Input: Granulosa cell tumor of the ovary associated with antecedent tamoxifen use. BACKGROUND: Increased attention has been focused recently on the estrogenic effects of tamoxifen. Review of the literature reveals an association between tamoxifen use and gynecologic tumors. CASE: A 52 - year - old postmenopausal woman was treated with tamoxifen for stage II estrogen receptor - positive breast carcinoma. Her aspartate transaminase and alanine transaminase levels increase markedly after 6 months of tamoxifen use. After an additional 17 months of elevated serum transaminases, the patient was found to have a stage Ic granulosa cell tumor of the ovary. CONCLUSION: Patients with tamoxifen - induced liver dysfunction may be at increased risk for granulosa cell tumors because of alterations in tamoxifen metabolism.

Granulosa cell tumor of the ovary

tumors

breast carcinoma

granulosa cell tumor of the ovary

liver dysfunction

granulosa cell tumors

tamoxifen

tamoxifen

tamoxifen

tamoxifen

estrogen

aspartate

alanine

tamoxifen

tamoxifen

tamoxifen

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

liver dysfunction

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary

tamoxifen

Granulosa cell tumor of the ovary

tamoxifen

granulosa cell tumor of the ovary


Input: A murine model of adenomyosis: the effects of hyperprolactinemia induced by fluoxetine hydrochloride, a selective serotonin reuptake inhibitor, on adenomyosis induction in Wistar albino rats. OBJECTIVE: The aim of this study was to investigate whether fluoxetine given to castrated and noncastrated rats caused hyperprolactinemia and its effects with respect to adenomyosis. DESIGN: Fluoxetine, a serotonin reuptake inhibitor, was given to Wistar Albino rats for 98 days to produce hyperprolactinemia. The drug was given to two groups consisting of castrated and noncastrated rats and compared to two groups of castrated and noncastrated controls. Prolactin levels were measured and the uteri of the rats were removed for histopathological analysis at the end of 98 days. SETTING: Marmara University School of Medicine, Department of Histology and Embryology, Zeynep Kamil Women and Children' s Hospital. MAIN OUTCOME MEASURES: Serum prolactin levels, uterine histopathology. RESULTS: The prolactin levels of castrated and noncastrated groups treated with fluoxetine were statistically significantly higher when compared to their respective control groups. Histological studies revealed 11 cases of adenomyosis, all within the noncastrated group receiving fluoxetine. CONCLUSION: It was suggested that high serum prolactin levels cause degeneration of myometrial cells in the presence of ovarian steroids that results in a myometrial invasion by endometrial stroma. This invasion eventually progresses to adenomyosis.

adenomyosis

hyperprolactinemia

adenomyosis

hyperprolactinemia

adenomyosis

hyperprolactinemia

adenomyosis

adenomyosis

fluoxetine hydrochloride

serotonin

fluoxetine

Fluoxetine

serotonin

fluoxetine

fluoxetine

steroids

fluoxetine hydrochloride

hyperprolactinemia

fluoxetine hydrochloride

hyperprolactinemia

fluoxetine hydrochloride

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

Fluoxetine

hyperprolactinemia

Fluoxetine

hyperprolactinemia

Fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine

hyperprolactinemia

fluoxetine hydrochloride

adenomyosis

fluoxetine hydrochloride

adenomyosis

fluoxetine hydrochloride

adenomyosis

fluoxetine hydrochloride

adenomyosis

fluoxetine hydrochloride

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

Fluoxetine

adenomyosis

Fluoxetine

adenomyosis

Fluoxetine

adenomyosis

Fluoxetine

adenomyosis

Fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis

fluoxetine

adenomyosis


Input: Effects of deliberate hypotension induced by labetalol with isoflurane on neuropsychological function. The effect of deliberate hypotension on brain function measured by neuropsychological tests was studied in 41 adult patients. Twenty - four patients were anaesthetized for middle - ear surgery with deliberate hypotension induced by labetalol with isoflurane (hypotensive group). Seventeen patients without hypotension served as a control group. The mean arterial pressure was 77 + / - 2 mmHg (10. 3 + / - 0. 3 kPa) before hypotension and 50 + / - 0 mmHg (6. 7 + / - 0. 0 kPa) during hypotension in the hypotensive group, and 86 + / - 2 mmHg (11. 5 + / - 0. 3 kPa) during anaesthesia in the control group. The following psychological tests were performed: four subtests of the Wechsler Adult Intelligence Scale (similarities, digit span, vocabulary and digit symbol), Trail - Making tests A and B, Zung tests (self - rating anxiety scale and self - rating depression scale) and two - part memory test battery with immediate and delayed recall. The tests were performed preoperatively and 2 days postoperatively. There were no statistically significant differences between the groups in any of the tests in the changes from preoperative value to postoperative value. The results indicate that hypotension induced by labetalol with isoflurane has no significant harmful effects on mental functions compared to normotensive anaesthesia.

hypotension

hypotension

hypotension

hypotensive

hypotension

hypotension

hypotension

hypotensive

anxiety

depression

hypotension

labetalol

isoflurane

labetalol

isoflurane

labetalol

isoflurane

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

labetalol

hypotension

labetalol

hypotension

labetalol

hypotensive

labetalol

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotensive

isoflurane

hypotension


Input: Auditory disturbance associated with interscalene brachial plexus block. We performed an audiometric study in 20 patients who underwent surgery of the shoulder region under an interscalene brachial plexus block (IBPB). Bupivacaine 0. 75% with adrenaline was given followed by a 24 - hr continuous infusion of 0. 25% bupivacaine. Three audiometric threshold measurements (0. 25 - 18 kHz) were made: the first before IBPB, the second 2 - 6 h after surgery and the third on the first day after operation. In four patients hearing impairment on the side of the block was demonstrated after operation, in three measurements on the day of surgery and in one on the following day. The frequencies at which the impairment occurred varied between patients; in one only low frequencies (0. 25 - 0. 5 kHz) were involved. The maximum change in threshold was 35 dB at 6 kHz measured at the end of the continuous infusion of bupivacaine. This patient had hearing threshold changes (15 - 20 dB) at 6 - 10 kHz on the opposite side also. IBPB may cause transient auditory dysfunction in the ipsilateral ear, possibly via an effect on sympathetic innervation.

Bupivacaine

adrenaline

bupivacaine

bupivacaine

hearing impairment

auditory dysfunction

Bupivacaine

hearing impairment

bupivacaine

hearing impairment

bupivacaine

hearing impairment

adrenaline

hearing impairment


Input: Midazolam compared with thiopentone as an induction agent. In patients premedicated with scopolamine + morphine (+ 5 mg nitrazepam the evening before surgery), the sleep - inducing effect of midazolam 0. 15 mg / kg i. v. was clearly slower in onset than that of thiopentone 4. 67 mg / kg i. v. Somewhat fewer cardiovascular and local sequelae were found in the midazolam group, but, although apnoea occurred less often in the midazolam group it lasted longer. On the whole, the differences between midazolam and thiopentone had no apparent clinical consequences. Midazolam is a new alternative agent for induction in combination anaesthesia.

Midazolam

thiopentone

scopolamine

morphine

nitrazepam

midazolam

thiopentone

midazolam

midazolam

midazolam

thiopentone

Midazolam

apnoea

Midazolam

apnoea

midazolam

apnoea

midazolam

apnoea

midazolam

apnoea

midazolam

apnoea

Midazolam

apnoea

thiopentone

apnoea

thiopentone

apnoea

thiopentone

apnoea


Input: Cardiotoxic and possible leukemogenic effects of adriamycin in nonhuman primates. 10 monkeys (macaques) received adriamycin by monthly intravenous injections at 12 mg / m2 (1 mg / kg). 8 of the 10 monkeys developed congestive heart failure at an average cumulative adriamycin dose (310 mg / m2) well below that considered the safe upper limit (550 mg / m2) in man. Histologically, the myocardial lesions resembled those found in human anthracycline - induced cardiomyopathy. 1 of the 10 monkeys developed acute myeloblastic leukemia after receiving 324 mg / m2 of adriamycin; the 10th monkey is alive and well 26 months after the last dose of drug. Our results suggest that adriamycin is a more potent cardiotoxin in monkeys than in man, and that leukemia may be a consequence of prolonged treatment with this drug.

Cardiotoxic

congestive heart failure

myocardial lesions

cardiomyopathy

acute myeloblastic leukemia

leukemia

adriamycin

adriamycin

adriamycin

anthracycline

adriamycin

adriamycin

adriamycin

congestive heart failure

adriamycin

congestive heart failure

adriamycin

congestive heart failure

adriamycin

congestive heart failure

adriamycin

congestive heart failure

adriamycin

acute myeloblastic leukemia

adriamycin

acute myeloblastic leukemia

adriamycin

acute myeloblastic leukemia

adriamycin

acute myeloblastic leukemia

adriamycin

acute myeloblastic leukemia


Input: Doxorubicin cardiomyopathy in children with left - sided Wilms tumor. Two children with Wilms tumor of the left kidney experienced severe anthracycline cardiomyopathy after irradiation to the tumor bed and conventional dosage of doxorubicin. The cardiomyopathy is attributed 1) to the fact that radiation fields for left Wilms tumor include the lower portion of the heart and 2) to the interaction of doxorubicin and irradiation on cardiac muscle. It is recommended that doxorubicin dosage be sharply restricted in children with Wilms tumor of the left kidney who receive postoperative irradiation.

