Input: Population - based study of risk of venous thromboembolism associated with various oral contraceptives. BACKGROUND: Four studies published since December, 1995, reported that the incidence of venous thromboembolism (VTE) was higher in women who used oral contraceptives (OCs) containing the third - generation progestagens gestodene or desogestrel than in users of OCs containing second - generation progestagens. However, confounding and bias in the design of these studies may have affected the findings. The aim of our study was to re - examine the association between risk of VTE and OC use with a different study design and analysis to avoid some of the bias and confounding of the earlier studies. METHODS: We used computer records of patients from 143 general practices in the UK. The study was based on the medical records of about 540, 000 women born between 1941 and 1981. All women who had a recorded diagnosis of deep - vein thrombosis, venous thrombosis not otherwise specified, or pulmonary embolus during the study period, and who had been treated with an anticoagulant were identified as potential cases of VTE. We did a cohort analysis to estimate and compare incidence of VTE in users of the main OC preparations, and a nested case - control study to calculate the odds ratios of VTE associated with use of different types of OC, after adjustment for potential confounding factors. In the case - control study, we matched cases to controls by exact year of birth, practice, and current use of OCs. We used a multiple logistic regression model that included body - mass index, number of cycles, change in type of OC prescribed within 3 months of the event, previous pregnancy, and concurrent disease. FINDINGS: 85 women met the inclusion criteria for VTE, two of whom were users of progestagen - only OCs. Of the 83 cases of VTE associated with use of combined OCs, 43 were recorded as deep - vein thrombosis, 35 as pulmonary thrombosis, and five as venous thrombosis not otherwise specified. The crude rate of VTE per 10, 000 woman - years was 4. 10 in current users of any OC, 3. 10 in users of second - generation OCs, and 4. 96 in users of third - generation preparations. After adjustment for age, the rate ratio of VTE in users of third - generation relative to second - generation OCs was 1. 68 (95% CI 1. 04 - 2. 75). Logistic regression showed no significant difference in the risk of VTE between users of third - generation and second - generation OCs. Among users of third - generation progestagens, the risk of VTE was higher in users of desogestrel with 20 g ethinyloestradiol than in users of gestodene or desogestrel with 30 g ethinyloestradiol. With all second - generation OCs as the reference, the odds ratios for VTE were 3. 49 (1. 21 - 10. 12) for desogestrel plus 20 g ethinyloestradiol and 1. 18 (0. 66 - 2. 17) for the other third - generation progestagens. INTERPRETATION: The previously reported increase in odds ratio associated with third - generation OCs when compared with second - generation products is likely to have been the result of residual confounding by age. The increased odds ratio associated with products containing 20 micrograms ethinyloestradiol and desogestrel compared with the 30 micrograms product is biologically implausible, and is likely to be the result of preferential prescribing and, thus, confounding.

venous thromboembolism

venous thromboembolism

VTE

VTE

deep - vein thrombosis

venous thrombosis

VTE

VTE

VTE

VTE

VTE

deep - vein thrombosis

thrombosis

venous thrombosis

VTE

VTE

VTE

VTE

VTE

oral contraceptives

oral contraceptives

OCs

progestagens

gestodene

desogestrel

OCs

progestagens

OC

OC

OC

OCs

OC

progestagen

OCs

OCs

OC

OCs

OCs

OCs

progestagens

desogestrel

ethinyloestradiol

gestodene

desogestrel

ethinyloestradiol

OCs

desogestrel

ethinyloestradiol

progestagens

OCs

ethinyloestradiol

desogestrel

oral contraceptives

venous thromboembolism

oral contraceptives

venous thromboembolism

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

venous thromboembolism

oral contraceptives

venous thromboembolism

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

oral contraceptives

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OC

venous thromboembolism

OC

venous thromboembolism

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

venous thromboembolism

OC

venous thromboembolism

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

venous thromboembolism

OC

venous thromboembolism

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OC

venous thromboembolism

OC

venous thromboembolism

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OC

venous thromboembolism

OC

venous thromboembolism

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OC

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

venous thromboembolism

OCs

venous thromboembolism

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE

OCs

VTE


Input: MK - 801 augments pilocarpine - induced electrographic seizure but protects against brain damage in rats. 1. The authors examined the anticonvulsant effects of MK - 801 on the pilocarpine - induced seizure model. Intraperitoneal injection of pilocarpine (400 mg / kg) induced tonic and clonic seizure. Scopolamine (10 mg / kg) and pentobarbital (5 mg / kg) prevented development of pilocarpine - induced behavioral seizure but MK - 801 (0. 5 mg / kg) did not. 2. An electrical seizure measured with hippocampal EEG appeared in the pilocarpine - treated group. Scopolamine and pentobarbital blocked the pilocarpine - induced electrographic seizure, MK - 801 treatment augmented the electrographic seizure induced by pilocarpine. 3. Brain damage was assessed by examining the hippocampus microscopically. Pilocarpine produced neuronal death in the hippocampus, which showed pyknotic changes. Pentobarbital, scopolamine and MK - 801 protected the brain damage by pilocarpine, though in the MK - 801 - treated group, the pyramidal cells of hippocampus appeared darker than normal. In all treatments, granule cells of the dentate gyrus were not affected. 4. These results indicate that status epilepticus induced by pilocarpine is initiated by cholinergic overstimulation and propagated by glutamatergic transmission, the elevation of which may cause brain damage through an excitatory NMDA receptor - mediated mechanism.

MK - 801

pilocarpine

MK - 801

pilocarpine

pilocarpine

Scopolamine

pentobarbital

pilocarpine

MK - 801

pilocarpine

Scopolamine

pentobarbital

pilocarpine

MK - 801

pilocarpine

Pilocarpine

Pentobarbital

scopolamine

MK - 801

pilocarpine

MK - 801

pilocarpine

NMDA

seizure

brain damage

seizure

tonic and clonic seizure

seizure

seizure

seizure

seizure

Brain damage

neuronal death

brain damage

status epilepticus

brain damage

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

Pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

neuronal death

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

Pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

status epilepticus

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

Pilocarpine

seizure

Pilocarpine

seizure

Pilocarpine

tonic and clonic seizure

Pilocarpine

seizure

Pilocarpine

seizure

Pilocarpine

seizure

Pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

tonic and clonic seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

pilocarpine

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

tonic and clonic seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure

MK - 801

seizure


Input: Paclitaxel, 5 - fluorouracil, and folinic acid in metastatic breast cancer: BRE - 26, a phase II trial. 5 - Fluorouracil plus folinic acid and paclitaxel (Taxol; Bristol - Myers Squibb Company, Princeton, NJ) are effective salvage therapies for metastatic breast cancer patients. Paclitaxel and 5 - fluorouracil have additive cytotoxicity in MCF - 7 cell lines. We performed a phase II trial of paclitaxel 175 mg / m2 over 3 hours on day I followed by folinic acid 300 mg over 1 hour before 5 - fluorouracil 350 mg / m2 on days 1 to 3 every 28 days (TFL) in women with metastatic breast cancer. Analysis is reported on 37 patients with a minimum of 6 months follow - up who received a total of 192 cycles of TFL: nine cycles (5%) were associated with grade 3 / 4 neutropenia requiring hospitalization; seven (4%) cycles in two patients required granulocyte colony - stimulating factor due to neutropenia; no patient required platelet transfusions. Grade 3 / 4 nonhematologic toxicities were uncommon. Among the 34 patients evaluable for response, there were three complete responses (9%) and 18 partial responses (53%) for an overall response rate of 62%. Of the 19 evaluable patients with prior doxorubicin exposure, 11 (58%) responded compared with nine of 15 (60%) without prior doxorubicin. Plasma paclitaxel concentrations were measured at the completion of paclitaxel infusion and at 24 hours in 19 patients. TFL is an active, well - tolerated regimen in metastatic breast cancer.

