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Biomedical subjects

R Estruch

Publications and source records attributed to R Estruch.

101 records · Page 6Linked to original sources
PubMed1981

[Legionnaires' disease. First observations in Catalonia (author's transl)].

The authors report the first two cases of legionnaires' disease from Catalonia. Both patients were chronic bronchitic males, and the cases were sporadic. The onset of the disease was characterized by a febrile illness with muscle and joint pains, respiratory symptoms (cough and mucous sputum production), and mental changes. There were no digestive complaints. Pulmonary consolidation occurred in both patients in the left upper lobe. Blood chemistries disclosed the existence of an absolute lymphopenia, altered liver function tests, and elevated CPK levels. Bacterial cultures of blood and sputum, respiratory virus screening (influenza A and B, parainfluenza 1, 2 and 3, and adenoviruses), and tests for Mycoplasma pneumoniae, Coxiella burnetti and Chlamydia psittaci were all negative. Antibody titers against Legionella pneumophila by indirect immunofluorescence were 1/1024 (positive) for serotype 1 and 1/1024 (positive) for serotype II in one patient, and 1/1024 (positive) for serotype I and 1/128 (negative) for serotype II in the other patient. The authors review the epidemiological, clinical, biochemical and diagnostic aspects of legionnaires' disease, which knowledge will undoubtedly allow to detect an increasing number of cases.

Bronchitis↗
PubMed1981

[Hodgkin's disease presenting as an hepatic disease. Report of two cases (author's transl)].

During the course of Hodgkin's disease there is a low incidence of clinical manifestations of liver involvement: less than 15% of the patients present jaundice at some time during the evolution of their disease. The initial manifestation of Hodgkin's disease as an hepatic illness is a rare event. Two such cases are herein reported. The first patient was a 68 year-old male with a febrile illness of one month duration who 15 days before admission presented painless jaundice, dark urine, and discolored stools. The clinical work-up pointed to the possible existence of an extrahepatic cholestasis. At laparotomy a normal biliary tree was found, and surgical liver biopsy disclosed severe tissue cholestasis and a granulomatous portal reaction constituted by white blood cells, eosinophiles and histiocytes, most of them atypical and some showing features of Reed-Sternberg cells. The second patient was a 21 year-old male with a febrile illness of four months duration who developed jaundice and progressive mental obtundation one week before admission. The biochemical studies demonstrated severe pancytopenia and signs of advanced liver failure. Percutaneous liver biopsy disclosed a normal hepatic architecture and the presence of numerous atypical histiocytes in the portal areas. Lymphography showed sizeable pelvic and paraaortic lymph nodes. Subsequent laparotomy for lymph node biopsy confirmed the diagnosis of Hodgkin's disease, nodular sclerosis type. The authors suggest that hepatic Hodgkin's disease must be considered in the differential diagnosis of any febrile illness with jaundice.

Adult↗
PubMedDate not supplied

High alcohol intake as a risk and prognostic factor for community-acquired pneumonia.

OBJECTIVE: To evaluate whether high alcohol intake is an independent risk factor for community-acquired pneumonia in middle-aged people and whether it confers a poor prognosis. METHODS: A two-phase study was performed. Risk factors for community-acquired pneumonia were evaluated in a case-control study of 50 patients and 50 controls. Prognostic factors and microbiologic and clinical features were then evaluated in a cohort study of the 50 middle-aged patients with community-acquired pneumonia. RESULTS: In the first study, the only independent risk factor for community-acquired pneumonia was high alcohol intake (P < .02). In the second study, patients with chronic alcoholism had a higher incidence of pneumonia caused by gram-negative bacilli (P < .03), as well as a higher incidence of Candida albicans (P < .03), Staphylococcus aureus (P < .0001), and gram-negative bacilli (P < .001) in the cultures of pharyngeal smears than did the nonalcoholics. Compared with nonalcoholic patients, alcoholic patients with pneumonia showed more severe clinical symptoms (P < .02), required longer intravenous treatment (P < .02) and longer hospital stay (P < .01), and had multilobar involvement and pleural effusion (both P < .01), as well as slower resolution of pulmonary infiltrates. The only prognostic factor for mortality was high alcohol intake (P < .03). CONCLUSIONS: High alcohol intake is the main risk factor for developing community-acquired pneumonia in middle-aged people. This situation also confers a worse prognosis in these patients, who should be treated with broad-spectrum antibiotics for a longer period.

Adult↗
PubMedDate not supplied

Chronic alcohol consumption increases serum levels of circulating endothelial cell/leucocyte adhesion molecules E-selectin and ICAM-1.

A group of 30 chronic alcoholics without alcohol-related diseases and 30 controls (teetotallers) were selected to measure serum levels of endothelial adhesion molecules (AMs) (ICAM-1, VCAM-1, and E-selectin). ICAM-1 and E-selectin serum levels were higher in alcoholics, whereas VCAM-1 serum levels were similar in both groups. There was a significant correlation between daily alcohol intake and serum level of ICAM-1 (r = 0.49, P = 0.003) and E-selectin (r = 0.41, P = 0.02). A significant positive correlation between E-selectin and total lifetime dose of ethanol was also observed (r = 0.52, P = 0.003). These changes in serum levels of endothelial AMs of chronic alcoholics may reflect endothelial and/or immune activation, and could interfere with the reactions between immune cells and the endothelium.

Adult↗
PubMedDate not supplied

Acute ethanol treatment decreases intracellular calcium-ion transients in mouse single skeletal muscle fibres in vitro.

Alcohol misuse frequently leads to muscle weakness, which may also occur in the setting of acute and chronic alcoholic myopathies. At the cellular level, ethanol has been found to interfere with signalling mechanisms in cardiac myocytes, skeletal myotubes, and smooth muscle cells. In this study, we focused on the effects of ethanol on the intracellular calcium ([Ca(2+)](i)) transients responsible for excitation-contraction (EC) coupling in isolated mouse skeletal fibres loaded with the fluorescent Ca(2+) indicator fura-2. Following electrical stimulation, ethanol caused a significant reversible dose-dependent reduction in [Ca(2+)](i) transient amplitude, already significant at 100 mM ethanol (P = 0.03), without modifying resting [Ca(2+)](i). Evaluating the potential loci for the effects of ethanol, we indirectly measured sarcolemmal Ca(2+) entry by monitoring Mn(2+)-quenching of intracellular fura-2 via the nitrendipine-sensitive Ca(2+) channels during electrical pacing. Ethanol at doses of 20 mM and greater caused a dose-dependent reduction in the rate of fura-2 quenching (all at P<0.05). Moreover, the intracellular pool of Ca(2+) releasable by caffeine was found to be reduced at a minimum of 300 mM ethanol (P = 0.05). We conclude that ethanol reduces the [Ca(2+)](i) transients underlying EC coupling in single mouse skeletal muscle fibres. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca(2+) influx via voltage-operated Ca(2+)-channels and, to a lesser extent, to a reduction in the Ca(2+) sarcoplasmic reticulum loading state. This inhibitory effect of ethanol may be implicated in the development of muscle weakness with alcohol consumption.

Animals↗