Doxorubicin

anthracycline

doxorubicin

doxorubicin

doxorubicin

cardiomyopathy

Wilms tumor

Wilms tumor

cardiomyopathy

tumor

cardiomyopathy

Wilms tumor

Wilms tumor

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy


Input: Promotional effects of testosterone and dietary fat on prostate carcinogenesis in genetically susceptible rats. Germfree (GF) Lobund strain Wistar (LW) rats, fed vegetable diet L - 485, have developed prostate adenocarcinomas spontaneously (10% incidence) at average age 34 months. Conventional LW rats, implanted with testosterone at age 4 months, developed a higher incidence of prostate cancer after an average interval of 14 months: 24% had developed gross tumors, and 40% when it included microscopic tumors. Preliminary results indicate that testosterone - treated LW rats that were fed the same diet, which was supplemented with corn oil up to 20% fat, developed prostate cancer after intervals of 6 - 12 months. Aged GF Sprague - Dawley (SD) rats have not developed prostate cancer spontaneously. Conventional SD rats fed diet L - 485 and treated with testosterone developed only prostatitis. Experimental designs should consider genetic susceptibility as a basic prerequisite for studies on experimental prostate cancer.

testosterone

testosterone

testosterone

testosterone

carcinogenesis

prostate adenocarcinomas

prostate cancer

tumors

tumors

prostate cancer

prostate cancer

prostatitis

prostate cancer

testosterone

prostate adenocarcinomas

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate adenocarcinomas

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate adenocarcinomas

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate adenocarcinomas

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostate cancer

testosterone

prostatitis

testosterone

prostatitis

testosterone

prostatitis

testosterone

prostatitis


Input: Mitomycin C associated hemolytic uremic syndrome. Mitomycin C associated Hemolytic Uremic Syndrome (HUS) is a potentially fatal but uncommon condition that is not yet widely recognised. It consists of microangiopathic hemolytic anemia, thrombocytopenia and progressive renal failure associated with mitomycin C treatment and affects about 10% of patients treated with this agent. The renal failure usually develops about 8 - 10 mth after start of mitomycin C treatment and the mortality is approximately 60% from renal failure or pulmonary edema. Renal lesions are similar to those seen in idiopathic HUS and include arteriolar fibrin thrombi, expanded subendothelial zones in glomerular capillary walls, ischemic wrinkling of glomerular basement membranes and mesangiolysis. The mechanism of action is postulated as mitomycin C - induced endothelial cell damage. We describe the clinical course and pathological findings in a 65 yr - old man with gastric adenocarcinoma who developed renal failure and thrombocytopenia while on treatment with mitomycin C and died in pulmonary edema.

Mitomycin C

Mitomycin C

mitomycin C

mitomycin C

mitomycin C

mitomycin C

hemolytic uremic syndrome

Hemolytic Uremic Syndrome

HUS

hemolytic anemia

thrombocytopenia

renal failure

renal failure

renal failure

pulmonary edema

Renal lesions

HUS

thrombi

ischemic

gastric adenocarcinoma

renal failure

thrombocytopenia

pulmonary edema

Mitomycin C

renal failure

Mitomycin C

renal failure

Mitomycin C

renal failure

Mitomycin C

Renal lesions

Mitomycin C

renal failure

Mitomycin C

renal failure

Mitomycin C

renal failure

Mitomycin C

renal failure

Mitomycin C

Renal lesions

Mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

Renal lesions

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

Renal lesions

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

Renal lesions

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

renal failure

mitomycin C

Renal lesions

mitomycin C

renal failure

Mitomycin C

hemolytic uremic syndrome

Mitomycin C

Hemolytic Uremic Syndrome

Mitomycin C

HUS

Mitomycin C

HUS

Mitomycin C

hemolytic uremic syndrome

Mitomycin C

Hemolytic Uremic Syndrome

Mitomycin C

HUS

Mitomycin C

HUS

mitomycin C

hemolytic uremic syndrome

mitomycin C

Hemolytic Uremic Syndrome

mitomycin C

HUS

mitomycin C

HUS

mitomycin C

hemolytic uremic syndrome

mitomycin C

Hemolytic Uremic Syndrome

mitomycin C

HUS

mitomycin C

HUS

mitomycin C

hemolytic uremic syndrome

mitomycin C

Hemolytic Uremic Syndrome

mitomycin C

HUS

mitomycin C

HUS

mitomycin C

hemolytic uremic syndrome

mitomycin C

Hemolytic Uremic Syndrome

mitomycin C

HUS

mitomycin C

HUS


Input: Continuous ambulatory ECG monitoring during fluorouracil therapy: a prospective study. Although there have been anecdotal reports of cardiac toxicity associated with fluorouracil (5 - FU) therapy, this phenomenon has not been studied in a systematic fashion. We prospectively performed continuous ambulatory ECG monitoring on 25 patients undergoing 5 - FU infusion for treatment of solid tumors in order to assess the incidence of ischemic ST changes. Patients were monitored for 23 + / - 4 hours before 5 - FU infusion, and 98 + / - 9 hours during 5 - FU infusion. Anginal episodes were rare: only one patient had angina (during 5 - FU infusion). However, asymptomatic ST changes (greater than or equal to 1 mm ST deviation) were common: six of 25 patients (24%) had ST changes before 5 - FU infusion v 17 (68%) during 5 - FU infusion (P less than. 002). The incidence of ischemic episodes per patient per hour was 0. 05 + / - 0. 02 prior to 5 - FU infusion v 0. 13 + / - 0. 03 during 5 - FU infusion (P less than. 001); the duration of ECG changes was 0. 6 + / - 0. 3 minutes per patient per hour before 5 - FU v 1. 9 + / - 0. 5 minutes per patient per hour during 5 - FU (P less than. 01). ECG changes were more common among patients with known coronary artery disease. There were two cases of sudden death, both of which occurred at the end of the chemotherapy course. We conclude that 5 - FU infusion is associated with a significant increase in silent ST segment deviation suggestive of ischemia, particularly among patients with coronary artery disease. The mechanism and clinical significance of these ECG changes remain to be determined.

fluorouracil

fluorouracil

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

5 - FU

cardiac toxicity

tumors

ischemic

Anginal

angina

ischemic

coronary artery disease

sudden death

ischemia

coronary artery disease

fluorouracil

Anginal

fluorouracil

angina

fluorouracil

Anginal

fluorouracil

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

5 - FU

Anginal

5 - FU

angina

fluorouracil

ischemic

fluorouracil

ischemic

fluorouracil

ischemia

fluorouracil

ischemic

fluorouracil

ischemic

fluorouracil

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia

5 - FU

ischemic

5 - FU

ischemic

5 - FU

ischemia


Input: Lethal anuria complicating high dose ifosfamide chemotherapy in a breast cancer patient with an impaired renal function. A sixty - year - old woman with advanced breast cancer, previously treated with cisplatin, developed an irreversible lethal renal failure with anuria, the day after 5 g / m2 bolus ifosfamide. Postrenal failure was excluded by echography. A prerenal component could have contributed to renal failure because of a transient hypotension, due to an increasing ascitis, occurring just before anuria. However, correction of the hemodynamic parameters did not improve renal function. Ifosfamide is a known nephrotoxic drug with demonstrated tubulopathies. We strongly suspect that this lethal anuria was mainly due to ifosfamide, occurring in a patient having received previous cisplatin chemotherapy and with poor kidney perfusion due to transient hypotension. We recommend careful use of ifosfamide in patients pretreated with nephrotoxic chemotherapy and inadequate renal perfusion.

anuria

breast cancer

impaired renal function

breast cancer

renal failure

anuria

Postrenal failure

renal failure

hypotension

anuria

nephrotoxic

tubulopathies

anuria

hypotension

nephrotoxic

ifosfamide

cisplatin

ifosfamide

Ifosfamide

ifosfamide

cisplatin

ifosfamide

ifosfamide

impaired renal function

ifosfamide

Postrenal failure

ifosfamide

nephrotoxic

ifosfamide

tubulopathies

ifosfamide

nephrotoxic

ifosfamide

impaired renal function

ifosfamide

Postrenal failure

ifosfamide

nephrotoxic

ifosfamide

tubulopathies

ifosfamide

nephrotoxic

Ifosfamide

impaired renal function

Ifosfamide

Postrenal failure

Ifosfamide

nephrotoxic

Ifosfamide

tubulopathies

Ifosfamide

nephrotoxic

ifosfamide

impaired renal function

ifosfamide

Postrenal failure

ifosfamide

nephrotoxic

ifosfamide

tubulopathies

ifosfamide

nephrotoxic

ifosfamide

impaired renal function

ifosfamide

Postrenal failure

ifosfamide

nephrotoxic

ifosfamide

tubulopathies

ifosfamide

nephrotoxic

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

Ifosfamide

anuria

Ifosfamide

anuria

Ifosfamide

anuria

Ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria

ifosfamide

anuria


Input: Central vein thrombosis and topical dipivalyl epinephrine. A report is given on an 83 - year - old female who acquired central vein thrombosis in her seeing eye one day after having started topical medication with dipivalyl epinephrine for advanced glaucoma discovered in the other eye. From present knowledge about the effects of adrenergic eye drops on ocular blood circulation, it is difficult to suggest an association between the two events, which may be coincidental only.

vein thrombosis

vein thrombosis

glaucoma

dipivalyl epinephrine

dipivalyl epinephrine

dipivalyl epinephrine

vein thrombosis

dipivalyl epinephrine

vein thrombosis

dipivalyl epinephrine

vein thrombosis

dipivalyl epinephrine

vein thrombosis


Input: Amelioration of bendrofluazide - induced hypokalemia by timolol. The beta adrenergic blocking drug, timolol, tended to correct the hypokalemia of short - term bendrofluazide treatment in 6 healthy male subjects and although the effect was small it was significant. Timolol also reduced the rise in plasma aldosterone and urine potassium excretion following bendrofluazide and increased the urine sodium / potassium ratio. There was no evidence of a shift of potassium from the intracellular to the extracellular space.

