Input: Severe congestive heart failure patient on amiodarone presenting with myxedemic coma: a case report. This is a case report of myxedema coma secondary to amiodarone - induced hypothyroidism in a patient with severe congestive heart failure (CHF). To our knowledge and after reviewing the literature there is one case report of myxedema coma during long term amiodarone therapy. Myxedema coma is a life threatening condition that carries a mortality reaching as high as 20% with treatment. The condition is treated with intravenous thyroxine (T4) or intravenous tri - iodo - thyronine (T3). Patients with CHF on amiodarone may suffer serious morbidity and mortality from hypothyroidism, and thus may deserve closer follow up for thyroid stimulating hormone (TSH) levels. This case report carries an important clinical application given the frequent usage of amiodarone among CHF patients. The myriad clinical presentation of myxedema coma and its serious morbidity and mortality stresses the need to suspect this clinical syndrome among CHF patients presenting with hypotension, weakness or other unexplained symptoms.

congestive heart failure

myxedemic coma

myxedemic

coma

myxedema coma

myxedema

coma

hypothyroidism

congestive heart failure

CHF

myxedema coma

myxedema

coma

Myxedema coma

Myxedema

coma

CHF

hypothyroidism

CHF

myxedema coma

myxedema

coma

CHF

hypotension

weakness

amiodarone

amiodarone

amiodarone

thyroxine

tri - iodo - thyronine

amiodarone

amiodarone

amiodarone

myxedemic coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

Myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedemic coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

Myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedemic coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

Myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedemic coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

Myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedemic coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

Myxedema coma

amiodarone

coma

amiodarone

myxedema coma

amiodarone

coma

amiodarone

myxedemic

amiodarone

myxedema

amiodarone

myxedema

amiodarone

Myxedema

amiodarone

myxedema

amiodarone

myxedemic

amiodarone

myxedema

amiodarone

myxedema

amiodarone

Myxedema

amiodarone

myxedema

amiodarone

myxedemic

amiodarone

myxedema

amiodarone

myxedema

amiodarone

Myxedema

amiodarone

myxedema

amiodarone

myxedemic

amiodarone

myxedema

amiodarone

myxedema

amiodarone

Myxedema

amiodarone

myxedema

amiodarone

myxedemic

amiodarone

myxedema

amiodarone

myxedema

amiodarone

Myxedema

amiodarone

myxedema

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism

amiodarone

hypothyroidism


Input: Fear - potentiated startle, but not light - enhanced startle, is enhanced by anxiogenic drugs. RATIONALE AND OBJECTIVES: The light - enhanced startle paradigm (LES) is suggested to model anxiety, because of the non - specific cue and the long - term effect. In contrast, the fear - potentiated startle (FPS) is suggested to model conditioned fear. However, the pharmacological profiles of these two paradigms are very similar. The present study investigated the effects of putative anxiogenic drugs on LES and FPS and aimed at determining the sensitivity of LES for anxiogenic drugs and to potentially showing a pharmacological differentiation between these two paradigms. METHODS: Male Wistar rats received each dose of the alpha (2) - adrenoceptor antagonist yohimbine (0. 25 - 1. 0mg / kg), the 5 - HT (2C) receptor agonist m - chlorophenylpiperazine (mCPP, 0. 5 - 2. 0mg / kg) or the GABA (A) inverse receptor agonist pentylenetetrazole (PTZ, 3 - 30mg / kg) and were subsequently tested in either LES or FPS. RESULTS: None of the drugs enhanced LES, whereas mCPP increased percentage FPS and yohimbine increased absolute FPS values. Furthermore, yohimbine increased baseline startle amplitude in the LES, while mCPP suppressed baseline startle in both the LES and FPS and PTZ suppressed baseline startle in the FPS. CONCLUSIONS: In contrast to findings in the FPS paradigm, none of the drugs were able to exacerbate the LES response. Thus, a clear pharmacological differentiation was found between LES and FPS.

startle

startle

startle

anxiety

startle

startle

startle

startle

yohimbine

5 - HT

m - chlorophenylpiperazine

mCPP

GABA

pentylenetetrazole

PTZ

mCPP

yohimbine

yohimbine

mCPP

PTZ

pentylenetetrazole

startle

pentylenetetrazole

startle

pentylenetetrazole

startle

pentylenetetrazole

startle

pentylenetetrazole

startle

pentylenetetrazole

startle

pentylenetetrazole

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

PTZ

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

yohimbine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

m - chlorophenylpiperazine

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle

mCPP

startle


Input: Proteinase 3 - antineutrophil cytoplasmic antibody - (PR3 - ANCA) positive necrotizing glomerulonephritis after restarting sulphasalazine treatment. A 59 - year - old woman with ulcerative colitis developed red eyes, pleural effusion, eosinophilia and urinary abnormalities after restarting of sulphasalazine treatment. Light microscopy of a kidney biopsy revealed segmental necrotizing glomerulonephritis without deposition of immunoglobulin or complement. Proteinase 3 - antineutrophil cytoplasmic antibody (PR3 - ANCA) titer was elevated at 183 ELISA units (EU) in sera (normal range less than 10 EU), myeloperoxidase - ANCA was negative. PR3 - ANCA titer was 250 and 1, 070 EU in pleural effusions on right and left side, respectively. Although cessation of sulphasalazine treatment resulted in improvements in fever, red eyes, chest pain, titer of C - reactive protein and volume of the pleural effusions, we initiated steroid therapy, because PR3 - ANCA titer rose to 320 EU, eosinophil count increased to 1, 100 cells / microl, and the pleural effusion remained. One month after steroid therapy, the pleural effusion disappeared, and PR3 - ANCA titer normalized 3 months later. This case suggests that sulphasalazine can induce PR3 - ANCA - positive necrotizing glomerulonephritis.

glomerulonephritis

ulcerative colitis

red eyes

pleural effusion

eosinophilia

urinary abnormalities

segmental necrotizing glomerulonephritis

pleural effusions

fever

red eyes

chest pain

pleural effusions

pleural effusion

pleural effusion

glomerulonephritis

sulphasalazine

sulphasalazine

sulphasalazine

steroid

steroid

sulphasalazine

sulphasalazine

fever

sulphasalazine

fever

sulphasalazine

fever

sulphasalazine

fever

sulphasalazine

segmental necrotizing glomerulonephritis

sulphasalazine

segmental necrotizing glomerulonephritis

sulphasalazine

segmental necrotizing glomerulonephritis

sulphasalazine

segmental necrotizing glomerulonephritis

sulphasalazine

pleural effusion

sulphasalazine

pleural effusions

sulphasalazine

pleural effusions

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusions

sulphasalazine

pleural effusions

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusions

sulphasalazine

pleural effusions

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion

sulphasalazine

pleural effusions

sulphasalazine

pleural effusions

sulphasalazine

pleural effusion

sulphasalazine

pleural effusion


Input: Is phenytoin administration safe in a hypothermic child? A male neonate with a Chiari malformation and a leaking myelomeningocoele underwent ventriculoperitoneal shunt insertion followed by repair of myelomeningocoele. During anaesthesia and surgery, he inadvertently became moderately hypothermic. Intravenous phenytoin was administered during the later part of the surgery for seizure prophylaxis. Following phenytoin administration, the patient developed acute severe bradycardia, refractory to atropine and adrenaline. The cardiac depressant actions of phenytoin and hypothermia can be additive. Administration of phenytoin in the presence of hypothermia may lead to an adverse cardiac event in children. As phenytoin is a commonly used drug, clinicians need to be aware of this interaction.

phenytoin

phenytoin

phenytoin

atropine

adrenaline

phenytoin

phenytoin

phenytoin

hypothermic

Chiari malformation

hypothermic

seizure

bradycardia

hypothermia

hypothermia

phenytoin

bradycardia

phenytoin

bradycardia

phenytoin

bradycardia

phenytoin

bradycardia

phenytoin

bradycardia

phenytoin

bradycardia


Input: Amisulpride related tic - like symptoms in an adolescent schizophrenic. Tic disorders can be effectively treated by atypical antipsychotics such as risperidone, olanzapine and ziprasidone. However, there are two case reports that show tic - like symptoms, including motor and phonic variants, occurring during treatment with quetiapine or clozapine. We present a 15 - year - old girl schizophrenic who developed frequent involuntary eye - blinking movements after 5 months of amisulpride treatment (1000 mg per day). The tic - like symptoms resolved completely after we reduced the dose of amisulpride down to 800 mg per day. However, her psychosis recurred after the dose reduction. We then placed her on an additional 100 mg per day of quetiapine. She has been in complete remission under the combined medications for more than one year and maintains a fair role function. No more tic - like symptoms or other side effects have been reported. Together with previously reported cases, our patient suggests that tic - like symptoms might occur in certain vulnerable individuals during treatment with atypical antipsychotics such as quetiapine, clozapine, or amisulpride.