Paclitaxel

5 - fluorouracil

folinic acid

5 - Fluorouracil

folinic acid

paclitaxel

Taxol

Paclitaxel

5 - fluorouracil

paclitaxel

folinic acid

5 - fluorouracil

granulocyte colony - stimulating factor

doxorubicin

doxorubicin

paclitaxel

paclitaxel

breast cancer

breast cancer

cytotoxicity

breast cancer

neutropenia

neutropenia

toxicities

breast cancer

folinic acid

neutropenia

folinic acid

neutropenia

folinic acid

neutropenia

folinic acid

neutropenia

folinic acid

neutropenia

folinic acid

neutropenia

Paclitaxel

neutropenia

Paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

Taxol

neutropenia

Taxol

neutropenia

Paclitaxel

neutropenia

Paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

paclitaxel

neutropenia

5 - fluorouracil

neutropenia

5 - fluorouracil

neutropenia

5 - Fluorouracil

neutropenia

5 - Fluorouracil

neutropenia

5 - fluorouracil

neutropenia

5 - fluorouracil

neutropenia

5 - fluorouracil

neutropenia

5 - fluorouracil

neutropenia


Input: Efficacy and proarrhythmia with the use of d, l - sotalol for sustained ventricular tachyarrhythmias. This study prospectively evaluated the clinical efficacy, the incidence of torsades de pointes, and the presumable risk factors for torsades de pointes in patients treated with d, l - sotalol for sustained ventricular tachyarrhythmias. Eighty - one consecutive patients (54 with coronary artery disease, and 20 with dilated cardiomyopathy) with inducible sustained ventricular tachycardia or ventricular fibrillation received oral d, l - sotalol to prevent induction of the ventricular tachyarrhythmia. During oral loading with d, l - sotalol, continuous electrocardiographic (ECG) monitoring was performed. Those patients in whom d, l - sotalol prevented induction of ventricular tachycardia or ventricular fibrillation were discharged with the drug and followed up on an outpatient basis for 21 + / - 18 months. Induction of the ventricular tachyarrhythmia was prevented by oral d, l - sotalol in 35 (43%) patients; the ventricular tachyarrhythmia remained inducible in 40 (49%) patients; and two (2. 5%) patients did not tolerate even 40 mg of d, l - sotalol once daily. Four (5%) patients had from torsades de pointes during the initial oral treatment with d, l - sotalol. Neither ECG [sinus - cycle length (SCL), QT or QTc interval, or U wave] nor clinical parameters identified patients at risk for torsades de pointes. However, the oral dose of d, l - sotalol was significantly lower in patients with torsades de pointes (200 + / - 46 vs. 328 + / - 53 mg / day; p = 0. 0017). Risk factors associated with the development of torsades de pointes were the appearance of an U wave (p = 0. 049), female gender (p = 0. 015), and significant dose - corrected changes of SCL, QT interval, and QTc interval (p < 0. 05). During follow - up, seven (20%) patients had a nonfatal ventricular tachycardia recurrence, and two (6%) patients died suddenly. One female patient with stable cardiac disease had recurrent torsades de pointes after 2 years of successful treatment with d, l - sotalol. Torsades de pointes occurred early during treatment even with low doses of oral d, l - sotalol. Pronounced changes in the surface ECG (cycle length, QT, and QTc) in relation to the dose of oral d, l - sotalol might identify a subgroup of patients with an increased risk for torsades de pointes. Other ECG parameters before the application of d, l - sotalol did not identify patients at increased risk for torsades de pointes. Recurrence rates of ventricular tachyarrhythmias are high despite complete suppression of the arrhythmia during programmed stimulation. Therefore programmed electrical stimulation in the case of d, l - sotalol seems to be of limited prognostic value.

proarrhythmia

ventricular tachyarrhythmias

torsades de pointes

torsades de pointes

ventricular tachyarrhythmias

coronary artery disease

dilated cardiomyopathy

ventricular tachycardia

ventricular fibrillation

ventricular tachyarrhythmia

ventricular tachycardia

ventricular fibrillation

ventricular tachyarrhythmia

ventricular tachyarrhythmia

torsades de pointes

torsades de pointes

torsades de pointes

torsades de pointes

ventricular tachycardia

cardiac disease

torsades de pointes

Torsades de pointes

torsades de pointes

torsades de pointes

ventricular tachyarrhythmias

arrhythmia

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

Torsades de pointes

d, l - sotalol

torsades de pointes

d, l - sotalol

torsades de pointes


Input: Chronic hyperprolactinemia and changes in dopamine neurons. The tuberoinfundibular dopaminergic (TIDA) system is known to inhibit prolactin (PRL) secretion. In young animals this system responds to acute elevations in serum PRL by increasing its activity. However, this responsiveness is lost in aging rats with chronically high serum PRL levels. The purpose of this study was to induce hyperprolactinemia in rats for extended periods of time and examine its effects on dopaminergic systems in the brain. Hyperprolactinemia was induced by treatment with haloperidol, a dopamine receptor antagonist, and Palkovits' microdissection technique in combination with high - performance liquid chromatography was used to measure neurotransmitter concentrations in several areas of the brain. After 6 months of hyperprolactinemia, dopamine (DA) concentrations in the median eminence (ME) increased by 84% over the control group. Nine months of hyperprolactinemia produced a 50% increase in DA concentrations in the ME over the control group. However, DA response was lost if a 9 - month long haloperidol - induced hyperprolactinemia was followed by a 1 1 / 2 month - long extremely high increase in serum PRL levels produced by implantation of MMQ cells under the kidney capsule. There was no change in the levels of DA, norepinephrine (NE), serotonin (5 - HT), or their metabolites in the arcuate nucleus (AN), medial preoptic area (MPA), caudate putamen (CP), substantia nigra (SN), and zona incerta (ZI), except for a decrease in 5 - hydroxyindoleacetic acid (5 - HIAA) in the AN after 6 - months of hyperprolactinemia and an increase in DA concentrations in the AN after 9 - months of hyperprolactinemia. These results demonstrate that hyperprolactinemia specifically affects TIDA neurons and these effects vary, depending on the duration and intensity of hyperprolactinemia. The age - related decrease in hypothalamic dopamine function may be associated with increases in PRL secretion.

hyperprolactinemia

hyperprolactinemia

Hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

hyperprolactinemia

dopamine

haloperidol

dopamine

dopamine

DA

DA

DA

haloperidol

DA

norepinephrine

NE

serotonin

5 - HT

5 - hydroxyindoleacetic acid

5 - HIAA

DA

dopamine

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

Hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

Hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia


Input: Treatment - related disseminated necrotizing leukoencephalopathy with characteristic contrast enhancement of the white matter. This report describes unique contrast enhancement of the white matter on T1 - weighted magnetic resonance images of two patients with disseminated necrotizing leukoencephalopathy, which developed from acute lymphoblastic leukemia treated with high - dose methotrexate. In both patients, the enhancement was more pronounced near the base of the brain than at the vertex. Necropsy of the first case revealed loss of myelination and necrosis of the white matter. Possible mechanisms causing such a leukoencephalopathy are discussed.

leukoencephalopathy

leukoencephalopathy

acute lymphoblastic leukemia

loss of myelination

necrosis

leukoencephalopathy

methotrexate

methotrexate

loss of myelination

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

leukoencephalopathy

methotrexate

necrosis


Input: Thrombotic complications in acute promyelocytic leukemia during all - trans - retinoic acid therapy. A case of acute renal failure, due to occlusion of renal vessels in a patient with acute promyelocytic leukemia (APL) treated with all - trans - retinoic acid (ATRA) and tranexamic acid has been described recently. We report a case of acute renal failure in an APL patient treated with ATRA alone. This case further supports the concern about thromboembolic complications associated with ATRA therapy in APL patients. The patients, a 43 - year - old man, presented all the signs and symptoms of APL and was included in a treatment protocol with ATRA. After 10 days of treatment, he developed acute renal failure that was completely reversible after complete remission of APL was achieved and therapy discontinued. We conclude that ATRA is a valid therapeutic choice for patients with APL, although the procoagulant tendency is not completely corrected. Thrombotic events, however, could be avoided by using low - dose heparin.