bendrofluazide

timolol

timolol

bendrofluazide

Timolol

aldosterone

potassium

bendrofluazide

sodium

potassium

potassium

hypokalemia

hypokalemia

bendrofluazide

hypokalemia

bendrofluazide

hypokalemia

bendrofluazide

hypokalemia

bendrofluazide

hypokalemia

bendrofluazide

hypokalemia

bendrofluazide

hypokalemia


Input: A cross - sectional evaluation of the effect of risperidone and selective serotonin reuptake inhibitors on bone mineral density in boys. OBJECTIVE: The aim of the present study was to investigate the effect of risperidone - induced hyperprolactinemia on trabecular bone mineral density (BMD) in children and adolescents. METHOD: Medically healthy 7 - to 17 - year - old males chronically treated, in a naturalistic setting, with risperidone were recruited for this cross - sectional study through child psychiatry outpatient clinics between November 2005 and June 2007. Anthropometric measurements and laboratory testing were conducted. The clinical diagnoses were based on chart review, and developmental and treatment history was obtained from the medical record. Volumetric BMD of the ultradistal radius was measured using peripheral quantitative computed tomography, and areal BMD of the lumbar spine was estimated using dual - energy x - ray absorptiometry. RESULTS: Hyperprolactinemia was present in 49% of 83 boys (n = 41) treated with risperidone for a mean of 2. 9 years. Serum testosterone concentration increased with pubertal status but was not affected by hyperprolactinemia. As expected, bone mineral content and BMD increased with sexual maturity. After adjusting for the stage of sexual development and height and BMI z scores, serum prolactin was negatively associated with trabecular volumetric BMD at the ultradistal radius (P <. 03). Controlling for relevant covariates, we also found treatment with selective serotonin reuptake inhibitors (SSRIs) to be associated with lower trabecular BMD at the radius (P =. 03) and BMD z score at the lumbar spine (P <. 05). These findings became more marked when the analysis was restricted to non - Hispanic white patients. Of 13 documented fractures, 3 occurred after risperidone and SSRIs were started, and none occurred in patients with hyperprolactinemia. CONCLUSIONS: This is the first study to link risperidone - induced hyperprolactinemia and SSRI treatment to lower BMD in children and adolescents. Future research should evaluate the longitudinal course of this adverse event to determine its temporal stability and whether a higher fracture rate ensues.

risperidone

serotonin

risperidone

risperidone

risperidone

testosterone

serotonin

risperidone

risperidone

hyperprolactinemia

Hyperprolactinemia

hyperprolactinemia

fractures

hyperprolactinemia

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

Hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia

risperidone

hyperprolactinemia


Input: Seizures associated with levofloxacin: case presentation and literature review. PURPOSE: We present a case of a patient who developed seizures shortly after initiating treatment with levofloxacin and to discuss the potential drug - drug interactions related to the inhibition of cytochrome P450 (CYP) 1A2 in this case, as well as in other cases, of levofloxacin - induced seizures. METHODS: Several biomedical databases were searched including MEDLINE, Cochrane and Ovid. The main search terms utilized were case report and levofloxacin. The search was limited to studies published in English. RESULTS: Six cases of levofloxacin - induced seizures have been reported in the literature. Drug - drug interactions related to the inhibition of CYP1A2 by levofloxacin are likely involved in the clinical outcome of these cases. CONCLUSIONS: Clinicians are exhorted to pay close attention when initiating levofloxacin therapy in patients taking medications with epileptogenic properties that are CYP1A2 substrates.

Seizures

seizures

seizures

seizures

levofloxacin

levofloxacin

levofloxacin

levofloxacin

levofloxacin

levofloxacin

levofloxacin

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

Seizures

levofloxacin

seizures

levofloxacin

seizures

levofloxacin

seizures


Input: Mice lacking mPGES - 1 are resistant to lithium - induced polyuria. Cyclooxygenase - 2 activity is required for the development of lithium - induced polyuria. However, the involvement of a specific, terminal prostaglandin (PG) isomerase has not been evaluated. The present study was undertaken to assess lithium - induced polyuria in mice deficient in microsomal prostaglandin E synthase - 1 (mPGES - 1). A 2 - wk administration of LiCl (4 mmol. kg (- 1). day (- 1) ip) in mPGES - 1 + / + mice led to a marked polyuria with hyposmotic urine. This was associated with elevated renal mPGES - 1 protein expression and increased urine PGE (2) excretion. In contrast, mPGES - 1 - / - mice were largely resistant to lithium - induced polyuria and a urine concentrating defect, accompanied by nearly complete blockade of high urine PGE (2) and cAMP output. Immunoblotting, immunohistochemistry, and quantitative (q) RT - PCR consistently detected a significant decrease in aquaporin - 2 (AQP2) protein expression in both the renal cortex and medulla of lithium - treated + / + mice. This decrease was significantly attenuated in the - / - mice. qRT - PCR detected similar patterns of changes in AQP2 mRNA in the medulla but not in the cortex. Similarly, the total protein abundance of the Na - K - 2Cl cotransporter (NKCC2) in the medulla but not in the cortex of the + / + mice was significantly reduced by lithium treatment. In contrast, the dowregulation of renal medullary NKCC2 expression was significantly attenuated in the - / - mice. We conclude that mPGES - 1 - derived PGE (2) mediates lithium - induced polyuria likely via inhibition of AQP2 and NKCC2 expression.

lithium

lithium

prostaglandin

PG

lithium

prostaglandin E

LiCl

PGE (2)

lithium

PGE (2)

lithium

K

lithium

PGE (2)

lithium

polyuria

polyuria

polyuria

polyuria

polyuria

polyuria

LiCl

polyuria

LiCl

polyuria

LiCl

polyuria

LiCl

polyuria

LiCl

polyuria

LiCl

polyuria


Input: Identification of a simple and sensitive microplate method for the detection of oversulfated chondroitin sulfate in heparin products. Heparin is a commonly implemented anticoagulant used to treat critically ill patients. Recently, a number of commercial lots of heparin products were found to be contaminated with an oversulfated chondroitin sulfate (OSCS) derivative that could elicit a hypotensive response in pigs following a single high - dose infusion. Using both contaminated heparin products and the synthetically produced derivative, we showed that the OSCS produces dose - dependent hypotension in pigs. The no observed effect level (NOEL) for this contaminant appears to be approximately 1mg / kg, corresponding to a contamination level of approximately 3%. We also demonstrated that OSCS can be identified in heparin products using a simple, inexpensive, commercially available heparin enzyme immunoassay (EIA) kit that has a limit of detection of approximately 0. 1%, well below the NOEL. This kit may provide a useful method to test heparin products for contamination with oversulfated GAG derivatives.

chondroitin sulfate

heparin

Heparin

heparin

chondroitin sulfate

heparin

heparin

heparin

heparin

hypotensive

hypotension

chondroitin sulfate

hypotensive

chondroitin sulfate

hypotension

chondroitin sulfate

hypotensive

chondroitin sulfate

hypotension


Input: Doxorubicin cardiomyopathy - induced inflammation and apoptosis are attenuated by gene deletion of the kinin B1 receptor. Clinical use of the anthracycline doxorubicin (DOX) is limited by its cardiotoxic effects, which are attributed to the induction of apoptosis. To elucidate the possible role of the kinin B1 receptor (B1R) during the development of DOX cardiomyopathy, we studied B1R knockout mice (B1R (- / -)) by investigating cardiac inflammation and apoptosis after induction of DOX - induced cardiomyopathy. DOX control mice showed cardiac dysfunction measured by pressure - volume loops in vivo. This was associated with a reduced activation state of AKT, as well as an increased bax / bcl2 ratio in Western blots, indicating cardiac apoptosis. Furthermore, mRNA levels of the proinflammatory cytokine interleukin 6 were increased in the cardiac tissue. In DOX B1R (- / -) mice, cardiac dysfunction was improved compared to DOX control mice, which was associated with normalization of the bax / bcl - 2 ratio and interleukin 6, as well as AKT activation state. These findings suggest that B1R is detrimental in DOX cardiomyopathy in that it mediates the inflammatory response and apoptosis. These insights might have useful implications for future studies utilizing B1R antagonists for treatment of human DOX cardiomyopathy.

Doxorubicin

anthracycline

doxorubicin

DOX

DOX

DOX

DOX

DOX

DOX

DOX

DOX

cardiomyopathy

inflammation

cardiotoxic

cardiomyopathy

inflammation

cardiomyopathy

cardiac dysfunction

cardiac apoptosis

cardiac dysfunction

cardiomyopathy

cardiomyopathy

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

Doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

doxorubicin

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy

DOX

cardiomyopathy


Input: Hepatotoxicity associated with sulfasalazine in inflammatory arthritis: A case series from a local surveillance of serious adverse events. BACKGROUND: Spontaneous reporting systems for adverse drug reactions (ADRs) are handicapped by under - reporting and limited detail on individual cases. We report an investigation from a local surveillance for serious adverse drug reactions associated with disease modifying anti - rheumatic drugs that was triggered by the occurrence of liver failure in two of our patients. METHODS: Serious ADR reports have been solicited from local clinicians by regular postcards over the past seven years. Patients', who had hepatotoxicity on sulfasalazine and met a definition of a serious ADR, were identified. Two clinicians reviewed structured case reports and assessed causality by consensus and by using a causality assessment instrument. The likely frequency of hepatotoxicity with sulfasalazine was estimated by making a series of conservative assumptions. RESULTS: Ten cases were identified: eight occurred during surveillance. Eight patients were hospitalised, two in hepatic failure - one died after a liver transplant. All but one event occurred within 6 weeks of treatment. Seven patients had a skin rash, three eosinophilia and one interstitial nephritis. Five patients were of Black British of African or Caribbean descent. Liver enzymes showed a hepatocellular pattern in four cases and a mixed pattern in six. Drug - related hepatotoxicity was judged probable or highly probable in 8 patients. The likely frequency of serious hepatotoxicity with sulfasalazine was estimated at 0. 4% of treated patients. CONCLUSION: Serious hepatotoxicity associated with sulfasalazine appears to be under - appreciated and intensive monitoring and vigilance in the first 6 weeks of treatment is especially important.