Amisulpride

risperidone

olanzapine

ziprasidone

quetiapine

clozapine

amisulpride

amisulpride

quetiapine

quetiapine

clozapine

amisulpride

tic - like symptoms

schizophrenic

Tic disorders

tic - like symptoms

schizophrenic

involuntary eye - blinking movements

tic - like symptoms

psychosis

tic - like symptoms

tic - like symptoms

Amisulpride

tic - like symptoms

Amisulpride

Tic disorders

Amisulpride

tic - like symptoms

Amisulpride

tic - like symptoms

Amisulpride

tic - like symptoms

Amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

Tic disorders

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

Tic disorders

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

Tic disorders

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms

amisulpride

tic - like symptoms


Input: Comparison of developmental toxicology of aspirin (acetylsalicylic acid) in rats using selected dosing paradigms. BACKGROUND: Analysis of the literature for nonsteroidal anti - inflammatory drugs (NSAIDs) suggests that a low incidence of developmental anomalies occurs in rats given NSAIDs on specific days during organogenesis. Aspirin (acetylsalicylic acid [ASA]), an irreversible cyclooxygenase 1 and 2 inhibitor, induces developmental anomalies when administered to Wistar rats on gestational day (GD) 9, 10, or 11 (Kimmel CA, Wilson JG, Schumacher HJ. Teratology 4: 15 - 24, 1971). There are no published ASA studies using the multiple dosing paradigm of GDs 6 to 17. Objectives of the current study were to compare results between Sprague - Dawley (SD) and Wistar strains when ASA is administered on GD 9, 10, or 11; to compare the malformation patterns following single and multiple dosings during organogenesis in SD rats; and to test the hypothesis that maternal gastrointestinal toxicity confounds the detection of low incidence malformations with ASA when a multiple dosing paradigm is used. METHODS: ASA was administered as a single dose on GD 9 (0, 250, 500, or 625 mg / kg), 10 (0, 500, 625, or 750 mg / kg), or 11 (0, 500, 750, or 1000 mg / kg) and from GD 6 to GD 17 (0, 50, 125, or 250 mg / kg a day) in the multiple dose study to SD rats. Animals were killed on GD 21, and fetuses were examined viscerally. RESULTS: The literature evaluation suggested that NSAIDs induce ventricular septal defects (VSDs) and midline defects (MDs) in rats and diaphragmatic hernia (DH), MDs, and VSDs in rabbits (Cook JC et al., 2003); hence, the present study focused on these malformations, even though ASA induces several other low - incidence malformations. In single dose studies, DH, MD, and VSD were induced on GDs 9 and 10. VSD also was noted following treatment on GD 11. In contrast, DH and MD were noted in the multiple dose study design only in the high - dose group, and VSD was noted across all dose groups. CONCLUSIONS: High concordance in major developmental anomalies between Wistar and SD rats were noted with the exception of VSD in the SD rats and hydrocephalus in the Wistar rats. Variations and malformations were similar when ASA was administered as a single dose or during the period of organogenesis (GDs 6 to 17). It was also evident that, by titrating the dose to achieve a maximum tolerated dose, malformations that normally occur at low incidence, as reported from previous single dose studies, could also be induced with ASA given at multiple doses.

aspirin

acetylsalicylic acid

Aspirin

acetylsalicylic acid

ASA

ASA

ASA

ASA

ASA

ASA

ASA

ASA

developmental anomalies

developmental anomalies

gastrointestinal toxicity

malformations

ventricular septal defects

VSDs

midline defects

MDs

diaphragmatic hernia

DH

MDs

VSDs

malformations

malformations

DH

MD

VSD

VSD

DH

MD

VSD

developmental anomalies

VSD

hydrocephalus

malformations

malformations

aspirin

diaphragmatic hernia

aspirin

DH

aspirin

DH

aspirin

DH

acetylsalicylic acid

diaphragmatic hernia

acetylsalicylic acid

DH

acetylsalicylic acid

DH

acetylsalicylic acid

DH

Aspirin

diaphragmatic hernia

Aspirin

DH

Aspirin

DH

Aspirin

DH

acetylsalicylic acid

diaphragmatic hernia

acetylsalicylic acid

DH

acetylsalicylic acid

DH

acetylsalicylic acid

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

ASA

diaphragmatic hernia

ASA

DH

ASA

DH

ASA

DH

aspirin

developmental anomalies

aspirin

developmental anomalies

aspirin

malformations

aspirin

malformations

aspirin

malformations

aspirin

developmental anomalies

aspirin

malformations

aspirin

malformations

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

Aspirin

developmental anomalies

Aspirin

developmental anomalies

Aspirin

malformations

Aspirin

malformations

Aspirin

malformations

Aspirin

developmental anomalies

Aspirin

malformations

Aspirin

malformations

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

acetylsalicylic acid

developmental anomalies

acetylsalicylic acid

malformations

acetylsalicylic acid

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

developmental anomalies

ASA

malformations

ASA

malformations

ASA

malformations

ASA

developmental anomalies

ASA

malformations

ASA

malformations

aspirin

ventricular septal defects

aspirin

VSDs

aspirin

VSDs

aspirin

VSD

aspirin

VSD

aspirin

VSD

aspirin

VSD

acetylsalicylic acid

ventricular septal defects

acetylsalicylic acid

VSDs

acetylsalicylic acid

VSDs

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

Aspirin

ventricular septal defects

Aspirin

VSDs

Aspirin

VSDs

Aspirin

VSD

Aspirin

VSD

Aspirin

VSD

Aspirin

VSD

acetylsalicylic acid

ventricular septal defects

acetylsalicylic acid

VSDs

acetylsalicylic acid

VSDs

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

acetylsalicylic acid

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD

ASA

ventricular septal defects

ASA

VSDs

ASA

VSDs

ASA

VSD

ASA

VSD

ASA

VSD

ASA

VSD


Input: Torsade de pointes induced by metoclopramide in an elderly woman with preexisting complete left bundle branch block. There is a growing list of drugs implicated in acquired long QT syndrome and torsade de pointes. However, the torsadogenic potential of metoclopramide, a commonly used antiemetic and prokinetic drug, has not been reported in the literature, despite its chemical similarity to procainamide. We report on a 92 - year - old woman with preexisting complete left bundle branch block who developed torsade de pointes after intravenous and oral administration of metoclopramide. This patient also developed torsade de pointes when cisapride and erythromycin were given simultaneously. These two episodes were suppressed successfully after discontinuing the offending drugs and administering class IB drugs. This is the first documentation that metoclopramide provokes torsade de pointes clinically. Metoclopramide should be used cautiously in patients with a risk of torsade de pointes.

Torsade de pointes

left bundle branch block

long QT syndrome

torsade de pointes

left bundle branch block

torsade de pointes

torsade de pointes

torsade de pointes

torsade de pointes

metoclopramide

metoclopramide

procainamide

metoclopramide

cisapride

erythromycin

metoclopramide

Metoclopramide

metoclopramide

Torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

Torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

Torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

Torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

metoclopramide

torsade de pointes

Metoclopramide

Torsade de pointes

Metoclopramide

torsade de pointes

Metoclopramide

torsade de pointes

Metoclopramide

torsade de pointes

Metoclopramide

torsade de pointes

Metoclopramide

torsade de pointes

erythromycin

Torsade de pointes

erythromycin

torsade de pointes

erythromycin

torsade de pointes

erythromycin

torsade de pointes

erythromycin

torsade de pointes

erythromycin

torsade de pointes

cisapride

Torsade de pointes

cisapride

torsade de pointes

cisapride

torsade de pointes

cisapride

torsade de pointes

cisapride

torsade de pointes

cisapride

torsade de pointes


Input: Apomorphine: an underutilized therapy for Parkinson' s disease. Apomorphine was the first dopaminergic drug ever used to treat symptoms of Parkinson' s disease. While powerful antiparkinsonian effects had been observed as early as 1951, the potential of treating fluctuating Parkinson' s disease by subcutaneous administration of apomorphine has only recently become the subject of systematic study. A number of small scale clinical trials have unequivocally shown that intermittent subcutaneous apomorphine injections produce antiparkinsonian benefit close if not identical to that seen with levodopa and that apomorphine rescue injections can reliably revert off - periods even in patients with complex on - off motor swings. Continuous subcutaneous apomorphine infusions can reduce daily off - time by more than 50% in this group of patients, which appears to be a stronger effect than that generally seen with add - on therapy with oral dopamine agonists or COMT inhibitors. Extended follow - up studies of up to 8 years have demonstrated long - term persistence of apomorphine efficacy. In addition, there is convincing clinical evidence that monotherapy with continuous subcutaneous apomorphine infusions is associated with marked reductions of preexisting levodopa - induced dyskinesias. The main side effects of subcutaneous apomorphine treatment are related to cutaneous tolerability problems, whereas sedation and psychiatric complications play a lesser role. Given the marked degree of efficacy of subcutaneous apomorphine treatment in fluctuating Parkinson' s disease, this approach seems to deserve more widespread clinical use.

