Input: Diuretics, potassium and arrhythmias in hypertensive coronary disease. It has been proposed that modest changes in plasma potassium can alter the tendency towards cardiac arrhythmias. If this were so, patients with coronary artery disease might be especially susceptible. Thus, myocardial electrical excitability was measured in patients with mild essential hypertension and known coronary artery disease after 8 weeks of treatment with a potassium - conserving diuretic (amiloride) and a similar period on a potassium - losing diuretic (chlorthalidone) in a randomised study. Plasma potassium concentrations were on average 1 mmol / L lower during the chlorthalidone phase compared to amiloride therapy. Blood pressure and volume states as assessed by bodyweight, plasma renin and noradrenaline (norepinephrine) concentrations were similar on the 2 regimens. Compared to amiloride treatment, the chlorthalidone phase was associated with an increased frequency of ventricular ectopic beats (24 - hour Holter monitoring) and a higher Lown grading, increased upslope and duration of the monophasic action potential, prolonged ventricular effective refractory period, and increased electrical instability during programmed ventricular stimulation. The above results indicate that because potassium - losing diuretic therapy can increase myocardial electrical excitability in patients with ischaemic heart disease, even minor falls in plasma potassium concentrations are probably best avoided in such patients.

potassium

potassium

potassium

amiloride

potassium

chlorthalidone

potassium

chlorthalidone

amiloride

noradrenaline

norepinephrine

amiloride

chlorthalidone

potassium

potassium

arrhythmias

hypertensive

coronary disease

cardiac arrhythmias

coronary artery disease

hypertension

coronary artery disease

ventricular ectopic beats

ischaemic heart disease

chlorthalidone

ventricular ectopic beats

chlorthalidone

ventricular ectopic beats

chlorthalidone

ventricular ectopic beats


Input: GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental. No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg / kg, i. v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg / kg, i. v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2. 5 mg / kg, i. v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

GABA

naloxone

thiopental

naloxone

thiopental

thiopental

GABA

glutamate

aspartate

glycine

thiosemicarbazide

thiopental

thiopental

GABA

glutamate

amino acids

Naloxone

glutamate

GABA

naloxone

thiopental

GABA

respiratory paralysis

respiratory paralysis

respiratory paralysis

respiratory arrest

respiratory paralysis

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis

thiopental

respiratory paralysis


Input: National project on the prevention of mother - to - infant infection by hepatitis B virus in Japan. In Japan, a nationwide prevention program against mother - to - infant infection by hepatitis B virus (HBV) started in 1985. This program consists of double screenings of pregnant women and prophylactic treatment to the infants born to both hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive mothers. These infants are treated with two injections of hepatitis B immune globulin (HBIG) and at least three injections of plasma derived hepatitis B vaccine. We sent questionnaires about the numbers of each procedure or examination during nine months of investigation period to each local government in 1986 and 1987. 93. 4% pregnant women had the chance to be examined for HBsAg, and the positive rate was 1. 4 to 1. 5%. The HBeAg positive rate in HBsAg positive was 23 to 26%. The HBsAg positive rate in neonates and in infants before two months were 3% and 2% respectively. Some problems may arise, because 27 to 30% of infants need the fourth vaccination in some restricted areas.

infection by hepatitis B virus

infection by hepatitis B virus

hepatitis B

hepatitis B surface antigen

HBsAg

hepatitis B e antigen

HBeAg

hepatitis B vaccine

HBsAg

HBeAg

HBsAg

HBsAg

hepatitis B e antigen

infection by hepatitis B virus

hepatitis B e antigen

infection by hepatitis B virus

hepatitis B e antigen

hepatitis B

HBeAg

infection by hepatitis B virus

HBeAg

infection by hepatitis B virus

HBeAg

hepatitis B

HBeAg

infection by hepatitis B virus

HBeAg

infection by hepatitis B virus

HBeAg

hepatitis B

hepatitis B surface antigen

infection by hepatitis B virus

hepatitis B surface antigen

infection by hepatitis B virus

hepatitis B surface antigen

hepatitis B

HBsAg

infection by hepatitis B virus

HBsAg

infection by hepatitis B virus

HBsAg

hepatitis B

HBsAg

infection by hepatitis B virus

HBsAg

infection by hepatitis B virus

HBsAg

hepatitis B

HBsAg

infection by hepatitis B virus

HBsAg

infection by hepatitis B virus

HBsAg

hepatitis B

HBsAg

infection by hepatitis B virus

HBsAg

infection by hepatitis B virus

HBsAg

hepatitis B


Input: Nociceptive effects induced by intrathecal administration of prostaglandin D2, E2, or F2 alpha to conscious mice. The effects of intrathecal administration of prostaglandins on pain responses in conscious mice were evaluated by using hot plate and acetic acid writhing tests. Prostaglandin D2 (0. 5 - 3 ng / mouse) had a hyperalgesic action on the response to a hot plate during a 3 - 60 min period after injection. Prostaglandin E2 showed a hyperalgesic effect at doses of 1 pg to 10 ng / mouse, but the effect lasted shorter (3 - 30 min) than that of prostaglandin D2. Similar results were obtained by acetic acid writhing tests. The hyperalgesic effect of prostaglandin D2 was blocked by simultaneous injection of a substance P antagonist (greater than or equal to 100 ng) but not by AH6809, a prostanoid EP1 - receptor antagonist. Conversely, prostaglandin E2 - induced hyperalgesia was blocked by AH6809 (greater than or equal to 500 ng) but not by the substance P antagonist. Prostaglandin F2 alpha had little effect on pain responses. These results demonstrate that both prostaglandin D2 and prostaglandin E2 exert hyperalgesia in the spinal cord, but in different ways.

prostaglandin D2, E2, or F2 alpha

prostaglandin D2

prostaglandin D2, E2

prostaglandin D2, E2, or F2 alpha

prostaglandins

acetic acid

Prostaglandin D2

Prostaglandin E2

pg

prostaglandin D2

acetic acid

prostaglandin D2

prostaglandin E2

Prostaglandin F2 alpha

prostaglandin D2

prostaglandin E2

pain

hyperalgesic

hyperalgesic

hyperalgesic

hyperalgesia

pain

hyperalgesia

prostaglandin D2, E2, or F2 alpha

hyperalgesic

prostaglandin D2, E2, or F2 alpha

hyperalgesic

prostaglandin D2, E2, or F2 alpha

hyperalgesic

prostaglandin D2, E2, or F2 alpha

hyperalgesia

prostaglandin D2, E2, or F2 alpha

hyperalgesia

prostaglandin D2, E2

hyperalgesic

prostaglandin D2, E2

hyperalgesic

prostaglandin D2, E2

hyperalgesic

prostaglandin D2, E2

hyperalgesia

prostaglandin D2, E2

hyperalgesia

Prostaglandin E2

hyperalgesic

Prostaglandin E2

hyperalgesic

Prostaglandin E2

hyperalgesic

Prostaglandin E2

hyperalgesia

Prostaglandin E2

hyperalgesia

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesia

prostaglandin E2

hyperalgesia

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesic

prostaglandin E2

hyperalgesia

prostaglandin E2

hyperalgesia

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesia

Prostaglandin D2

hyperalgesic

Prostaglandin D2

hyperalgesic

Prostaglandin D2

hyperalgesic

Prostaglandin D2

hyperalgesia

Prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesic

prostaglandin D2

hyperalgesia

prostaglandin D2

hyperalgesia


Input: Swallowing - induced atrial tachyarrhythmia triggered by salbutamol: case report and review of the literature. CASE: A 49 - year - old patient experienced chest discomfort while swallowing. On electrocardiogram, episodes of atrial tachyarrhythmia were recorded immediately after swallowing; 24 - hour Holter monitoring recorded several events. The arrhythmia resolved after therapy with atenolol, but recurred a year later. The patient noticed that before these episodes he had been using an inhalator of salbutamol. After stopping the beta - agonist, and after a week with the atenolol, the arrhythmia disappeared. DISCUSSION: Swallowing - induced atrial tachyarrhythmia (SIAT) is a rare phenomenon. Fewer than 50 cases of SIAT have been described in the literature. This article summarizes all the cases published, creating a comprehensive review of the current knowledge and approach to SIAT. It discusses demographics, clinical characteristics and types of arrhythmia, postulated mechanisms of SIAT, and different treatment possibilities such as medications, surgery, and radiofrequency catheter ablation (RFCA). CONCLUSION: Salbutamol is presented here as a possible trigger for SIAT. Although it is difficult to define causality in a case report, it is logical to think that a beta - agonist like salbutamol (known to induce tachycardia) may be the trigger of adrenergic reflexes originating in the esophagus while swallowing and that a beta - blocker such as atenolol (that blocks the adrenergic activity) may relieve it.

atrial tachyarrhythmia

atrial tachyarrhythmia

arrhythmia

arrhythmia

atrial tachyarrhythmia

SIAT

SIAT

SIAT

arrhythmia

SIAT

SIAT

tachycardia

salbutamol

atenolol

salbutamol

atenolol

Salbutamol

salbutamol

atenolol

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

Salbutamol

atrial tachyarrhythmia

Salbutamol

atrial tachyarrhythmia

Salbutamol

atrial tachyarrhythmia

Salbutamol

SIAT

Salbutamol

SIAT

Salbutamol

SIAT

Salbutamol

SIAT

Salbutamol

SIAT

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

atrial tachyarrhythmia

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT

salbutamol

SIAT


Input: Coenzyme Q10 treatment ameliorates acute cisplatin nephrotoxicity in mice. The nephroprotective effect of coenzyme Q10 was investigated in mice with acute renal injury induced by a single i. p. injection of cisplatin (5 mg / kg). Coenzyme Q10 treatment (10 mg / kg / day, i. p.) was applied for 6 consecutive days, starting 1 day before cisplatin administration. Coenzyme Q10 significantly reduced blood urea nitrogen and serum creatinine levels which were increased by cisplatin. Coenzyme Q10 significantly compensated deficits in the antioxidant defense mechanisms (reduced glutathione level and superoxide dismutase activity), suppressed lipid peroxidation, decreased the elevations of tumor necrosis factor - alpha, nitric oxide and platinum ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cisplatin administration. Also, histopathological renal tissue damage mediated by cisplatin was ameliorated by coenzyme Q10 treatment. Immunohistochemical analysis revealed that coenzyme Q10 significantly decreased the cisplatin - induced overexpression of inducible nitric oxide synthase, nuclear factor - kappaB, caspase - 3 and p53 in renal tissue. It was concluded that coenzyme Q10 represents a potential therapeutic option to protect against acute cisplatin nephrotoxicity commonly encountered in clinical practice.

