Input: Amiodarone - induced torsade de pointes during bladder irrigation: an unusual presentation - - a case report. The authors present a case of early (within 4 days) development of torsade de pointes (TdP) associated with oral amiodarone therapy. Consistent with other reports this case of TdP occurred in the context of multiple exacerbating factors including hypokalemia and digoxin excess. Transient prolongation of the QT during bladder irrigation prompted the episode of TdP. It is well known that bradycardia exacerbates acquired TdP. The authors speculate that the increased vagal tone during bladder irrigation, a vagal maneuver, in the context of amiodarone therapy resulted in amiodarone - induced proarrhythmia. In the absence of amiodarone therapy, a second bladder irrigation did not induce TdP despite hypokalemia and hypomagnesemia.

Amiodarone

amiodarone

digoxin

amiodarone

amiodarone

amiodarone

torsade de pointes

torsade de pointes

TdP

TdP

hypokalemia

TdP

bradycardia

TdP

proarrhythmia

TdP

hypokalemia

hypomagnesemia

Amiodarone

torsade de pointes

Amiodarone

torsade de pointes

Amiodarone

TdP

Amiodarone

TdP

Amiodarone

TdP

Amiodarone

TdP

Amiodarone

TdP

amiodarone

torsade de pointes

amiodarone

torsade de pointes

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

torsade de pointes

amiodarone

torsade de pointes

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

torsade de pointes

amiodarone

torsade de pointes

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

torsade de pointes

amiodarone

torsade de pointes

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP

amiodarone

TdP


Input: Acute renal insufficiency after high - dose melphalan in patients with primary systemic amyloidosis during stem cell transplantation. BACKGROUND: Patients with primary systemic amyloidosis (AL) have a poor prognosis. Median survival time from standard treatments is only 17 months. High - dose intravenous melphalan followed by peripheral blood stem cell transplant (PBSCT) appears to be the most promising therapy, but treatment mortality can be high. The authors have noted the development of acute renal insufficiency immediately after melphalan conditioning. This study was undertaken to further examine its risk factors and impact on posttransplant mortality. METHODS: Consecutive AL patients who underwent PBSCT were studied retrospectively. Acute renal insufficiency (ARI) after high - dose melphalan was defined by a minimum increase of 0. 5 mg / dL (44 micromol / L) in the serum creatinine level that is greater than 50% of baseline immediately after conditioning. Urine sediment score was the sum of the individual types of sediment identified on urine microscopy. RESULTS: Of the 80 patients studied, ARI developed in 18. 8% of the patients after high - dose melphalan. Univariate analysis identified age, hypoalbuminemia, heavy proteinuria, diuretic use, and urine sediment score (> 3) as risk factors. Age and urine sediment score remained independently significant risk factors in the multivariate analysis. Patients who had ARI after high - dose melphalan underwent dialysis more often (P = 0. 007), and had a worse 1 - year survival (P = 0. 03). CONCLUSION: The timing of renal injury strongly suggests melphalan as the causative agent. Ongoing tubular injury may be a prerequisite for renal injury by melphalan as evidenced by the active urinary sediment. Development of ARI adversely affected the outcome after PBSCT. Effective preventive measures may help decrease the treatment mortality of PBSCT in AL patients.

Acute renal insufficiency

primary systemic amyloidosis

primary systemic amyloidosis

AL

acute renal insufficiency

AL

Acute renal insufficiency

ARI

ARI

hypoalbuminemia

proteinuria

ARI

renal injury

tubular injury

renal injury

ARI

AL

melphalan

melphalan

melphalan

melphalan

creatinine

melphalan

melphalan

melphalan

melphalan

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI

melphalan

Acute renal insufficiency

melphalan

acute renal insufficiency

melphalan

Acute renal insufficiency

melphalan

ARI

melphalan

ARI

melphalan

ARI

melphalan

renal injury

melphalan

renal injury

melphalan

ARI


Input: Impaired fear recognition in regular recreational cocaine users. INTRODUCTION: The ability to read facial expressions is essential for normal human social interaction. The aim of the present study was to conduct the first investigation of facial expression recognition performance in recreational cocaine users. MATERIALS AND METHODS: Three groups, comprised of 21 cocaine naive participants (CN), 30 occasional cocaine (OC), and 48 regular recreational cocaine (RC) users, were compared. An emotional facial expression (EFE) task consisting of a male and female face expressing six basic emotions (happiness, surprise, sadness, anger, fear, and disgust) was administered. Mean percent accuracy and latencies for correct responses across eight presentations of each basic emotion were derived. Participants were also assessed with the " Eyes task " to investigate their ability to recognize more complex emotional states and the Symptom CheckList - 90 - Revised to measure psychopathology. RESULTS: There were no group differences in psychopathology or " eyes task " performance, but the RC group, who otherwise had similar illicit substance use histories to the OC group, exhibited impaired fear recognition accuracy compared to the OC and CN groups. The RC group also correctly identified anger, fear, happiness, and surprise, more slowly than CN, but not OC participants. The OC group was slower than CN when correctly identifying disgust. The selective deficit in fear recognition accuracy manifested by the RC group cannot be explained by the subacute effects of cocaine, or ecstasy, because recent and less recent users of these drugs within this group were similarly impaired. Possible parallels between RC users and psychopaths with respect to impaired fear recognition, amygdala dysfunction, and etiology are discussed.

Impaired fear recognition

impaired fear recognition

deficit in fear recognition

psychopaths

impaired fear recognition

amygdala dysfunction

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

ecstasy

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition

cocaine

Impaired fear recognition

cocaine

impaired fear recognition

cocaine

deficit in fear recognition

cocaine

impaired fear recognition


Input: Corneal ulcers associated with aerosolized crack cocaine use. PURPOSE: We report 4 cases of corneal ulcers associated with drug abuse. The pathogenesis of these ulcers and management of these patients are also reviewed. METHODS: Review of all cases of corneal ulcers associated with drug abuse seen at our institution from July 2006 to December 2006. RESULTS: Four patients with corneal ulcers associated with crack cocaine use were reviewed. All corneal ulcers were cultured, and the patients were admitted to the hospital for intensive topical antibiotic treatment. Each patient received comprehensive health care, including medical and substance abuse consultations. Streptococcal organisms were found in 3 cases and Capnocytophaga and Brevibacterium casei in 1 patient. The infections responded to antibiotic treatment. Two patients needed a lateral tarsorrhaphy for persistent epithelial defects. CONCLUSIONS: Aerosolized crack cocaine use can be associated with the development of corneal ulcers. Drug abuse provides additional challenges for management. Not only treatment of their infections but also the overall poor health of the patients and increased risk of noncompliance need to be addressed. Comprehensive care may provide the patient the opportunity to discontinue their substance abuse, improve their overall health, and prevent future corneal complications.

Corneal ulcers

corneal ulcers

drug abuse

ulcers

corneal ulcers

drug abuse

corneal ulcers

corneal ulcers

substance abuse

infections

epithelial defects

corneal ulcers

Drug abuse

infections

substance abuse

crack cocaine

crack cocaine

crack cocaine

crack cocaine

Corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

Corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

Corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers

crack cocaine

corneal ulcers


Input: Levetiracetam as an adjunct to phenobarbital treatment in cats with suspected idiopathic epilepsy. OBJECTIVE: To assess pharmacokinetics, efficacy, and tolerability of oral levetiracetam administered as an adjunct to phenobarbital treatment in cats with poorly controlled suspected idiopathic epilepsy. DESIGN - Open - label, noncomparative clinical trial. ANIMALS: 12 cats suspected to have idiopathic epilepsy that was poorly controlled with phenobarbital or that had unacceptable adverse effects when treated with phenobarbital. PROCEDURES: Cats were treated with levetiracetam (20 mg / kg [9. 1 mg / lb], PO, q 8 h). After a minimum of 1 week of treatment, serum levetiracetam concentrations were measured before and 2, 4, and 6 hours after drug administration, and maximum and minimum serum concentrations and elimination half - life were calculated. Seizure frequencies before and after initiation of levetiracetam treatment were compared, and adverse effects were recorded. RESULTS: Median maximum serum levetiracetam concentration was 25. 5 microg / mL, median minimum serum levetiracetam concentration was 8. 3 microg / mL, and median elimination half - life was 2. 9 hours. Median seizure frequency prior to treatment with levetiracetam (2. 1 seizures / mo) was significantly higher than median seizure frequency after initiation of levetiracetam treatment (0. 42 seizures / mo), and 7 of 10 cats were classified as having responded to levetiracetam treatment (ie, reduction in seizure frequency of > or = 50%). Two cats had transient lethargy and inappetence. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that levetiracetam is well tolerated in cats and may be useful as an adjunct to phenobarbital treatment in cats with idiopathic epilepsy.

