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Biomedical subjects

S Reus

Publications and source records attributed to S Reus.

14 recordsLinked to original sources
PubMed2002

A prospective study of the clarithromycin-digoxin interaction in elderly patients.

The study was a prospective observational trial carried out to assess the clarithromycin-digoxin interaction in elderly patients chronically taking digoxin. Digoxin concentrations were determined before and after concomitant treatment with clarithromycin. A Bayesian approach was used to calculate digoxin pharmacokinetics. In the seven patients who were studied there was a significant increase in digoxin concentration after 4-7 days of clarithromycin treatment; digoxin clearance and elimination rate constant were 56-60% lower and elimination half-life was 82% longer. The pharmacokinetic clarithromycin-digoxin interaction in the elderly may be much more frequent than has been assumed up to now.

Aged↗
PubMed2000

Progressive multifocal leukoencephalopathy treated with cidofovir in HIV-infected patients receiving highly active anti-retroviral therapy.

Progressive multifocal leukoencephalopathy (PML) has been a devastating disease for HIV-1-infected patients since the beginning of the AIDS pandemic. Currently, highly active antiretroviral therapy (HAART) seems to improve the outcome of PML in many patients. We describe two cases of PML whose course worsened in spite of HAART, but had a good response to cidofovir.

AIDS-Related Opportunistic Infections↗
PubMed2000

[Lipodystrophy and hyperglycemia produced by protease inhibitors].

BACKGROUND: HIV-1 protease inhibitors (PI) have been recently associated with a syndrome of anomalous body fat distribution or lipodystrophy (LD), which sometimes is associated to hyperglycemia. Many aspects of this syndrome remain obscure. The objective of the study is to describe the prevalence, clinical patterns, derangement of glucose metabolism associated and follow-up. METHODS: Patients taking at least one PI during January 1998 were asked a questionnaire about any body change, and a physical exam looking for fat changes was performed. In patients found to have LD, basal plasma glucose, cholesterol, triglycerides and cortisol were studied, and an oral glucose tolerance test (OGTT) was performed. In those cases with breast enlargement, prolactin and estradiol were measured. RESULTS: Among 272 patients, five cases (1.8%) of LD were detected. The syndrome appeared associated with all the IP available at the time of the study, a medium of 4.2 months after the introduction of the drug. The most common pattern was fat accumulation in abdomen and breast, and fat loss in arms, legs and face. Basal glycemia was normal in all 5 patients, but OGTT showed carbohydrate intolerance in two (both of them had family antecedents of type 2 diabetes mellitus). Only one patient need treatment withdrawal because of progressive deforming changes. CONCLUSIONS: The LD can appear in patients taking any IP. Body changes are usually self limited and in many patients PI don't need to be stopped.

Adult↗
PubMed1999

[Visceral leishmaniasis: a comparative study of patients with and without human immunodeficiency virus infection].

BACKGROUND: The changes that HIV coinfection can induce in clinical symptoms, response to treatment and prognosis of visceral Leishmaniasis (VL) are not well known. METHOD: We retrospectively describe the characteristics of VL in patients with and without HIV infection, between 1988-1998. RESULTS: Fifty episodes of VL were diagnosed in 40 patients. Nineteen (47.5%) were HIV coinfected, 57.8% of them have had an aids defining illness, and the median of CD4+ lymphocytes was 50/mm3. Clinical and laboratory data were similar to patients non HIV infected, except for lower levels of LDH (437 vs 578 U/ml; p = 0.02) and total lymphocytes (665 vs 1.500/mm3; p = 0.004) and higher levels of hemoglobin (9.8 vs 8.7 gr/dl; p = 0.01) and ESR (85 vs 44 mm; p = 0.01). The first episode of VL was diagnosed in 87.5% patients through bone marrow aspirate, and the other cases were diagnosed by biopsies of gum (2), lymph node (1) or liver (1). One patient was diagnosed clinically: he had a positive serology and a good response to antileishmanial therapy. Treatment failed in nine patients (22.5%), 7 HIV-coinfected. Eight patients died (20%), 6 HIV-coinfected. Five deaths were directly attributed to VL. Six coinfected patients (31.5%) relapsed and only one (4.7%) in the other group. CONCLUSIONS: We did not find major differences in clinical manifestations or laboratory data between the two groups. Biopsies of several tissues can be particularly helpful for diagnosis in immunocompromised patients with negative bone marrow aspirates. Failures, mortality and relapses are more common in HIV infected patients. VL coinfection usually affects HIV infected patients when they develop severe immunodepression.

AIDS-Related Opportunistic Infections↗
PubMed1998

Can alprostadil improve liver failure in HIV-infected patients with severe acute viral hepatitis?

Liver failure with hepatic encephalopathy during an acute viral hepatitis carries a very high mortality. Liver transplantation is the usual treatment, but for poor candidates for transplantation only supportive therapy is available. Two patients with HIV infection developed an acute B hepatitis with liver insufficiency and hepatic encephalopathy. After an alprostadil infusion was begun they improved quickly and made a full recovery. This drug merits further investigation.

Adult↗
PubMed1992

[Neonatal diabetes mellitus and microcephaly. Indications for autosomal recessive inheritance].

Still, there are a lot of questions about the pathogenesis of neonatal diabetes mellitus. In the author's opinion neonatal diabetes mellitus is a distinct entity which differs from the well-known types of diabetes in children (type 1 diabetes, MODY-diabetes) and transient neonatal hyperglycemia regarding pathogenesis, pathophysiology and prognosis. Casuistics of three children two of whom were sibs are reported in detail to demonstrate the characteristics of neonatal diabetes mellitus. Regarding the reported sibs we suppose genetic origin of the disease. Autosomal-recessive mode of inheritance must be assumed.

Abnormalities, Multiple↗