Hepatotoxicity

arthritis

liver failure

hepatotoxicity

hepatotoxicity

hepatic failure

skin rash

eosinophilia

interstitial nephritis

hepatotoxicity

hepatotoxicity

hepatotoxicity

sulfasalazine

sulfasalazine

sulfasalazine

sulfasalazine

sulfasalazine

sulfasalazine

Hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

Hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

Hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

Hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

Hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity

sulfasalazine

hepatotoxicity


Input: An evaluation of amikacin nephrotoxicity in the hematology / oncology population. Amikacin is an aminoglycoside commonly used to provide empirical double gram - negative treatment for febrile neutropenia and other suspected infections. Strategies of extended - interval and conventional dosing have been utilized extensively in the general medical population; however, data are lacking to support a dosing strategy in the hematology / oncology population. To evaluate amikacin - associated nephrotoxicity in an adult hematology / oncology population, a prospective, randomized, open - label trial was conducted at a university - affiliated medical center. Forty patients with a diagnosis consistent with a hematologic / oncologic disorder that required treatment with an aminoglycoside were randomized to either conventional or extended - interval amikacin. The occurrence of nephrotoxicity by means of an increase in serum creatinine and evaluation of efficacy via amikacin serum concentrations with respective pathogens were assessed. The occurrence of nephrotoxicity was similar between the conventional and extended - interval groups, at 10% and 5%, respectively (P = 1. 00). Six patients in the conventional group had a positive culture, compared with none in the extended - interval group (P = 0. 002). The occurrence of nephrotoxicity was similar between the two dosing regimens, but the distribution of risk factors was variable between the two groups. Efficacy could not be assessed.

amikacin

Amikacin

aminoglycoside

amikacin

aminoglycoside

amikacin

creatinine

amikacin

nephrotoxicity

febrile neutropenia

infections

nephrotoxicity

hematologic / oncologic disorder

hematologic / oncologic disorder

oncologic disorder

nephrotoxicity

nephrotoxicity

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

Amikacin

nephrotoxicity

Amikacin

nephrotoxicity

Amikacin

nephrotoxicity

Amikacin

nephrotoxicity

Amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity


Input: Memory function and serotonin transporter promoter gene polymorphism in ecstasy (MDMA) users. Although 3, 4 - methylenedioxymethamphetamine (MDMA or ecstasy) has been shown to damage brain serotonin (5 - HT) neurons in animals and possibly humans, little is known about the long - term consequences of MDMA - induced 5 - HT neurotoxic lesions on functions in which 5 - HT is involved, such as cognitive function. Because 5 - HT transporters play a key element in the regulation of synaptic 5 - HT transmission it may be important to control for the potential covariance effect of a polymorphism in the 5 - HT transporter promoter gene region (5 - HTTLPR) when studying the effects of MDMA as well as cognitive functioning. The aim of the study was to investigate the effects of moderate and heavy MDMA use on cognitive function, as well as the effects of long - term abstention from MDMA, in subjects genotyped for 5 - HTTLPR. A second aim of the study was to determine whether these effects differ for females and males. Fifteen moderate MDMA users (< 55 lifetime tablets), 22 heavy MDMA + users (> 55 lifetime tablets), 16 ex - MDMA + users (last tablet > 1 year ago) and 13 controls were compared on a battery of neuropsychological tests. DNA from peripheral nuclear blood cells was genotyped for 5 - HTTLPR using standard polymerase chain reaction methods. A significant group effect was observed only on memory function tasks (p = 0. 04) but not on reaction times (p = 0. 61) or attention / executive functioning (p = 0. 59). Heavy and ex - MDMA + users performed significantly poorer on memory tasks than controls. In contrast, no evidence of memory impairment was observed in moderate MDMA users. No significant effect of 5 - HTTLPR or gender was observed. While the use of MDMA in quantities that may be considered " moderate " is not associated with impaired memory functioning, heavy use of MDMA use may lead to long lasting memory impairments. No effect of 5 - HTTLPR or gender on memory function or MDMA use was observed.

serotonin

ecstasy

MDMA

3, 4 - methylenedioxymethamphetamine

MDMA

ecstasy

serotonin

5 - HT

MDMA

5 - HT

5 - HT

5 - HT

5 - HT

5 - HT

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

MDMA

neurotoxic lesions

memory impairment

impaired memory functioning

memory impairments

ecstasy

memory impairment

ecstasy

impaired memory functioning

ecstasy

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

3, 4 - methylenedioxymethamphetamine

memory impairment

3, 4 - methylenedioxymethamphetamine

impaired memory functioning

3, 4 - methylenedioxymethamphetamine

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

ecstasy

memory impairment

ecstasy

impaired memory functioning

ecstasy

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments

MDMA

memory impairment

MDMA

impaired memory functioning

MDMA

memory impairments


Input: Aging process of epithelial cells of the rat prostate lateral lobe in experimental hyperprolactinemia induced by haloperidol. The aim of the study was to examine the influence of hyperprolactinemia, induced by haloperidol (HAL) on age related morphology and function changes of epithelial cells in rat prostate lateral lobe. The study was performed on sexually mature male rats. Serum concentrations of prolactin (PRL) and testosterone (T) were measured. Tissue sections were evaluated with light and electron microscopy. Immunohistochemical reactions for Anti - Proliferating Cell Nuclear Antigen (PCNA) were performed. In rats of the experimental group, the mean concentration of: PRL was more than twice higher, whereas T concentration was almost twice lower than that in the control group. Light microscopy visualized the following: hypertrophy and epithelium hyperplasia of the glandular ducts, associated with increased PCNA expression. Electron microscopy revealed changes in columnar epithelial cells, concerning organelles, engaged in protein synthesis and secretion.

hyperprolactinemia

hyperprolactinemia

hypertrophy

hyperplasia

haloperidol

haloperidol

HAL

PRL

testosterone

T

PRL

T

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

haloperidol

hyperprolactinemia

HAL

hyperprolactinemia

HAL

hyperprolactinemia


Input: Does supplemental vitamin C increase cardiovascular disease risk in women with diabetes? BACKGROUND: Vitamin C acts as a potent antioxidant; however, it can also be a prooxidant and glycate protein under certain circumstances in vitro. These observations led us to hypothesize that a high intake of vitamin C in diabetic persons might promote atherosclerosis. OBJECTIVE: The objective was to examine the relation between vitamin C intake and mortality from cardiovascular disease. DESIGN: We studied the relation between vitamin C intake and mortality from total cardiovascular disease (n = 281), coronary artery disease (n = 175), and stroke (n = 57) in 1923 postmenopausal women who reported being diabetic at baseline. Diet was assessed with a food - frequency questionnaire at baseline, and subjects initially free of coronary artery disease were prospectively followed for 15 y. RESULTS: After adjustment for cardiovascular disease risk factors, type of diabetes medication used, duration of diabetes, and intakes of folate, vitamin E, and beta - carotene, the adjusted relative risks of total cardiovascular disease mortality were 1. 0, 0. 97, 1. 11, 1. 47, and 1. 84 (P for trend < 0. 01) across quintiles of total vitamin C intake from food and supplements. Adjusted relative risks of coronary artery disease were 1. 0, 0. 81, 0. 99, 1. 26, and 1. 91 (P for trend = 0. 01) and of stroke were 1. 0, 0. 52, 1. 23, 2. 22, and 2. 57 (P for trend < 0. 01). When dietary and supplemental vitamin C were analyzed separately, only supplemental vitamin C showed a positive association with mortality endpoints. Vitamin C intake was unrelated to mortality from cardiovascular disease in the nondiabetic subjects at baseline. CONCLUSION: A high vitamin C intake from supplements is associated with an increased risk of cardiovascular disease mortality in postmenopausal women with diabetes.