Levetiracetam

phenobarbital

levetiracetam

phenobarbital

phenobarbital

phenobarbital

levetiracetam

levetiracetam

levetiracetam

levetiracetam

levetiracetam

levetiracetam

levetiracetam

levetiracetam

levetiracetam

phenobarbital

idiopathic epilepsy

idiopathic epilepsy

idiopathic epilepsy

Seizure

seizure

seizures

seizure

seizures

seizure

lethargy

inappetence

idiopathic epilepsy

Levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy

levetiracetam

lethargy


Input: Bilateral haemorrhagic infarction of the globus pallidus after cocaine and alcohol intoxication. Cocaine is a risk factor for both ischemic and haemorrhagic stroke. We present the case of a 31 - year - old man with bilateral ischemia of the globus pallidus after excessive alcohol and intranasal cocaine use. Drug - related globus pallidus infarctions are most often associated with heroin. Bilateral basal ganglia infarcts after the use of cocaine, without concurrent heroin use, have never been reported. In our patient, transient cardiac arrhythmia or respiratory dysfunction related to cocaine and / or ethanol use were the most likely causes of cerebral hypoperfusion.

haemorrhagic infarction of the globus pallidus

haemorrhagic

infarction of the globus pallidus

ischemic and haemorrhagic stroke

ischemic and haemorrhagic stroke

haemorrhagic stroke

ischemia of the globus pallidus

globus pallidus infarctions

basal ganglia infarcts

cardiac arrhythmia

respiratory dysfunction

cerebral hypoperfusion

cocaine

alcohol

Cocaine

alcohol

cocaine

heroin

cocaine

heroin

cocaine

ethanol

heroin

haemorrhagic infarction of the globus pallidus

heroin

infarction of the globus pallidus

heroin

globus pallidus infarctions

heroin

basal ganglia infarcts

heroin

haemorrhagic infarction of the globus pallidus

heroin

infarction of the globus pallidus

heroin

globus pallidus infarctions

heroin

basal ganglia infarcts

cocaine

ischemia of the globus pallidus

Cocaine

ischemia of the globus pallidus

cocaine

ischemia of the globus pallidus

cocaine

ischemia of the globus pallidus

cocaine

ischemia of the globus pallidus

alcohol

ischemic and haemorrhagic stroke

alcohol

ischemic and haemorrhagic stroke

alcohol

ischemic and haemorrhagic stroke

alcohol

ischemic and haemorrhagic stroke

ethanol

ischemic and haemorrhagic stroke

ethanol

ischemic and haemorrhagic stroke

alcohol

haemorrhagic stroke

alcohol

haemorrhagic stroke

ethanol

haemorrhagic stroke


Input: Acute renal failure after high - dose methotrexate therapy in a patient with ileostomy. High - dose methotrexate (HD - MTX) is an important treatment for Burkitt lymphoma, but can cause hepatic and renal toxicity when its clearance is delayed. We report a case of acute renal failure after HD - MTX therapy in a patient with ileostomy, The patient was a 3 - year - old boy who had received a living - related liver transplantation for congenital biliary atresia. At day 833 after the transplantation, he was diagnosed with PTLD (post - transplantation lymphoproliferative disorder, Burkitt - type malignant lymphoma). During induction therapy, he suffered ileal perforation and ileostomy was performed. Subsequent HD - MTX therapy caused acute renal failure that required continuous hemodialysis. We supposed that intravascular hypovolemia due to substantial drainage from the ileostoma caused acute prerenal failure. After recovery of his renal function, we could safely treat the patient with HD - MTX therapy by controlling drainage from ileostoma with total parenteral nutrition.

Acute renal failure

Burkitt lymphoma

hepatic and renal toxicity

hepatic and renal toxicity

renal toxicity

acute renal failure

biliary atresia

PTLD

post - transplantation lymphoproliferative disorder

Burkitt - type malignant lymphoma

acute renal failure

hypovolemia

acute prerenal failure

methotrexate

methotrexate

MTX

MTX

MTX

MTX

methotrexate

Acute renal failure

methotrexate

acute renal failure

methotrexate

acute renal failure

methotrexate

Acute renal failure

methotrexate

acute renal failure

methotrexate

acute renal failure

MTX

Acute renal failure

MTX

acute renal failure

MTX

acute renal failure

MTX

Acute renal failure

MTX

acute renal failure

MTX

acute renal failure

MTX

Acute renal failure

MTX

acute renal failure

MTX

acute renal failure

MTX

Acute renal failure

MTX

acute renal failure

MTX

acute renal failure


Input: Antithrombotic drug use, cerebral microbleeds, and intracerebral hemorrhage: a systematic review of published and unpublished studies. BACKGROUND AND PURPOSE: Cerebral microbleeds (MB) are potential risk factors for intracerebral hemorrhage (ICH), but it is unclear if they are a contraindication to using antithrombotic drugs. Insights could be gained by pooling data on MB frequency stratified by antithrombotic use in cohorts with ICH and ischemic stroke (IS) / transient ischemic attack (TIA). METHODS: We performed a systematic review of published and unpublished data from cohorts with stroke or TIA to compare the presence of MB in: (1) antithrombotic users vs nonantithrombotic users with ICH; (2) antithrombotic users vs nonusers with IS / TIA; and (3) ICH vs ischemic events stratified by antithrombotic use. We also analyzed published and unpublished follow - up data to determine the risk of ICH in antithrombotic users with MB. RESULTS: In a pooled analysis of 1460 ICH and 3817 IS / TIA, MB were more frequent in ICH vs IS / TIA in all treatment groups, but the excess increased from 2. 8 (odds ratio; range, 2. 3 - 3. 5) in nonantithrombotic users to 5. 7 (range, 3. 4 - 9. 7) in antiplatelet users and 8. 0 (range, 3. 5 - 17. 8) in warfarin users (P difference = 0. 01). There was also an excess of MB in warfarin users vs nonusers with ICH (OR, 2. 7; 95% CI, 1. 6 - 4. 4; P < 0. 001) but none in warfarin users with IS / TIA (OR, 1. 3; 95% CI, 0. 9 - 1. 7; P = 0. 33; P difference = 0. 01). There was a smaller excess of MB in antiplatelet users vs nonusers with ICH (OR, 1. 7; 95% CI, 1. 3 - 2. 3; P < 0. 001), but findings were similar for antiplatelet users with IS / TIA (OR, 1. 4; 95% CI, 1. 2 - 1. 7; P < 0. 001; P difference = 0. 25). In pooled follow - up data for 768 antithrombotic users, presence of MB at baseline was associated with a substantially increased risk of subsequent ICH (OR, 12. 1; 95% CI, 3. 4 - 42. 5; P < 0. 001). CONCLUSIONS: The excess of MB in warfarin users with ICH compared to other groups suggests that MB increase the risk of warfarin - associated ICH. Limited prospective data corroborate these findings, but larger prospective studies are urgently required.

cerebral microbleeds

intracerebral hemorrhage

Cerebral microbleeds

MB

intracerebral hemorrhage

ICH

MB

ICH

ischemic stroke

IS

transient ischemic attack

TIA

stroke

TIA

MB

ICH

IS

TIA

ICH

ischemic

ICH

MB

ICH

IS

TIA

MB

ICH

IS

TIA

MB

ICH

IS

TIA

MB

ICH

IS

TIA

MB

ICH

MB

ICH

MB

ICH

warfarin

warfarin

warfarin

warfarin

warfarin

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

intracerebral hemorrhage

warfarin

intracerebral hemorrhage

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH

warfarin

ICH


Input: Verapamil stimulation test in hyperprolactinemia: loss of prolactin response in anatomic or functional stalk effect. AIM: Verapamil stimulation test was previously investigated as a tool for differential diagnosis of hyperprolactinemia, but with conflicting results. Macroprolactinemia was never considered in those previous studies. Here, we aimed to re - investigate the diagnostic value of verapamil in a population who were all screened for macroprolactinemia. Prolactin responses to verapamil in 65 female patients (age: 29. 9 + / - 8. 1 years) with hyperprolactinemia were tested in a descriptive, matched case - control study. METHODS: Verapamil 80 mg, p. o. was administered, and then PRL levels were measured at 8th and 16th hours, by immunometric chemiluminescence. Verapamil responsiveness was determined by peak percent change in basal prolactin levels (PRL). RESULTS: Verapamil significantly increased PRL levels in healthy controls (N. 8, PRL: 183%), macroprolactinoma (N. 8, PRL: 7%), microprolactinoma (N. 19, PRL: 21%), macroprolactinemia (N. 23, PRL: 126%), but not in pseudoprolactinoma (N. 8, PRL: 0. 8%), and risperidone - induced hyperprolactinemia (N. 7, PRL: 3%). ROC curve analysis revealed that unresponsiveness to verapamil defined as PRL < 7%, discriminated anatomical or functional stalk effect (sensitivity: 74%, specificity: 73%, AUC: 0. 855 + / - 0. 04, P < 0. 001, CI: 0. 768 - 0. 942) associated with pseudoprolactinoma or risperidone - induced hyperprolactinemia, respectively. CONCLUSION: Verapamil responsiveness is not a reliable finding for the differential diagnosis of hyperprolactinemia. However, verapamil unresponsiveness discriminates stalk effect (i. e., anatomically or functionally inhibited dopaminergic tonus) from other causes of hyperprolactinemia with varying degrees of responsiveness.

Verapamil

Verapamil

verapamil

verapamil

Verapamil

Verapamil

Verapamil

risperidone

verapamil

risperidone

Verapamil

verapamil

hyperprolactinemia

hyperprolactinemia

Macroprolactinemia

macroprolactinemia

hyperprolactinemia

macroprolactinoma

microprolactinoma

macroprolactinemia

pseudoprolactinoma

hyperprolactinemia

pseudoprolactinoma

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia


Input: Central action of narcotic analgesics. Part IV. Noradrenergic influences on the activity of analgesics in rats. The effect of clonidine, naphazoline and xylometazoline on analgesia induced by morphine, codeine, fentanyl and pentazocine, and on cataleptic effect of morphine, codine and fentanyl was studied in rats. The biochemical assays on the influence of four analgesics on the brain concentration and turnover of noradrenaline (NA) were also performed. It was found that three drugs stimulating central NA receptors failed to affect the analgesic ED50 of all antinociceptive agents and they enhanced catalepsy induced by morphine and fentanyl. Codeine catalepsy was increased by clonidine and decreased by naphazoline and xylometazoline. The brain concentration of NA was not changed by morphine and fentanyl, but one of the doses of codeine (45 mg / kg) slightly enhanced it. Pentazocine dose - dependently decreased the brain level of NA. The rate of NA turnover was not altered by analgesics except for the higher dose of fentanyl (0. 2 mg / kg) following which the disappearance of NA from the brain was diminished. The results are discussed in the light of various and non - uniform data from the literature. It is suggested that in rats the brain NA plays a less important function than the other monoamines in the behavioural activity of potent analgesics.