Apomorphine

Apomorphine

apomorphine

apomorphine

levodopa

apomorphine

apomorphine

dopamine

apomorphine

apomorphine

levodopa

apomorphine

apomorphine

Parkinson' s disease

Parkinson' s disease

Parkinson' s disease

dyskinesias

psychiatric

Parkinson' s disease

levodopa

dyskinesias

levodopa

dyskinesias


Input: Fatal excited delirium following cocaine use: epidemiologic findings provide new evidence for mechanisms of cocaine toxicity. We describe an outbreak of deaths from cocaine - induced excited delirium (EDDs) in Dade County, Florida between 1979 and 1990. From a registry of all cocaine - related deaths in Dade County, Florida, from 1969 - 1990, 58 EDDs were compared with 125 victims of accidental cocaine overdose without excited delirium. Compared with controls, EDDs were more frequently black, male, and younger. They were less likely to have a low body mass index, and more likely to have died in police custody, to have received medical treatment immediately before death, to have survived for a longer period, to have developed hyperthermia, and to have died in summer months. EDDs had concentrations of cocaine and benzoylecgonine in autopsy blood that were similar to those for controls. The epidemiologic findings are most consistent with the hypothesis that chronic cocaine use disrupts dopaminergic function and, when coupled with recent cocaine use, may precipitate agitation, delirium, aberrant thermoregulation, rhabdomyolysis, and sudden death.

delirium

toxicity

delirium

EDDs

EDDs

overdose

delirium

EDDs

hyperthermia

EDDs

agitation

delirium

rhabdomyolysis

sudden death

cocaine

cocaine

cocaine

cocaine

cocaine

cocaine

benzoylecgonine

cocaine

cocaine

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

rhabdomyolysis

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

sudden death

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

delirium

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium

cocaine

EDDs

cocaine

EDDs

cocaine

delirium


Input: Heparin - induced thrombocytopenia, thrombosis, and hemorrhage. Sixty - two patients with a heparin - induced thrombocytopenia are reported. Clinical manifestations of this disorder include hemorrhage or, more frequently, thromboembolic events in patients receiving heparin. Laboratory testing has revealed a falling platelet count, increased resistance to heparin, and aggregation of platelets by the patient' s plasma when heparin is added. Immunologic testing has demonstrated the presence of a heparin - dependent platelet membrane antibody. The 20 deaths, 52 hemorrhagic and thromboembolic complications, and 21 surgical procedures to manage the complications confirm the seriousness of the disorder. Specific risk factors have not been identified; therefore, all patients receiving heparin should be monitored. If the platelet count falls to less than 100, 000 / mm3, while the patient is receiving heparin, platelet aggregation testing, using the patient' s plasma, is indicated. Management consists of cessation of heparin, platelet anti - aggregating agents, and alternate forms of anticoagulation when indicated.

Heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

thrombocytopenia

thrombosis

hemorrhage

thrombocytopenia

hemorrhage

thromboembolic

a falling platelet count

hemorrhagic and thromboembolic complications

hemorrhagic and thromboembolic complications

thromboembolic complications

platelet aggregation

Heparin

thromboembolic

Heparin

hemorrhagic and thromboembolic complications

Heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

heparin

thromboembolic

heparin

hemorrhagic and thromboembolic complications

heparin

thromboembolic complications

Heparin

thrombocytopenia

Heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

Heparin

hemorrhage

Heparin

hemorrhage

Heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications

heparin

hemorrhage

heparin

hemorrhage

heparin

hemorrhagic and thromboembolic complications


Input: Cardiac toxicity of 5 - fluorouracil. Report of a case of spontaneous angina. We report a case of a patient with colon carcinoma and liver metastasis who presented chest pain after 5 - fluorouracil (5 - FU) administration. Clinical electrocardiographic evolution was similar to that observed in Prinzmetal' s angina, and chest pain promptly resolved with nifedipine. These data suggest that coronary spasm may be the cause of cardiotoxicity due to 5 - FU, and that calcium antagonists may probably be used in the prevention or treatment of 5 - FU cardiotoxicity.

Cardiac toxicity

angina

colon carcinoma

metastasis

chest pain

Prinzmetal' s angina

chest pain

coronary spasm

cardiotoxicity

cardiotoxicity

5 - fluorouracil

5 - fluorouracil

5 - FU

nifedipine

5 - FU

calcium

5 - FU

5 - fluorouracil

chest pain

5 - fluorouracil

chest pain

5 - fluorouracil

chest pain

5 - fluorouracil

chest pain

5 - FU

chest pain

5 - FU

chest pain

5 - FU

chest pain

5 - FU

chest pain

5 - FU

chest pain

5 - FU

chest pain

5 - fluorouracil

Prinzmetal' s angina

5 - fluorouracil

Prinzmetal' s angina

5 - FU

Prinzmetal' s angina

5 - FU

Prinzmetal' s angina

5 - FU

Prinzmetal' s angina


Input: Toxicity due to remission inducing drugs in rheumatoid arthritis. Association with HLA - B35 and Cw4 antigens. Twenty - five patients with rheumatoid arthritis (RA) who developed toxicity while taking remission inducing drugs and 30 without toxicity were studied for possible associations with class I and II HLA antigens. A strong association has been found between nephritis and dermatitis due to Tiopronin (a D - Penicillamine like compound) and class I antigens B35 - Cw4, and between dermatitis due to gold thiosulphate and B35. Compared to healthy controls a lower DR5 frequency was observed in patients with RA except for the Tiopronin related nephritis group.

Toxicity

rheumatoid arthritis

rheumatoid arthritis

RA

toxicity

toxicity

nephritis

dermatitis

dermatitis

RA

nephritis

Tiopronin

D - Penicillamine

gold

thiosulphate

Tiopronin

gold

dermatitis

gold

dermatitis

Tiopronin

nephritis

Tiopronin

nephritis

Tiopronin

nephritis

Tiopronin

nephritis

Tiopronin

dermatitis

Tiopronin

dermatitis

Tiopronin

dermatitis

Tiopronin

dermatitis


Input: Transient hemiparesis: a rare manifestation of diphenylhydantoin toxicity. Report of two cases. Among the common side effects of diphenylhydantoin (DPH) overdose, the most frequently encountered neurological signs are those of cerebellar dysfunction. Very rarely, the toxic neurological manifestations of this drug are of cerebral origin. Two patients are presented who suffered progressive hemiparesis due to DPH overdose. Both had brain surgery before DPH treatment. It is assumed that patients with some cerebral damage are liable to manifest DPH toxicity as focal neurological signs.

hemiparesis

toxicity

overdose

cerebellar dysfunction

hemiparesis

overdose

cerebral damage

toxicity

diphenylhydantoin

diphenylhydantoin

DPH

DPH

DPH

DPH

diphenylhydantoin

overdose

diphenylhydantoin

overdose

diphenylhydantoin

overdose

diphenylhydantoin

overdose

DPH

overdose

DPH

overdose

DPH

overdose

DPH

overdose

DPH

overdose

DPH

overdose

DPH

overdose

DPH

overdose

diphenylhydantoin

cerebellar dysfunction

diphenylhydantoin

cerebellar dysfunction

DPH

cerebellar dysfunction

DPH

cerebellar dysfunction

DPH

cerebellar dysfunction

DPH

cerebellar dysfunction

diphenylhydantoin

hemiparesis

diphenylhydantoin

hemiparesis

diphenylhydantoin

hemiparesis

diphenylhydantoin

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis

DPH

hemiparesis


Input: Nerve growth factor and prostaglandins in the urine of female patients with overactive bladder. PURPOSE: NGF and PGs in the bladder can be affected by pathological changes in the bladder and these changes can be detected in urine. We investigated changes in urinary NGF and PGs in women with OAB. MATERIALS AND METHODS: The study groups included 65 women with OAB and 20 without bladder symptoms who served as controls. Evaluation included patient history, urinalysis, a voiding diary and urodynamic studies. Urine samples were collected. NGF, PGE2, PGF2alpha and PGI2 were measured using enzyme - linked immunosorbent assay and compared between the groups. In addition, correlations between urinary NGF and PG, and urodynamic parameters in patients with OAB were examined. RESULTS: Urinary NGF, PGE2 and PGF2alpha were significantly increased in patients with OAB compared with controls (p < 0. 05). However, urinary PGI2 was not different between controls and patients with OAB. In patients with OAB urinary PGE2 positively correlated with volume at first desire to void and maximum cystometric capacity (p < 0. 05). Urinary NGF, PGF2alpha and PGI2 did not correlate with urodynamic parameters in patients with OAB. CONCLUSIONS: NGF and PGs have important roles in the development of OAB symptoms in female patients. Urinary levels of these factors may be used as markers to evaluate OAB symptoms.

prostaglandins

PGs

PGs

PG

PGs

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

overactive bladder

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB

OAB


Input: Acute low back pain during intravenous administration of amiodarone: a report of two cases. Amiodarone represents an effective antiarrhythmic drug for cardioversion of recent - onset atrial fibrillation (AF) and maintenance of sinus rhythm. We briefly describe two patients suffering from recent - onset atrial fibrillation, who experienced an acute devastating low back pain a few minutes after initiation of intravenous amiodarone loading. Notably, this side effect has not been ever reported in the medical literature. Clinicians should be aware of this reaction since prompt termination of parenteral administration leads to complete resolution.

low back pain

atrial fibrillation

AF

atrial fibrillation

low back pain

amiodarone

Amiodarone

amiodarone

amiodarone

low back pain

amiodarone

low back pain

Amiodarone

low back pain

Amiodarone

low back pain

amiodarone

low back pain

amiodarone

low back pain


Input: Postoperative myalgia after succinylcholine: no evidence for an inflammatory origin. A common side effect associated with succinylcholine is postoperative myalgia. The pathogenesis of this myalgia is still unclear; inflammation has been suggested but without convincing evidence. We designed the present study to investigate whether an inflammatory reaction contributes to this myalgia. The incidence and severity of succinylcholine - associated myalgia was determined in 64 patients pretreated with saline or dexamethasone before succinylcholine (n = 32 for each). Incidence and severity of myalgia did not differ significantly between the two groups: 15 patients in the dexamethasone group complained of myalgia compared with 18 patients in the saline group, and severe myalgia was reported by five patients and three patients, respectively (not significant). At 48 h after surgery, 12 patients in both groups still suffered from myalgia (not significant). In addition, interleukin - 6 (IL - 6) as an early marker of inflammation was assessed in a subgroup of 10 patients pretreated with saline. We found an increase of IL - 6 for only three patients, but only one patient reported myalgia; no relationship between myalgia and the increase of IL - 6 was found. In conclusion, there is no evidence for an inflammatory origin of succinylcholine - associated myalgia. IMPLICATIONS: Administration of dexamethasone before succinylcholine was not effective in decreasing the incidence or the severity of succinylcholine - induced postoperative myalgia. Furthermore, there was no significant relationship between postoperative myalgia and time course of interleukin - 6 concentrations, a marker of inflammation. Pretreatment with dexamethasone is not justified to prevent postoperative myalgia after succinylcholine.

