid mistakes in clinical interpretation of the EEG. On the other hand, enflurane may prove to be a safe fast acting activator of epileptic foci during corticography or depth electrode intraoperative recordings.

enflurane

enflurane

enflurane

enflurane

enflurane

enflurane

seizures

seizures

seizures

Epileptic

seizure

epileptic

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure

enflurane

seizures

enflurane

seizures

enflurane

seizures

enflurane

seizure


Input: Reversible cerebral lesions associated with tiazofurin usage: MR demonstration. Tiazofurin is an experimental chemotherapeutic agent currently undergoing clinical evaluation. We report our results with magnetic resonance (MR) in demonstrating reversible cerebral abnormalities concurrent with the use of this drug. The abnormalities on MR were correlated with findings on CT as well as with cerebral angiography. The utility of MR in the evaluation of patients receiving this new agent is illustrated.

cerebral lesions

cerebral abnormalities

tiazofurin

Tiazofurin

tiazofurin

cerebral lesions

tiazofurin

cerebral abnormalities

Tiazofurin

cerebral lesions

Tiazofurin

cerebral abnormalities


Input: Antagonism of diazepam - induced sedative effects by Ro15 - 1788 in patients after surgery under lumbar epidural block. A double - blind placebo - controlled investigation of efficacy and safety. The aim of this study was to assess the efficacy of Ro15 - 1788 and a placebo in reversing diazepam - induced effects after surgery under epidural block, and to evaluate the local tolerance and general safety of Ro15 - 1788. Fifty - seven patients were sedated with diazepam for surgery under epidural anaesthesia. Antagonism of diazepam - induced effects by Ro15 - 1788 was investigated postoperatively in a double - blind placebo - controlled trial. The patient' s subjective assessment of mood rating, an objective test of performance, a test for amnesia, and vital signs were recorded for up to 300 min after administration of the trial drug. No significant differences between the two groups were observed for mood rating, amnesia, or vital signs. The Ro15 - 1788 group showed a significant improvement in the performance test up to 120 min after administration of the drug. There was no evidence of reaction at the injection site.

diazepam

Ro15 - 1788

Ro15 - 1788

diazepam

Ro15 - 1788

diazepam

diazepam

Ro15 - 1788

Ro15 - 1788

amnesia

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia

diazepam

amnesia


Input: Enhanced stimulus - induced neurotransmitter overflow in epinephrine - induced hypertensive rats is not mediated by prejunctional beta - adrenoceptor activation. The present study examines the effect of 6 - day epinephrine treatment (100 micrograms / kg per h, s. c.) on stimulus - induced (1 Hz) endogenous neurotransmitter overflow from the isolated perfused kidney of vehicle - and epinephrine - treated rats. Renal catecholamine stores and stimulus - induced overflow in the vehicle - treated group consisted of norepinephrine only. However, epinephrine treatment resulted in the incorporation of epinephrine into renal catecholamine stores such that approximately 40% of the catecholamine present was epinephrine while the norepinephrine content was reduced by a similar degree. Total tissue catecholamine content of the kidney on a molar basis was unchanged. Stimulus - induced fractional overflow of neurotransmitter from the epinephrine - treated kidneys was approximately twice normal and consisted of both norepinephrine and epinephrine in proportions similar to those found in the kidney. This difference in fractional overflow between groups was not affected by neuronal and extraneuronal uptake blockade. Propranolol had no effect on stimulus - induced overflow in either group. Phentolamine increased stimulus - induced overflow in both groups although the increment in overflow was greater in the epinephrine - treated group. In conclusion, chronic epinephrine treatment results in enhanced fractional neurotransmitter overflow. However, neither alterations in prejunctional beta - adrenoceptor influences nor alterations in neuronal and extraneuronal uptake mechanisms appear to be responsible for this alteration. Furthermore, data obtained with phentolamine alone do not suggest alpha - adrenoceptor desensitization as the cause of the enhanced neurotransmitter overflow after epinephrine treatment.