clonidine

naphazoline

xylometazoline

morphine

codeine

fentanyl

pentazocine

morphine

codine

fentanyl

noradrenaline

morphine

fentanyl

Codeine

clonidine

naphazoline

xylometazoline

morphine

fentanyl

codeine

Pentazocine

fentanyl

monoamines

cataleptic

catalepsy

catalepsy

clonidine

cataleptic

clonidine

catalepsy

clonidine

catalepsy

clonidine

cataleptic

clonidine

catalepsy

clonidine

catalepsy

fentanyl

cataleptic

fentanyl

catalepsy

fentanyl

catalepsy

fentanyl

cataleptic

fentanyl

catalepsy

fentanyl

catalepsy

fentanyl

cataleptic

fentanyl

catalepsy

fentanyl

catalepsy

fentanyl

cataleptic

fentanyl

catalepsy

fentanyl

catalepsy

fentanyl

cataleptic

fentanyl

catalepsy

fentanyl

catalepsy

naphazoline

cataleptic

naphazoline

catalepsy

naphazoline

catalepsy

naphazoline

cataleptic

naphazoline

catalepsy

naphazoline

catalepsy

codeine

cataleptic

codeine

catalepsy

codeine

catalepsy

codine

cataleptic

codine

catalepsy

codine

catalepsy

Codeine

cataleptic

Codeine

catalepsy

Codeine

catalepsy

codeine

cataleptic

codeine

catalepsy

codeine

catalepsy

xylometazoline

cataleptic

xylometazoline

catalepsy

xylometazoline

catalepsy

xylometazoline

cataleptic

xylometazoline

catalepsy

xylometazoline

catalepsy

morphine

cataleptic

morphine

catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

catalepsy

morphine

catalepsy

morphine

cataleptic

morphine

catalepsy

morphine

catalepsy


Input: Modification by propranolol of cardiovascular effects of induced hypoglycaemia. The cardiovascular effects of hypoglycaemia, with and without beta - blockade, were compared in fourteen healthy men. Eight received insulin alone, and eight, including two of the original insulin - only group, were given propranolol and insulin. In the insulin - group the period of hypoglycaemia was associated with an increase in heart - rate and a fall in diastolic blood - pressure. In the propranolol - insulin group there was a significant fall in heart - rate in most subjects and an increase in diastolic pressure. Typical S - T / T changes occurred in the insulin - group but in none of the propranolol - insulin group. Hypertension in diabetics prone to hypoglycaemia attacks should not be treated with beta - blockers because these drugs may cause a sharp rise in blood - pressure in such patients.

propranolol

propranolol

propranolol

propranolol

hypoglycaemia

hypoglycaemia

hypoglycaemia

Hypertension

diabetics

hypoglycaemia

propranolol

Hypertension

propranolol

Hypertension

propranolol

Hypertension

propranolol

Hypertension


Input: Prevention and treatment of endometrial disease in climacteric women receiving oestrogen therapy. The treatment regimens are described in 74 patients with endometrial disease among 850 climacteric women receiving oestrogen therapy. Cystic hyperplasia was associated with unopposed oestrogen therapy without progestagen. Two courses of 21 days of 5 mg norethisterone daily caused reversion to normal in all 57 cases of cystic hyperplasia and 6 of the 8 cases of atypical hyperplasia. 4 cases of endometrial carcinoma referred from elsewhere demonstrated the problems of inappropriate and unsupervised unopposed oestrogen therapy and the difficulty in distinguishing severe hyperplasia from malignancy. Cyclical low - dose oestrogen therapy with 7 - - 13 days of progestagen does not seem to increase the risk of endometrial hyperplasia or carcinoma.

endometrial disease

endometrial disease

hyperplasia

hyperplasia

hyperplasia

endometrial carcinoma

hyperplasia

malignancy

endometrial hyperplasia

carcinoma

oestrogen

oestrogen

oestrogen

progestagen

norethisterone

oestrogen

oestrogen

progestagen

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia

oestrogen

hyperplasia


Input: Pure red cell aplasia, toxic dermatitis and lymphadenopathy in a patient taking diphenylhydantoin. A patient taking diphenylhydantoin for 3 weeks developed a generalized skin rash, lymphadenopathy and pure red cell aplasia. After withdrawal of the pharmacon all symptoms disappeared spontaneously. Skin rash is a well - known complication of diphenylhydantoin treatment as is benign and malignant lymphadenopathy. Pure red cell aplasia associated with diphenylhydantoin medication has been reported in 3 patients. The exact mechanism by which diphenylhydantoin exerts its toxic effects is not known. In this patient the time relation between the ingestion of diphenylhydantoin and the occurrence of the skin rash, lymphadenopathy and pure red cell aplasia is very suggestive of a direct connection.

Pure red cell aplasia

toxic dermatitis

lymphadenopathy

skin rash

lymphadenopathy

pure red cell aplasia

Skin rash

lymphadenopathy

Pure red cell aplasia

skin rash

lymphadenopathy

pure red cell aplasia

diphenylhydantoin

diphenylhydantoin

diphenylhydantoin

diphenylhydantoin

diphenylhydantoin

diphenylhydantoin

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

toxic dermatitis

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

lymphadenopathy

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia

diphenylhydantoin

Pure red cell aplasia

diphenylhydantoin

pure red cell aplasia


Input: Continuous infusion tobramycin combined with carbenicillin for infections in cancer patients. The cure rate of infections in cancer patients is adversely affected by neutropenia (less than 1, 000 / mm3). In particular, patients with severe neutropenia (less than 100 / mm3) have shown a poor response to antibiotics. To overcome the adverse effects of neutropenia, tobramycin was given by continuous infusion and combined with intermittent carbenicillin. Tobramycin was given to a total daily dose of 300 mg / m2 and carbenicillin was given at a dose of 5 gm every four hours. There were 125 infectious episodes in 116 cancer patients receiving myelosuppressive chemotherapy. The overall cure rate was 70%. Pneumonia was the most common infection and 61% of 59 episodes were cured. Gram - negative bacilli were the most common causative organisms and 69% of these infections were cured. The most common pathogen was Klebsiella pneumoniae and this, together with Escherichia coli and Pseudomonas aeruginosa, accounted for 74% of all gram - negative bacillary infections. Response was not influenced by the initial neutrophil count, with a 62% cure rate for 39 episodes associated with severe neutropenia. However, failure of the neutrophil count to increase during therapy adversely affected response. Azotemia was the major side effect recognized, and it occurred in 11% of episodes. Major azotemia (serum creatinine greater than 2. 5 mg / dl or BUN greater than 50 mg / dl) occurred in only 2%. Azotemia was not related to duration of therapy or serum tobramycin concentration. This antibiotic regimen showed both therapeutic efficacy and acceptable renal toxicity for these patients.

tobramycin

carbenicillin

tobramycin

carbenicillin

Tobramycin

carbenicillin

creatinine

tobramycin

infections

cancer

infections

cancer

neutropenia

neutropenia

neutropenia

cancer

Pneumonia

infection

infections

pneumoniae

gram - negative bacillary infections

neutropenia

Azotemia

azotemia

Azotemia

renal toxicity

tobramycin

Azotemia

tobramycin

azotemia

tobramycin

Azotemia

tobramycin

Azotemia

tobramycin

azotemia

tobramycin

Azotemia

Tobramycin

Azotemia

Tobramycin

azotemia

Tobramycin

Azotemia

tobramycin

Azotemia

tobramycin

azotemia

tobramycin

Azotemia

carbenicillin

Azotemia

carbenicillin

azotemia

carbenicillin

Azotemia

carbenicillin

Azotemia

carbenicillin

azotemia

carbenicillin

Azotemia

carbenicillin

Azotemia

carbenicillin

azotemia

carbenicillin

Azotemia


Input: Recurrent subarachnoid hemorrhage associated with aminocaproic acid therapy and acute renal artery thrombosis. Case report. Epsilon aminocaproic acid (EACA) has been used to prevent rebleeding in patients with subarachnoid hemorrhage (SAH). Although this agent does decrease the frequency of rebleeding, several reports have described thrombotic complications of EACA therapy. These complications have included clinical deterioration and intracranial vascular thrombosis in patients with SAH, arteriolar and capillary fibrin thrombi in patients with fibrinolytic syndromes treated with EACA, or other thromboembolic phenomena. Since intravascular fibrin thrombi are often observed in patients with fibrinolytic disorders, EACA should not be implicated in the pathogenesis of fibrin thrombi in patients with disseminated intravascular coagulation or other " consumption coagulopathies. " This report describes subtotal infarction of the kidney due to thrombosis of a normal renal artery. This occlusion occurred after EACA therapy in a patient with SAH and histopathological documentation of recurrent SAH. The corresponding clinical event was characterized by marked hypertension and abrupt neurological deterioration.