Postoperative myalgia

postoperative myalgia

myalgia

inflammation

myalgia

myalgia

myalgia

myalgia

myalgia

myalgia

inflammation

myalgia

myalgia

myalgia

postoperative myalgia

postoperative myalgia

inflammation

postoperative myalgia

succinylcholine

succinylcholine

succinylcholine

dexamethasone

succinylcholine

dexamethasone

succinylcholine

dexamethasone

succinylcholine

succinylcholine

dexamethasone

succinylcholine

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

Postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

postoperative myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia

succinylcholine

myalgia


Input: Levodopa - induced oromandibular dystonia in progressive supranuclear palsy. Levodopa - induced dyskinesias have been reported in Parkinson' s disease and multiple system atrophy. Cranial dystonias are rare in patients with progressive supranuclear palsy (PSP). In this report we describe an unusual case of reversible levodopa - induced Oromandibular dystonia (OMD) in a PSP patient to highlight the importance of recognizing this drug related complication in the management of PSP, and discuss the possible underlying pathophysiology.

Levodopa

Levodopa

levodopa

dystonia

progressive supranuclear palsy

dyskinesias

Parkinson' s disease

multiple system atrophy

dystonias

progressive supranuclear palsy

PSP

Oromandibular dystonia

OMD

PSP

PSP

Levodopa

dystonia

Levodopa

dystonias

Levodopa

dystonia

Levodopa

dystonias

levodopa

dystonia

levodopa

dystonias


Input: Protective effect of edaravone against streptomycin - induced vestibulotoxicity in the guinea pig. This study investigated alleviation of streptomycin - induced vestibulotoxicity by edaravone in guinea pigs. Edaravone, a free radical scavenger, has potent free radical quenching action and is used in clinical practice to treat cerebral infarction. Streptomycin was administered to the inner ear by osmotic pump for 24 h, and edaravone (n = 8) or saline (n = 6) was intraperitoneally injected once a day for 7 days. We observed horizontal vestibulo - ocular reflex as a marker of postoperative vestibular function. Animals injected with saline showed statistically smaller gains than those injected with edaravone. These results suggest that edaravone suppresses streptomycin - induced vestibulotoxicity.

edaravone

streptomycin

streptomycin

edaravone

Edaravone

Streptomycin

edaravone

edaravone

edaravone

streptomycin

vestibulotoxicity

vestibulotoxicity

cerebral infarction

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

Streptomycin

vestibulotoxicity

Streptomycin

vestibulotoxicity

Streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity

streptomycin

vestibulotoxicity


Input: Ketamine in war / tropical surgery (a final tribute to the racemic mixture). A technique of continuous intravenous anaesthesia with ketamine was used successfully during the Somalia civil war in 1994 and in north Uganda in 1999 for 64 operations in 62 patients, aged from 6 weeks to 70 years, undergoing limb and abdominal surgery including caesarian sections and interventions in neonates. Operations lasting up to 2h could be performed in the absence of sophisticated equipment such as pulse oximeters or ventilators in patients on spontaneous ventilation breathing air / oxygen only. After premedication with diazepam, glycopyrrolate and local anaesthesia, and induction with standard doses of ketamine, a maintenance dose of 10 - 20 microg / kg / min of ketamine proved safe and effective. Emphasis was placed on bedside clinical monitoring, relying heavily on the heart rate. Diazepam, unless contraindicated or risky, remains the only necessary complementary drug to ketamine as it buffers its cardiovascular response and decreases the duration and intensity of operative and postoperative hallucinations. Local anaesthetic blocks were useful in decreasing the requirement for postoperative analgesia. An antisialogue was usually unnecessary in operations lasting up to 2 h, glycopyrrolate being the best choice for its lowest psychotropic and chronotropic effects, especially in a hot climate. Experience in war / tropical settings suggests this technique could be useful in civilian contexts such as outdoor life - saving emergency surgery or in mass casualties where, e. g. amputation and rapid extrication were required.

Ketamine

ketamine

oxygen

diazepam

glycopyrrolate

ketamine

ketamine

Diazepam

ketamine

glycopyrrolate

hallucinations

analgesia

Ketamine

hallucinations

ketamine

hallucinations

ketamine

hallucinations

ketamine

hallucinations

ketamine

hallucinations


Input: Steroid structure and pharmacological properties determine the anti - amnesic effects of pregnenolone sulphate in the passive avoidance task in rats. Pregnenolone sulphate (PREGS) has generated interest as one of the most potent memory - enhancing neurosteroids to be examined in rodent learning studies, with particular importance in the ageing process. The mechanism by which this endogenous steroid enhances memory formation is hypothesized to involve actions on glutamatergic and GABAergic systems. This hypothesis stems from findings that PREGS is a potent positive modulator of N - methyl - d - aspartate receptors (NMDARs) and a negative modulator of gamma - aminobutyric acid (A) receptors (GABA (A) Rs). Moreover, PREGS is able to reverse the amnesic - like effects of NMDAR and GABA (A) R ligands. To investigate this hypothesis, the present study in rats examined the memory - altering abilities of structural analogs of PREGS, which differ in their modulation of NMDAR and / or GABA (A) R function. The analogs tested were: 11 - ketopregnenolone sulphate (an agent that is inactive at GABA (A) Rs and NMDARs), epipregnanolone ([3beta - hydroxy - 5beta - pregnan - 20 - one] sulphate, an inhibitor of both GABA (A) Rs and NMDARs), and a newly synthesized (-) PREGS enantiomer (which is identical to PREGS in effects on GABA (A) Rs and NMDARs). The memory - enhancing effects of PREGS and its analogs were tested in the passive avoidance task using the model of scopolamine - induced amnesia. Both PREGS and its (-) enantiomer blocked the effects of scopolamine. The results show that, unlike PREGS, 11 - ketopregnenolone sulphate and epipregnanolone sulphate failed to block the effect of scopolamine, suggesting that altering the modulation of NMDA receptors diminishes the memory - enhancing effects of PREGS. Moreover, enantioselectivity was demonstrated by the ability of natural PREGS to be an order of magnitude more effective than its synthetic enantiomer in reversing scopolamine - induced amnesia. These results identify a novel neuropharmacological site for the modulation of memory processes by neuroactive steroids.

Steroid

pregnenolone sulphate

Pregnenolone sulphate

PREGS

steroid

PREGS

N - methyl - d - aspartate

gamma - aminobutyric acid

GABA

PREGS

GABA

PREGS

GABA

11 - ketopregnenolone sulphate

GABA

epipregnanolone ([3beta - hydroxy - 5beta - pregnan - 20 - one] sulphate

GABA

PREGS

PREGS

GABA

PREGS

scopolamine

PREGS

scopolamine

PREGS

11 - ketopregnenolone sulphate

epipregnanolone sulphate

scopolamine

NMDA

PREGS

PREGS

scopolamine

steroids

amnesic

amnesic

amnesia

amnesia

scopolamine

amnesic

scopolamine

amnesic

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesic

scopolamine

amnesic

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesic

scopolamine

amnesic

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesic

scopolamine

amnesic

scopolamine

amnesia

scopolamine

amnesia


Input: Preliminary efficacy assessment of intrathecal injection of an American formulation of adenosine in humans. BACKGROUND: Preclinical studies of intrathecal adenosine suggest it may be effective in the treatment of acute and chronic pain in humans, and preliminary studies in volunteers and patients with a Swedish formulation of adenosine suggests it may be effective in hypersensitivity states but not with acute noxious stimulation. The purpose of this study was to screen for efficacy of a different formulation of adenosine marketed in the US, using both acute noxious stimulation and capsaicin - evoked mechanical hypersensitivity. METHODS: Following Food and Drug Administration and institutional review board approval and written informed consent, 65 volunteers were studied in two trials: an open - label, dose - escalating trial with intrathecal adenosine doses of 0. 25 - 2. 0 mg and a double - blind, placebo - controlled trial of adenosine, 2 mg. Cerebrospinal fluid was obtained for pharmacokinetic analysis, and pain ratings in response to acute heat stimuli and areas of mechanical hyperalgesia and allodynia after intradermal capsaicin injection were determined. RESULTS: Adenosine produced no effect on pain report to acute noxious thermal or chemical stimulation but reduced mechanical hyperalgesia and allodynia from intradermal capsaicin injection for at least 24 h. In contrast, residence time of adenosine in cerebrospinal fluid was short (< 4 h). CONCLUSIONS: These results show selective inhibition by intrathecal adenosine of hypersensitivity, presumed to reflect central sensitization in humans after peripheral capsaicin injection. The long - lasting effect is consistent with that observed in preliminary reports of patients with chronic neuropathic pain and is not due to prolonged residence of adenosine in cerebrospinal fluid.