Coenzyme Q10

cisplatin

coenzyme Q10

cisplatin

Coenzyme Q10

cisplatin

Coenzyme Q10

blood urea nitrogen

creatinine

cisplatin

Coenzyme Q10

reduced glutathione

superoxide

nitric oxide

platinum

selenium

zinc

cisplatin

cisplatin

coenzyme Q10

coenzyme Q10

cisplatin

nitric oxide

coenzyme Q10

cisplatin

nephrotoxicity

acute renal injury

tumor

necrosis

renal tissue damage

nephrotoxicity

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury

cisplatin

acute renal injury


Input: Metformin prevents experimental gentamicin - induced nephropathy by a mitochondria - dependent pathway. The antidiabetic drug metformin can diminish apoptosis induced by oxidative stress in endothelial cells and prevent vascular dysfunction even in nondiabetic patients. Here we tested whether it has a beneficial effect in a rat model of gentamicin toxicity. Mitochondrial analysis, respiration intensity, levels of reactive oxygen species, permeability transition, and cytochrome c release were assessed 3 and 6 days after gentamicin administration. Metformin treatment fully blocked gentamicin - mediated acute renal failure. This was accompanied by a lower activity of N - acetyl - beta - D - glucosaminidase, together with a decrease of lipid peroxidation and increase of antioxidant systems. Metformin also protected the kidney from histological damage 6 days after gentamicin administration. These in vivo markers of kidney dysfunction and their correction by metformin were complemented by in vitro studies of mitochondrial function. We found that gentamicin treatment depleted respiratory components (cytochrome c, NADH), probably due to the opening of mitochondrial transition pores. These injuries, partly mediated by a rise in reactive oxygen species from the electron transfer chain, were significantly decreased by metformin. Thus, our study suggests that pleiotropic effects of metformin can lessen gentamicin nephrotoxicity and improve mitochondrial homeostasis.

Metformin

gentamicin

metformin

gentamicin

oxygen

gentamicin

Metformin

gentamicin

Metformin

gentamicin

metformin

gentamicin

oxygen

metformin

metformin

gentamicin

nephropathy

vascular dysfunction

toxicity

acute renal failure

kidney dysfunction

nephrotoxicity

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: Sedation depth during spinal anesthesia and the development of postoperative delirium in elderly patients undergoing hip fracture repair. OBJECTIVE: To determine whether limiting intraoperative sedation depth during spinal anesthesia for hip fracture repair in elderly patients can decrease the prevalence of postoperative delirium. PATIENTS AND METHODS: We performed a double - blind, randomized controlled trial at an academic medical center of elderly patients (> or = 65 years) without preoperative delirium or severe dementia who underwent hip fracture repair under spinal anesthesia with propofol sedation. Sedation depth was titrated using processed electroencephalography with the bispectral index (BIS), and patients were randomized to receive either deep (BIS, approximately 50) or light (BIS, > or = 80) sedation. Postoperative delirium was assessed as defined by Diagnostic and Statistical Manual of Mental Disorders (Third Edition Revised) criteria using the Confusion Assessment Method beginning at any time from the second day after surgery. RESULTS: From April 2, 2005, through October 30, 2008, a total of 114 patients were randomized. The prevalence of postoperative delirium was significantly lower in the light sedation group (11 / 57 [19%] vs 23 / 57 [40%] in the deep sedation group; P =. 02), indicating that 1 incident of delirium will be prevented for every 4. 7 patients treated with light sedation. The mean + / - SD number of days of delirium during hospitalization was lower in the light sedation group than in the deep sedation group (0. 5 + / - 1. 5 days vs 1. 4 + / - 4. 0 days; P =. 01). CONCLUSION: The use of light propofol sedation decreased the prevalence of postoperative delirium by 50% compared with deep sedation. Limiting depth of sedation during spinal anesthesia is a simple, safe, and cost - effective intervention for preventing postoperative delirium in elderly patients that could be widely and readily adopted.

postoperative delirium

postoperative delirium

delirium

hip fracture

hip fracture

postoperative delirium

postoperative delirium

delirium

delirium

dementia

hip fracture

Postoperative delirium

Postoperative delirium

delirium

Mental Disorders

postoperative delirium

postoperative delirium

delirium

delirium

delirium

postoperative delirium

postoperative delirium

delirium

postoperative delirium

postoperative delirium

delirium

propofol

propofol

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

delirium

propofol

Postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

delirium

propofol

Postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

Postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

Postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium

propofol

postoperative delirium


Input: Sorafenib - induced acute myocardial infarction due to coronary artery spasm. A 65 - year - old man with advanced renal cell carcinoma was admitted due to continuing chest pain at rest. Two weeks before his admission, sorafenib had been started. He was diagnosed with non - ST - elevation myocardial infarction by laboratory data and electrocardiogram. Enhanced heart magnetic resonance imaging also showed subendocardial infarction. However, there was no stenosis in coronary arteries on angiography. Coronary artery spasm was induced by a provocative test. Cessation of sorafenib and administration of Ca - channel blocker and nitrates ameliorated his symptoms, but relapse occurred after resumption of sorafenib. Addition of oral nicorandil reduced his symptoms and maintained stable angina status. We report the first case of sorafenib - induced coronary artery spasm. Sorafenib is a multikinase inhibitor that targets signaling pathways necessary for cellular proliferation and survival. On the other hand, the Rho / ROCK pathway has an important role in the pathogenesis of coronary artery spasm. Our report may show an adverse effect on the Rho / ROCK pathway by sorafenib use.

Sorafenib

sorafenib

sorafenib

Ca

nitrates

sorafenib

nicorandil

sorafenib

Sorafenib

sorafenib

myocardial infarction

coronary artery spasm

renal cell carcinoma

chest pain

myocardial infarction

subendocardial infarction

Coronary artery spasm

stable angina

coronary artery spasm

coronary artery spasm

Sorafenib

coronary artery spasm

Sorafenib

Coronary artery spasm

Sorafenib

coronary artery spasm

Sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

Coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

Coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

Coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

Coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

Sorafenib

coronary artery spasm

Sorafenib

Coronary artery spasm

Sorafenib

coronary artery spasm

Sorafenib

coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

Coronary artery spasm

sorafenib

coronary artery spasm

sorafenib

coronary artery spasm


Input: Anxiogenic potential of ciprofloxacin and norfloxacin in rats. INTRODUCTION: The possible anxiogenic effects of fluoroquinolones, namely ciprofloxacin and norfloxacin, were investigated in adult Charles Foster albino rats of either sex, weighing 150 - 200 g. METHODS: The drugs were given orally, in doses of 50 mg / kg for five consecutive days and the experiments were performed on the fifth day. The tests included open - field exploratory behaviour, elevated plus maze and elevated zero maze, social interaction and novelty - suppressed feeding latency behaviour. RESULTS: The results indicate that ciprofloxacin - and norfloxacin - treated rats showed anxious behaviour in comparison to control rats in all the parameters studied. However, ciprofloxacin - and norfloxacin - treated rats did not differ significantly from each other in various behavioural parameters. CONCLUSION: The present experimental findings substantiate the clinically observed anxiogenic potential of ciprofloxacin and norfloxacin.

ciprofloxacin

norfloxacin

fluoroquinolones

ciprofloxacin

norfloxacin

ciprofloxacin

norfloxacin

ciprofloxacin

norfloxacin

ciprofloxacin

norfloxacin

anxious behaviour

norfloxacin

anxious behaviour

norfloxacin

anxious behaviour

norfloxacin

anxious behaviour

norfloxacin

anxious behaviour

norfloxacin

anxious behaviour

ciprofloxacin

anxious behaviour

ciprofloxacin

anxious behaviour

ciprofloxacin

anxious behaviour

ciprofloxacin

anxious behaviour

ciprofloxacin

anxious behaviour


Input: Myocardial Fas ligand expression increases susceptibility to AZT - induced cardiomyopathy. BACKGROUND: Dilated cardiomyopathy (DCM) and myocarditis occur in many HIV - infected individuals, resulting in symptomatic heart failure in up to 5% of patients. Highly active antiretroviral therapy (HAART) has significantly reduced morbidity and mortality of acquired immunodeficiency syndrome (AIDS), but has resulted in an increase in cardiac and skeletal myopathies. METHODS AND RESULTS: In order to investigate whether the HAART component zidovudine (3' - azido - 2', 3' - deoxythymidine; AZT) triggers the Fas - dependent cell - death pathway and cause cytoskeletal disruption in a murine model of DCM, 8 - week - old transgenic (expressing Fas ligand in the myocardium: FasL Tg) and non - transgenic (NTg) mice received water ad libitum containing different concentrations of AZT (0, 0. 07, 0. 2, and 0. 7 mg / ml). After 6 weeks, cardiac function was assessed by echocardiography and morphology was assessed by histopathologic and immunohistochemical methods. NTg and untreated FasL Tg mice showed little or no change in cardiac structure or function. In contrast, AZT - treated FasL Tg mice developed cardiac dilation and depressed cardiac function in a dose - dependent manner, with concomitant inflammatory infiltration of both ventricles. These changes were associated with an increased sarcolemmal expression of Fas and FasL, as well as increased activation of caspase 3, translocation of calpain 1 to the sarcolemma and sarcomere, and increased numbers of cells undergoing apoptosis. These were associated with changes in dystrophin and cardiac troponin I localization, as well as loss of sarcolemmal integrity. CONCLUSIONS: The expression of Fas ligand in the myocardium, as identified in HIV - positive patients, might increase the susceptibility to HAART - induced cardiomyopathy due to activation of apoptotic pathways, resulting in cardiac dilation and dysfunction.