subarachnoid hemorrhage

acute renal artery thrombosis

subarachnoid hemorrhage

SAH

thrombotic

intracranial vascular thrombosis

SAH

thrombi

thromboembolic phenomena

thrombi

thrombi

disseminated intravascular coagulation

consumption coagulopathies

infarction

thrombosis of a normal renal artery

SAH

SAH

hypertension

aminocaproic acid

Epsilon aminocaproic acid

EACA

EACA

EACA

EACA

EACA

Epsilon aminocaproic acid

subarachnoid hemorrhage

Epsilon aminocaproic acid

subarachnoid hemorrhage

Epsilon aminocaproic acid

SAH

Epsilon aminocaproic acid

SAH

Epsilon aminocaproic acid

SAH

Epsilon aminocaproic acid

SAH

EACA

subarachnoid hemorrhage

EACA

subarachnoid hemorrhage

EACA

SAH

EACA

SAH

EACA

SAH

EACA

SAH

EACA

subarachnoid hemorrhage

EACA

subarachnoid hemorrhage

EACA

SAH

EACA

SAH

EACA

SAH

EACA

SAH

EACA

subarachnoid hemorrhage

EACA

subarachnoid hemorrhage

EACA

SAH

EACA

SAH

EACA

SAH

EACA

SAH

EACA

subarachnoid hemorrhage

EACA

subarachnoid hemorrhage

EACA

SAH

EACA

SAH

EACA

SAH

EACA

SAH

EACA

subarachnoid hemorrhage

EACA

subarachnoid hemorrhage

EACA

SAH

EACA

SAH

EACA

SAH

EACA

SAH

Epsilon aminocaproic acid

acute renal artery thrombosis

Epsilon aminocaproic acid

thrombosis of a normal renal artery

EACA

acute renal artery thrombosis

EACA

thrombosis of a normal renal artery

EACA

acute renal artery thrombosis

EACA

thrombosis of a normal renal artery

EACA

acute renal artery thrombosis

EACA

thrombosis of a normal renal artery

EACA

acute renal artery thrombosis

EACA

thrombosis of a normal renal artery

EACA

acute renal artery thrombosis

EACA

thrombosis of a normal renal artery

Epsilon aminocaproic acid

thrombotic

Epsilon aminocaproic acid

thrombi

Epsilon aminocaproic acid

thrombi

Epsilon aminocaproic acid

thrombi

EACA

thrombotic

EACA

thrombi

EACA

thrombi

EACA

thrombi

EACA

thrombotic

EACA

thrombi

EACA

thrombi

EACA

thrombi

EACA

thrombotic

EACA

thrombi

EACA

thrombi

EACA

thrombi

EACA

thrombotic

EACA

thrombi

EACA

thrombi

EACA

thrombi

EACA

thrombotic

EACA

thrombi

EACA

thrombi

EACA

thrombi

Epsilon aminocaproic acid

intracranial vascular thrombosis

EACA

intracranial vascular thrombosis

EACA

intracranial vascular thrombosis

EACA

intracranial vascular thrombosis

EACA

intracranial vascular thrombosis

EACA

intracranial vascular thrombosis

Epsilon aminocaproic acid

hypertension

EACA

hypertension

EACA

hypertension

EACA

hypertension

EACA

hypertension

EACA

hypertension


Input: Long - term propranolol therapy in pregnancy: maternal and fetal outcome. Propranolol, a beta - adrenergic blocking agent, has found an important position in the practice of medicine. Its use in pregnancy, however, is an open question as a number of detrimental side effects have been reported in the fetus and neonate. Ten patients and 12 pregnancies are reported where chronic propranolol has been administered. Five patients with serial pregnancies with and without propranolol therapy are also examined. Maternal, fetal, and neonatal complications are examined. An attempt is made to differentiate drug - related complications from maternal disease - - related complications. We conclude that previously reported hypoglycemia, hyperbilirubinemia, polycythemia, neonatal apnea, and bradycardia are not invariable and cannot be statistically correlated with chronic propranolol therapy. Growth retardation, however, appears to be significant in both of our series.

propranolol

Propranolol

propranolol

propranolol

propranolol

hypoglycemia

hyperbilirubinemia

polycythemia

neonatal apnea

bradycardia

Growth retardation

propranolol

Growth retardation

Propranolol

Growth retardation

propranolol

Growth retardation

propranolol

Growth retardation

propranolol

Growth retardation


Input: Use of propranolol in the treatment of idiopathic orthostatic hypotension. Five patients with idiopathic orthostatic hypotension who had physiologic and biochemical evidence of severe autonomic dysfunction were included in the study. They all exhibited markedly reduced plasma catecholamines and plasma renin activity in both recumbent and upright positions and had marked hypersensitivity to the pressor effects of infused norepinephrine. Treatment with propanolol administered intravenously (1 - 5 mg) produced increases in supine and upright blood pressure in 4 of the 5 individuals with rises ranging from 11 / 6 to 22 / 11 mmHg. Chronic oral administration of propranolol (40 - 160 mg / day) also elevated the blood pressures of these individuals with increases in the order of 20 - 35 / 15 - 25 mmg being observed. In 1 patient, marked hypertension was induced by propranolol and the drug had to be withdrawn. It otherwise was well tolerated and no important side effects were observed. Treatment has been continued in 3 individuals for 6 - 13 months with persistence of the pressor effect, although there appears to have been some decrease in the degree of response with time. Hemodynamic measurements in 1 of the patients demonstrated an increase in total peripheral resistance and essentially no change in cardiac output following propranolol therapy. The studies suggest that propranolol is a useful drug in selected patients with severe idiopathic orthostatic hypotension.

propranolol

catecholamines

norepinephrine

propanolol

propranolol

propranolol

propranolol

propranolol

idiopathic orthostatic hypotension

idiopathic orthostatic hypotension

hypersensitivity

hypertension

idiopathic orthostatic hypotension

propranolol

hypertension

propanolol

hypertension

propranolol

hypertension

propranolol

hypertension

propranolol

hypertension

propranolol

hypertension


Input: Total intravenous anesthesia with etomidate. III. Some observations in adults. An investigation was undertaken to determine the dosage of etomidate required to maintain sleep in adults undergoing surgery under regional local anesthesia. Premedication of diazepam 10 mg and atropine 0. 5 mg was given, and sleep was induced and maintained by intermittent intravenous injections of etomidate 0. 1 / mg / kg, given whenever the patient would open his eyes on request. A mean overall dose of etomidate 17. 4 microgram / kg / min. was required to maintain sleep, but great individual variation occurred, with older patients requiring less drug. The investigation was discontinued after 18 patients because of the frequency and intensity of side - effects, particularly pain and myoclonia, which caused the technique to be abandoned in two cases. It is considered unlikely that etomidate will prove to be the hypnotic of choice for a totally intravenous anesthetic technique in adults because of the high incidence of myoclonia after prolonged administration. In several patients uncontrollable muscle movements persisted for many minutes after complete recovery of consciousness.

etomidate

etomidate

diazepam

atropine

etomidate

etomidate

etomidate

pain

myoclonia

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

myoclonia

etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain

etomidate

pain


Input: A method for the measurement of tremor, and a comparison of the effects of tocolytic beta - mimetics. A method permitting measurement of finger tremor as a displacement - time curve is described, using a test system with simple amplitude calibration. The coordinates of the inversion points of the displacement - time curves were transferred through graphical input equipment to punched tape. By means of a computer program, periods and amplitudes of tremor oscillations were calculated and classified. The event frequency for each class of periods and amplitudes was determined. The actions of fenoterol - hydrobromide, ritodrin - HCl and placebo given to 10 healthy subjects by intravenous infusion in a double - blind crossover study were tested by this method. At therapeutic doses both substances raised the mean tremor amplitude to about three times the control level. At the same time, the mean period within each class of amplitudes shortened by 10 - - 20 ms, whereas the mean periods calculated from all oscillations together did not change significantly. After the end of fenoterol - hydrobromide infusion, tremor amplitudes decreased significantly faster than those following ritodrin - HCl infusion.

tremor

tremor

tremor

tremor

tremor

fenoterol - hydrobromide

ritodrin - HCl

fenoterol - hydrobromide

ritodrin - HCl

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

fenoterol - hydrobromide

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor

ritodrin - HCl

tremor


Input: Bilateral retinal artery and choriocapillaris occlusion following the injection of long - acting corticosteroid suspensions in combination with other drugs: I. Clinical studies. Two well - documented cases of bilateral retinal artery and choriocapillaris occlusions with blindness following head and neck soft - tissue injection with methylprednisolone acetate in combination with lidocaine, epinephrine, or penicillin are reported. One case had only a unilateral injection. The acute observations included hazy sensorium, superior gaze palsy, pupillary abnormalities, and conjunctival hemorrhages with edema. Follow - up changes showed marked visual loss, constricted visual fields, optic nerve pallor, vascular attenuation, and chorioretinal atrophy. The literature is reviewed, and possible causes are discussed.

retinal artery and choriocapillaris occlusion

retinal artery and choriocapillaris occlusions

blindness

palsy

pupillary abnormalities

hemorrhages

edema

visual loss

chorioretinal atrophy

corticosteroid

methylprednisolone acetate

lidocaine

epinephrine

penicillin

methylprednisolone acetate

retinal artery and choriocapillaris occlusion

methylprednisolone acetate

retinal artery and choriocapillaris occlusions


Input: Cephalothin - induced immune hemolytic anemia. A patient with renal disease developed Coombs - positive hemolytic anemia while receiving cephalothin therapy. An anti - cephalothin IgG antibody was detected in the patient' s serum and in the eluates from her erythrocytes. In addition, nonimmunologic binding of normal and patient' s serum proteins to her own and cephalothin - coated normal red cells was demonstrated. Skin tests and in vitro lymphocyte stimulation revealed that the patient was sensitized to cephalothin and also to ampicillin. Careful investigation of drug - induced hemolytic anemias reveals the complexity of the immune mechanisms involved.

Cephalothin

cephalothin

cephalothin

cephalothin

cephalothin

ampicillin

hemolytic anemia

renal disease

hemolytic anemia

hemolytic anemias

Cephalothin

hemolytic anemia

Cephalothin

hemolytic anemia

Cephalothin

hemolytic anemias

cephalothin

hemolytic anemia

cephalothin

hemolytic anemia

cephalothin

hemolytic anemias

cephalothin

hemolytic anemia

cephalothin

hemolytic anemia

cephalothin

hemolytic anemias

cephalothin

hemolytic anemia

cephalothin

hemolytic anemia

cephalothin

hemolytic anemias

cephalothin

hemolytic anemia

cephalothin

hemolytic anemia

cephalothin

hemolytic anemias


Input: Kaliuretic effect of L - dopa treatment in parkinsonian patients. Hypokalemia, sometimes severe, was observed in some L - dopa - treated parkinsonian patients. The influence of L - dopa on the renal excretion of potassium was studied in 3 patients with hypokalemia and in 5 normokalemic patients by determination of renal plasma flow, glomerular filtration rate, plasma concentration of potassium and sodium as well as urinary excretion of potassium, sodium and aldosterone. L - Dopa intake was found to cause an increased excretion of potassium, and sometimes also of sodium, in the hypokalemic but not in the normokalemic patients. This effect on the renal function could be prohibited by the administration of a peripheral dopa decarbodylase inhibitor. It is not known why this effect occurred in some individuals but not in others, but our results indicate a correlation between aldosterone production and this renal effect of L - dopa.