adenosine

adenosine

adenosine

adenosine

capsaicin

adenosine

adenosine

capsaicin

Adenosine

capsaicin

adenosine

adenosine

capsaicin

adenosine

acute and chronic pain

acute and chronic pain

chronic pain

hypersensitivity

hypersensitivity

pain

mechanical hyperalgesia

allodynia

pain

mechanical hyperalgesia

allodynia

hypersensitivity

neuropathic pain

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia

capsaicin

mechanical hyperalgesia

capsaicin

allodynia


Input: Effect of lithium maintenance therapy on thyroid and parathyroid function. OBJECTIVES: To assess changes induced by lithium maintenance therapy on the incidence of thyroid, parathyroid and ion alterations. These were evaluated with respect to the duration of lithium therapy, age, sex, and family history (whether or not the patient had a first - degree relative with thyroid disease). DESIGN: Prospective study. SETTING: Affective Disorders Clinic at St. Mary' s Hospital, Montreal. PATIENTS: One hundred and one patients (28 men and 73 women) with bipolar disorder receiving lithium maintenance therapy ranging from 1 year' s to 32 years' duration. The control group consisted of 82 patients with no psychiatric or endocrinological diagnoses from the hospital' s out - patient clinics. OUTCOME MEASURES: Laboratory analyses of calcium, magnesium and thyroid - stimulating hormone levels performed before beginning lithium therapy and at biannual follow - up. RESULTS: Hypothyroidism developed in 40 patients, excluding 8 patients who were hypothyroid at baseline. All patients having first - degree relatives affected by thyroid illness had accelerated onset of hypothyroidism (3. 7 years after onset of lithium therapy) compared with patients without a family history (8. 6 years after onset of lithium therapy). Women over 60 years of age were more often affected by hypothyroidism than women under 60 years of age (34. 6% versus 31. 9%). Magnesium levels in patients on lithium treatment were unchanged from baseline levels. After lithium treatment, calcium levels were higher than either baseline levels or control levels. Thus, lithium treatment counteracted the decrease in plasma calcium levels associated with aging. CONCLUSIONS: Familial thyroid illness is a risk factor for hypothyroidism and hypercalcemia during lithium therapy.

lithium

lithium

lithium

lithium

calcium

magnesium

lithium

lithium

lithium

Magnesium

lithium

lithium

calcium

lithium

calcium

lithium

thyroid disease

bipolar disorder

psychiatric

Hypothyroidism

hypothyroid

thyroid illness

hypothyroidism

hypothyroidism

thyroid illness

hypothyroidism

hypercalcemia

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism

lithium

Hypothyroidism

lithium

hypothyroid

lithium

hypothyroidism

lithium

hypothyroidism

lithium

hypothyroidism


Input: Systemic toxicity following administration of sirolimus (formerly rapamycin) for psoriasis: association of capillary leak syndrome with apoptosis of lesional lymphocytes. BACKGROUND: Sirolimus (formerly rapamycin) is an immunosuppressive agent that interferes with T - cell activation. After 2 individuals with psoriasis developed a capillary leak syndrome following treatment with oral sirolimus lesional skin cells and activated peripheral blood cells were analyzed for induction of apoptosis. OBSERVATIONS: A keratome skin specimen from 1 patient with sirolimus - induced capillary leak syndrome had a 2. 3 - fold increase in percentage of apoptotic cells (to 48%) compared with an unaffected sirolimus - treated patient with psoriasis (21%). Activated peripheral blood T cells from patients with psoriasis tended to exhibit greater spontaneous or dexamethasone - induced apoptosis than did normal T cells, particularly in the presence of sirolimus. CONCLUSIONS: Severe adverse effects of sirolimus include fever, anemia, and capillary leak syndrome. These symptoms may be the result of drug - induced apoptosis of lesional leukocytes, especially activated T lymphocytes, and possibly release of inflammatory mediators. Because patients with severe psoriasis may develop capillary leak from various systemic therapies, clinical monitoring is advisable for patients with inflammatory diseases who are treated with immune modulators.

toxicity

psoriasis

capillary leak syndrome

psoriasis

capillary leak syndrome

capillary leak syndrome

psoriasis

psoriasis

fever

anemia

capillary leak syndrome

psoriasis

capillary leak

inflammatory diseases

sirolimus

rapamycin

Sirolimus

rapamycin

sirolimus

sirolimus

sirolimus

dexamethasone

sirolimus

sirolimus

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak

Sirolimus

capillary leak syndrome

Sirolimus

capillary leak syndrome

Sirolimus

capillary leak syndrome

Sirolimus

capillary leak syndrome

Sirolimus

capillary leak

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak syndrome

rapamycin

capillary leak

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak syndrome

sirolimus

capillary leak


Input: Contribution of the glycine site of NMDA receptors in rostral and intermediate - caudal parts of the striatum to the regulation of muscle tone in rats. The aim of the present study was to assess the contribution of the glycine site of NMDA receptors in the striatum to the regulation of muscle tone. Muscle tone was examined using a combined mechanoand electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat' s hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by haloperidol (2. 5 mg / kg i. p.). 5, 7 - dichlorokynurenic acid (5, 7 - DCKA), a selective glycine site antagonist, injected in doses of 2. 5 and 4. 5 microg / 0. 5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol - induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). 5, 7 - DCKA injected bilaterally in a dose of 4. 5 microg / 0. 5 microl into the intermediate - caudal region of the striatum of rats not pretreated with haloperidol had no effect on the muscle tone. The present results suggest that blockade of the glycine site of NMDA receptors in the rostral part of the striatum may be mainly responsible for the antiparkinsonian action of this drug.

glycine

NMDA

glycine

NMDA

haloperidol

5, 7 - dichlorokynurenic acid

5, 7 - DCKA

glycine

haloperidol

5, 7 - DCKA

haloperidol

glycine

NMDA

Muscle rigidity

muscle rigidity

haloperidol

Muscle rigidity

haloperidol

muscle rigidity

haloperidol

Muscle rigidity

haloperidol

muscle rigidity

haloperidol

Muscle rigidity

haloperidol

muscle rigidity


Input: Efficacy and tolerability of lovastatin in 3390 women with moderate hypercholesterolemia. OBJECTIVE: To evaluate the efficacy and safety of lovastatin in women with moderate hypercholesterolemia. DESIGN: The Expanded Clinical Evaluation of Lovastatin (EXCEL) Study, a multicenter, double - blind, diet - and placebo - controlled trial, in which participants were randomly assigned to receive placebo or lovastatin at doses of 20 or 40 mg once daily, or 20 or 40 mg twice daily for 48 weeks. SETTING: Ambulatory patients recruited by 362 participating centers throughout the United States. PATIENTS: Women (n = 3390) from the total cohort of 8245 volunteers. MEASUREMENTS: Plasma total, low - density lipoprotein (LDL), and high - density lipoprotein (HDL) cholesterol, and triglycerides; and laboratory and clinical evidence of adverse events monitored periodically throughout the study. RESULTS: Among women, lovastatin (20 to 80 mg / d) produced sustained (12 - to 48 - week), dose - related changes (P < 0. 001): decreases in LDL cholesterol (24% to 40%) and triglycerides (9% to 18%), and increases in HDL cholesterol (6. 7% to 8. 6%). Depending on the dose, from 82% to 95% of lovastatin - treated women achieved the National Cholesterol Education Program goal of LDL cholesterol levels less than 4. 14 mmol / L (160 mg / dL), and 40% to 87% achieved the goal of 3. 36 mmol / L (130 mg / dL). Successive transaminase elevations greater than three times the upper limit of normal occurred in 0. 1% of women and were dose dependent above the 20 - mg dose. Myopathy, defined as muscle symptoms with creatine kinase elevations greater than 10 times the upper limit of normal, was rare and associated with the highest recommended daily dose of lovastatin (80 mg). Estrogen - replacement therapy appeared to have no effect on either the efficacy or safety profile of lovastatin. CONCLUSION: Lovastatin is highly effective and generally well tolerated as therapy for primary hypercholesterolemia in women.

lovastatin

lovastatin

Lovastatin

lovastatin

cholesterol

triglycerides

lovastatin

cholesterol

triglycerides

cholesterol

lovastatin

Cholesterol

cholesterol

creatine

lovastatin

lovastatin

Lovastatin

hypercholesterolemia

hypercholesterolemia

Myopathy

hypercholesterolemia

lovastatin

Myopathy

lovastatin

Myopathy

Lovastatin

Myopathy

lovastatin

Myopathy

lovastatin

Myopathy

lovastatin

Myopathy

lovastatin

Myopathy

lovastatin

Myopathy

Lovastatin

Myopathy


Input: REM sleep deprivation changes behavioral response to catecholaminergic and serotonergic receptor activation in rats. The effects of REM sleep deprivation (REMD) on apomorphine - induced aggressiveness and quipazine - induced head twitches in rats were determined. Forty - eight hr of REMD increased apomorphine - induced aggressiveness, and reduced (immediately after completing of REMD) or increased (96 hr after completing of REMD) quipazine - induced head twitches. Results are discussed in terms of similarity to pharmacological effects of other antidepressive treatments.