Thrombotic

acute promyelocytic leukemia

acute renal failure

occlusion of renal vessels

acute promyelocytic leukemia

APL

acute renal failure

APL

thromboembolic

APL

APL

acute renal failure

APL

APL

Thrombotic

all - trans - retinoic acid

all - trans - retinoic acid

ATRA

tranexamic acid

ATRA

ATRA

ATRA

ATRA

heparin

all - trans - retinoic acid

Thrombotic

all - trans - retinoic acid

Thrombotic

all - trans - retinoic acid

Thrombotic

all - trans - retinoic acid

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

ATRA

Thrombotic

all - trans - retinoic acid

acute renal failure

all - trans - retinoic acid

acute renal failure

all - trans - retinoic acid

acute renal failure

all - trans - retinoic acid

acute renal failure

all - trans - retinoic acid

acute renal failure

all - trans - retinoic acid

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure

ATRA

acute renal failure


Input: Pupillary changes associated with the development of stimulant - induced mania: a case report. A 30 - year - old cocaine - dependent man who was a subject in a study evaluating the anticraving efficacy of the stimulant medication diethylpropion (DEP) became manic during his second week on the study drug. Pupillometric changes while on DEP, especially changes in the total power of pupillary oscillation, were dramatically different than those observed in the eight other study subjects who did not become manic. The large changes in total power of pupillary oscillation occurred a few days before the patient became fully manic. Such medication - associated changes in the total power of pupillary oscillation might be of utility in identifying persons at risk for manic - like adverse effects during the medical use of psychomotor stimulants or sympathomimetic agents.

mania

manic

pupillary oscillation

manic

pupillary oscillation

manic

pupillary oscillation

manic

cocaine

diethylpropion

DEP

DEP

diethylpropion

mania

diethylpropion

manic

diethylpropion

manic

diethylpropion

manic

diethylpropion

manic

DEP

mania

DEP

manic

DEP

manic

DEP

manic

DEP

manic

DEP

mania

DEP

manic

DEP

manic

DEP

manic

DEP

manic


Input: The negative mucosal potential: separating central and peripheral effects of NSAIDs in man. OBJECTIVE: We wanted to test whether assessment of both a central pain - related signal (chemo - somatosensory evoked potential, CSSEP) and a concomitantly recorded peripheral signal (negative mucosal potential, NMP) allows for separation of central and peripheral effects of NSAIDs. For this purpose, experimental conditions were created in which NSAIDs had previously been observed to produce effects on phasic and tonic pain by either central or peripheral mechanisms. METHODS: According to a double - blind, randomised, controlled, threefold cross - over design, 18 healthy subjects (11 males, 7 females; mean age 26 years) received either placebo, 400 mg ibuprofen, or 800 mg ibuprofen. Phasic pain was applied by means of short pulses of CO2 to the nasal mucosa (stimulus duration 500 ms, interval approximately 60 s), and tonic pain was induced in the nasal cavity by means of dry air of controlled temperature, humidity and flow rate (22 degrees C, 0% relative humidity, 145 ml. s - 1). Both CSSEPs as central and NMPs as peripheral correlates of pain were obtained in response to the CO2 stimuli. Additionally, the subjects rated the intensity of both phasic and tonic pain by means of visual analogue scales. RESULTS: As described earlier, administration of ibuprofen was followed by a decrease in tonic pain but - relative to placebo - an increase in correlates of phasic pain, indicating a specific effect of ibuprofen on the interaction between the pain stimuli under these special experimental conditions. Based on the similar behaviour of CSSEP and NMP, it was concluded that the pharmacological process underlying this phenomenon was localised in the periphery. By means of the simultaneous recording of interrelated peripheral and central electrophysiologic correlates of nociception, it was possible to separate central and peripheral effects of an NSAID. The major advantage of this pain model is the possibility of obtaining peripheral pain - related activity directly using a non - invasive technique in humans.

pain

pain

pain

pain

pain

pain

pain

pain

pain

pain

pain

ibuprofen

ibuprofen

ibuprofen

ibuprofen

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain

ibuprofen

pain


Input: Acute severe depression following peri - operative ondansetron. A 41 - year - old woman with a strong history of postoperative nausea and vomiting presented for abdominal hysterectomy 3 months after a previous anaesthetic where ondansetron prophylaxis had been used. She had developed a severe acute major depression disorder almost immediately thereafter, possibly related to the use of a serotonin antagonist. Nine years before she had experienced a self - limited puerperal depressive episode. Anaesthesia with a propofol infusion and avoidance of serotonin antagonists provided a nausea - free postoperative course without exacerbation of the depression disorder.

depression

postoperative nausea and vomiting

major depression disorder

depressive episode

nausea

depression disorder

ondansetron

ondansetron

serotonin

propofol

serotonin

ondansetron

major depression disorder

ondansetron

major depression disorder


Input: Hypertensive response during dobutamine stress echocardiography. Among 3, 129 dobutamine stress echocardiographic studies, a hypertensive response, defined as systolic blood pressure (BP) > or = 220 mm Hg and / or diastolic BP > or = 110 mm Hg, occurred in 30 patients (1%). Patients with this response more often had a history of hypertension and had higher resting systolic and diastolic BP before dobutamine infusion.

Hypertensive

hypertensive

hypertension

dobutamine

dobutamine

dobutamine

dobutamine

Hypertensive

dobutamine

hypertensive

dobutamine

hypertension

dobutamine

Hypertensive

dobutamine

hypertensive

dobutamine

hypertension

dobutamine

Hypertensive

dobutamine

hypertensive

dobutamine

hypertension


Input: Continuously nebulized albuterol in severe exacerbations of asthma in adults: a case - controlled study. A retrospective, case - controlled analysis comparing patients admitted to a medical intensive care unit with severe exacerbations of asthma who received continuously nebulized albuterol (CNA) versus intermittent albuterol (INA) treatments is reported. Forty matched pairs of patients with asthma are compared. CNA was administered for a mean of 11 + / - 10 hr. The incidence of cardiac dysrhythmias was similar between groups. Symptomatic hypokalemia did not occur. CNA patients had higher heart rates during treatment, which may reflect severity of illness. The incidence of intubation was similar. We conclude that CNA and INA demonstrated similar profiles with regard to safety, morbidity, and mortality.

albuterol

albuterol

albuterol

asthma

asthma

asthma

cardiac dysrhythmias

hypokalemia

albuterol

cardiac dysrhythmias

albuterol

cardiac dysrhythmias

albuterol

cardiac dysrhythmias


Input: Hyperosmolar nonketotic coma precipitated by lithium - induced nephrogenic diabetes insipidus. A 45 - year - old man, with a 10 - year history of manic depression treated with lithium, was admitted with hyperosmolar, nonketotic coma. He gave a five - year history of polyuria and polydipsia, during which time urinalysis had been negative for glucose. After recovery from hyperglycaemia, he remained polyuric despite normal blood glucose concentrations; water deprivation testing indicated nephrogenic diabetes insipidus, likely to be lithium - induced. We hypothesize that when this man developed type 2 diabetes, chronic polyuria due to nephrogenic diabetes insipidus was sufficient to precipitate hyperosmolar dehydration.

Hyperosmolar nonketotic coma

nephrogenic diabetes insipidus

manic depression

hyperosmolar, nonketotic coma

polyuria

polydipsia

hyperglycaemia

polyuric

nephrogenic diabetes insipidus

type 2 diabetes

polyuria

nephrogenic diabetes insipidus

dehydration

lithium

lithium

glucose

glucose

lithium

lithium

polyuria

lithium

polyuric

lithium

polyuria

lithium

polyuria

lithium

polyuric

lithium

polyuria

lithium

polyuria

lithium

polyuric

lithium

polyuria

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

Hyperosmolar nonketotic coma

lithium

hyperosmolar, nonketotic coma

lithium

Hyperosmolar nonketotic coma

lithium

hyperosmolar, nonketotic coma

lithium

Hyperosmolar nonketotic coma

lithium

hyperosmolar, nonketotic coma


Input: Effects of the intracoronary infusion of cocaine on left ventricular systolic and diastolic function in humans. BACKGROUND: In dogs, a large amount of intravenous cocaine causes a profound deterioration of left ventricular (LV) systolic function and an increase in LV end - diastolic pressure. This study was done to assess the influence of a high intracoronary cocaine concentration on LV systolic and diastolic function in humans. METHODS AND RESULTS: In 20 patients (14 men and 6 women aged 39 to 72 years) referred for cardiac catheterization for the evaluation of chest pain, we measured heart rate, systemic arterial pressure, LV pressure and its first derivative (dP / dt), and LV volumes and ejection fraction before and during the final 2 to 3 minutes of a 15 - minute intracoronary infusion of saline (n = 10, control subjects) or cocaine hydrochloride 1 mg / min (n = 10). No variable changed with saline. With cocaine, the drug concentration in blood obtained from the coronary sinus was 3. 0 + / - 0. 4 (mean + / - SD) mg / L, similar in magnitude to the blood cocaine concentration reported in abusers dying of cocaine intoxication. Cocaine induced no significant change in heart rate, LV dP / dt (positive or negative), or LV end - diastolic volume, but it caused an increase in systolic and mean arterial pressures, LV end - diastolic pressure, and LV end - systolic volume, as well as a decrease in LV ejection fraction. CONCLUSIONS: In humans, the intracoronary infusion of cocaine sufficient in amount to achieve a high drug concentration in coronary sinus blood causes a deterioration of LV systolic and diastolic performance.

cocaine

cocaine

cocaine

cocaine hydrochloride

cocaine

cocaine

cocaine

Cocaine

cocaine

deterioration of left ventricular (LV) systolic function

chest pain

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

cocaine hydrochloride

deterioration of left ventricular (LV) systolic function

cocaine hydrochloride

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance

Cocaine

deterioration of left ventricular (LV) systolic function

Cocaine

deterioration of LV systolic and diastolic performance

cocaine

deterioration of left ventricular (LV) systolic function

cocaine

deterioration of LV systolic and diastolic performance


Input: Heparin - induced thrombocytopenia, paradoxical thromboembolism, and other side effects of heparin therapy. Although several new anticoagulant drugs are in development, heparin remains the drug of choice for most anticoagulation needs. The clinical effects of heparin are meritorious, but side effects do exist. Important untoward effects of heparin therapy including heparin - induced thrombocytopenia, heparin - associated osteoporosis, eosinophilia, skin reactions, allergic reactions other than thrombocytopenia and alopecia will be discussed in this article.