AZT

zidovudine

3' - azido - 2', 3' - deoxythymidine

AZT

AZT

AZT

cardiomyopathy

Dilated cardiomyopathy

DCM

myocarditis

HIV - infected

heart failure

acquired immunodeficiency syndrome

AIDS

cardiac and skeletal myopathies

DCM

cardiac dilation

cardiomyopathy

cardiac dilation and dysfunction

cardiac dilation

cardiac dilation and dysfunction

AZT

Dilated cardiomyopathy

AZT

DCM

AZT

DCM

AZT

cardiac dilation

AZT

cardiac dilation and dysfunction

AZT

cardiac dilation

zidovudine

Dilated cardiomyopathy

zidovudine

DCM

zidovudine

DCM

zidovudine

cardiac dilation

zidovudine

cardiac dilation and dysfunction

zidovudine

cardiac dilation

3' - azido - 2', 3' - deoxythymidine

Dilated cardiomyopathy

3' - azido - 2', 3' - deoxythymidine

DCM

3' - azido - 2', 3' - deoxythymidine

DCM

3' - azido - 2', 3' - deoxythymidine

cardiac dilation

3' - azido - 2', 3' - deoxythymidine

cardiac dilation and dysfunction

3' - azido - 2', 3' - deoxythymidine

cardiac dilation

AZT

Dilated cardiomyopathy

AZT

DCM

AZT

DCM

AZT

cardiac dilation

AZT

cardiac dilation and dysfunction

AZT

cardiac dilation

AZT

Dilated cardiomyopathy

AZT

DCM

AZT

DCM

AZT

cardiac dilation

AZT

cardiac dilation and dysfunction

AZT

cardiac dilation

AZT

Dilated cardiomyopathy

AZT

DCM

AZT

DCM

AZT

cardiac dilation

AZT

cardiac dilation and dysfunction

AZT

cardiac dilation

AZT

cardiomyopathy

AZT

cardiomyopathy

zidovudine

cardiomyopathy

zidovudine

cardiomyopathy

3' - azido - 2', 3' - deoxythymidine

cardiomyopathy

3' - azido - 2', 3' - deoxythymidine

cardiomyopathy

AZT

cardiomyopathy

AZT

cardiomyopathy

AZT

cardiomyopathy

AZT

cardiomyopathy

AZT

cardiomyopathy

AZT

cardiomyopathy


Input: Valproate - induced chorea and encephalopathy in atypical nonketotic hyperglycinemia. Nonketotic hyperglycinemia is a disorder of amino acid metabolism in which a defect in the glycine cleavage system leads to an accumulation of glycine in the brain and other body compartments. In the classical form it presents as neonatal apnea, intractable seizures, and hypotonia, followed by significant psychomotor retardation. An important subset of children with nonketotic hyperglycinemia are atypical variants who present in a heterogeneous manner. This report describes a patient with mild language delay and mental retardation, who was found to have nonketotic hyperglycinemia following her presentation with acute encephalopathy and chorea shortly after initiation of valproate therapy.

Valproate

glycine

glycine

valproate

chorea

encephalopathy

nonketotic hyperglycinemia

Nonketotic hyperglycinemia

disorder of amino acid metabolism

apnea

seizures

hypotonia

psychomotor retardation

nonketotic hyperglycinemia

language delay

mental retardation

nonketotic hyperglycinemia

encephalopathy

chorea

Valproate

chorea

Valproate

chorea

valproate

chorea

valproate

chorea

Valproate

encephalopathy

Valproate

encephalopathy

valproate

encephalopathy

valproate

encephalopathy


Input: Microinjection of ritanserin into the CA1 region of hippocampus improves scopolamine - induced amnesia in adult male rats. The effect of ritanserin (5 - HT2 antagonist) on scopolamine (muscarinic cholinergic antagonist) - induced amnesia in Morris water maze (MWM) was investigated. Rats were divided into eight groups and bilaterally cannulated into CA1 region of the hippocampus. One week later, they received repeatedly vehicles (saline, DMSO, saline + DMSO), scopolamine (2 microg / 0. 5 microl saline / side; 30 min before training), ritanserin (2, 4 and 8 microg / 0. 5 microl DMSO / side; 20 min before training) and scopolamine (2 microg / 0. 5 microl; 30 min before ritanserin injection) + ritanserin (4 microg / 0. 5 microl DMSO) through cannulae each day. Animals were tested for four consecutive days (4 trial / day) in MWM during which the position of hidden platform was unchanged. In the fifth day, the platform was elevated above the water surface in another position to evaluate the function of motor, motivational and visual systems. The results showed a significant increase in escape latencies and traveled distances to find platform in scopolamine - treated group as compared to saline group. Ritanserin - treated rats (4 microg / 0. 5 microl / side) showed a significant decrease in the mentioned parameters as compared to DMSO - treated group. However, scopolamine and ritanserin co - administration resulted in a significant decrease in escape latencies and traveled distances as compared to the scopolamine - treated rats. Our findings show that microinjection of ritanserin into the CA1 region of the hippocampus improves the scopolamine - induced amnesia.

ritanserin

scopolamine

ritanserin

scopolamine

DMSO

DMSO

scopolamine

ritanserin

DMSO

scopolamine

ritanserin

ritanserin

DMSO

scopolamine

Ritanserin

DMSO

scopolamine

ritanserin

scopolamine

ritanserin

scopolamine

amnesia

amnesia

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia

scopolamine

amnesia


Input: Hypoxia in renal disease with proteinuria and / or glomerular hypertension. Despite the increasing need to identify and quantify tissue oxygenation at the cellular level, relatively few methods have been available. In this study, we developed a new hypoxia - responsive reporter vector using a hypoxia - responsive element of the 5' vascular endothelial growth factor untranslated region and generated a novel hypoxia - sensing transgenic rat. We then applied this animal model to the detection of tubulointerstitial hypoxia in the diseased kidney. With this model, we were able to identify diffuse cortical hypoxia in the puromycin aminonucleoside - induced nephrotic syndrome and focal and segmental hypoxia in the remnant kidney model. Expression of the hypoxia - responsive transgene increased throughout the observation period, reaching 2. 2 - fold at 2 weeks in the puromycin aminonucleoside model and 2. 6 - fold at 4 weeks in the remnant kidney model, whereas that of vascular endothelial growth factor showed a mild decrease, reflecting distinct behaviors of the two genes. The degree of hypoxia showed a positive correlation with microscopic tubulointerstitial injury in both models. Finally, we identified the localization of proliferating cell nuclear antigen - positive, ED - 1 - positive, and terminal dUTP nick - end labeled - positive cells in the hypoxic cortical area in the remnant kidney model. We propose here a possible pathological tie between chronic tubulointerstitial hypoxia and progressive glomerular diseases.

Hypoxia

renal disease

proteinuria

hypertension

hypoxia

hypoxia

hypoxia

hypoxia

diseased kidney

hypoxia

nephrotic syndrome

hypoxia

hypoxia

hypoxia

tubulointerstitial injury

hypoxic

hypoxia

glomerular diseases

puromycin aminonucleoside

puromycin aminonucleoside

puromycin aminonucleoside

Hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxic

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

Hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

hypoxic

puromycin aminonucleoside

hypoxia

puromycin aminonucleoside

nephrotic syndrome

puromycin aminonucleoside

nephrotic syndrome


Input: Consensus statement concerning cardiotoxicity occurring during haematopoietic stem cell transplantation in the treatment of autoimmune diseases, with special reference to systemic sclerosis and multiple sclerosis. Autologous haematopoietic stem cell transplantation is now a feasible and effective treatment for selected patients with severe autoimmune diseases. Worldwide, over 650 patients have been transplanted in the context of phase I and II clinical trials. The results are encouraging enough to begin randomised phase III trials. However, as predicted, significant transplant - related morbidity and mortality have been observed. This is primarily due to complications related to either the stage of the disease at transplant or due to infections. The number of deaths related to cardiac toxicity is low. However, caution is required when cyclophosphamide or anthracyclines such as mitoxantrone are used in patients with a possible underlying heart damage, for example, systemic sclerosis patients. In November 2002, a meeting was held in Florence, bringing together a number of experts in various fields, including rheumatology, cardiology, neurology, pharmacology and transplantation medicine. The object of the meeting was to analyse existing data, both published or available, in the European Group for Blood and Marrow Transplantation autoimmune disease database, and to propose a safe approach to such patients. A full cardiological assessment before and during the transplant emerged as the major recommendation.