vitamin C

Vitamin C

vitamin C

vitamin C

vitamin C

folate

vitamin E

beta - carotene

vitamin C

vitamin C

vitamin C

Vitamin C

vitamin C

cardiovascular disease

diabetes

diabetic

atherosclerosis

cardiovascular disease

cardiovascular disease

coronary artery disease

stroke

diabetic

coronary artery disease

cardiovascular disease

diabetes

diabetes

cardiovascular disease

coronary artery disease

stroke

cardiovascular disease

cardiovascular disease

diabetes

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

Vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease

vitamin C

cardiovascular disease


Input: Absolute and attributable risk of venous thromboembolism in women on combined cyproterone acetate and ethinylestradiol. OBJECTIVE: To achieve absolute risk estimates of venous thromboembolism (VTE) among women on cyproterone acetate plus ethinylestradiol (CPA / EE), and among women on combined oral contraceptives (COCs). METHODS: From the Danish National Register of Patients (NRP), 1996 to 1998, the records of 1. 1 million Danish women, ages 15 to 44 years, were searched for evidence of VTE. COC use was ascertained through mailed questionnaires. Sales statistics of COCs and CPA / EE were provided through Danish Drug Statistics. RESULTS: During the time frame of the study, 330 women were found to have had VTE while on COCs. Of these women, 67 were on levonorgestrel - containing COCs. Eleven were on CPA / EE. The corresponding absolute risk of VTE was 3. 4 (range, 3. 1 - 3. 8) per 10 000 women years among the women on COCs, 4. 2 (range, 3. 2 - 5. 2) per 10 000 women years among women on levonorgestrel - containing COCs, and 3. 1 (range, 1. 3 - 4. 9) per 10 000 women years among the women on CPA / EE. CONCLUSION: Our results suggest the absolute risk of VTE among Danish women on COCs is similar to that among women taking CPA / EE.

venous thromboembolism

venous thromboembolism

VTE

VTE

VTE

VTE

VTE

cyproterone acetate

ethinylestradiol

cyproterone acetate

ethinylestradiol

CPA

EE

combined oral contraceptives

COCs

COC

COCs

CPA

EE

COCs

levonorgestrel

COCs

CPA

EE

COCs

levonorgestrel

COCs

CPA

EE

COCs

CPA

EE

combined oral contraceptives

venous thromboembolism

combined oral contraceptives

venous thromboembolism

combined oral contraceptives

VTE

combined oral contraceptives

VTE

combined oral contraceptives

VTE

combined oral contraceptives

VTE

combined oral contraceptives

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COC

venous thromboembolism

COC

venous thromboembolism

COC

VTE

COC

VTE

COC

VTE

COC

VTE

COC

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

venous thromboembolism

COCs

venous thromboembolism

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE

COCs

VTE


Input: Effect of lindane on hepatic and brain cytochrome P450s and influence of P450 modulation in lindane induced neurotoxicity. Oral administration of lindane (2. 5, 5, 10 and 15 mg / kg, body weight) for 5 days was found to produce a dose - dependent increase in the activity of P450 dependent 7 - ethoxyresorufin - O - deethylase (EROD), 7 - pentoxyresorufin - O - dealkylase (PROD) and N - nitrosodimethylamine demethylase (NDMA - d) in rat brain and liver. A significant increase in the hepatic and brain P450 monooxygenases was also observed when the duration of exposure of low dose (2. 5 mg / kg) of lindane was increased from 5 days to 15 or 21 days. As observed with different doses, the magnitude of induction in the activity of P450 monooxygenases was several fold higher in liver microsomes when compared with the brain. Western blotting studies have indicated that the increase in the P450 enzymes could be due to the increase in the expression of P450 1A1 / 1A2, 2B1 / 2B2 and 2E1 isoenzymes. In vitro studies using organic inhibitors specific for individual P450 isoenzymes and antibody inhibition experiments have further demonstrated that the increase in the activity of PROD, EROD and NDMA - d are due to the increase in the levels of P450 2B1 / 2B2, 1A1 / 1A2 and 2E1 isoenzymes, respectively. Induction studies have further shown that while pretreatment of 3 - methylcholanthrene (MC), an inducer of P4501A1 / 1A2, did not produce any significant effect in the incidence of lindane induced convulsions, pretreatment with phenobarbital (PB), an inducer of P450 2B1 / 2B2 or ethanol, an inducer of P450 2E1 catalysed reactions, significantly increased the incidence of lindane induced convulsions. Similarly, when the P450 - mediated metabolism of lindane was blocked by cobalt chloride incidence of convulsions was increased in animals treated with lindane indicating that lindane per se or its metabolites formed by PB or ethanol inducible P450 isoenzymes are involved in its neurobehavioral toxicity.

lindane

lindane

lindane

N - nitrosodimethylamine

NDMA

lindane

NDMA

3 - methylcholanthrene

MC

lindane

phenobarbital

ethanol

lindane

lindane

cobalt chloride

lindane

lindane

ethanol

neurotoxicity

convulsions

convulsions

convulsions

toxicity

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions

lindane

convulsions


Input: Seizure associated with sleep deprivation and sustained - release bupropion. This case report describes a generalized seizure associated with sustained - release bupropion use and sleep deprivation. The subject, a 31 - year - old female smoker, was participating in a clinical trial evaluating an investigational medication for smoking cessation that used sustained - release bupropion as an active control. After 5 weeks of bupropion use, the subject experienced a generalized tonic clonic seizure after staying up nearly all night packing and moving to a new residence. The patient had no other risk factors for seizures. We suggest that sleep deprivation may add to the risk of bupropion - associated seizures.

Seizure

sleep deprivation

seizure

sleep deprivation

seizure

seizures

sleep deprivation

seizures

bupropion

bupropion

bupropion

bupropion

bupropion

bupropion

Seizure

bupropion

seizure

bupropion

seizure

bupropion

seizures

bupropion

seizures

bupropion

Seizure

bupropion

seizure

bupropion

seizure

bupropion

seizures

bupropion

seizures

bupropion

Seizure

bupropion

seizure

bupropion

seizure

bupropion

seizures

bupropion

seizures

bupropion

Seizure

bupropion

seizure

bupropion

seizure

bupropion

seizures

bupropion

seizures

bupropion

Seizure

bupropion

seizure

bupropion

seizure

bupropion

seizures

bupropion

seizures


Input: Nephrotoxic effects in high - risk patients undergoing angiography. BACKGROUND: The use of iodinated contrast medium can result in nephropathy. Whether iso - osmolar contrast medium is less nephrotoxic than low - osmolar contrast medium in high - risk patients is uncertain. METHODS: We conducted a randomized, double - blind, prospective, multicenter study comparing the nephrotoxic effects of an iso - osmolar, dimeric, nonionic contrast medium, iodixanol, with those of a low - osmolar, nonionic, monomeric contrast medium, iohexol. The study involved 129 patients with diabetes with serum creatinine concentrations of 1. 5 to 3. 5 mg per deciliter who underwent coronary or aortofemoral angiography. The primary end point was the peak increase from base line in the creatinine concentration during the three days after angiography. Other end points were an increase in the creatinine concentration of 0. 5 mg per deciliter or more, an increase of 1. 0 mg per deciliter or more, and a change in the creatinine concentration from day 0 to day 7. RESULTS: The creatinine concentration increased significantly less in patients who received iodixanol. From day 0 to day 3, the mean peak increase in creatinine was 0. 13 mg per deciliter in the iodixanol group and 0. 55 mg per deciliter in the iohexol group (P = 0. 001; the increase with iodixanol minus the increase with iohexol, - 0. 42 mg per deciliter [95 percent confidence interval, - 0. 73 to - 0. 22]). Two of the 64 patients in the iodixanol group (3 percent) had an increase in the creatinine concentration of 0. 5 mg per deciliter or more, as compared with 17 of the 65 patients in the iohexol group (26 percent) (P = 0. 002; odds ratio for such an increase in the iodixanol group, 0. 09 [95 percent confidence interval, 0. 02 to 0. 41]). No patient receiving iodixanol had an increase of 1. 0 mg per deciliter or more, but 10 patients in the iohexol group (15 percent) did. The mean change in the creatinine concentration from day 0 to day 7 was 0. 07 mg per deciliter in the iodixanol group and 0. 24 mg per deciliter in the iohexol group (P = 0. 003; value in the iodixanol group minus the value in the iohexol group, - 0. 17 mg per deciliter [95 percent confidence interval, - 0. 34 to - 0. 07]). CONCLUSIONS: Nephropathy induced by contrast medium may be less likely to develop in high - risk patients when iodixanol is used rather than a low - osmolar, nonionic contrast medium.

Nephrotoxic

nephropathy

nephrotoxic

nephrotoxic

diabetes

Nephropathy

iodixanol

iohexol

creatinine

creatinine

creatinine

creatinine

creatinine

iodixanol

creatinine

iodixanol

iohexol

iodixanol

iohexol

iodixanol

creatinine

iohexol

iodixanol

iodixanol

iohexol

creatinine

iodixanol

iohexol

iodixanol

iohexol

iodixanol

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy

iohexol

Nephrotoxic

iohexol

nephropathy

iohexol

nephrotoxic

iohexol

nephrotoxic

iohexol

Nephropathy


Input: Experimental cranial pain elicited by capsaicin: a PET study. Using a positron emission tomography (PET) study it was shown recently that in migraine without aura certain areas in the brain stem were activated during the headache state, but not in the headache free interval. It was suggested that this brain stem activation is inherent to the migraine attack itself and represents the so called' migraine generator'. To test this hypothesis we performed an experimental pain study in seven healthy volunteers, using the same positioning in the PET scanner as in the migraine patients. A small amount of capsaicin was administered subcutaneously in the right forehead to evoke a burning painful sensation in the first division of the trigeminal nerve. Increases of regional cerebral blood flow (rCBF) were found bilaterally in the insula, in the anterior cingulate cortex, the cavernous sinus and the cerebellum. Using the same stereotactic space limits as in the above mentioned migraine study no brain stem activation was found in the acute pain state compared to the pain free state. The increase of activation in the region of the cavernous sinus however, suggests that this structure is more likely to be involved in trigeminal transmitted pain as such, rather than in a specific type of headache as was suggested for cluster headache.

pain

migraine

headache

headache

migraine

migraine

pain

migraine

painful

migraine

pain

pain

pain

headache

cluster headache

capsaicin

capsaicin

capsaicin

pain

capsaicin

pain

capsaicin

painful

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

pain

capsaicin

painful

capsaicin

pain

capsaicin

pain

capsaicin

pain


Input: Neuroleptic malignant syndrome with risperidone. Neuroleptic malignant syndrome is thought to be a result of dopamine D2 receptor blockade in the striatum of the basal ganglia. Risperidone, a benzisoxazole derivative antipsychotic, has high serotonin 5 - HT2 receptor blockade and dose - related D2 receptor blockade. The high ratio is believed to impart the low frequency of extrapyramidal symptoms with risperidone at low dosages. With this low frequency of extrapyramidal symptoms, it was thought the frequency of neuroleptic malignant syndrome might also be lowered. A 73 - year - old woman developed neuroleptic malignant syndrome after monotherapy with risperidone. The syndrome reversed after discontinuing risperidone and starting treatment with dantrolene and bromocriptine. It appears that the protection from extrapyramidal side effects observed with risperidone does not ensure protection from neuroleptic malignant syndrome.