Heparin

heparin

heparin

heparin

heparin

heparin

heparin

thrombocytopenia

thromboembolism

thrombocytopenia

osteoporosis

eosinophilia

skin reactions

allergic reactions

thrombocytopenia

alopecia

Heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

Heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

Heparin

thromboembolism

heparin

thromboembolism

heparin

thromboembolism

heparin

thromboembolism

heparin

thromboembolism

heparin

thromboembolism

heparin

thromboembolism

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

Heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

Heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

Heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions


Input: Nonopaque crystal deposition causing ureteric obstruction in patients with HIV undergoing indinavir therapy. OBJECTIVE: We describe the unique CT features of ureteric calculi in six HIV - infected patients receiving indinavir, the most commonly used HIV protease inhibitor, which is associated with an increased incidence of urolithiasis. CONCLUSION: Ureteric obstruction caused by precipitated indinavir crystals may be difficult to diagnose with unenhanced CT. The calculi are not opaque, and secondary signs of obstruction may be absent or minimal and should be sought carefully. Images may need to be obtained using i. v. contrast material to enable diagnosis of ureteric stones or obstruction in patients with HIV infection who receive indinavir therapy.

ureteric obstruction

ureteric calculi

HIV - infected

urolithiasis

Ureteric obstruction

ureteric stones or obstruction

ureteric stones

ureteric stones or obstruction

HIV infection

indinavir

indinavir

indinavir

indinavir

indinavir

ureteric calculi

indinavir

ureteric stones or obstruction

indinavir

ureteric stones

indinavir

ureteric calculi

indinavir

ureteric stones or obstruction

indinavir

ureteric stones

indinavir

ureteric calculi

indinavir

ureteric stones or obstruction

indinavir

ureteric stones

indinavir

ureteric calculi

indinavir

ureteric stones or obstruction

indinavir

ureteric stones


Input: Ischemic colitis and sumatriptan use. Sumatriptan succinate, a serotonin - 1 (5 - hydroxytryptamine - 1) receptor agonist, is an antimigraine drug that is reported to act by selectively constricting intracranial arteries. Recently, vasopressor responses that are distinct from the cranial circulation have been demonstrated to occur in the systemic, pulmonary, and coronary circulations. Cases have been published of coronary vasospasm, myocardial ischemia, and myocardial infarction occurring after sumatriptan use. We report on the development of 8 serious cases of ischemic colitis in patients with migraine treated with sumatriptan.

Ischemic colitis

coronary vasospasm

myocardial ischemia

myocardial infarction

ischemic colitis

migraine

sumatriptan

Sumatriptan succinate

serotonin

5 - hydroxytryptamine

sumatriptan

sumatriptan

sumatriptan

Ischemic colitis

sumatriptan

ischemic colitis

Sumatriptan succinate

Ischemic colitis

Sumatriptan succinate

ischemic colitis

sumatriptan

Ischemic colitis

sumatriptan

ischemic colitis

sumatriptan

Ischemic colitis

sumatriptan

ischemic colitis


Input: Pallidotomy with the gamma knife: a positive experience. 51 patients with medically refractory Parkinson' s disease underwent stereotactic posteromedial pallidotomy between August 1993 and February 1997 for treatment of bradykinesia, rigidity, and L - DOPA - induced dyskinesias. In 29 patients, the pallidotomies were performed with the Leksell Gamma Knife and in 22 they were performed with the standard radiofrequency (RF) method. Clinical assessment as well as blinded ratings of Unified Parkinson' s Disease Rating Scale (UPDRS) scores were carried out pre - and postoperatively. Mean follow - up time is 20. 6 months (range 6 - 48) and all except 4 patients have been followed more than one year. 85 percent of patients with dyskinesias were relieved of symptoms, regardless of whether the pallidotomies were performed with the Gamma Knife or radiofrequency methods. About 2 / 3 of the patients in both Gamma Knife and radiofrequency groups showed improvements in bradykinesia and rigidity, although when considered as a group neither the Gamma Knife nor the radiofrequency group showed statistically significant improvements in UPDRS scores. One patient in the Gamma Knife group (3. 4%) developed a homonymous hemianopsia 9 months following treatment and 5 patients (27. 7%) in the radiofrequency group became transiently confused postoperatively. No other complications were seen. Gamma Knife pallidotomy is as effective as radiofrequency pallidotomy in controlling certain of the symptoms of Parkinson' s disease. It may be the only practical technique available in certain patients, such as those who take anticoagulants, have bleeding diatheses or serious systemic medical illnesses. It is a viable option for other patients as well.

Parkinson' s disease

bradykinesia

rigidity

dyskinesias

Parkinson' s Disease

dyskinesias

bradykinesia

rigidity

homonymous hemianopsia

Parkinson' s disease

bleeding

L - DOPA

L - DOPA

dyskinesias

L - DOPA

dyskinesias


Input: Neuroleptic malignant syndrome and methylphenidate. A 1 - year - old female presented with neuroleptic malignant syndrome probably caused by methylphenidate. She had defects in the supratentorial brain including the basal ganglia and the striatum (multicystic encephalomalacia) due to severe perinatal hypoxic - ischemic encephalopathy, which was considered to be a possible predisposing factor causing neuroleptic malignant syndrome. A dopaminergic blockade mechanism generally is accepted as the pathogenesis of this syndrome. However, methylphenidate is a dopamine agonist via the inhibition of uptake of dopamine, and therefore dopaminergic systems in the brainstem (mainly the midbrain) and the spinal cord were unlikely to participate in the onset of this syndrome. A relative gamma - aminobutyric acid - ergic deficiency might occur because diazepam, a gamma - aminobutyric acid - mimetic agent, was strikingly effective. This is the first reported patient with neuroleptic malignant syndrome probably caused by methylphenidate.

Neuroleptic malignant syndrome

neuroleptic malignant syndrome

multicystic encephalomalacia

hypoxic - ischemic encephalopathy

neuroleptic malignant syndrome

neuroleptic malignant syndrome

methylphenidate

methylphenidate

methylphenidate

dopamine

dopamine

gamma - aminobutyric acid

diazepam

gamma - aminobutyric acid

methylphenidate

methylphenidate

Neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

Neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

Neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

Neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome

methylphenidate

neuroleptic malignant syndrome


Input: Differential effects of 17alpha - ethinylestradiol on the neutral and acidic pathways of bile salt synthesis in the rat. Effects of 17alpha - ethinylestradiol (EE) on the neutral and acidic biosynthetic pathways of bile salt (BS) synthesis were evaluated in rats with an intact enterohepatic circulation and in rats with long - term bile diversion to induce BS synthesis. For this purpose, bile salt pool composition, synthesis of individual BS in vivo, hepatic activities, and expression levels of cholesterol 7alpha - hydroxylase (CYP7A), and sterol 27 - hydroxylase (CYP27), as well as of other enzymes involved in BS synthesis, were analyzed in rats treated with EE (5 mg / kg, 3 days) or its vehicle. BS pool size was decreased by 27% but total BS synthesis was not affected by EE in intact rats. Synthesis of cholate was reduced by 68% in EE - treated rats, while that of chenodeoxycholate was increased by 60%. The recently identified Delta22 - isomer of beta - muricholate contributed for 5. 4% and 18. 3% (P < 0. 01) to the pool in control and EE - treated rats, respectively, but could not be detected in bile after exhaustion of the pool. A clear reduction of BS synthesis was found in bile - diverted rats treated with EE, yet biliary BS composition was only minimally affected. Activity of CYP7A was decreased by EE in both intact and bile - diverted rats, whereas the activity of the CYP27 was not affected. Hepatic mRNA levels of CYP7A were significantly reduced by EE in bile - diverted rats only; CYP27 mRNA levels were not affected by EE. In addition, mRNA levels of sterol 12alpha - hydroxylase and lithocholate 6beta - hydroxylase were increased by bile diversion and suppressed by EE. This study shows that 17alpha - ethinylestradiol (EE) - induced intrahepatic cholestasis in rats is associated with selective inhibition of the neutral pathway of bile salt (BS) synthesis. Simultaneous impairment of other enzymes in the BS biosynthetic pathways may contribute to overall effects of EE on BS synthesis.