cardiotoxicity

autoimmune diseases

systemic sclerosis

multiple sclerosis

autoimmune diseases

infections

cardiac toxicity

heart damage

systemic sclerosis

autoimmune disease

cyclophosphamide

anthracyclines

mitoxantrone

mitoxantrone

heart damage

cyclophosphamide

heart damage


Input: Immunohistochemical study on inducible type of nitric oxide (iNOS), basic fibroblast growth factor (bFGF) and tumor growth factor - beta1 (TGF - beta1) in arteritis induced in rats by fenoldopam and theophylline, vasodilators. Arteritis induced in rats by vasodilators, fenoldopam and theophylline, was examined immunohistochemically for expressions of inducible type of nitric oxide synthase (iNOS), basic fibroblast growth factor (bFGF) and tumor growth factor - beta1 (TGF - beta1). Rats were administered fenoldopam for 24 hours by intravenous infusion with or without following repeated daily oral administrations of theophylline. Irrespective of theophylline administration, iNOS antigens were remarkably abundant in ED - 1 - positive cells on day 5 and 8 post - fenoldopam - infusion (DPI); bFGF antigens were remarkably abundant in ED - 1 - positive cells on 1 and 3 DPI; TGF - beta1 antigens were observed in ED - 1 - positive cells on and after 5 DPI. These results suggest that the peak expression of iNOS antigen was followed by that of bFGF antigen, and bFGF may have a suppressive effect on iNOS expression in these rat arteritis models. On the other hand, TGF - beta1 was not considered to have a suppressive effect on iNOS expression in these models.

nitric oxide

fenoldopam

theophylline

fenoldopam

theophylline

nitric oxide

fenoldopam

theophylline

theophylline

fenoldopam

tumor

arteritis

Arteritis

tumor

arteritis

fenoldopam

arteritis

fenoldopam

Arteritis

fenoldopam

arteritis

fenoldopam

arteritis

fenoldopam

Arteritis

fenoldopam

arteritis

fenoldopam

arteritis

fenoldopam

Arteritis

fenoldopam

arteritis

fenoldopam

arteritis

fenoldopam

Arteritis

fenoldopam

arteritis

theophylline

arteritis

theophylline

Arteritis

theophylline

arteritis

theophylline

arteritis

theophylline

Arteritis

theophylline

arteritis

theophylline

arteritis

theophylline

Arteritis

theophylline

arteritis

theophylline

arteritis

theophylline

Arteritis

theophylline

arteritis


Input: Low - molecular - weight heparin for the treatment of patients with mechanical heart valves. BACKGROUND: The interruption of oral anticoagulant (OAC) administration is sometimes indicated in patients with mechanical heart valves, mainly before noncardiac surgery, non - surgical interventions, and pregnancy. Unfractionated heparin (UH) is currently the substitute for selected patients. Low - molecular - weight heparin (LMWH) offers theoretical advantages over UH, but is not currently considered in clinical guidelines as an alternative to UH in patients with prosthetic valves. HYPOTHESIS: The aim of the present study was to review the data accumulated so far on the use of LMWH in this patient population and to discuss its applicability in common practice. METHODS: For this paper, the current medical literature on LMWH in patients with mechanical heart valves was extensively reviewed. RESULTS: There were eight series and six case reports. None of the studies was randomized, and only one was prospective. Data to establish the thromboembolic risk were incomplete. After excluding case reports, the following groups were constructed: (a) short - term administration, after valve insertion (n = 212); (b) short - term, perioperative (noncardiac) / periprocedural (n = 114); (c) long - term, due to intolerance to OAC (n = 16); (d) long - term, in pregnancy (n = 10). The incidence rate of thromboembolism was 0. 9% for all the studies and 0. 5, 0, 20, and 0% in groups a, b, c, and d, respectively; for hemorrhage, the overall rate was 3. 4% (3. 8, 2. 6, 10, and 0% for the respective groups). CONCLUSIONS: In patients with mechanical heart valves, short - term LMWH therapy compares favorably with UH. Data on mid - and long - term LMWH administration in these patients are sparse. Further randomized studies are needed to confirm the safety and precise indications for the use of LMWH in patients with mechanical heart valves.

Low - molecular - weight heparin

Unfractionated heparin

UH

Low - molecular - weight heparin

LMWH

UH

UH

LMWH

LMWH

LMWH

UH

LMWH

LMWH

thromboembolic

thromboembolism

hemorrhage

Low - molecular - weight heparin

hemorrhage

Low - molecular - weight heparin

hemorrhage

LMWH

hemorrhage

LMWH

hemorrhage

LMWH

hemorrhage

LMWH

hemorrhage

LMWH

hemorrhage

LMWH

hemorrhage

Low - molecular - weight heparin

thromboembolic

Low - molecular - weight heparin

thromboembolism

Low - molecular - weight heparin

thromboembolic

Low - molecular - weight heparin

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism

LMWH

thromboembolic

LMWH

thromboembolism


Input: Topiramate - induced nephrolithiasis. Topiramate is a recently developed antiepileptic medication that is becoming more widely prescribed because of its efficacy in treating refractory seizures. Urologists should be aware that this medication can cause metabolic acidosis in patients secondary to inhibition of carbonic anhydrase. In addition, a distal tubular acidification defect may result, thus impairing the normal compensatory drop in urine pH. These factors can lead to the development of calcium phosphate nephrolithiasis. We report the first two cases of topiramate - induced nephrolithiasis in the urologic literature.

Topiramate

Topiramate

calcium phosphate

topiramate

nephrolithiasis

refractory seizures

metabolic acidosis

nephrolithiasis

nephrolithiasis

Topiramate

nephrolithiasis

Topiramate

nephrolithiasis

Topiramate

nephrolithiasis

Topiramate

nephrolithiasis

Topiramate

nephrolithiasis

Topiramate

nephrolithiasis

topiramate

nephrolithiasis

topiramate

nephrolithiasis

topiramate

nephrolithiasis


Input: Spironolactone: is it a novel drug for the prevention of amphotericin B - related hypokalemia in cancer patients? OBJECTIVE: Nephrotoxicity is the major adverse effect of amphotericin B (AmB), often limiting administration of full dosage. Selective distal tubular epithelial toxicity seems to be responsible for the profound potassium wasting that is a major clinical side effect of treatment with AmB. Potassium depletion also potentiates the tubular toxicity of AmB. This study was designed to assess the ability of spironolactone to reduce potassium requirements and to prevent hypokalemia in neutropenic patients on AmB treatment. METHODS: In this study 26 patients with various hematological disorders were randomized to receive either intravenous AmB alone or AmB and oral spironolactone 100 mg twice daily when developing a proven or suspected fungal infection. RESULTS: Patients receiving concomitant AmB and spironolactone had significantly higher plasma potassium levels than those receiving AmB alone (P = 0. 0027). Those patients receiving AmB and spironolactone required significantly less potassium supplementation to maintain their plasma potassium within the normal range (P = 0. 022). Moreover, urinary potassium losses were significantly less in patients receiving AmB and spironolactone than those receiving AmB alone (P = 0. 040). CONCLUSION: This study showed that spironolactone can reduce potassium requirements and prevent hypokalemia by reducing urinary potassium loss in neutropenic patients on AmB treatment.

Spironolactone

amphotericin B

amphotericin B

AmB

potassium

AmB

Potassium

AmB

spironolactone

potassium

AmB

AmB

AmB

spironolactone

AmB

spironolactone

potassium

AmB

AmB

spironolactone

potassium

potassium

potassium

AmB

spironolactone

AmB

spironolactone

potassium

potassium

AmB

hypokalemia

cancer

Nephrotoxicity

toxicity

toxicity

hypokalemia

neutropenic

hematological disorders

fungal infection

hypokalemia

neutropenic

amphotericin B

hypokalemia

amphotericin B

hypokalemia

amphotericin B

hypokalemia

amphotericin B

hypokalemia

amphotericin B

hypokalemia

amphotericin B

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia

AmB

hypokalemia


Input: Dopamine D2 receptor signaling controls neuronal cell death induced by muscarinic and glutamatergic drugs. Dopamine (DA), through D1 / D2 receptor - mediated signaling, plays a major role in the control of epileptic seizures arising in the limbic system. Excitotoxicity leading to neuronal cell death in the affected areas is a major consequence of seizures at the cellular level. In this respect, little is known about the role of DA receptors in the occurrence of epilepsy - induced neuronal cell death. Here we analyze the occurrence of seizures and neurotoxicity in D2R - / - mice treated with the cholinergic agonist pilocarpine. We compared these results with those previously obtained with kainic acid (KA), a potent glutamate agonist. Importantly, D2R - / - mice develop seizures at doses of both drugs that are not epileptogenic for WT littermates and show greater neurotoxicity. However, pilocarpine - induced seizures result in a more widespread neuronal death in both WT and D2R - / - brains in comparison to KA. Thus, the absence of D2R lowers the threshold for seizures induced by both glutamate and acetylcholine. Moreover, the dopaminergic control of epilepsy - induced neurodegeneration seems to be mediated by distinct interactions of D2R signaling with these two neurotransmitters.