L - dopa

L - dopa

L - dopa

potassium

potassium

sodium

potassium

sodium

aldosterone

L - Dopa

potassium

sodium

aldosterone

L - dopa

parkinsonian

Hypokalemia

parkinsonian

hypokalemia

L - dopa

Hypokalemia

L - dopa

hypokalemia

L - dopa

Hypokalemia

L - dopa

hypokalemia

L - dopa

Hypokalemia

L - dopa

hypokalemia

L - Dopa

Hypokalemia

L - Dopa

hypokalemia

L - dopa

Hypokalemia

L - dopa

hypokalemia


Input: Phenytoin encephalopathy as probable idiosyncratic reaction: case report. A case of phenytoin (DPH) encephalopathy with increasing seizures and EEG and mental changes is described. Despite adequate oral dosage of DPH (5 mg / kg / daily) the plasma level was very low (2. 8 microgramg / ml). The encephalopathy was probably an idiosyncratic and not toxic or allergic reaction. In fact the concentration of free DPH was normal, the patient presented a retarded morbilliform rash during DPH treatment, the protidogram was normal, and an intradermic DPH injection had no local effect. The authors conclude that in a patient starting DPH treatment an unexpected increase in seizures, with EEG and mental changes occurring simultaneously, should alert the physician to the possible need for eliminating DPH from the therapeutic regimen, even if plasma concentrations are low.

Phenytoin

phenytoin

DPH

DPH

DPH

DPH

DPH

DPH

DPH

encephalopathy

encephalopathy

seizures

encephalopathy

rash

seizures

Phenytoin

encephalopathy

Phenytoin

encephalopathy

Phenytoin

encephalopathy

phenytoin

encephalopathy

phenytoin

encephalopathy

phenytoin

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy

DPH

encephalopathy


Input: Effects of exercise on the severity of isoproterenol - induced myocardial infarction. The effect of exercise on the severity of isoproterenol - induced myocardial infarction was studied in male rats. Ninety - three rats were randomly divided into three groups. The exercise - isoproterenol (E - 1) and exercise control (EC) groups exercised daily for thirty days on a treadmill at 1 mph, 2% grade while animals of the sedentary - isoproterenol (S - I) group remained sedentary. Eight animals were assigned to the sedentary control (SC) group which remained sedentary throughout the experimental period. Forty - eight hours after the final exercise period, S - I and E - I animals received a single subcutaneous injection of isoproterenol (250 mg / kg body weight). Animals of the S - I group exhibited significantly (Pp less than 0. 05) greater mortality from the effects of isoproterenol than animals of the E - I group. Serum CPK activity for E - I animals was significantly (p less than 0. 05) greater than for animals in the S - I and EC groups twenty hours following isoproterenol injection. No statistically significant differences were observed between the two isoproterenol treated groups for severity of the induced lesions, changes in heart weight, or heart weight to body weight ratios. The results indicated that exercise reduced the mortality associated with the effects of large dosages of isoproterenol but had little on the severity of the infarction.

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

isoproterenol

myocardial infarction

myocardial infarction

infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction

isoproterenol

myocardial infarction


Input: Effect of D - Glucarates on basic antibiotic - induced renal damage in rats. Dehydrated rats regularly develop acute renal failure following single injection of aminoglycoside antibiotics combined with dextran or of antibiotics only. Oral administration of 2, 5 - di - O - acetyl - D - glucaro - 1, 4 - 6, 3 - dilactone protected rats against renal failure induced by kanamycin - dextran. The protective effect was prevalent among D - glucarates, and also to other saccharic acid, hexauronic acids and hexaaldonic acids, although to a lesser degree, but not to a hexaaldose, sugar alcohols, substances inthe TCA cycle and other acidic compounds. D - Glucarates were effective against renal damage induced by peptide antibiotics as well as various aminoglycoside antibitocis. Dose - responses were observed in the protective effect of D - Glucarates. With a D - glucarate of a fixed size of dose, approximately the same degree of protection was obtained against renal damages induced by different basic antibiotics despite large disparities in administration doses of different antibiotics. D - Glucarates had the ability to prevent renal damage but not to cure it. Rats excreted acidic urine when they were spared from renal lesions by monosaccharides. The reduction effect of D - glucarates against nephrotoxicity of basic antibiotics was discussed.

D - Glucarates

aminoglycoside

2, 5 - di - O - acetyl - D - glucaro - 1, 4 - 6, 3 - dilactone

kanamycin

D - glucarates

saccharic acid

hexauronic acids

hexaaldonic acids

sugar alcohols

TCA

D - Glucarates

aminoglycoside

D - Glucarates

D - glucarate

D - Glucarates

monosaccharides

D - glucarates

renal damage

Dehydrated

acute renal failure

renal failure

renal damage

renal damages

renal damage

renal lesions

nephrotoxicity

aminoglycoside

acute renal failure

aminoglycoside

acute renal failure

kanamycin

acute renal failure


Input: Paraplegia following intrathecal methotrexate: report of a case and review of the literature. A patient who developed paraplegia following the intrathecal instillation of methotrexate is discribed. The ten previously reported cases of this unusual complication are reviewed. The following factors appear to predispose to the development of this complication: abnormal cerebrospinal dynamics related to the presence of central nervous system leukemia, and epidural cerebrospinal leakage; elevated cerebrospinal fluid methothexate concentration related to abnormal cerebrospinal fluid dynamics and to inappropriately high methotrexate doses based on body surface area calculations in older children and adults; the presence of neurotoxic preservatives in commercially available methotrexate preparations and diluents; and the use of methotrexate diluents of unphysiologic pH, ionic content and osmolarity. The role of methotrexate contaminants, local folate deficiency, and cranial irradiation in the pathogenesis of intrathecal methotrexate toxicity is unclear. The incidence of neurotoxicity may be reduced by employing lower doses of methotrexate in the presence of central nervous system leukemia, in older children and adults, and in the presence of epidural leakage. Only preservative - free methotrexate in Elliott' s B Solution at a concentration of not more than 1 mg / ml should be used for intrathecal administration. Periodic monitoring of cerebruspinal fluid methotrexate levels may be predictive of the development of serious neurotoxicity.

Paraplegia

paraplegia

central nervous system leukemia

neurotoxic

folate deficiency

toxicity

neurotoxicity

central nervous system leukemia

neurotoxicity

methotrexate

methotrexate

methothexate

methotrexate

methotrexate

methotrexate

methotrexate

methotrexate

methotrexate

methotrexate

methotrexate

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methothexate

Paraplegia

methothexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia

methotrexate

Paraplegia

methotrexate

paraplegia


Input: Centrally mediated cardiovascular effects of intracisternal application of carbachol in anesthetized rats. The pressor response to the intracisternal (i. c.) injection of carbachol (1 mug) in anesthetized rats was analyzed. This response was significantly reduced by the intravenous (i. v.) injection of guanethidine (5 mg), hexamethonium (10 mg) or phentolamine (5 mg), and conversely, potentiated by i. v. desmethylimipramine (0. 3 mg), while propranolol (0. 5 mg) i. v. selectively inhibited the enlargement of pulse pressure and the tachycardia following i. c. carbachol (1 mug). On the other hand, the pressor response to i. c. carbachol (1 mug) was almost completely blocked by i. c. atropine (3 mug) or hexamethonium (500 mug), and significantly reduced by i. c. chlorpromazine (50 mug) but significantly potentiated by i. c. desmethylimipramine (30 mug). The pressor response to i. c. carbachol (1 mug) remained unchanged after sectioning of the bilateral cervical vagal nerves but disappeared after sectioning of the spinal cord (C7 - C8). From the above result it is suggested that the pressor response to i. c. carbachol ortral and peripheral adrenergic mechanisms, and that the sympathetic trunk is the main pathway.

carbachol

carbachol

guanethidine

hexamethonium

phentolamine

desmethylimipramine

propranolol

carbachol

carbachol

atropine

hexamethonium

chlorpromazine

desmethylimipramine

carbachol

carbachol

enlargement of pulse pressure

tachycardia

carbachol

tachycardia

carbachol

tachycardia

carbachol

tachycardia

carbachol

tachycardia

carbachol

tachycardia

carbachol

tachycardia

carbachol

enlargement of pulse pressure

carbachol

enlargement of pulse pressure

carbachol

enlargement of pulse pressure

carbachol

enlargement of pulse pressure

carbachol

enlargement of pulse pressure

carbachol

enlargement of pulse pressure

desmethylimipramine

enlargement of pulse pressure

desmethylimipramine

enlargement of pulse pressure


Input: Hyperglycemic effect of amino compounds structurally related to caproate in rats. The chronic feeding of small amounts (0. 3 - 3% of diet weight) of certain amino derivatives of caproate resulted in hyperglycemia, an elevated glucose tolerance curve and, occasionally, glucosuria. Effective compounds included norleucine, norvaline, glutamate, epsilon - aminocaproate, methionine, and leucine.

Hyperglycemic

hyperglycemia

glucosuria

amino

caproate

amino

caproate

glucose

norleucine

norvaline

glutamate

epsilon - aminocaproate

methionine

leucine

amino

Hyperglycemic

amino

hyperglycemia

amino

Hyperglycemic

amino

hyperglycemia


Input: Fatty liver induced by tetracycline in the rat. Dose - response relationships and effect of sex. Dose - response relationships, biochemical mechanisms, and sex differences in the experimental fatty liver induced by tetracycline were studied in the intact rat and with the isolated perfused rat liver in vitro. In the intact male and female rat, no direct relationship was observed between dose of tetracycline and hepatic accumulation of triglyceride. With provision of adequate oleic acid as a substrate for the isolated perfused liver, a direct relationship was observed between dose of tetracycline and both accumulation of triglyceride in the liver and depression of output of triglyceride by livers from male and female rats. Marked differences were observed between female and male rats with regard to base line (control) hepatic concentration of triglyceride and output of triglyceride. Accumulation of hepatic triglyceride, as a per cent of control values, in response to graded doses of tetracycline, did not differ significantly between male, female and pregnant rat livers. However, livers from female, and especially pregnant female rats, were strikingly resistant to the effects of tetracycline on depression of output of triglyceride under these experimental conditions. These differences between the sexes could not be related to altered disposition of tetracycline or altered uptake of oleic acid. Depressed hepatic secretion of triglyceride accounted only for 30 to 50% of accumulated hepatic triglyceride, indicating that additional mechanisms must be involved in the production of the triglyceride - rich fatty liver in response to tetracycline.