REM sleep deprivation

REM sleep deprivation

REMD

aggressiveness

head twitches

REMD

aggressiveness

REMD

REMD

head twitches

apomorphine

quipazine

apomorphine

quipazine

quipazine

head twitches

quipazine

head twitches

quipazine

head twitches

quipazine

head twitches

apomorphine

aggressiveness

apomorphine

aggressiveness

apomorphine

aggressiveness

apomorphine

aggressiveness


Input: Extrapyramidal side effects and oral haloperidol: an analysis of explanatory patient and treatment characteristics. The incidence of extrapyramidal side effects (EPS) was evaluated in 98 patients treated with haloperidol. The incidence of parkinsonism was higher at higher doses of haloperidol and in younger patients. Prophylactic antiparkinsonian medication was effective in younger but not in older patients. However, these medications were more effective in both young and old patients when given after parkinsonism developed. Akathisia was controlled by the benzodiazepine lorazepam in 14 out of 16 patients, while prophylactic antiparkinsonians were ineffective. The present study points to patient characteristics that may be of significance in the development of EPS due to haloperidol.

haloperidol

haloperidol

haloperidol

benzodiazepine

lorazepam

haloperidol

parkinsonism

parkinsonism

Akathisia

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism

haloperidol

parkinsonism


Input: Hepatic veno - occlusive disease caused by 6 - thioguanine. Clinically reversible veno - occlusive disease of the liver developed in a 23 - year - old man with acute lymphocytic leukemia after 10 months of maintenance therapy with 6 - thioguanine. Serial liver biopsies showed the development and resolution of intense sinusoidal engorgement. Although this disease was clinically reversible, some subintimal fibrosis about the terminal hepatic veins persisted. This case presented a unique opportunity to observe the histologic features of clinically reversible hepatic veno - occlusive disease over time, and may be the first case of veno - occlusive related solely to 6 - thioguanine.

Hepatic veno - occlusive disease

veno - occlusive disease of the liver

acute lymphocytic leukemia

fibrosis

hepatic veno - occlusive disease

6 - thioguanine

6 - thioguanine

6 - thioguanine

6 - thioguanine

Hepatic veno - occlusive disease

6 - thioguanine

veno - occlusive disease of the liver

6 - thioguanine

hepatic veno - occlusive disease

6 - thioguanine

Hepatic veno - occlusive disease

6 - thioguanine

veno - occlusive disease of the liver

6 - thioguanine

hepatic veno - occlusive disease

6 - thioguanine

Hepatic veno - occlusive disease

6 - thioguanine

veno - occlusive disease of the liver

6 - thioguanine

hepatic veno - occlusive disease


Input: Treatment of ifosfamide - induced urothelial toxicity by oral administration of sodium 2 - mercaptoethane sulphonate (MESNA) to patients with inoperable lung cancer. The protective effect of oral administration of the thiol compound sodium 2 - mercaptoethane sulphonate (MESNA) against urothelial toxicity induced by ifosfamide (IF) was tested in a group of 45 patients with inoperable lung cancer under treatment with IF (2250 mg / m2 on days 2 - 5) as part of a polychemotherapy regimen repeated in a 4 - week cycle. MESNA was given orally on the days of treatment with IF in 3 doses of 840 mg / m2, each administered at 0 hr (= injection of IF), 4 hr and 8 hr p. i. Out of a total of 88 courses of this treatment we observed 10 episodes of asymptomatic microscopic haematuria and no episodes of gross haematuria. In this group of 45 patients under protection with MESNA there were 5 complete remissions and 9 partial remissions (total 31%). A further group of 25 patients under polychemotherapy with IF were treated by conventional prophylactic measures (raised fluid intake and forced diuresis). In this group there were 1 complete and 5 partial remissions (total 24%), but nearly all patients developed either gross haematuria and / or symptoms of bladder irritation (cystitis and pollakisuria). There were no appreciable differences between the MESNA series and the conventional prophylaxis series with respect to either haematological or systemic toxicity of the cytostatic treatment. Our results support the view that MESNA, given orally in conjunction with combined cytostatic regimens which include IF, simplifies the treatment and provides optimum protection for the urinary epithelium. Protection with oral MESNA is particularly suitable for outpatients.

ifosfamide

sodium 2 - mercaptoethane sulphonate

MESNA

thiol

sodium 2 - mercaptoethane sulphonate

MESNA

ifosfamide

IF

IF

MESNA

IF

IF

MESNA

IF

MESNA

MESNA

IF

MESNA

urothelial toxicity

lung cancer

urothelial toxicity

lung cancer

haematuria

haematuria

haematuria

bladder irritation

cystitis

pollakisuria

toxicity

ifosfamide

urothelial toxicity

ifosfamide

urothelial toxicity

ifosfamide

bladder irritation

ifosfamide

urothelial toxicity

ifosfamide

urothelial toxicity

ifosfamide

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation

IF

urothelial toxicity

IF

urothelial toxicity

IF

bladder irritation


Input: Time course alterations of QTC interval due to hypaque 76. Sequential measurement of QT interval during left ventricular angiography was made 30 seconds and one, three, five and ten minutes after injection of hypaque 76. The subjects were ten patients found to have normal left ventricles and coronary arteries. Significant QTC prolongation occurred in 30 seconds to one minute in association with marked hypotension and elevation of cardiac output.

hypaque 76

hypaque 76

QTC prolongation

hypotension

hypaque 76

hypotension

hypaque 76

hypotension

hypaque 76

QTC prolongation

hypaque 76

QTC prolongation


Input: Production of autochthonous prostate cancer in Lobund - Wistar rats by treatments with N - nitroso - N - methylurea and testosterone. More than 50% of Lobund - Wistar (L - W) strain rats developed large, palpable prostate adenocarcinomas (PAs) following treatments with N - nitroso - N - methylurea (CAS: 684 - 93 - 5) and testosterone propionate [(TP) CAS: 57 - 85 - 2], and most of the tumor - bearing rats manifested metastatic lesions. The incubation periods averaged 10. 6 months. Within the same timeframe, no L - W rat developed a similar palpable PA when treated only with TP. In L - W rats, TP acted as a tumor enhancement agent, with primary emphasis on the development of prostate cancer.

prostate cancer

prostate adenocarcinomas

PAs

tumor

PA

tumor

prostate cancer

N - nitroso - N - methylurea

testosterone

N - nitroso - N - methylurea

testosterone propionate

TP

TP

TP

testosterone propionate

prostate cancer

testosterone propionate

prostate adenocarcinomas

testosterone propionate

PAs

testosterone propionate

PA

testosterone propionate

prostate cancer

TP

prostate cancer

TP

prostate adenocarcinomas

TP

PAs

TP

PA

TP

prostate cancer

TP

prostate cancer

TP

prostate adenocarcinomas

TP

PAs

TP

PA

TP

prostate cancer

TP

prostate cancer

TP

prostate adenocarcinomas

TP

PAs

TP

PA

TP

prostate cancer

N - nitroso - N - methylurea

prostate cancer

N - nitroso - N - methylurea

prostate adenocarcinomas

N - nitroso - N - methylurea

PAs

N - nitroso - N - methylurea

PA

N - nitroso - N - methylurea

prostate cancer

N - nitroso - N - methylurea

prostate cancer

N - nitroso - N - methylurea

prostate adenocarcinomas

N - nitroso - N - methylurea

PAs

N - nitroso - N - methylurea

PA

N - nitroso - N - methylurea

prostate cancer


Input: A dystonia - like syndrome after neuropeptide (MSH / ACTH) stimulation of the rat locus ceruleus. The movement disorder investigated in these studies has some features in common with human idiopathic dystonia, and information obtained in these studies may be of potential clinical benefit. The present experimental results indicated that peptidergic stimulation of the LC resulted in a NE - mediated inhibition of cerebellar Purkinje cells located at terminals of the ceruleo - cerebellar pathway. However, it is not certain as to the following: (a) what receptors were stimulated by the ACTH N - terminal fragments at the LC that resulted in this disorder; (b) whether NE, released onto Purkinje cell synapses located at terminals of the ceruleo - cerebellar pathway, did indeed cause the long - term depression at Purkinje cell synapses (previously described by others) that resulted in the long duration of the movement disorder; (c) whether the inhibition of inhibitory Purkinje cells resulted in disinhibition or increased excitability of the unilateral cerebellar fastigial or interpositus nuclei, the output targets of the Purkinje cell axons, that may have been an important contributing factor to this disorder. These questions are currently being investigated.