Dopamine

Dopamine

DA

DA

pilocarpine

kainic acid

KA

glutamate

pilocarpine

KA

glutamate

acetylcholine

epileptic seizures

Excitotoxicity

seizures

epilepsy

seizures

neurotoxicity

seizures

neurotoxicity

seizures

seizures

epilepsy

neurodegeneration

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizures

kainic acid

seizures

kainic acid

seizures

kainic acid

seizures

kainic acid

seizures

kainic acid

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures

KA

seizures


Input: Treatment of risperidone - induced hyperprolactinemia with a dopamine agonist in children. BACKGROUND: Risperidone, a potent antagonist of both serotonergic (5HT2A) and dopaminergic D2 receptors is associated with hyperprolactinemia in adults and children. Chronically elevated prolactin levels in children with prolactinomas may be associated with arrested growth and development resulting in either delayed puberty or short stature. These possibilities stress the importance of developing a safe and effective approach to drug - induced hyperprolactinemia in youth. We report the successful treatment of risperidone - induced hyperprolactinemia with cabergoline in youth. METHODS: We undertook a retrospective case review of four children with risperidone - induced hyperprolactinemia treated with cabergoline. RESULTS: Four males (age 6 - 11 years) with Diagnostic and Statistical Manual of Mental Disorders (fourth edition) bipolar disorder or psychoses, with risperidone - induced elevations in serum prolactin levels (57. 5 - 129 ng / mL, normal 5 - 15 ng / mL), were treated with cabergoline (mean dose 2. 13 + / - 0. 09 mg / week). When serum prolactin levels normalized in all four subjects (mean 11. 2 + / - 10. 9 ng / mL), the cabergoline dose was reduced to 1 mg / week in three of four subjects. The mean duration of therapy with cabergoline was 523. 5 + / - 129. 7 days, and the mean duration of therapy with risperidone was 788. 5 + / - 162. 5 days. Cabergoline was well tolerated without adverse effects. CONCLUSIONS: Cabergoline may be useful for the treatment of risperidone - induced hyperprolactinemia in youth; however, further research is needed.

risperidone

dopamine

Risperidone

risperidone

cabergoline

risperidone

cabergoline

risperidone

cabergoline

cabergoline

cabergoline

risperidone

Cabergoline

Cabergoline

risperidone

hyperprolactinemia

hyperprolactinemia

prolactinomas

delayed puberty

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

Mental Disorders

bipolar disorder

psychoses

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

Risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia


Input: Cholestatic jaundice associated with the use of metformin. We report a patient who developed cholestatic jaundice shortly after initiation of treatment with metformin hydrochloride. Ultrasound of the liver and abdominal CT were normal. An ERCP showed normal biliary anatomy. A percutaneous liver biopsy was obtained showing marked cholestasis, with portal edema, ductular proliferation, and acute inflammation. Metformin hydrochloride was discontinued, and the patient' s jaundice resolved slowly over a period of several months. Given the onset of his jaundice 2 wk after the initiation of metformin, we believe that this case represents an example of metformin - associated hepatotoxicity, the first such case reported.

Cholestatic jaundice

cholestatic jaundice

cholestasis

edema

inflammation

jaundice

jaundice

hepatotoxicity

metformin

metformin hydrochloride

Metformin hydrochloride

metformin

metformin

metformin

Cholestatic jaundice

metformin

cholestatic jaundice

metformin hydrochloride

Cholestatic jaundice

metformin hydrochloride

cholestatic jaundice

Metformin hydrochloride

Cholestatic jaundice

Metformin hydrochloride

cholestatic jaundice

metformin

Cholestatic jaundice

metformin

cholestatic jaundice

metformin

Cholestatic jaundice

metformin

cholestatic jaundice

metformin

cholestasis

metformin hydrochloride

cholestasis

Metformin hydrochloride

cholestasis

metformin

cholestasis

metformin

cholestasis


Input: Electro - oculography, electroretinography, visual evoked potentials, and multifocal electroretinography in patients with vigabatrin - attributed visual field constriction. PURPOSE: Symptomatic visual field constriction thought to be associated with vigabatrin has been reported. The current study investigated the visual fields and visual electrophysiology of eight patients with known vigabatrin - attributed visual field loss, three of whom were reported previously. Six of the patients were no longer receiving vigabatrin. METHODS: The central and peripheral fields were examined with the Humphrey Visual Field Analyzer. Full visual electrophysiology, including flash electroretinography (ERG), pattern electroretinography, multifocal ERG using the VERIS system, electro - oculography, and flash and pattern visual evoked potentials, was undertaken. RESULTS: Seven patients showed marked visual field constriction with some sparing of the temporal visual field. The eighth exhibited concentric constriction. Most electrophysiological responses were usually just within normal limits; two patients had subnormal Arden electro - oculography indices; and one patient showed an abnormally delayed photopic b wave. However, five patients showed delayed 30 - Hz flicker b waves, and seven patients showed delayed oscillatory potentials. Multifocal ERG showed abnormalities that sometimes correlated with the visual field appearance and confirmed that the deficit occurs at the retinal level. CONCLUSION: Marked visual field constriction appears to be associated with vigabatrin therapy. The field defects and some electrophysiological abnormalities persist when vigabatrin therapy is withdrawn.

vigabatrin

vigabatrin

vigabatrin

vigabatrin

vigabatrin

vigabatrin

visual field constriction

visual field constriction

visual field loss

visual field constriction

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field constriction

vigabatrin

visual field loss

vigabatrin

visual field constriction

vigabatrin

visual field constriction


Input: Conversion to rapamycin immunosuppression in renal transplant recipients: report of an initial experience. BACKGROUND: The aim of this study is to evaluate the effects of RAPA conversion in patients undergoing cyclosporine (CsA) or tacrolimus (Tac) toxicity. METHODS: Twenty renal transplant recipients were switched to fixed dose rapamycin (RAPA) (5 mg / day) 0 to 204 months posttransplant. Drug monitoring was not initially used to adjust doses. The indications for switch were chronic CsA or Tac nephrotoxicity (12), acute CsA or Tac toxicity (3), severe facial dysmorphism (2), posttransplant lymphoproliferative disorder (PTLD) in remission (2), and hepatotoxicity in 1. Follow - up is 7 to 24 months. RESULTS: In the 12 patients switched because of chronic nephrotoxicity there was a significant decrease in serum creatinine [233 + / - 34 to 210 + / - 56 micromol / liter (P < 0. 05) at 6 months]. Facial dysmorphism improved in two patients. No relapse of PTLD was observed. Five patients developed pneumonia (two Pneumocystis carinii pneumonia, one infectious mononucleosis with polyclonal PTLD lung infiltrate) and two had bronchiolitis obliterans. There were no deaths. RAPA was discontinued in four patients, because of pneumonia in two, PTLD in one, and oral aphtous ulcers in one. RAPA levels were high (> 15 ng / ml) in 7 of 13 (54%) patients. CONCLUSIONS: RAPA conversion provides adequate immunosuppression to enable CsA withdrawal. However, when converting patients to RAPA drug levels should be monitored to avoid over - immunosuppression and adequate antiviral and Pneumocystis carinii pneumonia prophylaxis should be given.

rapamycin

RAPA

cyclosporine

CsA

tacrolimus

Tac

rapamycin

RAPA

CsA

Tac

CsA

Tac

creatinine

RAPA

RAPA

RAPA

CsA

RAPA

toxicity

nephrotoxicity

toxicity

facial dysmorphism

posttransplant lymphoproliferative disorder

PTLD

hepatotoxicity

nephrotoxicity

Facial dysmorphism

PTLD

pneumonia

Pneumocystis carinii pneumonia

infectious mononucleosis

PTLD

bronchiolitis obliterans

pneumonia

PTLD

aphtous ulcers

Pneumocystis carinii pneumonia

tacrolimus

nephrotoxicity

tacrolimus

nephrotoxicity

Tac

nephrotoxicity

Tac

nephrotoxicity

Tac

nephrotoxicity

Tac

nephrotoxicity

Tac

nephrotoxicity

Tac

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity

CsA

nephrotoxicity


Input: Worsening of levodopa - induced dyskinesias by motor and mental tasks. Ten patients who had Parkinson' s disease with disabling dyskinesia were included in this study to evaluate the role of mental (mental calculation) and motor (flexion / extension of right fingers, flexion / extension of left fingers, flexion / extension of the neck, speaking aloud) tasks on the worsening of peak - dose dyskinesia following administration of an effective single dose of apomorphine. Compared with the score at rest (1. 3 + / - 0. 3), a significant aggravation of the dyskinesia score was observed during speaking aloud (5. 2 + / - 1. 1, p < 0. 05), movements of right (4. 5 + / - 1. 0, p < 0. 05) and left (3. 7 + / - 0. 8, p < 0. 05) fingers, movements of the neck (5. 1 + / - 1. 0, p < 0. 05), and mental calculation (3. 1 + / - 1. 0, p < 0. 05). These results suggest that activation tasks such as " speaking aloud " could be used for objective assessment of dyskinesia severity.

levodopa

apomorphine

dyskinesias

Parkinson' s disease

dyskinesia

dyskinesia

dyskinesia

dyskinesia

apomorphine

dyskinesias

apomorphine

dyskinesia

apomorphine

dyskinesia

apomorphine

dyskinesia

apomorphine

dyskinesia

levodopa

dyskinesias

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesia


Input: Structural and functional impairment of mitochondria in adriamycin - induced cardiomyopathy in mice: suppression of cytochrome c oxidase II gene expression. The use of adriamycin (ADR) in cancer chemotherapy has been limited due to its cumulative cardiovascular toxicity. Earlier observations that ADR interacts with mitochondrial cytochrome c oxidase (COX) and suppresses its enzyme activity led us to investigate ADR' s action on the cardiovascular functions and heart mitochondrial morphology in Balb - c mice i. p. treated with ADR for several weeks. At various times during treatment, the animals were assessed for cardiovascular functions by electrocardiography and for heart tissue damage by electron microscopy. In parallel, total RNA was extracted from samples of dissected heart and analyzed by Northern blot hybridization to determine the steady - state level of three RNA transcripts encoded by the COXII, COXIII, and COXIV genes. Similarly, samples obtained from the liver of the same animals were analyzed for comparative studies. Our results indicated that 1) treatment of mice with ADR caused cardiovascular arrhythmias characterized by bradycardia, extension of ventricular depolarization time (tQRS), and failure of QRS at high concentrations (10 - 14 mg / kg body weight cumulative dose); 2) the heart mitochondria underwent swelling, fusion, dissolution, and / or disruption of mitochondrial cristae after several weeks of treatment. Such abnormalities were not observed in the mitochondria of liver tissue; and 3) among the three genes of COX enzyme examined, only COXII gene expression was suppressed by ADR treatment, mainly after 8 weeks in both heart and liver. Knowing that heart mitochondria represent almost 40% of heart muscle by weight, we conclude that the deteriorating effects of ADR on cardiovascular function involve mitochondrial structural and functional impairment.