17alpha - ethinylestradiol

bile salt

17alpha - ethinylestradiol

EE

bile salt

BS

BS

bile salt

BS

cholesterol

sterol

BS

EE

BS

BS

EE

cholate

EE

chenodeoxycholate

EE

BS

EE

BS

EE

EE

EE

sterol

EE

17alpha - ethinylestradiol

EE

bile salt

BS

BS

EE

BS

intrahepatic cholestasis

17alpha - ethinylestradiol

intrahepatic cholestasis

17alpha - ethinylestradiol

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis

17alpha - ethinylestradiol

intrahepatic cholestasis

EE

intrahepatic cholestasis

EE

intrahepatic cholestasis


Input: Glibenclamide - sensitive hypotension produced by helodermin assessed in the rat. The effects of helodermin, a basic 35 - amino acid peptide isolated from the venom of a lizard salivary gland, on arterial blood pressure and heart rate were examined in the rat, focusing on the possibility that activation of ATP sensitive K + (K (ATP)) channels is involved in the responses. The results were also compared with those of vasoactive intestinal polypeptide (VIP). Helodermin produced hypotension in a dose - dependent manner with approximately similar potency and duration to VIP. Hypotension induced by both peptides was significantly attenuated by glibenclamide, which abolished a levcromakalim - produced decrease in arterial blood pressure. Oxyhemoglobin did not affect helodermin - induced hypotension, whereas it shortened the duration of acetylcholine (ACh) - produced hypotension. These findings suggest that helodermin - produced hypotension is partly attributable to the activation of glibenclamide - sensitive K + channels (K (ATP) channels), which presumably exist on arterial smooth muscle cells. EDRF (endothelium - derived relaxing factor) / nitric oxide does not seem to play an important role in the peptide - produced hypotension.

Glibenclamide

helodermin

helodermin

amino acid

ATP

K

K

ATP

Helodermin

glibenclamide

levcromakalim

helodermin

acetylcholine

ACh

helodermin

glibenclamide

K

K

ATP

nitric oxide

hypotension

hypotension

Hypotension

hypotension

hypotension

hypotension

hypotension

acetylcholine

hypotension

acetylcholine

hypotension

acetylcholine

Hypotension

acetylcholine

hypotension

acetylcholine

hypotension

acetylcholine

hypotension

acetylcholine

hypotension

ACh

hypotension

ACh

hypotension

ACh

Hypotension

ACh

hypotension

ACh

hypotension

ACh

hypotension

ACh

hypotension

levcromakalim

hypotension

levcromakalim

hypotension

levcromakalim

Hypotension

levcromakalim

hypotension

levcromakalim

hypotension

levcromakalim

hypotension

levcromakalim

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

Hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

Hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

Helodermin

hypotension

Helodermin

hypotension

Helodermin

Hypotension

Helodermin

hypotension

Helodermin

hypotension

Helodermin

hypotension

Helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

Hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

Hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension

helodermin

hypotension


Input: Long - term efficacy and adverse event of nifedipine sustained - release tablets for cyclosporin A - induced hypertension in patients with psoriasis. Thirteen psoriatic patients with hypertension during the course of cyclosporin A therapy were treated for 25 months with a calcium channel blocker, sustained - release nifedipine, to study the clinical antihypertensive effects and adverse events during treatment with both drugs. Seven of the 13 patients had exhibited a subclinical hypertensive state before cyclosporin A therapy. Both systolic and diastolic blood pressures of these 13 patients were decreased significantly after 4 weeks of nifedipine therapy, and blood pressure was maintained within the normal range thereafter for 25 months. The adverse events during combined therapy with cyclosporin A and nifedipine included an increase in blood urea nitrogen levels in 9 of the 13 patients and development of gingival hyperplasia in 2 of the 13 patients. Our findings indicate that sustained - release nifedipine is useful for hypertensive psoriatic patients under long - term treatment with cyclosporin A, but that these patients should be monitored for gingival hyperplasia.

nifedipine

cyclosporin A

cyclosporin A

calcium

nifedipine

cyclosporin A

nifedipine

cyclosporin A

nifedipine

blood urea nitrogen

nifedipine

cyclosporin A

hypertension

psoriasis

psoriatic

hypertension

hypertensive

gingival hyperplasia

hypertensive

psoriatic

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

gingival hyperplasia

cyclosporin A

hypertension

cyclosporin A

hypertension

cyclosporin A

hypertensive

cyclosporin A

hypertensive

cyclosporin A

hypertension

cyclosporin A

hypertension

cyclosporin A

hypertensive

cyclosporin A

hypertensive

cyclosporin A

hypertension

cyclosporin A

hypertension

cyclosporin A

hypertensive

cyclosporin A

hypertensive

cyclosporin A

hypertension

cyclosporin A

hypertension

cyclosporin A

hypertensive

cyclosporin A

hypertensive

cyclosporin A

hypertension

cyclosporin A

hypertension

cyclosporin A

hypertensive

cyclosporin A

hypertensive

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia

nifedipine

gingival hyperplasia


Input: Torsade de pointes ventricular tachycardia during low dose intermittent dobutamine treatment in a patient with dilated cardiomyopathy and congestive heart failure. The authors describe the case of a 56 - year - old woman with chronic, severe heart failure secondary to dilated cardiomyopathy and absence of significant ventricular arrhythmias who developed QT prolongation and torsade de pointes ventricular tachycardia during one cycle of intermittent low dose (2. 5 mcg / kg per min) dobutamine. This report of torsade de pointes ventricular tachycardia during intermittent dobutamine supports the hypothesis that unpredictable fatal arrhythmias may occur even with low doses and in patients with no history of significant rhythm disturbances. The mechanisms of proarrhythmic effects of Dubutamine are discussed.

Torsade de pointes

ventricular tachycardia

dilated cardiomyopathy

congestive heart failure

heart failure

dilated cardiomyopathy

ventricular arrhythmias

QT prolongation

torsade de pointes

ventricular tachycardia

torsade de pointes

ventricular tachycardia

arrhythmias

dobutamine

dobutamine

dobutamine

Dubutamine

dobutamine

Torsade de pointes

dobutamine

torsade de pointes

dobutamine

torsade de pointes

dobutamine

Torsade de pointes

dobutamine

torsade de pointes

dobutamine

torsade de pointes

dobutamine

Torsade de pointes

dobutamine

torsade de pointes

dobutamine

torsade de pointes

Dubutamine

Torsade de pointes

Dubutamine

torsade de pointes

Dubutamine

torsade de pointes


Input: Positive skin tests in late reactions to radiographic contrast media. In the last few years delayed reactions several hours after the injection of radiographic and contrast materials (PRC) have been described with increasing frequency. The authors report two observations on patients with delayed reactions in whom intradermoreactions (IDR) and patch tests to a series of ionic and non ionic PRC were studied. After angiography by the venous route in patient n degree 1 a biphasic reaction with an immediate reaction (dyspnea, loss of consciousness) and delayed macro - papular rash appeared, whilst patient n degree 2 developed a generalised sensation of heat, persistent pain at the site of injection immediately and a generalised macro - papular reaction after 24 hours. The skin tests revealed positive delayed reactions of 24 hours and 48 hours by IDR and patch tests to only some PRC with common chains in their structures. The positive skin tests are in favour of immunological reactions and may help in diagnosis of allergy in the patients.

