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Biomedical subjects

M L Horton

Publications and source records attributed to M L Horton.

At least 19 recordsLinked to original sources
PubMed1993

Fatal and nonfatal hepatotoxicity associated with flutamide.

OBJECTIVE: To identify and describe patients with hepatotoxicity possibly caused by flutamide, an antiandrogen drug. DESIGN: Case series of reports, submitted to the Adverse Drug Event Reporting System of the Food and Drug Administration. SETTING: Outpatient clinics and physicians' offices in the United States. PATIENTS: Nineteen patients treated with flutamide for prostate cancer or benign prostatic hypertrophy (for Investigation of a New Drug or off-label use). MEASUREMENTS: Evidence of increased liver enzyme levels, hyperbilirubinemia, associated clinical symptoms, and diagnoses of cholestatic hepatitis. Autopsy reports were used when available. RESULTS: From the time of marketing of flutamide in February 1989 through March 1991, the Food and Drug Administration received reports of 19 patients in the United States who developed serious hepatotoxicity while using flutamide. Fourteen patients had resolution of abnormal liver function test results after discontinuing or decreasing the dose of flutamide, but five patients died of progressive liver disease. Autopsy reports from three patients and abnormal pathologic results from three other patients (reported to the Food and Drug Administration or in the medical literature) showed hepatocellular necrosis and possibly cholestasis. Thorough work-ups excluded other possible causes than flutamide. CONCLUSIONS: Flutamide appears to cause hepatotoxic effects in certain patients. Physicians should tell patients to immediately report to physicians nausea, vomiting, fatigue, jaundice, and other signs and symptoms of liver injury.

Adverse Drug Reaction Reporting Systems↗
PubMed1991

Cystinuria in a cat.

A 10-month-old male Siamese cat with dysuria was determined to have cystine crystalluria. Many small calculi composed entirely of cystine were found in the urinary bladder. Measurement of serum and urine amino acids and calculation of fractional reabsorption of amino acids indicated reabsorption defects for cystine, ornithine, lysine, and arginine. Urinary acidification, fractional reabsorption of glucose, and fractional reabsorption of electrolytes were normal. Diagnoses of cystinuria and cystine urolithiasis were made on the basis of low fractional reabsorption of cystine and dibasic amino acids and the detection of cystine calculi in the urinary bladder.

Absorption↗
PubMed1991

Modulation of monomethylhydrazine-induced seizures by ivermectin.

Exposure to monomethylhydrazine (MMH), a common rocket propellant, can cause dose-related central nervous system (CNS) disturbances ranging from tremors to tonic-clonic convulsions to death. MMH inhibits gamma-aminobutyric acid (GABA) synthesis in the CNS. Diazepam (BZ) acts at the GABA receptor site, and it is also here that ivermectin (AVM) is pharmacologically active. Mice were injected with 30 mg/kg MMH. Groups of 12 mice each were then given varying doses of AVM (5, 10 and 15 mg/kg), or AVM + BZ combinations (5 mg/kg AVM with 5 mg/kg BZ, 10 mg/kg AVM with 5 mg/kg BZ). Time to first convulsion and time to death were recorded over the next 7 h and all groups were monitored over the next 7 days. Times to convulsion were not altered with AVM alone, but death was significantly prevented with AVM dosages. A treatment of 10 mg/kg AVM with 5 mg/kg BZ resulted in no seizures or deaths.

Animals↗
PubMed1986

Surgical treatment of nutcracker esophagus.

The "nutcracker esophagus" has become a commonly diagnosed esophageal motility disorder due to the advent of the more accurate low-compliance perfusion system. The disorder is characterized by high-amplitude peristaltic contractions often of prolonged duration and manifested by dysphagia and chest pain. Typically, symptomatic control is achieved with medical management. We report a case of "nutcracker esophagus" that was refractory to conventional modes of treatment but responded with symptomatic and manometric resolution after an extended esophagomyotomy.

Deglutition Disorders↗
PubMed1986

Femoral venipuncture for collection of multiple blood samples in the nonanesthetized rat.

A technique for blood collection via the femoral vein was developed for use in nonanesthetized rats. The technique was useful for single or serial blood collection. Volumes of 0.1 to 1 ml were collected for serum biochemical or venous blood gas determinations. The technique was effective, reproducible, did not require anesthesia, and was less stressful than other methods of blood collection in the rat.

Alanine Transaminase↗
PubMed1975

The treatment of ethylene glycol toxicosis with pyrazole.

Rats and dogs were protected from the effects of lethal doses of ingested ethylene glycol (EG) with pyrazole (P), an inhibitor of liver alcohol dehydrogenase. Rats given 1.35 ml/100 g of EG followed by 2.2 mmol/kg of P i.p. at 6 and 30 hours postingestion survived. Untreated control animals died. Dogs were given either 10.0 or 12.5 ml/kg of EG and treatment was begun 6 hours later. The control treatment consised of NaHC03 administered i.v. according to the calculated base deficit, B-complex vitamins with ascorbic acid, hydrocortisone, and 5 per cent glucose in water. The addition postexposure to this treatment of 0.9 mmol/kg of P and 0.5 mmol/kg of P at 6 and 30 hours, respectively, constituted the experimental therapy. In summary: with 10 ml/kg of EG, no P, 2 of 5 dogs survived; 12.5 ml/kg of EG, no P, 0/1; 10 ml/kg of EG plus P, 9/11; 12.5 ml/kg of EG plus P, 12/22. Dogs that succumbed had large numbers of oxalate crystals in their kidneys at necropsy. The surviving dogs had few oxalate crystals in their kidneys at the time of unilateral nephrectomy (2 weeks postexposure) or necropsy (30 days postexposure). Several clinical factors were identified as useful prognostic indicators in the treatment of EG poisoning. The results suggested that pyrazole, despite its marked toxicity, may be of clinically significant value in the treatment of ethylene glycol poisoning when therapy is initiated withing 6 hours of exposure.

Animals↗