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Biomedical subjects

M A Pizarro

Publications and source records attributed to M A Pizarro.

12 recordsLinked to original sources
PubMed2001

Flutamide-induced hepatotoxicity: report of a case series.

OBJECTIVE: To evaluate the characteristics of flutamide induced hepatotoxicity. MATERIAL AND METHODS: In this retrospective study we have analyzed all cases of flutamide hepatotoxicity submitted to the Andalucian Registry of drug-induced liver disease. Data were collected using a structured reporting form. Causality assessment was performed using two clinical scales: the standard CIOMS scale and the recently developed María and Victorino scale. RESULTS: Nine of 185 patients (4.9%) were identified. In 8 male patients, mean age 75 years (range 65-83), flutamide was indicated for palliative therapy of disseminated prostatic carcinoma, and in one young female (14 years) was given for the treatment of facial hirsutism. The mean duration of the flutamide therapy was 151 days (range 4-443). All patients presented with overt liver injury, the most frequent features being asthenia, anorexia, weight loss, nausea, vomiting and jaundice. No patient showed hypersensitivity features. In two patients (22%) the hepatic damage evolved to fulminant liver failure, one of them undergoing a liver transplantation and the other subsequently died. An additional patient died of a non-hepatic related cause when his liver function was improving. Causality assessment by the two clinical scales did not exclude any case, but the two patients who died where classified as unlikely by the María and Victorino scale. CONCLUSIONS: Flutamide can induce severe acute hepatitis, probably due to an idiosyncratic metabolic mechanism. Liver tests monitoring should probably be mandatory during the first months of flutamide therapy and the drug withdrawn if transaminases began to increase.

Adolescent↗
PubMed2001

Validity of early colonoscopy for the treatment of adenomas missed by initial endoscopic examination.

OBJECTIVE: To determine whether the features of adenomas identified in a first endoscopic examination may predict the presence of polyps with advanced pathological features that may have gone unnoticed and whether early colonoscopy may benefit these patients. MATERIAL AND METHODS: We examined 133 patients with diagnosis of colonic adenomas who had undergone complete colonoscopy and endoscopic polypectomy. All of them underwent colonoscopic follow-up at 3 years. Seventy nine patients underwent colonoscopic follow-up both at 6 months and at 3 years, while 54 patients underwent just colonoscopic follow-up at 3 years and 47 just at 6 months. RESULTS: Fifteen per cent of the patients analyzed developed polyps with pathological features after 6 months. The size and histological analysis of the polyps detected in the initial colonoscopic examination did not affect these results (p < 0.05). The number of polyps was statistically significant: patients with 3 or more polyps in the initial colonoscopic examination presented more polyps with pathological features after six months (25.8 versus 5.8%, p = 0002). This follow-up examination at 3 years did not reveal a higher occurrence of polyps with pathological features in any of the two groups of patients, namely, those who had undergone early colonoscopy and those who had not. CONCLUSIONS: Patients with multiple polyps have greater probability of developing synchronous polyps with some pathological features which may have gone unnoticed. Since early examination has not shown to provide a benefit for these patients, the first follow-up colonoscopy should be performed at 3 years, particularly if the initial colonoscopy is negative.

Adenoma↗
PubMed1975

Potentiation of adrenocortical response upon intermittent stimulation with corticotropin in normal subjects.

Modifications of adrenocortical steroidogenic response to ACTH as a consequence of acute prior exposure to this hormone, were studied in 106 normal subjects divided in 15 experimental groups. Adrenocortical response was assessed by the changes in plasma cortisol level and in urinary excretion of cortisol, 17-ketogenic and 17-ketosteroids; in some experiments plasma 11-deoxycortisol, corticosterone, progesterone and 17-hydroxyprogesterone were determined as well, together with urinary excretion of the unconjugated form of 11-deoxycortisol and corticosterone. Slow (8-h) intravenous administration of ACTH in amounts producing maximal response, leaves the adrenal cortex in a hyperresponsive state in case of further stimulation for up to 3 days, while the adrenocortical secretion comes back to baseline in the meantime. This potentiation phenomenon seems to concern essentially cortisol secretion since, among the compounds measured only cortisol and 11-deoxycortisol secretions increased progressively in amplitude when ACTH was administered repeatedly. Futhermore the degree of ACTH-induced adrenocortical hyperresponsiveness was found to depend on the amount of ACTH injected and on the time during which the adrenal cells are exposed to high peptide hormone concentrations. Increased adrenocortical responsiveness to ACTH persists when endogenous corticotropin secretion was suppressed for a few days by dexamethasone in normal subjects. Thus the potentiation phenomenon is not critically dependent on continued exposure of adrenal cells to endogenous corticotropin.

Adrenal Cortex↗