contrast media

contrast materials

PRC

PRC

PRC

dyspnea

loss of consciousness

macro - papular rash

pain

allergy

contrast media

pain

contrast materials

pain

PRC

pain

PRC

pain

PRC

pain

contrast media

macro - papular rash

contrast materials

macro - papular rash

PRC

macro - papular rash

PRC

macro - papular rash

PRC

macro - papular rash

contrast media

dyspnea

contrast materials

dyspnea

PRC

dyspnea

PRC

dyspnea

PRC

dyspnea

contrast media

loss of consciousness

contrast materials

loss of consciousness

PRC

loss of consciousness

PRC

loss of consciousness

PRC

loss of consciousness


Input: Risk of transient hyperammonemic encephalopathy in cancer patients who received continuous infusion of 5 - fluorouracil with the complication of dehydration and infection. From 1986 to 1998, 29 cancer patients who had 32 episodes of transient hyperammonemic encephalopathy related to continuous infusion of 5 - fluorouracil (5 - FU) were identified. None of the patients had decompensated liver disease. Onset of hyperammonemic encephalopathy varied from 0. 5 to 5 days (mean: 2. 6 + / - 1. 3 days) after the initiation of chemotherapy. Plasma ammonium level ranged from 248 to 2387 microg% (mean: 626 + / - 431 microg%). Among the 32 episodes, 26 (81%) had various degrees of azotemia, 18 (56%) occurred during bacterial infections and 14 (44%) without infection occurred during periods of dehydration. Higher plasma ammonium levels and more rapid onset of hyperammonemia were seen in 18 patients with bacterial infections (p = 0. 003 and 0. 0006, respectively) and in nine patients receiving high daily doses (2600 or 1800 mg / m2) of 5 - FU (p = 0. 0001 and < 0. 0001, respectively). In 25 out of 32 episodes (78%), plasma ammonium levels and mental status returned to normal within 2 days after adequate management. In conclusion, hyperammonemic encephalopathy can occur in patients receiving continuous infusion of 5 - FU. Azotemia, body fluid insufficiency and bacterial infections were frequently found in these patients. It is therefore important to recognize this condition in patients receiving continuous infusion of 5 - FU.

hyperammonemic encephalopathy

hyperammonemic

encephalopathy

cancer

dehydration

infection

cancer

hyperammonemic encephalopathy

hyperammonemic

encephalopathy

liver disease

hyperammonemic encephalopathy

hyperammonemic

encephalopathy

azotemia

bacterial infections

infection

dehydration

hyperammonemia

bacterial infections

hyperammonemic encephalopathy

hyperammonemic

encephalopathy

Azotemia

bacterial infections

5 - fluorouracil

5 - fluorouracil

5 - FU

ammonium

ammonium

5 - FU

ammonium

5 - FU

5 - FU

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemia

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - fluorouracil

hyperammonemia

5 - fluorouracil

hyperammonemic encephalopathy

5 - fluorouracil

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemia

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemia

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemia

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - FU

hyperammonemia

5 - FU

hyperammonemic encephalopathy

5 - FU

hyperammonemic

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - fluorouracil

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy

5 - FU

encephalopathy


Input: The effects of quinine and 4 - aminopyridine on conditioned place preference and changes in motor activity induced by morphine in rats. 1. The effects of two unselective potassium (K (+) -) channel blockers, quinine (12. 5, 25 and 50 mg / kg) and 4 - aminopyridine (1 and 2 mg / kg), on conditioned place preference and biphasic changes in motor activity induced by morphine (10 mg / kg) were tested in Wistar rats. Quinine is known to block voltage -, calcium - and ATP - sensitive K (+) - channels while 4 - aminopyridine is known to block voltage - sensitive K (+) - channels. 2. In the counterbalanced method, quinine attenuated morphine - induced place preference, whereas 4 - aminopyridine was ineffective. In the motor activity test measured with an Animex - activity meter neither of the K (+) - channel blockers affected morphine - induced hypoactivity, but both K (+) - channel blockers prevented morphine - induced secondary hyperactivity. 3. These results suggest the involvement of quinine - sensitive but not 4 - aminopyridine - sensitive K (+) - channels in morphine reward. It is also suggested that the blockade of K (+) - channels sensitive to these blockers is not sufficient to prevent morphine - induced hypoactivity whereas morphine - induced hyperactivity seems to be connected to both quinine - and 4 - aminopyridine - sensitive K (+) - channels.

quinine

4 - aminopyridine

morphine

potassium

K

quinine

4 - aminopyridine

morphine

Quinine

calcium

ATP

K

4 - aminopyridine

K

quinine

morphine

4 - aminopyridine

K

morphine

K

morphine

quinine

4 - aminopyridine

K

morphine

K

morphine

morphine

quinine

4 - aminopyridine

K

hypoactivity

hyperactivity

hypoactivity

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity

morphine

hyperactivity


Input: Nociceptin / orphanin FQ and nocistatin on learning and memory impairment induced by scopolamine in mice. 1. Nociceptin, also known as orphanin FQ, is an endogenous ligand for the orphan opioid receptor - like receptor 1 (ORL1) and involves in various functions in the central nervous system (CNS). On the other hand, nocistatin is recently isolated from the same precursor as nociceptin and blocks nociceptin - induced allodynia and hyperalgesia. 2. Although ORL1 receptors which display a high degree of sequence homology with classical opioid receptors are abundant in the hippocampus, little is known regarding their role in learning and memory. 3. The present study was designed to investigate whether nociceptin / orphanin FQ and nocistatin could modulate impairment of learning and memory induced by scopolamine, a muscarinic cholinergic receptor antagonist, using spontaneous alternation of Y - maze and step - down type passive avoidance tasks in mice. 4. While nocistatin (0. 5 - 5. 0 nmol mouse - 1, i. c. v.) administered 30 min before spontaneous alternation performance or the training session of the passive avoidance task, had no effect on spontaneous alternation or passive avoidance behaviours, a lower per cent alternation and shorter median step - down latency in the retention test were obtained in nociceptin (1. 5 and / or 5. 0 nmol mouse - 1, i. c. v.) - treated normal mice. 5. Administration of nocistatin (1. 5 and / or 5. 0 nmol mouse - 1, i. c. v.) 30 min before spontaneous alternation performance or the training session of the passive avoidance task, attenuated the scopolamine - induced impairment of spontaneous alternation and passive avoidance behaviours. 6. These results indicated that nocistatin, a new biologically active peptide, ameliorates impairments of spontaneous alternation and passive avoidance induced by scopolamine, and suggested that these peptides play opposite roles in learning and memory.

Nociceptin

orphanin FQ

nocistatin

scopolamine

Nociceptin

orphanin FQ

nocistatin

nociceptin

nociceptin

nociceptin

orphanin FQ

nocistatin

scopolamine

nocistatin

nociceptin

nocistatin

scopolamine

nocistatin

scopolamine

learning and memory impairment

learning and memory impairment

memory impairment

allodynia

hyperalgesia

impairment of learning and memory

impairment of learning

impairment of learning and memory

scopolamine

learning and memory impairment

scopolamine

memory impairment

scopolamine

impairment of learning and memory

scopolamine

impairment of learning and memory

scopolamine

learning and memory impairment

scopolamine

memory impairment

scopolamine

impairment of learning and memory

scopolamine

impairment of learning and memory

scopolamine

learning and memory impairment

scopolamine

memory impairment

scopolamine

impairment of learning and memory

scopolamine

impairment of learning and memory

scopolamine

learning and memory impairment

scopolamine

memory impairment

scopolamine

impairment of learning and memory

scopolamine

impairment of learning and memory

scopolamine

learning and memory impairment

scopolamine

impairment of learning

scopolamine

learning and memory impairment

scopolamine

impairment of learning

scopolamine

learning and memory impairment

scopolamine

impairment of learning

scopolamine

learning and memory impairment

scopolamine

impairment of learning


Input: Meloxicam - induced liver toxicity. We report the case of a female patient with rheumatoid arthritis who developed acute cytolytic hepatitis due to meloxicam. Recently introduced in Belgium, meloxicam is the first nonsteroidal antiinflammatory drug with selective action on the inducible form of cyclooxygenase 2. The acute cytolytic hepatitis occurred rapidly after meloxicam administration and was associated with the development of antinuclear antibodies suggesting a hypersensitivity mechanism. This first case of meloxicam related liver toxicity demonstrates the potential of this drug to induce hepatic damage.