Fatty liver

fatty liver

depression

depression

fatty liver

tetracycline

tetracycline

tetracycline

triglyceride

oleic acid

tetracycline

triglyceride

triglyceride

triglyceride

triglyceride

triglyceride

tetracycline

tetracycline

triglyceride

tetracycline

oleic acid

triglyceride

triglyceride

triglyceride

tetracycline

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver

tetracycline

Fatty liver

tetracycline

fatty liver

tetracycline

fatty liver


Input: Fatal myeloencephalopathy due to intrathecal vincristine administration. Vincristine was accidentally given intrathecally to a child with leukaemia, producing sensory and motor dysfunction followed by encephalopathy and death. Separate times for administering vincristine and intrathecal therapy is recommended.

myeloencephalopathy

leukaemia

sensory and motor dysfunction

encephalopathy

vincristine

Vincristine

vincristine

vincristine

sensory and motor dysfunction

Vincristine

sensory and motor dysfunction

vincristine

sensory and motor dysfunction

vincristine

myeloencephalopathy

vincristine

encephalopathy

Vincristine

myeloencephalopathy

Vincristine

encephalopathy

vincristine

myeloencephalopathy

vincristine

encephalopathy


Input: Progesterone potentiation of bupivacaine arrhythmogenicity in pentobarbital - anesthetized rats and beating rat heart cell cultures. The effects of progesterone treatment on bupivacaine arrhythmogenicity in beating rat heart myocyte cultures and on anesthetized rats were determined. After determining the bupivacaine AD50 (the concentration of bupivacaine that caused 50% of all beating rat heart myocyte cultures to become arrhythmic), we determined the effect of 1 - hour progesterone HCl exposure on myocyte contractile rhythm. Each concentration of progesterone (6. 25, 12. 5, 25, and 50 micrograms / ml) caused a significant and concentration - dependent reduction in the AD50 for bupivacaine. Estradiol treatment also increased the arrhythmogenicity of bupivacaine in myocyte cultures, but was only one fourth as potent as progesterone. Neither progesterone nor estradiol effects on bupivacaine arrhythmogenicity were potentiated by epinephrine. Chronic progesterone pretreatment (5 mg / kg / day for 21 days) caused a significant increase in bupivacaine arrhythmogenicity in intact pentobarbital - anesthetized rats. There was a significant decrease in the time to onset of arrhythmia as compared with control nonprogesterone - treated rats (6. 2 + / - 1. 3 vs. 30. 8 + / - 2. 5 min, mean + / - SE). The results of this study indicate that progesterone can potentiate bupivacaine arrhythmogenicity both in vivo and in vitro. Potentiation of bupivacaine arrhythmia in myocyte cultures suggests that this effect is at least partly mediated at the myocyte level.

Progesterone

bupivacaine

pentobarbital

progesterone

bupivacaine

bupivacaine

bupivacaine

progesterone

HCl

progesterone

bupivacaine

Estradiol

bupivacaine

progesterone

progesterone

estradiol

bupivacaine

epinephrine

progesterone

bupivacaine

pentobarbital

progesterone

bupivacaine

bupivacaine

arrhythmic

arrhythmia

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

bupivacaine

arrhythmic

bupivacaine

arrhythmia

bupivacaine

arrhythmia

Estradiol

arrhythmic

Estradiol

arrhythmia

Estradiol

arrhythmia

estradiol

arrhythmic

estradiol

arrhythmia

estradiol

arrhythmia

Progesterone

arrhythmic

Progesterone

arrhythmia

Progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia

progesterone

arrhythmic

progesterone

arrhythmia

progesterone

arrhythmia


Input: Acute renal failure occurring during intravenous desferrioxamine therapy: recovery after haemodialysis. A patient with transfusion - dependent thalassemia was undergoing home intravenous desferrioxamine (DFX) treatment by means of a totally implanted system because of his poor compliance with the nightly subcutaneous therapy. Due to an accidental malfunctioning of the infusion pump, the patient was inadvertently administered a toxic dosage of the drug which caused renal insufficiency. Given the progressive deterioration of the symptoms and of the laboratory values, despite adequate medical treatment, a decision was made to introduce haemodialytical therapy in order to remove the drug and therapy reduce the nephrotoxicity. From the results obtained, haemodialysis can therefore be suggested as a useful therapy in rare cases of progressive acute renal failure caused by desferrioxamine.

Acute renal failure

thalassemia

renal insufficiency

nephrotoxicity

acute renal failure

desferrioxamine

desferrioxamine

DFX

desferrioxamine

desferrioxamine

renal insufficiency

desferrioxamine

renal insufficiency

DFX

renal insufficiency

desferrioxamine

renal insufficiency


Input: Neuroleptic - associated hyperprolactinemia. Can it be treated with bromocriptine? Six stable psychiatric outpatients with hyperprolactinemia and amenorrhea / oligomenorrhea associated with their neuroleptic medications were treated with bromocriptine. Daily dosages of 5 - 10 mg corrected the hyperprolactinemia and restored menstruation in four of the six patients. One woman, however, developed worsened psychiatric symptoms while taking bromocriptine, and it was discontinued. Thus, three of six patients had their menstrual irregularity successfully corrected with bromocriptine. This suggests that bromocriptine should be further evaluated as potential therapy for neuroleptic - associated hyperprolactinemia and amenorrhea / galactorrhea.

Neuroleptic

bromocriptine

neuroleptic medications

bromocriptine

bromocriptine

bromocriptine

bromocriptine

neuroleptic

hyperprolactinemia

hyperprolactinemia

amenorrhea

oligomenorrhea

hyperprolactinemia

psychiatric symptoms

hyperprolactinemia

amenorrhea

galactorrhea

bromocriptine

psychiatric symptoms

bromocriptine

psychiatric symptoms

bromocriptine

psychiatric symptoms

bromocriptine

psychiatric symptoms

bromocriptine

psychiatric symptoms

Neuroleptic

amenorrhea

Neuroleptic

amenorrhea

neuroleptic medications

amenorrhea

neuroleptic medications

amenorrhea

neuroleptic

amenorrhea

neuroleptic

amenorrhea

Neuroleptic

oligomenorrhea

neuroleptic medications

oligomenorrhea

neuroleptic

oligomenorrhea

Neuroleptic

hyperprolactinemia

Neuroleptic

hyperprolactinemia

Neuroleptic

hyperprolactinemia

Neuroleptic

hyperprolactinemia

neuroleptic medications

hyperprolactinemia

neuroleptic medications

hyperprolactinemia

neuroleptic medications

hyperprolactinemia

neuroleptic medications

hyperprolactinemia

neuroleptic

hyperprolactinemia

neuroleptic

hyperprolactinemia

neuroleptic

hyperprolactinemia

neuroleptic

hyperprolactinemia


Input: Ethacrynic acid - induced convulsions and brain neurotransmitters in mice. Intracerebroventricular injection of ethacrynic acid (50% convulsive dose; 50 micrograms / mouse) accelerated the synthesis / turnover of 5 - hydroxytryptamine (5 - HT) but suppressed the synthesis of gamma - aminobutyric acid and acetylcholine in mouse brain. These effects were completely antagonized by pretreatment with a glutamate / N - methyl - D - aspartate antagonist, aminophosphonovaleric acid. In ethacrynic acid - induced convulsions, these neurotransmitter systems may be differentially modulated, probably through activation of glutaminergic neurons in the brain.

Ethacrynic acid

ethacrynic acid

5 - hydroxytryptamine

5 - HT

gamma - aminobutyric acid

acetylcholine

glutamate

N - methyl - D - aspartate

aminophosphonovaleric acid

ethacrynic acid

convulsions

convulsive

convulsions

Ethacrynic acid

convulsions

Ethacrynic acid

convulsive

Ethacrynic acid

convulsions

ethacrynic acid

convulsions

ethacrynic acid

convulsive

ethacrynic acid

convulsions

ethacrynic acid

convulsions

ethacrynic acid

convulsive

ethacrynic acid

convulsions


Input: Pharmacology of gamma - aminobutyric acidA receptor complex after the in vivo administration of the anxioselective and anticonvulsant beta - carboline derivative abecarnil. In rodents, the effect of the beta - carboline derivative isopropyl - 6 - benzyloxy - 4 - methoxymethyl - beta - carboline - 3 - carboxylate (abecarrnil), a new ligand for benzodiazepine receptors possessing anxiolytic and anticonvulsant properties, was evaluated on the function of central gamma - aminobutyric acid (GABA) A receptor complex, both in vitro and in vivo. Added in vitro to rat cortical membrane preparation, abecarnil increased [3H] GABA binding, enhanced muscimol - stimulated 36Cl - uptake and reduced the binding of t - [35S] butylbicyclophosphorothionate ([35S] TBPS). These effects were similar to those induced by diazepam, whereas the partial agonist Ro 16 - 6028 (tert - butyl - (S) - 8 - bromo - 11, 12, 13, 13a - tetrahydro - 9 - oxo - 9H - imidazo [1, 5 - a] - pyrrolo - [2, 1 - c] [1, 4] benzodiazepine - 1 - carboxylate) showed very weak efficacy in these biochemical tests. After i. p. injection to rats, abecarnil and diazepam decreased in a time - dependent and dose - related (0. 25 - 20 mg / kg i. p.) manner [35S] TBPS binding measured ex vivo in the cerebral cortex. Moreover, both drugs at the dose of 0. 5 mg / kg antagonized completely the convulsant activity and the increase of [35S] TBPS binding induced by isoniazide (350 mg / kg s. c.) as well as the increase of [35S] TBPS binding induced by foot - shock stress. To better correlate the biochemical and the pharmacological effects, we studied the action of abecarnil on [35S] TBPS binding, exploratory motility and on isoniazid - induced biochemical and pharmacological effects in mice. In these animals, abecarnil produced a paralleled dose - dependent (0. 05 - 1 mg / kg i. p.) reduction of both motor behavior and cortical [35S] TBPS binding. Moreover, 0. 05 mg / kg of this beta - carboline reduced markedly the increase of [35S] TBPS binding and the convulsions induced by isoniazid (200 mg / kg s. c.). (ABSTRACT TRUNCATED AT 250 WORDS)

gamma - aminobutyric acidA

beta - carboline

abecarnil

beta - carboline

isopropyl - 6 - benzyloxy - 4 - methoxymethyl - beta - carboline - 3 - carboxylate

abecarrnil

benzodiazepine

gamma - aminobutyric acid

GABA

abecarnil

GABA

muscimol

t - [35S] butylbicyclophosphorothionate

[35S] TBPS

diazepam

Ro 16 - 6028

tert - butyl - (S) - 8 - bromo - 11, 12, 13, 13a - tetrahydro - 9 - oxo - 9H - imidazo [1, 5 - a] - pyrrolo - [2, 1 - c] [1, 4] benzodiazepine - 1 - carboxylate

abecarnil

diazepam

[35S] TBPS

[35S] TBPS

isoniazide

[35S] TBPS

abecarnil

[35S] TBPS

isoniazid

abecarnil

beta - carboline

[35S] TBPS

isoniazid

convulsions

isoniazide

convulsions

isoniazid

convulsions

isoniazid

convulsions


Input: Recurrent myocardial infarction in a postpartum patient receiving bromocriptine. Myocardial infarction in puerperium is infrequently reported. Spasm, coronary dissection, or atheromatous etiology has been described. Bromocriptine has been implicated in several previous case reports of myocardial infarction in the puerperium. Our case (including an inadvertent rechallenge) suggests such a relationship. Although generally regarded as " safe, " possible serious cardiac effects of bromocriptine should be acknowledged.