Neuroleptic malignant syndrome

Neuroleptic malignant syndrome

extrapyramidal symptoms

extrapyramidal symptoms

neuroleptic malignant syndrome

neuroleptic malignant syndrome

neuroleptic malignant syndrome

risperidone

dopamine

Risperidone

benzisoxazole

serotonin

risperidone

risperidone

risperidone

dantrolene

bromocriptine

risperidone

risperidone

Neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

Risperidone

Neuroleptic malignant syndrome

Risperidone

Neuroleptic malignant syndrome

Risperidone

neuroleptic malignant syndrome

Risperidone

neuroleptic malignant syndrome

Risperidone

neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

Neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome

risperidone

neuroleptic malignant syndrome


Input: Hepatic and extrahepatic angiotensinogen gene expression in rats with acute nephrotic syndrome. Plasma concentration and urine excretion of the renin - angiotensin system proteins are altered in rats with nephrotic syndrome (NS). In this work the messenger ribonucleic acid (mRNA) levels of angiotensinogen (Ao) were analyzed with the slot - blot hybridization technique in liver and other extrahepatic tissues: kidney, heart, brain, and adrenal gland from control, nephrotic, and pair - fed (PF) rats. NS was induced by a single injection of puromycin amino - nucleoside (PAN). Although a great urinary excretion and half - normal plasma levels of Ao were observed on day 6 after PAN injection, when NS was clearly established, hepatic Ao mRNA levels did not change. Furthermore, the Ao mRNA levels did not change in any of the extrahepatic tissues studied on day 6, nor did its hepatic levels at days 1, 3, 5, or 7 after PAN injection. These data suggest that the hepatic and extrahepatic Ao mRNA levels are unaltered during the development of the acute NS induced by PAN.

nephrotic syndrome

nephrotic syndrome

NS

nephrotic

NS

NS

NS

angiotensin

puromycin amino - nucleoside

PAN

PAN

PAN

PAN

puromycin amino - nucleoside

nephrotic syndrome

puromycin amino - nucleoside

nephrotic syndrome

puromycin amino - nucleoside

NS

puromycin amino - nucleoside

nephrotic

puromycin amino - nucleoside

NS

puromycin amino - nucleoside

NS

puromycin amino - nucleoside

NS

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

NS

PAN

nephrotic

PAN

NS

PAN

NS

PAN

NS

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

NS

PAN

nephrotic

PAN

NS

PAN

NS

PAN

NS

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

NS

PAN

nephrotic

PAN

NS

PAN

NS

PAN

NS

PAN

nephrotic syndrome

PAN

nephrotic syndrome

PAN

NS

PAN

nephrotic

PAN

NS

PAN

NS

PAN

NS


Input: Cyclophosphamide associated bladder cancer - - a highly aggressive disease: analysis of 12 cases. PURPOSE: We gained knowledge of the etiology, treatment and prevention of cyclophosphamide associated urothelial cancer. MATERIALS AND METHODS: The medical records of 6 men and 6 women (mean age 55 years) with cyclophosphamide associated bladder cancer were reviewed. RESULTS: All tumors were grade 3 or 4 transitional cell carcinoma. Of the 5 patients initially treated with endoscopic resection alone only 1 is alive without disease. Of the 6 patients who underwent early cystectomy 4 were alive at 24 to 111 months. The remaining patient with extensive cancer underwent partial cystectomy for palliation and died 3 months later. CONCLUSIONS: Cyclophosphamide associated bladder tumor is an aggressive disease. However, long - term survival is possible when radical cystectomy is performed for bladder tumors with any sign of invasion and for recurrent high grade disease, even when noninvasive.

Cyclophosphamide

cyclophosphamide

cyclophosphamide

Cyclophosphamide

bladder cancer

urothelial cancer

bladder cancer

tumors

carcinoma

cancer

bladder tumor

bladder tumors

Cyclophosphamide

bladder cancer

Cyclophosphamide

bladder cancer

Cyclophosphamide

bladder tumor

Cyclophosphamide

bladder tumors

cyclophosphamide

bladder cancer

cyclophosphamide

bladder cancer

cyclophosphamide

bladder tumor

cyclophosphamide

bladder tumors

cyclophosphamide

bladder cancer

cyclophosphamide

bladder cancer

cyclophosphamide

bladder tumor

cyclophosphamide

bladder tumors

Cyclophosphamide

bladder cancer

Cyclophosphamide

bladder cancer

Cyclophosphamide

bladder tumor

Cyclophosphamide

bladder tumors


Input: Leg and back pain after spinal anaesthesia involving hyperbaric 5% lignocaine. Fifty - four patients, aged 27 - 90 years, who were given lignocaine 5% in 6. 8% glucose solution for spinal anaesthesia were studied. Thirteen of these patients experienced pain in the legs and / or back after recovery from anaesthesia. The patients affected were younger (p < 0. 05) and the site of the dural puncture was higher (p < 0. 01) than those individuals without pain. Five of the 13 patients (38%) with pain and seven of the 41 patients (17%) without pain admitted to a high alcohol intake, which might be a contributing factor. Leg and / or back pain is associated with the intrathecal use of hyperbaric 5% lignocaine.

Leg and back pain

pain in the legs and / or back

pain

pain

pain

Leg and / or back pain

lignocaine

lignocaine

glucose

alcohol

lignocaine

lignocaine

Leg and back pain

lignocaine

pain in the legs and / or back

lignocaine

Leg and / or back pain

lignocaine

Leg and back pain

lignocaine

pain in the legs and / or back

lignocaine

Leg and / or back pain

lignocaine

Leg and back pain

lignocaine

pain in the legs and / or back

lignocaine

Leg and / or back pain


Input: Acute blood pressure elevations with caffeine in men with borderline systemic hypertension. Whether the vasoconstrictive actions of caffeine are enhanced in hypertensive persons has not been demonstrated. Thus, caffeine (3. 3 mg / kg) versus placebo was tested in 48 healthy men (aged 20 to 35 years) selected after screening on 2 separate occasions. Borderline hypertensive men (n = 24) were selected with screening systolic blood pressure (BP) of 140 to 160 mm Hg and / or diastolic BP 90 to 99 mm Hg. Low - risk controls (n = 24) reported no parental history of hypertension and had screening BP < 130 / 85 mm Hg. Participants were then tested on 2 occasions after 12 - hour abstinence from caffeine in each of 2 protocols; this required a total of 4 laboratory visits. Caffeine - induced changes in diastolic BP were 2 to 3 times larger in borderline subjects than in controls (+ 8. 4 vs + 3. 8 mm Hg, p < 0. 0001), and were attributable to larger changes in impedance - derived measures of systemic vascular resistance (+ 135 vs + 45 dynes. s. cm - 5, p < 0. 004). These findings were consistent and reached significance in both protocols. The percentage of borderline subjects in whom diastolic BP changes exceeded the median control response was 96%. Consequently, whereas all participants exhibited normotensive levels during the resting predrug baseline, 33% of borderline subjects achieved hypertensive BP levels after caffeine ingestion. Thus, in borderline hypertensive men, exaggerated responses to caffeine were: selective for diastolic BP, consistent with greater vasoconstriction, replicated in 2 protocols, and representative of nearly all borderline hypertensives. We suspect that the potential for caffeine to stabilize high resistance states in susceptible persons suggests that its use may facilitate their disease progression, as well as hinder accurate diagnosis and treatment.

caffeine

caffeine

caffeine

caffeine

Caffeine

caffeine

caffeine

caffeine

hypertension

hypertensive

hypertensive

hypertension

hypertensive

hypertensive

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

Caffeine

hypertension

Caffeine

hypertensive

Caffeine

hypertensive

Caffeine

hypertension

Caffeine

hypertensive

Caffeine

hypertensive

Caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertension

caffeine

hypertensive

caffeine

hypertensive

caffeine

hypertensives


Input: Hallucinations and ifosfamide - induced neurotoxicity. BACKGROUND: Hallucinations as a symptom of central neurotoxicity are a known but poorly described side effect of ifosfamide. Most cases of ifosfamide - induced hallucinations have been reported with other mental status changes. METHODS: The authors interviewed six persons with ifosfamide - induced hallucinations in the presence of a clear sensorium. All patients were receiving high - dose ifosfamide as part of their bone marrow transplant procedure. RESULTS: Hallucinations occurred only when the patient' s eyes were closed and, in all but one case, were reported as disturbing or frightening. Underreporting of these hallucinations by patients is likely. CONCLUSIONS: Hallucinations may be the sole or first manifestation of neurotoxicity. The incidence may be dose and infusion - time related. The clinician should be alerted for possible ifosfamide - induced hallucinations, which may occur without other signs of neurotoxicity. " Eyes - closed " hallucinatory experiences appear to be an unusual feature of this presentation. Patients anxious about this experience respond well to support and education about this occurrence. Optimal pharmacologic management of disturbed patients is unclear. If agitation becomes marked, high - potency neuroleptics (i. e., haloperidol) may be effective.