dystonia

movement disorder

dystonia

depression

movement disorder

MSH

ACTH

ACTH

MSH

dystonia

MSH

dystonia

ACTH

dystonia

ACTH

dystonia

ACTH

dystonia

ACTH

dystonia


Input: Dexmedetomidine, acting through central alpha - 2 adrenoceptors, prevents opiate - induced muscle rigidity in the rat. The highly - selective alpha - 2 adrenergic agonist dexmedetomidine (D - MED) is capable of inducing muscle flaccidity and anesthesia in rats and dogs. Intense generalized muscle rigidity is an undesirable side effect of potent opiate agonists. Although the neurochemistry of opiate - induced rigidity has yet to be fully elucidated, recent work suggests a role for a central adrenergic mechanism. In the present study, the authors determined if treatment with D - MED prevents the muscle rigidity caused by high - dose alfentanil anesthesia in the rat. Animals (n = 42) were treated intraperitoneally with one of the following six regimens: 1) L - MED (the inactive L - isomer of medetomidine), 30 micrograms / kg; 2) D - MED, 10 micrograms / kg; 3) D - MED, 30 micrograms / kg; 4) D - MED [30 micrograms / kg] and the central - acting alpha - 2 antagonist, idazoxan [10 mg / kg]; 5) D - MED [30 micrograms / kg] and the peripheral - acting alpha - 2 antagonist DG - 5128 [10 mg / kg], or; 6) saline. Baseline electromyographic activity was recorded from the gastrocnemius muscle before and after drug treatment. Each rat was then injected with alfentanil (ALF, 0. 5 mg / kg sc). ALF injection resulted in a marked increase in hindlimb EMG activity in the L - MED treatment group which was indistinguishable from that seen in animals treated with saline. In contrast, D - MED prevented alfentanil - induced muscle rigidity in a dose - dependent fashion. The small EMG values obtained in the high - dose D - MED group were comparable with those recorded in earlier studies from control animals not given any opiate. The high - dose D - MED animals were flaccid, akinetic, and lacked a startle response during the entire experimental period. (ABSTRACT TRUNCATED AT 250 WORDS)

Dexmedetomidine

dexmedetomidine

D - MED

D - MED

alfentanil

medetomidine

D - MED

D - MED

D - MED

idazoxan

D - MED

DG - 5128

alfentanil

ALF

ALF

D - MED

alfentanil

D - MED

D - MED

muscle rigidity

muscle flaccidity

muscle rigidity

rigidity

muscle rigidity

muscle rigidity

akinetic

startle

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

ALF

muscle rigidity

ALF

muscle rigidity

ALF

rigidity

ALF

muscle rigidity

ALF

muscle rigidity

ALF

muscle rigidity

ALF

muscle rigidity

ALF

rigidity

ALF

muscle rigidity

ALF

muscle rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity

alfentanil

rigidity

alfentanil

muscle rigidity

alfentanil

muscle rigidity


Input: Seizure activity with imipenem therapy: incidence and risk factors. Two elderly patients with a history of either cerebral vascular accident (CVA) or head trauma and no evidence of renal disease developed seizures while receiving maximum doses of imipenem / cilastatin. Neither patient had reported previous seizures or seizure - like activity nor was receiving anticonvulsant agents. All seizures were controlled with therapeutic doses of phenytoin. Both patients had received maximum doses of other beta - lactam antibiotics without evidence of seizure activity.

Seizure

cerebral vascular accident

CVA

head trauma

renal disease

seizures

seizures

seizure

seizures

seizure

imipenem

imipenem / cilastatin

phenytoin

beta - lactam

imipenem / cilastatin

Seizure

imipenem / cilastatin

seizures

imipenem / cilastatin

seizures

imipenem / cilastatin

seizure

imipenem / cilastatin

seizures

imipenem / cilastatin

seizure


Input: The ability of insulin treatment to reverse or prevent the changes in urinary bladder function caused by streptozotocin - induced diabetes mellitus. 1. The effects of insulin treatment on in vivo and in vitro urinary bladder function in streptozotocin - diabetic rats were investigated. 2. Diabetes of 2 months duration resulted in decreases in body weight and increases in fluid consumption, urine volume, frequency of micturition, and average volume per micturition; effects which were prevented by insulin treatment. 3. Insulin treatment also prevented the increases in contractile responses of bladder body strips from diabetic rats to nerve stimulation, ATP, and bethanechol. 4. Diabetes of 4 months duration also resulted in decreases in body weight, and increases in fluid consumption, urine volume, frequency of micturition, and average volume per micturition, effects which were reversed by insulin treatment for the final 2 months of the study. 5. Insulin treatment reversed the increases in contractile responses of bladder body strips from diabetic rats to nerve stimulation, ATP, and bethanechol. 6. The data indicate that the effects of streptozotocin - induced diabetes on urinary bladder function are both prevented and reversed by insulin treatment.

streptozotocin

streptozotocin

ATP

bethanechol

ATP

bethanechol

streptozotocin

diabetes mellitus

diabetic

Diabetes

diabetic

Diabetes

diabetic

diabetes

streptozotocin

diabetes mellitus

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

diabetes

streptozotocin

diabetes mellitus

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

diabetes

streptozotocin

diabetes mellitus

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

Diabetes

streptozotocin

diabetic

streptozotocin

diabetes


Input: Delayed institution of hypertension during focal cerebral ischemia: effect on brain edema. The effect of induced hypertension instituted after a 2 - h delay following middle cerebral artery occlusion (MCAO) on brain edema formation and histochemical injury was studied. Under isoflurane anesthesia, the MCA of 14 spontaneously hypertensive rats was occluded. In the control group (n = 7), the mean arterial pressure (MAP) was not manipulated. In the hypertensive group (n = 7), the MAP was elevated by 25 - 30 mm Hg beginning 2 h after MCAO. Four hours after MCAO, the rats were killed and the brains harvested. The brains were sectioned along coronal planes spanning the distribution of ischemia produced by MCAO. Specific gravity (SG) was determined in the subcortex and in two sites in the cortex (core and periphery of the ischemic territory). The extent of neuronal injury was determined by 2, 3, 5 - triphenyltetrazolium staining. In the ischemic core, there was no difference in SG in the subcortex and cortex in the two groups. In the periphery of the ischemic territory, SG in the cortex was greater (less edema accumulation) in the hypertensive group (1. 041 + / - 0. 001 vs 1. 039 + / - 0. 001, P less than 0. 05). The area of histochemical injury (as a percent of the cross - sectional area of the hemisphere) was less in the hypertensive group (33 + / - 3% vs 21 + / - 2%, P less than 0. 05). The data indicate that phenylephrine - induced hypertension instituted 2 h after MCAO does not aggravate edema in the ischemic core, that it improves edema in the periphery of the ischemic territory, and that it reduces the area of histochemical neuronal dysfunction.

hypertension

cerebral ischemia

brain edema

hypertension

middle cerebral artery occlusion

MCAO

brain edema

hypertensive

hypertensive

MCAO

MCAO

ischemia

MCAO

ischemic

neuronal injury

ischemic

ischemic

edema

hypertensive

hypertensive

hypertension

MCAO

edema

ischemic

edema

ischemic

neuronal dysfunction

isoflurane

2, 3, 5 - triphenyltetrazolium

phenylephrine

phenylephrine

hypertension

phenylephrine

hypertension

phenylephrine

hypertensive

phenylephrine

hypertensive

phenylephrine

hypertensive

phenylephrine

hypertensive

phenylephrine

hypertension


Input: Amiodarone pulmonary toxicity. Amiodarone is an effective antiarrhythmic agent whose utility is limited by many side - effects, the most problematic being pneumonitis. The pulmonary toxicity of amiodarone is thought to result from direct injury related to the intracellular accumulation of phospholipid and T cell - mediated hypersensitivity pneumonitis. The clinical and radiographic features of amiodarone - induced pulmonary toxicity are characteristic but nonspecific. The diagnosis depends on exclusion of other entities, such as heart failure, infection, and malignancy. While withdrawal of amiodarone leads to clinical improvement in majority of cases, this is not always possible or advisable. Dose reduction or concomitant steroid therapy may have a role in selected patients.

Amiodarone

Amiodarone

amiodarone

amiodarone

amiodarone

steroid

pulmonary toxicity

pneumonitis

pulmonary toxicity

hypersensitivity pneumonitis

hypersensitivity

pneumonitis

pulmonary toxicity

heart failure

infection

malignancy

Amiodarone

pneumonitis

Amiodarone

pneumonitis

amiodarone

pneumonitis

amiodarone

pneumonitis

amiodarone

pneumonitis

Amiodarone

hypersensitivity pneumonitis

Amiodarone

hypersensitivity

Amiodarone

hypersensitivity pneumonitis

Amiodarone

hypersensitivity

amiodarone

hypersensitivity pneumonitis

amiodarone

hypersensitivity

amiodarone

hypersensitivity pneumonitis

amiodarone

hypersensitivity

amiodarone

hypersensitivity pneumonitis

amiodarone

hypersensitivity


Input: Light chain proteinuria and cellular mediated immunity in rifampin treated patients with tuberculosis. Light chain proteinuria was found in 9 of 17 tuberculosis patients treated with rifampin. Concomitant assay of cellular mediated immunity in these patients using skin test antigen and a lymphokine in vitro test provided results that were different. Response to Varidase skin test antigen was negative for all eight tuberculosis patients tested, but there occurred a hyper - responsiveness of the lymphocytes of these eight patients to phytomitogen (PHA - P). as well as of those of seven other tuberculous patients. This last finding may be related to time of testing and / or endogenous serum binding of rifampin which could have inhibited mitogen activity for the lymphocyte.