myocardial infarction

Myocardial infarction

Spasm

myocardial infarction

bromocriptine

Bromocriptine

bromocriptine

bromocriptine

myocardial infarction

bromocriptine

Myocardial infarction

bromocriptine

myocardial infarction

Bromocriptine

myocardial infarction

Bromocriptine

Myocardial infarction

Bromocriptine

myocardial infarction

bromocriptine

myocardial infarction

bromocriptine

Myocardial infarction

bromocriptine

myocardial infarction


Input: Asterixis induced by carbamazepine therapy. There are very few reports about asterixis as a side effect of treatment with psychopharmacologic agents. In this report we present four patients treated with a combination of different psychotropic drugs, in whom asterixis was triggered either by adding carbamazepine (CBZ) to a treatment regimen, or by increasing its dosage. Neither dosage nor serum levels of CBZ were in a higher range. We consider asterixis to be an easily overlooked sign of neurotoxicity, which may occur even at low or moderate dosage levels, if certain drugs as lithium or clozapine are used in combination with CBZ.

Asterixis

asterixis

asterixis

asterixis

neurotoxicity

carbamazepine

carbamazepine

CBZ

CBZ

lithium

clozapine

CBZ

lithium

Asterixis

lithium

asterixis

lithium

asterixis

lithium

asterixis

clozapine

Asterixis

clozapine

asterixis

clozapine

asterixis

clozapine

asterixis


Input: Pharmacodynamics of the hypotensive effect of levodopa in parkinsonian patients. Blood pressure effects of i. v. levodopa were examined in parkinsonian patients with stable and fluctuating responses to levodopa. The magnitude of the hypotensive effect of levodopa was concentration dependent and was fit to an Emax model in fluctuating responders. Stable responders demonstrated a small hypotensive response. Baseline blood pressures were higher in fluctuating patients; a higher baseline blood pressure correlated with greater hypotensive effects. Antiparkinsonian effects of levodopa temporally correlated with blood pressure changes. Phenylalanine, a large neutral amino acid (LNAA) competing with levodopa for transport across the blood - brain barrier, reduced the hypotensive and antiparkinsonian effects of levodopa. We conclude that levodopa has a central hypotensive action that parallels the motor effects in fluctuating patients. The hypotensive effect appears to be related to the higher baseline blood pressure we observed in fluctuating patients relative to stable patients.

hypotensive

parkinsonian

parkinsonian

hypotensive

hypotensive

hypotensive

hypotensive

hypotensive

hypotensive

levodopa

levodopa

levodopa

levodopa

levodopa

Phenylalanine

amino acid

levodopa

levodopa

levodopa

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive

levodopa

hypotensive


Input: Syndrome of inappropriate secretion of antidiuretic hormone after infusional vincristine. A 77 - year - old woman with refractory multiple myeloma was treated with a 4 - day continuous intravenous infusion of vincristine and doxorubicin and 4 days of oral dexamethasone. Nine days after her second cycle she presented with lethargy and weakness associated with hyponatremia. Evaluation revealed the syndrome of inappropriate secretion of antidiuretic hormone, which was attributed to the vincristine infusion. After normal serum sodium levels returned, further doxorubicin and dexamethasone chemotherapy without vincristine did not produce this complication.

Syndrome of inappropriate secretion of antidiuretic hormone

multiple myeloma

lethargy

weakness

hyponatremia

syndrome of inappropriate secretion of antidiuretic hormone

vincristine

vincristine

doxorubicin

dexamethasone

vincristine

sodium

doxorubicin

dexamethasone

vincristine

vincristine

Syndrome of inappropriate secretion of antidiuretic hormone

vincristine

syndrome of inappropriate secretion of antidiuretic hormone

vincristine

Syndrome of inappropriate secretion of antidiuretic hormone

vincristine

syndrome of inappropriate secretion of antidiuretic hormone

vincristine

Syndrome of inappropriate secretion of antidiuretic hormone

vincristine

syndrome of inappropriate secretion of antidiuretic hormone

vincristine

Syndrome of inappropriate secretion of antidiuretic hormone

vincristine

syndrome of inappropriate secretion of antidiuretic hormone


Input: Heart failure: to digitalise or not? The view against. Despite extensive clinical experience the role of digoxin is still not well defined. In patients with atrial fibrillation digoxin is beneficial for ventricular rate control. For patients in sinus rhythm and heart failure the situation is less clear. Digoxin has a narrow therapeutic: toxic ratio and concentrations are affected by a number of drugs. Also, digoxin has undesirable effects such as increasing peripheral resistance and myocardial demands, and causing arrhythmias. There is a paucity of data from well - designed trials. The trials that are available are generally small with limitations in design and these show variation in patient benefit. More convincing evidence is required showing that digoxin improves symptoms or exercise capacity. Furthermore, no trial has had sufficient power to evaluate mortality. Pooled analysis of the effects of other inotropic drugs shows an excess mortality and there is a possibility that digoxin may increase mortality after myocardial infarction (MI). Angiotensin - converting enzyme (ACE) inhibitors should be used first as they are safer, do not require blood level monitoring, modify progression of disease, relieve symptoms, improve exercise tolerance and reduce mortality. Caution should be exercised in using digoxin until large mortality trials are completed showing either benefit or harm. Until then digoxin should be considered a third - line therapy.

Heart failure

atrial fibrillation

heart failure

arrhythmias

myocardial infarction

MI

digoxin

digoxin

Digoxin

digoxin

digoxin

digoxin

Angiotensin

digoxin

digoxin

digoxin

arrhythmias

digoxin

arrhythmias

Digoxin

arrhythmias

digoxin

arrhythmias

digoxin

arrhythmias

digoxin

arrhythmias

digoxin

arrhythmias

digoxin

arrhythmias


Input: Intravascular hemolysis and acute renal failure following intermittent rifampin therapy. Renal failure is a rare complication associated with the use of rifampin. Intravascular hemolysis leading to acute renal failure following rifampin therapy is extremely rare. Two patients with leprosy who developed hemolysis and acute renal failure following rifampin are reported.

hemolysis

acute renal failure

Renal failure

hemolysis

acute renal failure

leprosy

hemolysis

acute renal failure

rifampin

rifampin

rifampin

rifampin

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

acute renal failure

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis

rifampin

hemolysis


Input: Zidovudine - induced hepatitis. A case of acute hepatitis induced by zidovudine in a 38 - year - old patient with AIDS is presented. The mechanism whereby the hepatitis was induced is not known. However, the patient tolerated well an alternative reverse transcriptase inhibitor, 2' 3' dideoxyinosine. Physicians caring for patients with AIDS should be aware of this hitherto rarely reported complication.

Zidovudine

zidovudine

2' 3' dideoxyinosine

hepatitis

hepatitis

AIDS

hepatitis

AIDS

Zidovudine

hepatitis

Zidovudine

hepatitis

Zidovudine

hepatitis

zidovudine

hepatitis

zidovudine

hepatitis

zidovudine

hepatitis


Input: Thoracic hematomyelia secondary to coumadin anticoagulant therapy: a case report. A case of thoracic hematomyelia secondary to anticoagulant therapy is presented. Clinical features, similar to 2 other previously reported cases, are discussed. A high index of suspicion may lead to a quick diagnostic procedure and successful decompressive surgery.

Thoracic hematomyelia

thoracic hematomyelia

coumadin

coumadin

Thoracic hematomyelia

coumadin

thoracic hematomyelia


Input: Mania associated with fluoxetine treatment in adolescents. Fluoxetine, a selective serotonin reuptake inhibitor, is gaining increased acceptance in the treatment of adolescent depression. Generally safe and well tolerated by adults, fluoxetine has been reported to induce mania. The cases of five depressed adolescents, 14 - 16 years of age, who developed mania during pharmacotherapy with fluoxetine, are reported here. Apparent risk factors for the development of mania or hypomania during fluoxetine pharmacotherapy in this population were the combination of attention - deficit hyperactivity disorder and affective instability; major depression with psychotic features; a family history of affective disorder, especially bipolar disorder; and a diagnosis of bipolar disorder. Further study is needed to determine the optimal dosage and to identify risk factors that increase individual vulnerability to fluoxetine induced mania in adolescents.