Meloxicam

meloxicam

meloxicam

meloxicam

meloxicam

liver toxicity

rheumatoid arthritis

hepatitis

hepatitis

hypersensitivity

liver toxicity

hepatic damage

Meloxicam

hypersensitivity

meloxicam

hypersensitivity

meloxicam

hypersensitivity

meloxicam

hypersensitivity

meloxicam

hypersensitivity

Meloxicam

liver toxicity

Meloxicam

hepatitis

Meloxicam

hepatitis

Meloxicam

liver toxicity

Meloxicam

hepatic damage

meloxicam

liver toxicity

meloxicam

hepatitis

meloxicam

hepatitis

meloxicam

liver toxicity

meloxicam

hepatic damage

meloxicam

liver toxicity

meloxicam

hepatitis

meloxicam

hepatitis

meloxicam

liver toxicity

meloxicam

hepatic damage

meloxicam

liver toxicity

meloxicam

hepatitis

meloxicam

hepatitis

meloxicam

liver toxicity

meloxicam

hepatic damage

meloxicam

liver toxicity

meloxicam

hepatitis

meloxicam

hepatitis

meloxicam

liver toxicity

meloxicam

hepatic damage


Input: Induction of apoptosis by remoxipride metabolites in HL60 and CD34 + / CD19 - human bone marrow progenitor cells: potential relevance to remoxipride - induced aplastic anemia. The antipsychotic agent, remoxipride [(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide] has been associated with acquired aplastic anemia. We have examined the ability of remoxipride, three pyrrolidine ring metabolites and five aromatic ring metabolites of the parent compound to induce apoptosis in HL60 cells and human bone marrow progenitor (HBMP) cells. Cells were treated for 0 - 24 h with each compound (0 - 200 microM). Apoptosis was assessed by fluorescence microscopy in Hoechst 33342 - and propidium iodide stained cell samples. Results were confirmed by determination of internucleosomal DNA fragmentation using gel electrophoresis for HL60 cell samples and terminal deoxynucleotidyl transferase assay in HBMP cells. The catechol and hydroquinone metabolites, NCQ436 and NCQ344, induced apoptosis in HL60 and HBMP cells in a time - and concentration dependent manner, while the phenols, NCR181, FLA873, and FLA797, and the derivatives formed by oxidation of the pyrrolidine ring, FLA838, NCM001, and NCL118, had no effect. No necrosis was observed in cells treated with NCQ436 but NCQ344 had a biphasic effect in both cell types, inducing apoptosis at lower concentrations and necrosis at higher concentrations. These data show that the catechol and hydroquinone metabolites of remoxipride have direct toxic effects in HL60 and HBMP cells, leading to apoptosis, while the phenol metabolites were inactive. Similarly, benzene - derived catechol and hydroquinone, but not phenol, induce apoptosis in HBMP cells [Moran et al., Mol. Pharmacol., 50 (1996) 610 - 615]. We propose that remoxipride and benzene may induce aplastic anemia via production of similar reactive metabolites and that the ability of NCQ436 and NCQ344 to induce apoptosis in HBMP cells may contribute to the mechanism underlying acquired aplastic anemia that has been associated with remoxipride.

remoxipride

remoxipride

remoxipride

(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide

remoxipride

pyrrolidine

Hoechst 33342

propidium iodide

catechol

hydroquinone

phenols

pyrrolidine

catechol

hydroquinone

remoxipride

phenol

benzene

catechol

hydroquinone

phenol

remoxipride

benzene

remoxipride

aplastic anemia

aplastic anemia

necrosis

necrosis

aplastic anemia

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide

aplastic anemia

(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide

aplastic anemia

(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide

aplastic anemia

(S) - (-) - 3 - bromo - N - [(1 - ethyl - 2 - pyrrolidinyl) methyl] - 2, 6 - dimethoxybenz amide

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

remoxipride

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia

benzene

aplastic anemia


Input: Synthesis and preliminary pharmacological investigations of 1 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazine derivatives as potential atypical antipsychotic agents in mice. In research towards the development of new atypical antipsychotic agents, one strategy is that the dopaminergic system can be modulated through manipulation of the serotonergic system. The synthesis and preliminary pharmacological evaluation of a series of potential atypical antipsychotic agents based on the structure of 1 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazine (7) is described. Compound 7e, 5 - {2 - [4 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazinyl] ethyl} - 2, 3 - dihy dro - 1H - indol - 2 - one, from this series showed significant affinities at the 5 - HT1A and 5 - HT2A receptors and moderate affinity at the D2 receptor. 7e exhibits a high reversal of catalepsy induced by haloperidol indicating its atypical antipsychotic nature.

1 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazine

1 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazine

5 - {2 - [4 - (1, 2 - dihydro - 2 - acenaphthylenyl) piperazinyl] ethyl} - 2, 3 - dihy dro - 1H - indol - 2 - one

haloperidol

catalepsy

haloperidol

catalepsy


Input: Sub - chronic inhibition of nitric - oxide synthesis modifies haloperidol - induced catalepsy and the number of NADPH - diaphorase neurons in mice. RATIONALE: NG - nitro - L - arginine (L - NOARG), an inhibitor of nitric - oxide synthase (NOS), induces catalepsy in mice. This effect undergoes rapid tolerance, showing a significant decrease after 2 days of sub - chronic L - NOARG treatment. Nitric oxide (NO) has been shown to influence dopaminergic neurotransmission in the striatum. Neuroleptic drugs such as haloperidol, which block dopamine receptors, also cause catalepsy in rodents. OBJECTIVES: To investigate the effects of subchronic L - NOARG treatment in haloperidol - induced catalepsy and the number of NOS neurons in areas related to motor control. METHODS: Male albino Swiss mice were treated sub - chronically (twice a day for 4 days) with L - NOARG (40 mg / kg i. p.) or haloperidol (1 mg / kg i. p.). Catalepsy was evaluated at the beginning and the end of the treatments. Reduced nicotinamide adenine dinucleotide phosphate - diaphorase (NADPH - d) histochemistry was also employed to visualize NOS as an index of enzyme expression in mice brain regions related to motor control. RESULTS: L - NOARG sub - chronic administration produced tolerance of L - NOARG and of haloperidol - induced catalepsy. It also induced an increase in the number of NADPH - d - positive cells in the dorsal part of the caudate and accumbens nuclei compared with haloperidol and in the pedunculopontine tegmental nucleus compared with saline. In contrast, there was a decrease in NADPH - d neuron number in the substantia nigra, pars compacta in both haloperidol - treated and L - NOARG - treated animals. CONCLUSIONS: The results give further support to the hypothesis that NO plays a role in motor behavior control and suggest that it may take part in the synaptic changes produced by antipsychotic treatment.

nitric - oxide

haloperidol

NADPH

NG - nitro - L - arginine

L - NOARG

nitric - oxide

L - NOARG

Nitric oxide

NO

haloperidol

dopamine

L - NOARG

haloperidol

L - NOARG

haloperidol

nicotinamide adenine dinucleotide phosphate

NADPH

L - NOARG

L - NOARG

haloperidol

NADPH

haloperidol

NADPH

haloperidol

L - NOARG

NO

catalepsy

catalepsy

catalepsy

catalepsy

Catalepsy

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

catalepsy

haloperidol

Catalepsy

haloperidol

catalepsy


Input: Prolonged left ventricular dysfunction occurs in patients with coronary artery disease after both dobutamine and exercise induced myocardial ischaemia. OBJECTIVE: To determine whether pharmacological stress leads to prolonged but reversible left ventricular dysfunction in patients with coronary artery disease, similar to that seen after exercise. DESIGN: A randomised crossover study of recovery time of systolic and diastolic left ventricular function after exercise and dobutamine induced ischaemia. SUBJECTS: 10 patients with stable angina, angiographically proven coronary artery disease, and normal left ventricular function. INTERVENTIONS: Treadmill exercise and dobutamine stress were performed on different days. Quantitative assessment of systolic and diastolic left ventricular function was performed using transthoracic echocardiography at baseline and at regular intervals after each test. RESULTS: Both forms of stress led to prolonged but reversible systolic and diastolic dysfunction. There was no difference in the maximum double product (p = 0. 53) or ST depression (p = 0. 63) with either form of stress. After exercise, ejection fraction was reduced at 15 and 30 minutes compared with baseline (mean (SEM), - 5. 6 (1. 5)%, p < 0. 05; and - 6. 1 (2. 2)%, p < 0. 01), and at 30 and 45 minutes after dobutamine (- 10. 8 (1. 8)% and - 5. 5 (1. 8)%, both p < 0. 01). Regional analysis showed a reduction in the worst affected segment 15 and 30 minutes after exercise (- 27. 9 (7. 2)% and - 28. 6 (5. 7)%, both p < 0. 01), and at 30 minutes after dobutamine (- 32 (5. 3)%, p < 0. 01). The isovolumic relaxation period was prolonged 45 minutes after each form of stress (p < 0. 05). CONCLUSIONS: In patients with coronary artery disease, dobutamine induced ischaemia results in prolonged reversible left ventricular dysfunction, presumed to be myocardial stunning, similar to that seen after exercise. Dobutamine induced ischaemia could therefore be used to study the pathophysiology of this phenomenon further in patients with coronary artery disease.