Hallucinations

neurotoxicity

Hallucinations

neurotoxicity

hallucinations

hallucinations

Hallucinations

hallucinations

Hallucinations

neurotoxicity

hallucinations

neurotoxicity

hallucinatory

agitation

ifosfamide

ifosfamide

ifosfamide

ifosfamide

ifosfamide

ifosfamide

haloperidol

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory

ifosfamide

Hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

Hallucinations

ifosfamide

hallucinations

ifosfamide

hallucinatory


Input: Chlorpropamide - induced optic neuropathy. A 65 - year - old woman with adult - onset diabetes treated with chlorpropamide (Diabenese) had a toxic optic neuropathy that resolved with discontinuation of chlorpropamide therapy. Visual loss occurs in diabetics for a variety of reasons, and accurate diagnosis is necessary to institute appropriate therapy. The possibility of a drug - induced optic neuropathy should be considered in the differential diagnosis of visual loss in diabetics.

Chlorpropamide

chlorpropamide

Diabenese

chlorpropamide

optic neuropathy

adult - onset diabetes

toxic optic neuropathy

Visual loss

diabetics

optic neuropathy

visual loss

diabetics

Chlorpropamide

optic neuropathy

Chlorpropamide

toxic optic neuropathy

Chlorpropamide

optic neuropathy

chlorpropamide

optic neuropathy

chlorpropamide

toxic optic neuropathy

chlorpropamide

optic neuropathy

Diabenese

optic neuropathy

Diabenese

toxic optic neuropathy

Diabenese

optic neuropathy

chlorpropamide

optic neuropathy

chlorpropamide

toxic optic neuropathy

chlorpropamide

optic neuropathy


Input: Levodopa - induced dyskinesia and thalamotomy. Levodopa - induced dyskinesia of the limbs in thirteen cases of Parkinsonism, which was choreic, ballistic or dystonic in type, was alleviated almost completely by stereotaxic surgery using a microelectrode technique for the ventralis oralis anterior and posterior nuclei of the thalamus, but much less by the ventralis intermedius nucleus. Control of levodopa - induced dyskinesias by thalamic lesions in the course of routine treatment of Parkinsonism is discussed.

Levodopa

Levodopa

levodopa

dyskinesia

dyskinesia

Parkinsonism

dystonic

dyskinesias

thalamic lesions

Parkinsonism

Levodopa

dyskinesia

Levodopa

dyskinesia

Levodopa

dyskinesias

Levodopa

dyskinesia

Levodopa

dyskinesia

Levodopa

dyskinesias

levodopa

dyskinesia

levodopa

dyskinesia

levodopa

dyskinesias


Input: Factors associated with nephrotoxicity and clinical outcome in patients receiving amikacin. Data from 60 patients treated with amikacin were analyzed for factors associated with nephrotoxicity. In 42 of these patients, data were examined for factors associated with clinical outcome. Variables evaluated included patient weight, age, sex, serum creatinine level, creatinine clearance, duration of therapy, total dose, mean daily dose, organism minimum inhibitory concentration (MIC), mean peak levels, mean trough levels, mean area under the serum concentration - time curve (AUC), total AUC, mean AUC greater than MIC, total AUC greater than MIC, mean Schumacher' s intensity factor (IF), total IF, In (mean maximum concentration [Cmax] / MIC). Model - dependent pharmacokinetic parameters were calculated by computer based on a one - compartment model. When the parameters were examined individually, duration of therapy and total AUC correlated significantly (P less than. 05) with nephrotoxicity. In contrast, a stepwise discriminant function analysis identified only duration of therapy (P less than. 001) as an important factor. Based on this model and on Bayes' theorem, the predictive accuracy of identifying " nephrotoxic " patients increased from 0. 17 to 0. 39. When examined individually, mean IF, MIC, total dose, mean daily dose, and ln (mean Cmax / MIC) correlated significantly (P less than. 05) with cure. In contrast, a simultaneous multivariable analysis identified IF, MIC, and total dose according to one model and ln (mean Cmax / MIC) according to a second statistical model of parameters selected to have the greatest prospective value. Based on Bayes' theorem and the first model, the predictive accuracy of identifying patients not cured increased from 0. 19 to 0. 83. For the second model, the predictive accuracy increased from 0. 19 to 0. 50. (ABSTRACT TRUNCATED AT 250 WORDS)

nephrotoxicity

nephrotoxicity

nephrotoxicity

nephrotoxic

amikacin

amikacin

creatinine

creatinine

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxic

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxicity

amikacin

nephrotoxic


Input: Cardiac transplantation: improved quality of survival with a modified immunosuppressive protocol. The effects on renal function on two different immunosuppressive protocols were evaluated retrospectively in two subsequent groups of heart transplant recipients. In group I, cyclosporine was given before the procedure at a loading dose of 17. 5 mg / kg and then continued after the procedure to keep a whole blood level about 1000 ng / ml. In group II, cyclosporine was started only after the procedure at a lower dosage and was complemented by azathioprine, which was used for the first postoperative week. Group II showed a better perioperative renal function as determined by serum blood urea nitrogen and serum creatinine levels. Group II also showed a significant decrease of chronic nephrotoxicity secondary to long - term therapy with cyclosporine. Despite this improvement in late renal function, group II still shows a slow rise in serum creatinine. We think that even these lower dosages of cyclosporine can cause chronic nephrotoxicity and that further modification of the immunosuppressive regimen is required to completely abolish this toxic side effect.

cyclosporine

cyclosporine

azathioprine

urea nitrogen

creatinine

cyclosporine

creatinine

cyclosporine

nephrotoxicity

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity

cyclosporine

nephrotoxicity


Input: Reversible cholestasis with bile duct injury following azathioprine therapy. A case report. A 67 - year - old patient, with primary polymyositis and without previous evidence of liver disease, developed clinical and biochemical features of severe cholestasis 3 months after initiation of azathioprine therapy. Liver biopsy showed cholestasis with both cytological and architectural alterations of interlobular bile ducts. Azathioprine withdrawal resulted after 7 weeks in the resolution of clinical and biochemical abnormalities. It is believed that this is the first reported case of reversible azathioprine - induced cholestasis associated with histological evidence of bile duct injury.

cholestasis

bile duct injury

polymyositis

liver disease

cholestasis

cholestasis

cholestasis

bile duct injury

azathioprine

azathioprine

Azathioprine

azathioprine

azathioprine

cholestasis

azathioprine

bile duct injury

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

bile duct injury

azathioprine

cholestasis

azathioprine

bile duct injury

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

bile duct injury

Azathioprine

cholestasis

Azathioprine

bile duct injury

Azathioprine

cholestasis

Azathioprine

cholestasis

Azathioprine

cholestasis

Azathioprine

bile duct injury

azathioprine

cholestasis

azathioprine

bile duct injury

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

cholestasis

azathioprine

bile duct injury


Input: Renal function and hemodynamics during prolonged isoflurane - induced hypotension in humans. The effect of isoflurane - induced hypotension on glomerular function and renal blood flow was investigated in 20 human subjects. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by inulin and para - aminohippurate (PAH) clearance, respectively. Anesthesia was maintained with fentanyl, nitrous oxide, oxygen, and isoflurane. Hypotension was induced for 236. 9 + / - 15. 1 min by increasing the isoflurane inspired concentration to maintain a mean arterial pressure of 59. 8 + / - 0. 4 mmHg. GFR and ERPF decreased with the induction of anesthesia but not significantly more during hypotension. Postoperatively, ERPF returned to preoperative values, whereas GFR was higher than preoperative values. Renal vascular resistance increased during anesthesia but decreased when hypotension was induced, allowing the maintenance of renal blood flow. We conclude that renal compensatory mechanisms are preserved during isoflurane - induced hypotension and that renal function and hemodynamics quickly return to normal when normotension is resumed.

isoflurane

isoflurane

para - aminohippurate

PAH

fentanyl

nitrous oxide

oxygen

isoflurane

isoflurane

isoflurane

hypotension

hypotension

Hypotension

hypotension

hypotension

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

Hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

Hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

Hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

Hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

Hypotension

isoflurane

hypotension

isoflurane

hypotension

isoflurane

hypotension


Input: Debrisoquine phenotype and the pharmacokinetics and beta - 2 receptor pharmacodynamics of metoprolol and its enantiomers. The metabolism of the cardioselective beta - blocker metoprolol is under genetic control of the debrisoquine / sparteine type. The two metabolic phenotypes, extensive (EM) and poor metabolizers (PM), show different stereoselective metabolism, resulting in apparently higher beta - 1 adrenoceptor antagonistic potency of racemic metoprolol in EMs. We investigated if the latter also applies to the beta - 2 adrenoceptor antagonism by metoprolol. The drug effect studied was the antagonism by metoprolol of terbutaline - induced hypokalemia. By using pharmacokinetic pharmacodynamic modeling the pharmacodynamics of racemic metoprolol and the active S - isomer, were quantitated in EMs and PMs in terms of IC50 values, representing metoprolol plasma concentrations resulting in half - maximum receptor occupancy. Six EMs received 0. 5 mg of terbutaline s. c. on two different occasions: 1) 1 hr after administration of a placebo and 2) 1 hr after 150 mg of metoprolol p. o. Five PMs were studied according to the same protocol, except for a higher terbutaline dose (0. 75 mg) on day 2. Blood samples for the analysis of plasma potassium, terbutaline, metoprolol (racemic, R - and S - isomer), and alpha - hydroxymetoprolol concentrations were taken at regular time intervals, during 8 hr after metoprolol. In PMs, metoprolol increased the terbutaline area under the plasma concentration vs. time curve (+ 67%). Higher metoprolol / alpha - hydroxymetoprolol ratios in PMs were predictive for higher R - / S - isomer ratios of unchanged drug. There was a difference in metoprolol potency with higher racemic metoprolol IC50 values in PMs (72 + / - 7 ng. ml - 1) than EMs (42 + / - 8 ng. ml - 1, P less than. 001). (ABSTRACT TRUNCATED AT 250 WORDS)