Mania

depression

mania

depressed

mania

mania

hypomania

attention - deficit hyperactivity disorder

depression

psychotic

affective disorder

bipolar disorder

bipolar disorder

mania

fluoxetine

Fluoxetine

serotonin

fluoxetine

fluoxetine

fluoxetine

fluoxetine

fluoxetine

Mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

hypomania

fluoxetine

bipolar disorder

fluoxetine

bipolar disorder

fluoxetine

mania

Fluoxetine

Mania

Fluoxetine

mania

Fluoxetine

mania

Fluoxetine

mania

Fluoxetine

hypomania

Fluoxetine

bipolar disorder

Fluoxetine

bipolar disorder

Fluoxetine

mania

fluoxetine

Mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

hypomania

fluoxetine

bipolar disorder

fluoxetine

bipolar disorder

fluoxetine

mania

fluoxetine

Mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

hypomania

fluoxetine

bipolar disorder

fluoxetine

bipolar disorder

fluoxetine

mania

fluoxetine

Mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

hypomania

fluoxetine

bipolar disorder

fluoxetine

bipolar disorder

fluoxetine

mania

fluoxetine

Mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

mania

fluoxetine

hypomania

fluoxetine

bipolar disorder

fluoxetine

bipolar disorder

fluoxetine

mania


Input: Gemfibrozil - lovastatin therapy for primary hyperlipoproteinemias. The specific aim of this retrospective, observational study was to assess safety and efficacy of long - term (21 months / patient), open - label, gemfibrozil - lovastatin treatment in 80 patients with primary mixed hyperlipidemia (68% of whom had atherosclerotic vascular disease). Because ideal lipid targets were not reached (low - density lipoprotein (LDL) cholesterol less than 130 mg / dl, high - density lipoprotein (HDL) cholesterol greater than 35 mg / dl, or total cholesterol / HDL cholesterol less than 4. 5 mg / dl) with diet plus a single drug, gemfibrozil (1. 2 g / day) - lovastatin (primarily 20 or 40 mg) treatment was given. Follow - up visits were scheduled with 2 - drug therapy every 6 to 8 weeks, an average of 10. 3 visits per patient, with 741 batteries of 6 liver function tests and 714 creatine phosphokinase levels measured. Only 1 of the 4, 446 liver function tests (0. 02%), a gamma glutamyl transferase, was greater than or equal to 3 times the upper normal limit. Of the 714 creatine phosphokinase levels, 9% were high; only 1 (0. 1%) was greater than or equal to 3 times the upper normal limit. With 2 - drug therapy, mean total cholesterol decreased 22% from 255 to 200 mg / dl, triglyceride levels decreased 35% from 236 to 154 mg / dl, LDL cholesterol decreased 26% from 176 to 131 mg / dl, and the total cholesterol / HDL cholesterol ratio decreased 24% from 7. 1 to 5. 4, all p less than or equal to 0. 0001. Myositis, attributable to the drug combination and symptomatic enough to discontinue it, occurred in 3% of patients, and in 1% with concurrent high creatine phosphokinase (769 U / liter); no patients had rhabdomyolysis or myoglobinuria. (ABSTRACT TRUNCATED AT 250 WORDS)

Gemfibrozil

lovastatin

gemfibrozil

lovastatin

cholesterol

cholesterol

cholesterol

cholesterol

gemfibrozil

lovastatin

creatine

creatine

cholesterol

triglyceride

cholesterol

cholesterol

cholesterol

creatine

hyperlipoproteinemias

hyperlipidemia

atherosclerotic vascular disease

Myositis

rhabdomyolysis

myoglobinuria

Gemfibrozil

Myositis

gemfibrozil

Myositis

gemfibrozil

Myositis

lovastatin

Myositis

lovastatin

Myositis

lovastatin

Myositis


Input: Hepatocellular carcinoma in Fanconi' s anemia treated with androgen and corticosteroid. The case of an 11 - year - old boy is reported who was known to have Fanconi' s anemia for 3 years and was treated with androgens, corticosteroids and transfusions. Two weeks before his death he was readmitted because of aplastic crisis with septicemia and marked abnormalities in liver function and died of hemorrhagic bronchopneumonia. At autopsy peliosis and multiple hepatic tumors were found which histologically proved to be well - differentiated hepatocellular carcinoma. This case contributes to the previous observations that non - metastasizing hepatic neoplasms and peliosis can develop in patients with androgen - and corticosteroid - treated Fanconi' s anemia.

Hepatocellular carcinoma

Fanconi' s anemia

Fanconi' s anemia

septicemia

hemorrhagic bronchopneumonia

peliosis

hepatic tumors

hepatocellular carcinoma

hepatic neoplasms

peliosis

Fanconi' s anemia

androgen

corticosteroid

androgens

corticosteroids

androgen

corticosteroid

corticosteroid

peliosis

corticosteroid

peliosis

corticosteroids

peliosis

corticosteroids

peliosis

corticosteroid

peliosis

corticosteroid

peliosis

androgen

peliosis

androgen

peliosis

androgens

peliosis

androgens

peliosis

androgen

peliosis

androgen

peliosis

corticosteroid

Hepatocellular carcinoma

corticosteroid

hepatocellular carcinoma

corticosteroids

Hepatocellular carcinoma

corticosteroids

hepatocellular carcinoma

corticosteroid

Hepatocellular carcinoma

corticosteroid

hepatocellular carcinoma

androgen

Hepatocellular carcinoma

androgen

hepatocellular carcinoma

androgens

Hepatocellular carcinoma

androgens

hepatocellular carcinoma

androgen

Hepatocellular carcinoma

androgen

hepatocellular carcinoma


Input: Chronic lesion of rostral ventrolateral medulla in spontaneously hypertensive rats. We studied the effects of chronic selective neuronal lesion of rostral ventrolateral medulla on mean arterial pressure, heart rate, and neurogenic tone in conscious, unrestrained spontaneously hypertensive rats. The lesions were placed via bilateral microinjections of 30 nmol / 200 nl N - methyl - D - aspartic acid. The restimulation of this area with N - methyl - D - aspartic acid 15 days postlesion failed to produce a pressor response. One day postlesion, the resting mean arterial pressure was significantly decreased in lesioned rats when compared with sham rats (100 + / - 7 versus 173 + / - 4 mm Hg, p less than 0. 05). Fifteen days later, the lesioned group still showed values significantly lower than the sham group (150 + / - 6 versus 167 + / - 5 mm Hg, p less than 0. 05). No significant heart rate differences were observed between the sham and lesioned groups. The ganglionic blocker trimethaphan (5 mg / kg i. v.) caused similar reductions in mean arterial pressure in both lesioned and sham groups. The trimethaphan - induced hypotension was accompanied by a significant bradycardia in lesioned rats (- 32 + / - 13 beats per minute) but a tachycardia in sham rats (+ 33 + / - 12 beats per minute) 1 day postlesion. Therefore, rostral ventrolateral medulla neurons appear to play a significant role in maintaining hypertension in conscious spontaneously hypertensive rats. Spinal or suprabulbar structures could be responsible for the gradual recovery of the hypertension in the lesioned rats.

hypertensive

hypertensive

hypotension

bradycardia

tachycardia

hypertension

hypertensive

hypertension

N - methyl - D - aspartic acid

N - methyl - D - aspartic acid

trimethaphan

trimethaphan

trimethaphan

hypotension

trimethaphan

hypotension

trimethaphan

tachycardia

trimethaphan

tachycardia


Input: Damage of substantia nigra pars reticulata during pilocarpine - induced status epilepticus in the rat: immunohistochemical study of neurons, astrocytes and serum - protein extravasation. The substantia nigra has a gating function controlling the spread of epileptic seizure activity. Additionally, in models of prolonged status epilepticus the pars reticulata of substantia nigra (SNR) suffers from a massive lesion which may arise from a massive metabolic derangement and hyperexcitation developing in the activated SNR. In this study, status epilepticus was induced by systemic injection of pilocarpine in rats. The neuropathology of SNR was investigated using immunohistochemical techniques with the major emphasis on the time - course of changes in neurons and astrocytes. Animals surviving 20, 30, 40, 60 min, 2, 3, 6 hours, 1, 2, and 3 days after induction of status epilepticus were perfusion - fixed, and brains processed for immunohistochemical staining of SNR. Nissl - staining and antibodies against the neuron - specific calcium - binding protein, parvalbumin, served to detect neuronal damage in SNR. Antibodies against the astroglia - specific cytoskeletal protein, glial fibrillary acidic protein (GFAP), and against the glial calcium - binding protein, S - 100 protein, were used to assess the status of astrocytes. Immunohistochemical staining for serum - albumin and immunoglobulins in brain tissue was taken as indicator of blood - brain barrier disturbances and vasogenic edema formation. Immunohistochemical staining indicated loss of GFAP - staining already at 30 min after induction of seizures in an oval focus situated in the center of SNR while sparing medial and lateral aspects. At 1 h there was additional vacuolation in S - 100 protein staining. By 2 hours, parvalbumin - staining changed in the central SNR indicating neuronal damage, and Nissl - staining visualized some neuronal distortion. Staining for serum - proteins occurred in a patchy manner throughout the forebrain during the first hours. By 6 h, vasogenic edema covered the lesioned SNR. By 24 h, glial and neuronal markers indicated a massive lesion in the center of SNR. By 48 - 72 h, astrocytes surrounding the lesion increased in size, and polymorphic phagocytotic cells invaded the damaged area. In a further group of animals surviving 1 to 5 days, conventional paraffin - sections confirmed the neuronal and glial damage of SNR. Additional pathology of similar quality was found in the globus pallidus. Since astrocytes were always damaged in parallel with neurons in SNR it is proposed that the anatomical and functional interrelationship between neurons and astrocytes is particularly tight in SNR. Both cell elements may suffer in common from metabolic disturbance and neurotransmitter dysfunction as occur during massive status epilepticus.

Damage of substantia nigra pars reticulata

status epilepticus

epileptic seizure

prolonged status epilepticus

metabolic derangement

status epilepticus

status epilepticus

neuronal damage

vasogenic edema

seizures

neuronal damage

vasogenic edema

lesioned SNR

damage of SNR

neurotransmitter dysfunction

status epilepticus

pilocarpine

pilocarpine

calcium

calcium

pilocarpine

Damage of substantia nigra pars reticulata

pilocarpine

lesioned SNR

pilocarpine

damage of SNR

pilocarpine

Damage of substantia nigra pars reticulata

pilocarpine

lesioned SNR

pilocarpine

damage of SNR

pilocarpine

status epilepticus

pilocarpine

prolonged status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

prolonged status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

neurotransmitter dysfunction

pilocarpine

neurotransmitter dysfunction