left ventricular dysfunction

coronary artery disease

myocardial ischaemia

left ventricular dysfunction

coronary artery disease

ischaemia

stable angina

coronary artery disease

depression

coronary artery disease

ischaemia

left ventricular dysfunction

myocardial stunning

ischaemia

coronary artery disease

dobutamine

dobutamine

dobutamine

dobutamine

dobutamine

dobutamine

Dobutamine

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

dobutamine

left ventricular dysfunction

Dobutamine

left ventricular dysfunction

Dobutamine

left ventricular dysfunction

Dobutamine

left ventricular dysfunction

dobutamine

myocardial stunning

dobutamine

myocardial stunning

dobutamine

myocardial stunning

dobutamine

myocardial stunning

dobutamine

myocardial stunning

dobutamine

myocardial stunning

Dobutamine

myocardial stunning


Input: Anorexigens and pulmonary hypertension in the United States: results from the surveillance of North American pulmonary hypertension. BACKGROUND: The use of appetite suppressants in Europe has been associated with the development of primary pulmonary hypertension (PPH). Recently, fenfluramine appetite suppressants became widely used in the United States but were withdrawn in September 1997 because of concerns over adverse effects. MATERIALS AND METHODS: We conducted a prospective surveillance study on patients diagnosed with pulmonary hypertension at 12 large referral centers in North America. Data collected on patients seen from September 1, 1996, to December 31, 1997, included the cause of the pulmonary hypertension and its severity. Patients with no identifiable cause of pulmonary hypertension were classed as PPH. A history of drug exposure also was taken with special attention on the use of antidepressants, anorexigens, and amphetamines. RESULTS: Five hundred seventy - nine patients were studied, 205 with PPH and 374 with pulmonary hypertension from other causes (secondary pulmonary hypertension [SPH]). The use of anorexigens was common in both groups. However, of the medications surveyed, only the fenfluramines had a significant preferential association with PPH as compared with SPH (adjusted odds ratio for use > 6 months, 7. 5; 95% confidence interval, 1. 7 to 32. 4). The association was stronger with longer duration of use when compared to shorter duration of use and was more pronounced in recent users than in remote users. An unexpectedly high (11. 4%) number of patients with SPH had used anorexigens. CONCLUSION: The magnitude of the association with PPH, the increase of association with increasing duration of use, and the specificity for fenfluramines are consistent with previous studies indicating that fenfluramines are causally related to PPH. The high prevalence of anorexigen use in patients with SPH also raises the possibility that these drugs precipitate pulmonary hypertension in patients with underlying conditions associated with SPH.

pulmonary hypertension

pulmonary hypertension

primary pulmonary hypertension

PPH

pulmonary hypertension

pulmonary hypertension

pulmonary hypertension

PPH

PPH

pulmonary hypertension

pulmonary hypertension

PPH

PPH

PPH

pulmonary hypertension

fenfluramine

amphetamines

fenfluramines

fenfluramines

fenfluramines

fenfluramine

pulmonary hypertension

fenfluramine

pulmonary hypertension

fenfluramine

primary pulmonary hypertension

fenfluramine

PPH

fenfluramine

pulmonary hypertension

fenfluramine

pulmonary hypertension

fenfluramine

pulmonary hypertension

fenfluramine

PPH

fenfluramine

PPH

fenfluramine

pulmonary hypertension

fenfluramine

pulmonary hypertension

fenfluramine

PPH

fenfluramine

PPH

fenfluramine

PPH

fenfluramine

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

primary pulmonary hypertension

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

primary pulmonary hypertension

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

primary pulmonary hypertension

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension

fenfluramines

pulmonary hypertension

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

PPH

fenfluramines

pulmonary hypertension


Input: Clinical aspects of heparin - induced thrombocytopenia and thrombosis and other side effects of heparin therapy. Heparin, first used to prevent the clotting of blood in vitro, has been clinically used to treat thrombosis for more than 50 years. Although several new anticoagulant drugs are in development, heparin remains the anticoagulant of choice to treat acute thrombotic episodes. The clinical effects of heparin are meritorious, but side effects do exist. Bleeding is the primary untoward effect of heparin. Major bleeding is of primary concern in patients receiving heparin therapy. However, additional important untoward effects of heparin therapy include heparin - induced thrombocytopenia, heparin - associated osteoporosis, eosinophilia, skin reactions, allergic reactions other than thrombocytopenia, alopecia, transaminasemia, hyperkalemia, hypoaldosteronism, and priapism. These side effects are relatively rare in a given individual, but given the extremely widespread use of heparin, some are quite common, particularly HITT and osteoporosis. Although reasonable incidences of many of these side effects can be " softly " deduced from current reports dealing with unfractionated heparin, at present the incidences of these side effects with newer low molecular weight heparins appear to be much less common. However, only longer experience will more clearly define the incidence of each side effect with low molecular weight preparations.

heparin

heparin

Heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparin

heparins

thrombocytopenia

thrombosis

thrombosis

thrombotic

Bleeding

bleeding

thrombocytopenia

osteoporosis

eosinophilia

skin reactions

allergic reactions

thrombocytopenia

alopecia

hyperkalemia

hypoaldosteronism

priapism

HITT

osteoporosis

heparin

skin reactions

heparin

skin reactions

Heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparin

skin reactions

heparins

skin reactions

heparin

allergic reactions

heparin

allergic reactions

Heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparin

allergic reactions

heparins

allergic reactions

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

thrombocytopenia

Heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

thrombocytopenia

heparin

HITT

heparins

thrombocytopenia

heparins

thrombocytopenia

heparins

thrombocytopenia

heparins

HITT

heparin

hyperkalemia

heparin

hyperkalemia

Heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparin

hyperkalemia

heparins

hyperkalemia

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

Heparin

osteoporosis

Heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparin

osteoporosis

heparins

osteoporosis

heparins

osteoporosis

heparin

priapism

heparin

priapism

Heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparin

priapism

heparins

priapism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

Heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparin

hypoaldosteronism

heparins

hypoaldosteronism

heparin

eosinophilia

heparin

eosinophilia

Heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparin

eosinophilia

heparins

eosinophilia

heparin

alopecia

heparin

alopecia

Heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparin

alopecia

heparins

alopecia


Input: A case of bilateral optic neuropathy in a patient on tacrolimus (FK506) therapy after liver transplantation. PURPOSE: To report a case of bilateral optic neuropathy in a patient receiving tacrolimus (FK 506, Prograf; Fujisawa USA, Inc, Deerfield, Illinois) for immunosuppression after orthotropic liver transplantation. METHOD: Case report. In a 58 - year - old man receiving tacrolimus after orthotropic liver transplantation, serial neuro - ophthalmologic examinations and laboratory studies were performed. RESULTS: The patient had episodic deterioration of vision in both eyes, with clinical features resembling ischemic optic neuropathies. Deterioration of vision occurred despite discontinuation of the tacrolimus. CONCLUSION: Tacrolimus and other immunosuppressive agents may be associated with optic nerve toxicity.

optic neuropathy

optic neuropathy

ischemic optic neuropathies

Deterioration of vision

optic nerve toxicity

tacrolimus

tacrolimus

FK 506

tacrolimus

tacrolimus

Tacrolimus

tacrolimus

optic neuropathy

tacrolimus

optic neuropathy

tacrolimus

optic nerve toxicity

optic neuropathy

optic neuropathy

optic nerve toxicity

tacrolimus

optic neuropathy

tacrolimus

optic neuropathy

tacrolimus

optic nerve toxicity

FK 506

optic neuropathy

FK 506

optic neuropathy

FK 506

optic nerve toxicity

tacrolimus

optic neuropathy

tacrolimus

optic neuropathy

tacrolimus

optic nerve toxicity

tacrolimus

optic neuropathy

tacrolimus

optic neuropathy

tacrolimus

optic nerve toxicity

Tacrolimus

optic neuropathy

Tacrolimus

optic neuropathy

Tacrolimus

optic nerve toxicity