Structural and functional impairment of mitochondria

cardiomyopathy

cancer

cardiovascular toxicity

cardiovascular arrhythmias

bradycardia

swelling

mitochondrial structural and functional impairment

adriamycin

adriamycin

ADR

ADR

ADR

ADR

ADR

ADR

ADR

adriamycin

Structural and functional impairment of mitochondria

adriamycin

mitochondrial structural and functional impairment

adriamycin

Structural and functional impairment of mitochondria

adriamycin

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

ADR

Structural and functional impairment of mitochondria

ADR

mitochondrial structural and functional impairment

adriamycin

bradycardia

adriamycin

bradycardia

ADR

bradycardia

ADR

bradycardia

ADR

bradycardia

ADR

bradycardia

ADR

bradycardia

ADR

bradycardia

ADR

bradycardia


Input: Enhanced bradycardia induced by beta - adrenoceptor antagonists in rats pretreated with isoniazid. High doses of isoniazid increase hypotension induced by vasodilators and change the accompanying reflex tachycardia to bradycardia, an interaction attributed to decreased synthesis of brain gamma - aminobutyric acid (GABA). In the present study, the possible enhancement by isoniazid of bradycardia induced by beta - adrenoceptor antagonists was determined in rats anaesthetised with chloralose - urethane. Isoniazid significantly increased bradycardia after propranolol, pindolol, labetalol and atenolol, as well as after clonidine, but not after hexamethonium or carbachol. Enhancement was not observed in rats pretreated with methylatropine or previously vagotomised. These results are compatible with interference by isoniazid with GABAergic inhibition of cardiac parasympathetic tone. Such interference could be exerted centrally, possibly at the nucleus ambiguus, or peripherally at the sinus node.

bradycardia

hypotension

tachycardia

bradycardia

bradycardia

bradycardia

isoniazid

isoniazid

gamma - aminobutyric acid

GABA

isoniazid

chloralose

urethane

Isoniazid

propranolol

pindolol

labetalol

atenolol

clonidine

hexamethonium

carbachol

methylatropine

isoniazid

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

Isoniazid

bradycardia

Isoniazid

bradycardia

Isoniazid

bradycardia

Isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

bradycardia

isoniazid

hypotension

isoniazid

hypotension

isoniazid

hypotension

Isoniazid

hypotension

isoniazid

hypotension


Input: Epileptogenic activity of folic acid after drug induces SLE (folic acid and epilepsy) OBJECTIVE: To study the effect of folic acid - containing multivitamin supplementation in epileptic women before and during pregnancy in order to determine the rate of structural birth defects and epilepsy - related side effects. STUDY DESIGN: First a randomised trial, later periconception care including in total 12225 females. RESULTS: Of 60 epileptic women with periconceptional folic acid (0. 8 mg) - containing multivitamin supplementation, no one developed epilepsy - related side effects during the periconception period. One epileptic woman delivered a newborn with cleft lip and palate. Another patient exhibited with a cluster of seizures after the periconception period using another multivitamin. This 22 - year - old epileptic woman was treated continuously by carbamazepine and a folic acid (1 mg) - containing multivitamin from the 20th week of gestation. She developed status epilepticus and later symptoms of systemic lupus erythematodes. Her pregnancy ended with stillbirth. CONCLUSIONS: The epileptic pregnant patient' s autoimmune disease (probably drug - induced lupus) could damage the blood - brain barrier, therefore the therapeutic dose (> or = 1 mg) of folic acid triggered a cluster of seizures. Physiological dose (< 1 mg) of folic acid both in healthy and 60 epileptic women, all without any autoimmune disease, did not increase the risk for epileptic seizures.

folic acid

folic acid

folic acid

folic acid

carbamazepine

folic acid

folic acid

folic acid

SLE

epilepsy

epileptic

birth defects

epilepsy

epileptic

epilepsy

epileptic

cleft lip and palate

cleft lip

cleft lip and palate

seizures

epileptic

status epilepticus

systemic lupus erythematodes

stillbirth

epileptic

autoimmune disease

lupus

seizures

epileptic

autoimmune disease

epileptic seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

seizures

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus

folic acid

SLE

folic acid

systemic lupus erythematodes

folic acid

lupus


Input: Effects of cisapride on symptoms and postcibal small - bowel motor function in patients with irritable bowel syndrome. BACKGROUND: Irritable bowel syndrome is a common cause of abdominal pain and discomfort and may be related to disordered gastrointestinal motility. Our aim was to assess the effects of long - term treatment with a prokinetic agent, cisapride, on postprandial jejunal motility and symptoms in the irritable bowel syndrome (IBS). METHODS: Thirty - eight patients with IBS (constipation - predominant, n = 17; diarrhoea - predominant, n = 21) underwent 24 - h ambulatory jejunal manometry before and after 12 week' s treatment [cisapride, 5 mg three times daily (n = 19) or placebo (n = 19)]. RESULTS: In diarrhoea - predominant patients significant differences in contraction characteristics were observed between the cisapride and placebo groups. In cisapride - treated diarrhoea - predominant patients the mean contraction amplitude was higher (29. 3 + / - 3. 2 versus 24. 9 + / - 2. 6 mm Hg, cisapride versus placebo (P < 0. 001); pretreatment, 25. 7 + / - 6. 0 mm Hg), the mean contraction duration longer (3. 4 + / - 0. 2 versus 3. 0 + / - 0. 2 sec, cisapride versus placebo (P < 0. 001); pretreatment, 3. 1 + / - 0. 5 sec), and the mean contraction frequency lower (2. 0 + / - 0. 2 versus 2. 5 + / - 0. 4 cont. / min, cisapride versus placebo (P < 0. 001); pretreatment, 2. 5 + / - 1. 1 cont. / min] than patients treated with placebo. No significant differences in jejunal motility were found in the constipation - predominant IBS group. Symptoms were assessed by using a visual analogue scale before and after treatment. Symptom scores relating to the severity of constipation were lower in cisapride - treated constipation - predominant IBS patients [score, 54 + / - 5 versus 67 + / - 14 mm, cisapride versus placebo (P < 0. 05); pretreatment, 62 + / - 19 mm]. Diarrhoea - predominant IBS patients had a higher pain score after cisapride therapy [score, 55 + / - 15 versus 34 + / - 12 mm, cisapride versus placebo (P < 0. 05); pretreatment, 67 + / - 19 mm]. CONCLUSION: Cisapride affects jejunal contraction characteristics and some symptoms in IBS.

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

cisapride

Cisapride

irritable bowel syndrome

Irritable bowel syndrome

abdominal pain

disordered gastrointestinal motility

irritable bowel syndrome

IBS

IBS

constipation

diarrhoea

diarrhoea

diarrhoea

constipation

IBS

constipation

constipation

IBS

Diarrhoea

IBS

pain

IBS

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

cisapride

abdominal pain

Cisapride

abdominal pain


Input: Clarithromycin - induced ventricular tachycardia. Clarithromycin is a relatively new macrolide antibiotic that offers twice - daily dosing. It differs from erythromycin only in the methylation of the hydroxyl group at position 6. Although the side - effect profile of erythromycin is established, including gastroenteritis and interactions with other drugs subject to hepatic mixed - function oxidase metabolism, experience with the newer macrolides is still being recorded. Cardiotoxicity has been demonstrated after both intravenous and oral administration of erythromycin but has never been reported with the newer macrolides. We report a case of ventricular dysrhythmias that occurred after six therapeutic doses of clarithromycin. The dysrhythmias resolved after discontinuation of the drug.