epinephrine

epinephrine

epinephrine

catecholamine

norepinephrine

epinephrine

epinephrine

catecholamine

catecholamine

epinephrine

norepinephrine

catecholamine

epinephrine

norepinephrine

epinephrine

Propranolol

Phentolamine

epinephrine

epinephrine

phentolamine

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive

epinephrine

hypertensive


Input: Ocular manifestations of juvenile rheumatoid arthritis. We followed 210 cases of juvenile rheumatoid arthritis closely for eleven years. Thirty - six of the 210 patients (17. 2%) developed iridocyclitis. Iridocyclitis was seen most frequently in young female patients (0 to 4 years) with the monoarticular or pauciatricular form of the arthritis. However, 30% of the patients developed uveitis after 16 years of age. Although 61% of patients had a noncontributory ocular history on entry, 42% had active uveitis on entry. Our approach was effective in detecting uveitis in new cases and exacerbations of uveitis in established cases. Forty - four percent of patients with uveitis had one or more identifiable signs or symptoms, such as red eye, ocular pain, decreased visual acuity, or photophobia, in order of decreasing frequency. Even after early detection and prompt treatment, 41% of cases of uveitis did not respond to more than six months of intensive topical treatment with corticosteroids and mydriatics. Despite this, there was a dramatic decrease in the 50% incidence of blinding complications of uveitis cited in earlier studies. Cataract and band keratopathy occurred in only 22 and 13% of our group, respectively. We used chloroquine or hydroxychloroquine in 173 of 210 cases and found only one case of chorioretinopathy attributable to these drugs. Systemically administered corticosteroids were used in 75 of 210 cases; a significant number of posterior subcapsular cataracts was found. Typical keratoconjunctivitis sicca developed in three of the uveitis cases. This association with uveitis and JRA was not noted previously. Surgical treatment of cataracts, band keratopathy, and glaucoma achieved uniformly discouraging results.

juvenile rheumatoid arthritis

juvenile rheumatoid arthritis

iridocyclitis

Iridocyclitis

arthritis

uveitis

uveitis

uveitis

uveitis

uveitis

ocular pain

decreased visual acuity

photophobia

uveitis

uveitis

Cataract

band keratopathy

chorioretinopathy

cataracts

keratoconjunctivitis

uveitis

uveitis

cataracts

band keratopathy

glaucoma

corticosteroids

chloroquine

hydroxychloroquine

corticosteroids

hydroxychloroquine

chorioretinopathy


Input: Water intoxication associated with oxytocin administration during saline - induced abortion. Four cases of water intoxication in connection with oxytocin administration during saline - induced abortions are described. The mechanism of water intoxication is discussed in regard to these cases. Oxytocin administration during midtrimester - induced abortions is advocated only if it can be carried out under careful observations of an alert nursing staff, aware of the symptoms of water intoxication and instructed to watch the diuresis and report such early signs of the syndrome as asthenia, muscular irritability, or headaches. The oxytocin should be given only in Ringers lactate or, alternately, in Ringers lactate and a 5 per cent dextrose and water solutions. The urinary output should be monitored and the oxytocin administration discontinued and the serum electrolytes checked if the urinary output decreases. The oxytocin should not be administered in excess of 36 hours. If the patient has not aborted by then the oxytocin should be discontinued for 10 to 12 hours in order to perform electrolyte determinations and correct any electrolyte imbalance.

Water intoxication

abortion

water intoxication

abortions

water intoxication

abortions

water intoxication

asthenia

irritability

headaches

oxytocin

oxytocin

Oxytocin

oxytocin

lactate

lactate

dextrose

oxytocin

oxytocin

oxytocin

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

Oxytocin

Water intoxication

Oxytocin

water intoxication

Oxytocin

water intoxication

Oxytocin

water intoxication

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

Water intoxication

oxytocin

water intoxication

oxytocin

water intoxication

oxytocin

water intoxication