Debrisoquine

metoprolol

metoprolol

debrisoquine

sparteine

metoprolol

metoprolol

metoprolol

terbutaline

metoprolol

metoprolol

terbutaline

metoprolol

terbutaline

potassium

terbutaline

metoprolol

alpha - hydroxymetoprolol

metoprolol

metoprolol

terbutaline

metoprolol

alpha - hydroxymetoprolol

metoprolol

metoprolol

hypokalemia

terbutaline

hypokalemia

terbutaline

hypokalemia

terbutaline

hypokalemia

terbutaline

hypokalemia

terbutaline

hypokalemia


Input: Cefotetan - induced immune hemolytic anemia. Immune hemolytic anemia due to a drug - adsorption mechanism has been described primarily in patients receiving penicillins and first - generation cephalosporins. We describe a patient who developed anemia while receiving intravenous cefotetan. Cefotetan - dependent antibodies were detected in the patient' s serum and in an eluate prepared from his red blood cells. The eluate also reacted weakly with red blood cells in the absence of cefotetan, suggesting the concomitant formation of warm - reactive autoantibodies. These observations, in conjunction with clinical and laboratory evidence of extravascular hemolysis, are consistent with drug - induced hemolytic anemia, possibly involving both drug - adsorption and autoantibody formation mechanisms. This case emphasizes the need for increased awareness of hemolytic reactions to all cephalosporins.

Cefotetan

penicillins

cephalosporins

cefotetan

Cefotetan

cefotetan

cephalosporins

hemolytic anemia

hemolytic anemia

anemia

hemolysis

hemolytic anemia

Cefotetan

hemolytic anemia

Cefotetan

hemolytic anemia

Cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

Cefotetan

hemolytic anemia

Cefotetan

hemolytic anemia

Cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia

cefotetan

hemolytic anemia


Input: Acute renal failure subsequent to the administration of rifampicin. A follow - up study of cases reported earlier. A clinical presentation is made of a 2 - 3 year follow - up of six cases of acute renal failure that have been reported earlier. The patients had developed transient renal failure after the intermittent administration of rifampicin. The stage of olig - anuria lasted for 1 - 3 weeks, and five of the patients were treated by hemodialysis. Two of the patients died due to unrelated causes during the follow - up period. The four patients re - examined were clinically cured. Pathologic findings by light microscopy and immunofluorescence at biopsy were scarce. Nothing abnormal was seen by electron microscopy in two of the cases studied. Renal function was normal. In three cases the excretion at 131I - hippuran renography was slightly slowed. Although in the acute stage the renal lesions histologically appeared toxic, evidence suggestive of an immunological mechanism cannot be excluded.

Acute renal failure

acute renal failure

renal failure

anuria

renal lesions

rifampicin

rifampicin

rifampicin

Acute renal failure

rifampicin

acute renal failure

rifampicin

Acute renal failure

rifampicin

acute renal failure


Input: Type B hepatitis after needle - stick exposure: prevention with hepatitis B immune globulin. Final report of the Veterans Administration Cooperative Study. Hepatitis B immune globulin (HBIG) and immune serum globulin (ISG) were examined in a randomized, double - blind trial to assess their relative efficacies in preventing type B hepatitis after needle - stick exposure to hepatitis B surface antigen (HBsAG) - positive donors. Clinical hepatitis developed in 1. 4% of HBIG and in 5. 9% of ISG recipients (P = 0. 016), and seroconversion (anti - HBs) occurred in 5. 6% and 20. 7% of them respectively (P less than 0. 001). Mild and transient side - effects were noted in 3. 0% of ISG and in 3. 2% of HBIG recipients. Available donor sera were examined for DNA polymerase (DNAP) and e antigen and antibody (HBeAg; anti - HBE). Both DNAP and HBeAg showed a highly statistically significant correlation with the infectivity of HBsAg - positive donors. Hepatitis B immune globulin remained significantly superior to ISG in preventing type B hepatitis even when the analysis was confined to these two high - risk subgroups. The efficacy of ISG in preventing type B hepatitis cannot be ascertained because a true placebo group was not included.

Type B hepatitis

hepatitis B

Hepatitis B

type B hepatitis

hepatitis

Hepatitis B

type B hepatitis

type B hepatitis

hepatitis B surface antigen

HBsAG

HBeAg

HBeAg

HBsAg

HBeAg

Type B hepatitis

HBeAg

hepatitis B

HBeAg

Hepatitis B

HBeAg

type B hepatitis

HBeAg

Hepatitis B

HBeAg

type B hepatitis

HBeAg

type B hepatitis

HBeAg

Type B hepatitis

HBeAg

hepatitis B

HBeAg

Hepatitis B

HBeAg

type B hepatitis

HBeAg

Hepatitis B

HBeAg

type B hepatitis

HBeAg

type B hepatitis


Input: Serotonin syndrome from venlafaxine - tranylcypromine interaction. Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine - MAOI interaction that resulted in the serotonin syndrome in a 23 - y - old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1 / 2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120 / 67 mm Hg, heart rate 127 / min, respiratory rate 28 / min, and temperature 97 F. After 180 mg of diazepam i. v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non - immune thrombocytopenia which resolved. The patient' s maximal temperature was 101. 2 F and his CPK remained < 500 units / L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.

Serotonin syndrome

muscle rigidity

salivation

confusion

agitation

hyperthermia

serotonin syndrome

depression

tremors

rigidity

myoclonic jerks

rigidity

salivation

muscle rigidity

hypoventilation

paralyzed

muscle rigidity

thrombocytopenia

rhabdomyolysis

paralysis

venlafaxine

tranylcypromine

serotonin

serotonin

serotonin

Venlafaxine

serotonin

norepinephrine

venlafaxine

tranylcypromine

venlafaxine

diazepam

venlafaxine

hyperthermia

Venlafaxine

hyperthermia

venlafaxine

hyperthermia

venlafaxine

hyperthermia

venlafaxine

thrombocytopenia

Venlafaxine

thrombocytopenia

venlafaxine

thrombocytopenia

venlafaxine

thrombocytopenia

venlafaxine

Serotonin syndrome

venlafaxine

serotonin syndrome

Venlafaxine

Serotonin syndrome

Venlafaxine

serotonin syndrome

venlafaxine

Serotonin syndrome

venlafaxine

serotonin syndrome

venlafaxine

Serotonin syndrome

venlafaxine

serotonin syndrome

tranylcypromine

hyperthermia

tranylcypromine

hyperthermia

tranylcypromine

myoclonic jerks

tranylcypromine

myoclonic jerks

venlafaxine

muscle rigidity

venlafaxine

rigidity

venlafaxine

rigidity

venlafaxine

muscle rigidity

venlafaxine

muscle rigidity

Venlafaxine

muscle rigidity

Venlafaxine

rigidity

Venlafaxine

rigidity

Venlafaxine

muscle rigidity

Venlafaxine

muscle rigidity

venlafaxine

muscle rigidity

venlafaxine

rigidity

venlafaxine

rigidity

venlafaxine

muscle rigidity

venlafaxine

muscle rigidity

venlafaxine

muscle rigidity

venlafaxine

rigidity

venlafaxine

rigidity

venlafaxine

muscle rigidity

venlafaxine

muscle rigidity

venlafaxine

myoclonic jerks

Venlafaxine

myoclonic jerks

venlafaxine

myoclonic jerks

venlafaxine

myoclonic jerks

venlafaxine

confusion

Venlafaxine

confusion

venlafaxine

confusion

venlafaxine

confusion

venlafaxine

tremors

Venlafaxine

tremors

venlafaxine

tremors

venlafaxine

tremors

tranylcypromine

tremors

tranylcypromine

tremors

tranylcypromine

Serotonin syndrome

tranylcypromine

serotonin syndrome

tranylcypromine

Serotonin syndrome

tranylcypromine

serotonin syndrome

venlafaxine

salivation

venlafaxine

salivation

Venlafaxine

salivation

Venlafaxine

salivation

venlafaxine

salivation

venlafaxine

salivation

venlafaxine

salivation

venlafaxine

salivation

tranylcypromine

confusion

tranylcypromine

confusion

tranylcypromine

thrombocytopenia

tranylcypromine

thrombocytopenia

tranylcypromine

salivation

tranylcypromine

salivation

tranylcypromine

salivation

tranylcypromine

salivation

tranylcypromine

muscle rigidity

tranylcypromine

rigidity

tranylcypromine

rigidity

tranylcypromine

muscle rigidity

tranylcypromine

muscle rigidity

tranylcypromine

muscle rigidity

tranylcypromine

rigidity

tranylcypromine

rigidity

tranylcypromine

muscle rigidity

tranylcypromine

muscle rigidity