Clarithromycin

Clarithromycin

macrolide

erythromycin

erythromycin

macrolides

erythromycin

macrolides

clarithromycin

ventricular tachycardia

gastroenteritis

Cardiotoxicity

ventricular dysrhythmias

dysrhythmias

erythromycin

gastroenteritis

erythromycin

gastroenteritis

erythromycin

gastroenteritis

Clarithromycin

ventricular tachycardia

Clarithromycin

ventricular tachycardia

clarithromycin

ventricular tachycardia


Input: Persistent nephrogenic diabetes insipidus following lithium therapy. We report the case of a patient who developed severe hypernatraemic dehydration following a head injury. Ten years previously he had been diagnosed to have lithium - induced nephrogenic diabetes insipidus, and lithium therapy had been discontinued. He remained thirsty and polyuric despite cessation of lithium and investigations on admission showed him to have normal osmoregulated thirst and vasopressin secretion, with clear evidence of nephrogenic diabetes insipidus. Lithium induced nephrogenic diabetes insipidus is considered to be reversible on cessation of therapy but polyuria persisted in this patient for ten years after lithium was stopped. We discuss the possible renal mechanisms and the implications for management of patients with lithium - induced nephrogenic diabetes insipidus.

nephrogenic diabetes insipidus

dehydration

head injury

nephrogenic diabetes insipidus

polyuric

nephrogenic diabetes insipidus

nephrogenic diabetes insipidus

polyuria

nephrogenic diabetes insipidus

lithium

lithium

lithium

lithium

vasopressin

Lithium

lithium

lithium

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

Lithium

nephrogenic diabetes insipidus

Lithium

nephrogenic diabetes insipidus

Lithium

nephrogenic diabetes insipidus

Lithium

nephrogenic diabetes insipidus

Lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

nephrogenic diabetes insipidus

lithium

polyuric

lithium

polyuria

lithium

polyuric

lithium

polyuria

lithium

polyuric

lithium

polyuria

lithium

polyuric

lithium

polyuria

Lithium

polyuric

Lithium

polyuria

lithium

polyuric

lithium

polyuria

lithium

polyuric

lithium

polyuria


Input: Late cardiotoxicity after treatment for a malignant bone tumor. Cardiac function was assessed in long - term survivors of malignant bone tumors who were treated according to Rosen' s T5 or T10 protocol, both including doxorubicin. Thirty - one patients, age 10 - 45 years (median age 17. 8 years) were evaluated 2. 3 - 14. 1 years (median 8. 9 years) following completion of treatment. Cumulative doses of doxorubicin were 225 - 550 mg / m2 (median dose 360). The evaluation consisted of a history, physical examination, electrocardiogram (ECG), signal averaged ECG, 24 - hour ambulatory ECG, echocardiography and radionuclide angiography. Eighteen of 31 (58%) patients showed cardiac toxicity, defined as having one or more of the following abnormalities: late potentials, complex ventricular arrhythmias, left ventricular dilation, decreased shortening fraction, or decreased ejection fraction. The incidence of cardiac abnormalities increased with length of follow - up (P < or =. 05). No correlation could be demonstrated between cumulative dose of doxorubicin and cardiac status, except for heart rate variability. When adjusted to body surface area, the left ventricular posterior wall thickness (LVPW index) was decreased in all patients. The incidence of doxorubicin - induced cardiotoxicity is high and increases with follow - up, irrespective of cumulative dose. Life - long cardiac follow - up in these patients is warranted. The results of our study suggest that heart rate variability and LVPW index could be sensitive indicators for cardiotoxicity.

cardiotoxicity

bone tumor

bone tumors

cardiac toxicity

ventricular arrhythmias

ventricular dilation

cardiac abnormalities

cardiotoxicity

cardiotoxicity

Rosen' s T5 or T10 protocol

doxorubicin

doxorubicin

doxorubicin

doxorubicin

doxorubicin

cardiac abnormalities

doxorubicin

cardiac abnormalities

doxorubicin

cardiac abnormalities

doxorubicin

cardiac abnormalities


Input: Venous complications of midazolam versus diazepam. Although some studies have suggested fewer venous complications are associated with midazolam than with diazepam for endoscopic procedures, this variable has not been well documented. We prospectively evaluated the incidence of venous complications after intravenous injection of diazepam or midazolam in 122 consecutive patients undergoing colonoscopy and esophagogastroduodenoscopy. Overall, venous complications were more frequent with diazepam (22 of 62 patients) than with midazolam (4 of 60 patients) (p < 0. 001). A palpable venous cord was present in 23% (14 of 62) of patients in the diazepam group, compared with 2% (1 of 60 patients) in the midazolam group (p < 0. 002). Pain at the injection site occurred in 35% (22 of 62) of patients in the diazepam group compared with 7% (4 of 60 patients) in the midazolam group (p < 0. 001). Swelling and warmth at the injection site were not significantly different between the two groups. Smoking, nonsteroidal anti - inflammatory drug use, intravenous catheter site, dwell time of the needle, alcohol use, and pain during the injection had no effect on the incidence of venous complications.

Venous complications

venous complications

venous complications

venous complications

Pain

Swelling

pain

venous complications

midazolam

diazepam

midazolam

diazepam

diazepam

midazolam

diazepam

midazolam

diazepam

midazolam

diazepam

midazolam

alcohol

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

Venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

diazepam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

Venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications

midazolam

venous complications


Input: Tetany and rhabdomyolysis due to surreptitious furosemide - - importance of magnesium supplementation. Diuretics may induce hypokalemia, hypocalcemia and hypomagnesemia. While severe hypokalemia may cause muscle weakness, severe hypomagnesemia is associated with muscle spasms and tetany which cannot be corrected by potassium and calcium supplementation alone (1, 2). Surreptitious diuretic ingestion has been described, mainly in women who are concerned that they are obese or edematous. Symptomatic hypokalemia has been reported in such patients (3 - 7) and in one case hypocalcemia was observed (8), but the effects of magnesium depletion were not noted in these patients.

Tetany

rhabdomyolysis

hypokalemia

hypocalcemia

hypomagnesemia

hypokalemia

muscle weakness

hypomagnesemia

muscle spasms

tetany

obese

edematous

hypokalemia

hypocalcemia

furosemide

magnesium

potassium

calcium

magnesium

furosemide

rhabdomyolysis

furosemide

Tetany

furosemide

tetany


Input: Loss of glutamate decarboxylase mRNA - containing neurons in the rat dentate gyrus following pilocarpine - induced seizures. In situ hybridization methods were used to determine if glutamic acid decarboxylase (GAD) mRNA - containing neurons within the hilus of the dentate gyrus are vulnerable to seizure - induced damage in a model of chronic seizures. Sprague - Dawley rats were injected intraperitoneally with pilocarpine, and the hippocampal formation was studied histologically at 1, 2, 4, and 8 week intervals after pilocarpine - induced seizures. In situ hybridization histochemistry, using a digoxigenin - labeled GAD cRNA probe, demonstrated a substantial decrease in the number of GAD mRNA - containing neurons in the hilus of the dentate gyrus in the pilocarpine - treated rats as compared to controls at all time intervals. Additional neuronanatomical studies, including cresyl violet staining, neuronal degeneration methods, and histochemical localization of glial fibrillary acidic protein, suggested that the decrease in the number of GAD mRNA - containing neurons was related to neuronal loss rather than to a decrease in GAD mRNA levels. The loss of GAD mRNA - containing neurons in the hilus contrasted with the relative preservation of labeled putative basket cells along the inner margin of the granule cell layer. Quantitative analyses of labeled neurons in three regions of the dentate gyrus in the 1 and 2 week groups showed statistically significant decreases in the mean number of GAD mRNA - containing neurons in the hilus of both groups of experimental animals. No significant differences were found in the molecular layer or the granule cell layer, which included labeled neurons along the lower margin of the granule cell layer. The results indicate that, in this model, a subpopulation of GAD mRNA - containing neurons within the dentate gyrus is selectively vulnerable to seizure - induced damage. Such differential vulnerability appears to be another indication of the heterogeneity of GABA neurons.

glutamate

pilocarpine

glutamic acid

pilocarpine

pilocarpine

digoxigenin

pilocarpine

cresyl violet

GABA

seizures

seizure

seizures

seizures

neuronal degeneration

neuronal loss

seizure

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

seizures

pilocarpine

seizures

pilocarpine

seizure

pilocarpine

neuronal degeneration

pilocarpine

neuronal loss

pilocarpine

neuronal degeneration

pilocarpine

neuronal loss

pilocarpine

neuronal degeneration

pilocarpine

neuronal loss

pilocarpine

neuronal degeneration

pilocarpine

neuronal loss


Input: Protective effect of misoprostol on indomethacin induced renal dysfunction in elderly patients. OBJECTIVE: To evaluate the possible protective effects of misoprostol on renal function in hospitalized elderly patients treated with indomethacin. METHODS: Forty - five hospitalized elderly patients (> 65 years old) who required therapy with nonsteroidal antiinflammatory drugs (NSAID) were randomly assigned to receive either indomethacin, 150 mg / day (Group A), or indomethacin 150 mg / day plus misoprostol at 0. 6 mg / day (Group B). Laboratory variables of renal function [serum creatinine, blood urea nitrogen (BUN) and electrolytes] were evaluated before initiation of therapy and every 2 days, until termination of the study (a period of at least 6 days). Response to treatment was estimated by the visual analog scale for severity of pain. RESULTS: Forty - two patients completed the study, 22 in Group A and 20 in Group B. BUN and creatinine increased by > 50% of baseline levels in 54 and 45% of Group A patients, respectively, compared to only 20 and 10% of Group B patients (p < 0. 05). Potassium (K) increment of 0. 6 mEq / l or more was observed in 50% of Group A, but in only 15% of Group B patients (p < 0. 05). The mean increments in BUN, creatinine, and K were reduced by 63, 80, and 42%, respectively, in Group B patients compared to Group A. Response to treatment did not differ significantly between the 2 groups. CONCLUSION: Hospitalized elderly patients are at risk for developing indomethacin related renal dysfunction. Addition of misoprostol can minimize this renal impairment without affecting pain control.