proteinuria

tuberculosis

proteinuria

tuberculosis

tuberculosis

tuberculous

rifampin

rifampin

rifampin

rifampin

proteinuria

rifampin

proteinuria

rifampin

proteinuria

rifampin

proteinuria

rifampin

proteinuria

rifampin

proteinuria


Input: Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction. To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal - sodium diet and four a low - sodium (17 mmol / day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal - sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low - sodium group the highest deficit was 276 mmol on day 13. The normal - sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low - sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic - induced potassium loss, presumably by an increased activity of the renin - angiotensin - aldosterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.

potassium

chlorthalidone

sodium

potassium

Chlorthalidone

sodium

sodium

potassium

aldosterone

potassium

sodium

potassium

potassium

sodium

sodium

aldosterone

sodium

aldosterone

sodium

potassium

angiotensin

aldosterone

sodium

potassium

hypokalaemia

hypertension

hypokalaemia

hypertension

hypokalaemia

chlorthalidone

hypokalaemia

chlorthalidone

hypokalaemia

chlorthalidone

hypokalaemia

Chlorthalidone

hypokalaemia

Chlorthalidone

hypokalaemia

Chlorthalidone

hypokalaemia


Input: Dynamic response of blood vessel in acute renal failure. In this study we postulated that during acute renal failure induced by gentamicin the transient or dynamic response of blood vessels could be affected, and that antioxidants can prevent the changes in dynamic responses of blood vessels. The new approach to ex vivo blood vessel experiments in which not only the end points of vessels response within the time interval is considered, but also dynamics of this response, was used in this paper. Our results confirm the alteration in dynamic response of blood vessels during the change of pressure in gentamicin - treated animals. The beneficial effects of vitamin C administration to gentamicin - treated animals are also confirmed through: lower level of blood urea and creatinine and higher level of potassium. The pressure dynamic responses of isolated blood vessels show a faster pressure change in gentamicin - treated animals (8. 07 + / - 1. 7 s vs. 5. 64 + / - 0. 18 s). Vitamin C administration induced slowdown of pressure change back to the control values. The pressure dynamic properties, quantitatively defined by comparative pressure dynamic and total pressure dynamic, confirm the alteration in dynamic response of blood vessels during the change of pressure in gentamicin - treated animals and beneficial effects of vitamin C administration.

acute renal failure

acute renal failure

gentamicin

gentamicin

vitamin C

gentamicin

urea

creatinine

potassium

gentamicin

Vitamin C

gentamicin

vitamin C

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure

gentamicin

acute renal failure


Input: The hemodynamics of oxytocin and other vasoactive agents during neuraxial anesthesia for cesarean delivery: findings in six cases. Oxytocin is a commonly used uterotonic that can cause significant and even fatal hypotension, particularly when given as a bolus. The resulting hypotension can be produced by a decrease in systemic vascular resistance or cardiac output through a decrease in venous return. Parturients with normal volume status, heart valves and pulmonary vasculature most often respond to this hypotension with a compensatory increase in heart rate and stroke volume. Oxytocin - induced hypotension at cesarean delivery may be incorrectly attributed to blood loss. Pulse power analysis (also called " pulse contour analysis ") of an arterial pressure wave form allows continuous evaluation of systemic vascular resistance and cardiac output in real time, thereby elucidating the causative factors behind changes in blood pressure. Pulse power analysis was conducted in six cases of cesarean delivery performed under neuraxial anesthesia. Hypotension in response to oxytocin was associated with a decrease in systemic vascular resistance and a compensatory increase in stroke volume, heart rate and cardiac output. Pulse power analysis may be helpful in determining the etiology of and treating hypotension during cesarean delivery under neuraxial anesthesia.

oxytocin

Oxytocin

Oxytocin

oxytocin

hypotension

hypotension

hypotension

stroke

hypotension

blood loss

Hypotension

stroke

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

Hypotension

oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

Hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

hypotension

Oxytocin

Hypotension

Oxytocin

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

hypotension

oxytocin

Hypotension

oxytocin

hypotension


Input: Exaggerated expression of inflammatory mediators in vasoactive intestinal polypeptide knockout (VIP - / -) mice with cyclophosphamide (CYP) - induced cystitis. Vasoactive intestinal polypeptide (VIP) is an immunomodulatory neuropeptide distributed in micturition pathways. VIP (- / -) mice exhibit altered bladder function and neurochemical properties in micturition pathways after cyclophosphamide (CYP) - induced cystitis. Given VIP' s role as an anti - inflammatory mediator, we hypothesized that VIP (- / -) mice would exhibit enhanced inflammatory mediator expression after cystitis. A mouse inflammatory cytokine and receptor RT2 profiler array was used to determine regulated transcripts in the urinary bladder of wild type (WT) and VIP (- / -) mice with or without CYP - induced cystitis (150 mg / kg; i. p.; 48 h). Four binary comparisons were made: WT control versus CYP treatment (48 h), VIP (- / -) control versus CYP treatment (48 h), WT control versus VIP (- / -) control, and WT with CYP treatment (48 h) versus VIP (- / -) with CYP treatment (48 h). The genes presented represent (1) greater than 1. 5 - fold change in either direction and (2) the p value is less than 0. 05 for the comparison being made. Several regulated genes were validated using enzyme - linked immunoassays including IL - 1beta and CXCL1. CYP treatment significantly (p < or = 0. 001) increased expression of CXCL1 and IL - 1beta in the urinary bladder of WT and VIP (- / -) mice, but expression in VIP (- / -) mice with CYP treatment was significantly (p < or = 0. 001) greater (4. 2 - to 13 - fold increase) than that observed in WT urinary bladder (3. 6 - to 5 - fold increase). The data suggest that in VIP (- / -) mice with bladder inflammation, inflammatory mediators are increased above that observed in WT with CYP. This shift in balance may contribute to increased bladder dysfunction in VIP (- / -) mice with bladder inflammation and altered neurochemical expression in micturition pathways.

cyclophosphamide

CYP

cyclophosphamide

CYP

CYP

CYP

CYP

CYP

CYP

CYP

CYP

CYP

cystitis

cystitis

cystitis

cystitis

bladder inflammation

bladder dysfunction

bladder inflammation

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

cyclophosphamide

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis

CYP

cystitis


Input: Intraocular pressure in patients with uveitis treated with fluocinolone acetonide implants. OBJECTIVE: To report the incidence and management of elevated intraocular pressure (IOP) in patients with uveitis treated with the fluocinolone acetonide (FA) intravitreal implant. DESIGN: Pooled data from 3 multicenter, double - masked, randomized, controlled, phase 2b / 3 clinical trials evaluating the safety and efficacy of the 0. 59 - mg or 2. 1 - mg FA intravitreal implant or standard therapy were analyzed. RESULTS: During the 3 - year follow - up, 71. 0% of implanted eyes had an IOP increase of 10 mm Hg or more than baseline and 55. 1%, 24. 7%, and 6. 2% of eyes reached an IOP of 30 mm Hg or more, 40 mm Hg or more, and 50 mm Hg or more, respectively. Topical IOP - lowering medication was administered in 74. 8% of implanted eyes, and IOP - lowering surgeries, most of which were trabeculectomies (76. 2%), were performed on 36. 6% of implanted eyes. Intraocular pressure - lowering surgeries were considered a success (postoperative IOP of 6 - 21 mm Hg with or without additional IOP - lowering medication) in 85. 1% of eyes at 1 year. The rate of hypotony (IOP < / = 5 mm Hg) following IOP - lowering surgery (42. 5%) was not different from that of implanted eyes not subjected to surgery (35. 4%) (P =. 09). CONCLUSION: Elevated IOP is a significant complication with the FA intravitreal implant but may be controlled with medication and surgery.

uveitis

elevated intraocular pressure

uveitis

hypotony

fluocinolone acetonide

fluocinolone acetonide

FA

FA

fluocinolone acetonide

elevated intraocular pressure

fluocinolone acetonide

elevated intraocular pressure

FA

elevated intraocular pressure

FA

elevated intraocular pressure


Input: Pallidal stimulation: an alternative to pallidotomy? A resurgence of interest in the surgical treatment of Parkinson' s disease (PD) came with the rediscovery of posteroventral pallidotomy by Laitinen in 1985. Laitinen' s procedure improved most symptoms in drug - resistant PD, which engendered wide interest in the neurosurgical community. Another lesioning procedure, ventrolateral thalamotomy, has become a powerful alternative to stimulate the nucleus ventralis intermedius, producing high long - term success rates and low morbidity rates. Pallidal stimulation has not met with the same success. According to the literature pallidotomy improves the " on " symptoms of PD, such as dyskinesias, as well as the " off " symptoms, such as rigidity, bradykinesia, and on - off fluctuations. Pallidal stimulation improves bradykinesia and rigidity to a minor extent; however, its strength seems to be in improving levodopa - induced dyskinesias. Stimulation often produces an improvement in the hyper - or dyskinetic upper limbs, but increases the " freezing " phenomenon in the lower limbs at the same time. Considering the small increase in the patient' s independence, the high costs of bilateral implants, and the difficulty most patients experience in handling the devices, the question arises as to whether bilateral pallidal stimulation is a real alternative to pallidotomy.

Parkinson' s disease

PD

PD

PD

dyskinesias

rigidity

bradykinesia

bradykinesia

rigidity

dyskinesias

hyper - or dyskinetic

levodopa

levodopa

dyskinesias

levodopa

dyskinesias

levodopa

hyper - or dyskinetic