misoprostol

indomethacin

misoprostol

indomethacin

indomethacin

indomethacin

misoprostol

creatinine

blood urea nitrogen

BUN

BUN

creatinine

Potassium

K

BUN

creatinine

K

indomethacin

misoprostol

renal dysfunction

pain

renal dysfunction

renal impairment

pain

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal impairment

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal impairment

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal impairment

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal impairment

indomethacin

renal dysfunction

indomethacin

renal dysfunction

indomethacin

renal impairment


Input: Nephrotoxic effects of aminoglycoside treatment on renal protein reabsorption and accumulation. To quantify the effects of gentamicin, kanamycin and netilmicin on renal protein reabsorption and accumulation, these drugs were administered to rats intraperitoneally (30 mg / kg / day) for 7, 14 or 21 days. Scanning electron microscopy of the glomerular endothelia, urinary measurements of sodium, potassium, endogenous lysozyme, N - acetyl - beta - D - glucosaminidase (NAG) as well as clearance and accumulation experiments after i. v. administration of egg - white lysozyme and measurements of inulin clearance (GFR) were done in each treatment group. Gentamicin administration decreased diameter, density and shape of endothelial fenestrae. Kanamycin and netilmicin appeared to have no effect at the dose used. All three aminoglycosides decreased GFR and increased urinary excretion of sodium and potassium. While gentamicin and kanamycin decreased the percentage reabsorption and accumulation of lysozyme after i. v. administration of egg - white lysozyme netilmicin had no effect. Daily excretion of total protein, endogenous lysozyme and NAG increased only after treatment with kanamycin and gentamicin. Thus, aminoglycosides may act as nephrotoxicants at glomerular and / or tubular level inducing impairment of renal reabsorption and accumulation of proteins.

Nephrotoxic

impairment of renal reabsorption

aminoglycoside

gentamicin

kanamycin

netilmicin

sodium

potassium

Gentamicin

Kanamycin

netilmicin

aminoglycosides

sodium

potassium

gentamicin

kanamycin

netilmicin

kanamycin

gentamicin

aminoglycosides

kanamycin

Nephrotoxic

kanamycin

impairment of renal reabsorption

Kanamycin

Nephrotoxic

Kanamycin

impairment of renal reabsorption

kanamycin

Nephrotoxic

kanamycin

impairment of renal reabsorption

kanamycin

Nephrotoxic

kanamycin

impairment of renal reabsorption

gentamicin

Nephrotoxic

gentamicin

impairment of renal reabsorption

Gentamicin

Nephrotoxic

Gentamicin

impairment of renal reabsorption

gentamicin

Nephrotoxic

gentamicin

impairment of renal reabsorption

gentamicin

Nephrotoxic

gentamicin

impairment of renal reabsorption


Input: Pharmacology of GYKI - 41 099 (chlorpropanol, Tobanum) a new potent beta - adrenergic antagonist. The compound GYKI - 41 099, as a beta - adrenergic antagonist, is 3 - 8 times more potent than propranolol in vitro and in vivo. Its antiarrhythmic effectiveness surpasses that of propranolol and pindolol inhibiting the ouabain arrhythmia in dogs and cats. GYKI - 41 900 has a negligible cardiodepressant activity; it is not cardioselective. The compound shows a rapid and long lasting effect. There was a prolonged elimination of the radioactivity after the injection of 14C - 41 099 to rats and dogs. The half life of the unlabeled substance in humans was more than 10 hours.

GYKI - 41 099

chlorpropanol

Tobanum

GYKI - 41 099

propranolol

propranolol

pindolol

ouabain

GYKI - 41 900

14C - 41 099

arrhythmia

ouabain

arrhythmia


Input: Chorea associated with oral contraception. Three patients developed chorea while receiving oral contraceptives. Two were young patients whose chorea developed long after treatment had been started and disappeared soon after it had been discontinued. The third patient had acute amphetamine - induced chorea after prolonged oral contraception. Prolonged administration of female sex hormones is a possible cause of chorea in women who have not previously had chorea or rheumatic fever.

Chorea

chorea

chorea

chorea

chorea

chorea

rheumatic fever

oral contraception

oral contraceptives

amphetamine

oral contraception

oral contraception

Chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

oral contraceptives

Chorea

oral contraceptives

chorea

oral contraceptives

chorea

oral contraceptives

chorea

oral contraceptives

chorea

oral contraceptives

chorea

oral contraception

Chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

oral contraception

chorea

amphetamine

Chorea

amphetamine

chorea

amphetamine

chorea

amphetamine

chorea

amphetamine

chorea

amphetamine

chorea


Input: Reversal of ammonia coma in rats by L - dopa: a peripheral effect. Ammonia coma was produced in rats within 10 to 15 minutes of an intraperitonealinjection of 1. 7 mmol NH4CL. This coma was prevented with 1. 68 mmol L - dopa given by gastric intubation 15 minutes before the ammonium salt injection. The effect of L - dopa was correlated with a decrease in blood and brain ammonia, an increase in brain dopamine, and an increase in renal excretion of ammonia and urea. Intraventricular infusion of dopamine sufficient to raise the brain dopamine to the same extent did not prevent the ammonia coma nor affect the blood and brain ammonia concentrations. Bilateral nephrectomy eliminated the beneficial effect of L - dopa on blood and brain ammonia and the ammonia coma was not prevented. Thus, the reduction in blood and brain ammonia and the prevention of ammonia coma after L - dopa, can be accounted for by the peripheral effect of dopamine on renal function rather than its central action. These results provide a reasonable explanation for the beneficial effects observed in some encephalopathic patients receiving L - dopa.

ammonia

L - dopa

Ammonia

L - dopa

ammonium salt

L - dopa

ammonia

dopamine

ammonia

urea

dopamine

dopamine

ammonia

ammonia

L - dopa

ammonia

ammonia

ammonia

ammonia

L - dopa

dopamine

L - dopa

coma

coma

coma

coma

coma

coma

encephalopathic

coma

coma

coma

coma

coma

coma


Input: Heparin - induced thrombocytopenia after liver transplantation. BACKGROUND: Unfractionated heparin sodium (UFH) or low - molecular weight heparin (LMWH) is used in anticoagulant protocols at several institutions to prevent thrombosis after liver transplantation. Heparin - induced thrombocytopenia (HIT) is an adverse immune - mediated reaction to heparin, resulting in platelet count decreases of more than 50%. The frequencies of HIT after liver transplantation and platelet factor 4 / heparin - reactive antibody (HIT antibody) positivity in liver transplantation patients, however, are unknown. PATIENTS AND METHODS: The 32 men and 20 women underwent living donor liver transplantation. We started LMWH (25 IU / kg / h) on postoperative day (POD) 1, switching to UFH (5000 U / d) on POD 2 or 3. The dose of UFH was changed according to the activated clotting time level. HIT antibody levels were measured the day before surgery and on POD 7 and 14. Platelet count was measured daily for 3 weeks. RESULTS: The average platelet counts preoperatively, and on POD 7, 14, and 21 were 65, 88, 149, and 169 x 10 (9) / L, respectively. Two patients developed hepatic artery thrombosis on POD 11 and 19, respectively, although they were HIT antibody - negative and their platelet counts were stable. In 2 other patients, the platelet count decreased suddenly from 107 x 10 (9) / L on POD 4 to 65 x 10 (9) / L on POD 6 and from 76 x 10 (9) / L on POD 7 to 33 x 10 (9) / L on POD 9, respectively. The heparin - induced platelet aggregation test was negative in these patients. The percentage of HIT antibody - positive patients was 0. 5% preoperatively, 5. 6% on POD 7, and 5. 6% on POD 14. None of the subjects / patients developed UFH - related HIT. CONCLUSIONS: In our series, the occurrence of HIT after liver transplantation was uncommon.

Heparin

Unfractionated heparin sodium

UFH

low - molecular weight heparin

Heparin

heparin

heparin

UFH

UFH

heparin

UFH

thrombocytopenia

thrombosis

thrombocytopenia

HIT

HIT

HIT

HIT

thrombosis

HIT

platelet aggregation

HIT

HIT

HIT

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Unfractionated heparin sodium

thrombocytopenia

Unfractionated heparin sodium

thrombocytopenia

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

Unfractionated heparin sodium

HIT

UFH

thrombocytopenia

UFH

thrombocytopenia

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

Heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

UFH

thrombocytopenia

UFH

thrombocytopenia

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

thrombocytopenia

UFH

thrombocytopenia

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

heparin

HIT

UFH

thrombocytopenia

UFH

thrombocytopenia

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT

UFH

HIT


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

PTU

propylthiouracil

PTU

PTU

vasculitis

Turner Syndrome

Graves' disease

purpura

vasculitis

Turner syndrome

Graves' disease

purpuric lesions

vasculitis

hyperthyroidism

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

propylthiouracil

vasculitis

propylthiouracil

vasculitis

propylthiouracil

vasculitis

propylthiouracil

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis

PTU

vasculitis


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

Succinylcholine

succinylcholine

Sch

propofol

masseter muscle rigidity

Masseter muscle rigidity

malignant hyperthermia

masseter muscle rigidity

masseter muscle rigidity

jaw of steel

malignant hyperthermia

Succinylcholine

masseter muscle rigidity

Succinylcholine

Masseter muscle rigidity

Succinylcholine

masseter muscle rigidity

Succinylcholine

masseter muscle rigidity

Succinylcholine

jaw of steel

succinylcholine

masseter muscle rigidity

succinylcholine

Masseter muscle rigidity

succinylcholine

masseter muscle rigidity

succinylcholine

masseter muscle rigidity

succinylcholine

jaw of steel

Sch

masseter muscle rigidity

Sch

Masseter muscle rigidity

Sch

masseter muscle rigidity

Sch

masseter muscle rigidity

Sch

jaw of steel