[Pulmonary infection by Mycobacterium xenopi in a patient with positive HIV].
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Biomedical subjects
Publications and source records attributed to M L Alberola.
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BACKGROUND: In recent studies, the hypothesis has been raised that the mechanisms by which aspirin acts as a protective anti-ischemic agent exceed the inhibition of platelet thromboxane A2 synthesis. Recently, new data have been obtained disclosing a platelet-antiaggregating effect by neutrophils, which occurs through a nitric oxide (NO)/cGMP-dependent pathway. METHODS AND RESULTS: The present study, using platelets and neutrophils from normal subjects, was undertaken to assess the putative effect of aspirin on the neutrophil-mediated, platelet-inactivating effect. Aspirin facilitated the inhibitory effect of neutrophils on platelet activation by thrombin, ADP, or epinephrine. This effect was equally evident in vitro and in blood samples of normal individuals taking aspirin. A significant stimulation of NO-mediated mechanisms in the presence of aspirin was disclosed by different methods, as follows: (1) the increased metabolism of arginine to citrulline, (2) the increase of cGMP in the platelet/neutrophil system, and (3) the inhibitory action of the L-arginine (L-Arg)-competitive analogue L-NMMA, which was reversed by L-Arg. The effect of aspirin appeared to be related to cyclooxygenase inhibition, since it was reproduced by using indomethacin. The vasoconstricting peptide endothelin-1 (ET-1) reversed the effect of aspirin through the endogenous production of platelet-activating factor (PAF) by neutrophils, as judged by the marked inhibitory effect of the PAF antagonist BN-52021. CONCLUSIONS: Our results show that a significant part of the effect of aspirin on platelet activation involves a neutrophil-mediated, NO/cGMP-dependent mechanism. The presence of ET-1 counterbalances these effects of neutrophils on platelet activation, therefore acting as an indirect proactivating agent. These results add new elements for interpreting the effects of aspirin on the interactions between blood cells, with special reference to high endothelin states (for example, ischemia/reperfusion processes).
Hepatitis C virus (HCV) infection is highly prevalent in the chronic renal failure population treated in dialysis units. Transmission of HCV via blood transfusions is becoming an increasing problem, but, nevertheless, the routes by which this transmission occurs are incompletely known. We have searched for the presence of HCV RNA by the polymerase chain reaction (PCR) in serum and dialysis ultrafiltrate in 12 hemodialysis and 5 continuous ambulatory peritoneal dialysis (CAPD) patients, all of whom were HCV-antibody-positive. Serum PCR were positive for HCV RNA in all the cases, whereas PCR performed on samples of hemodialysis ultrafiltrate or peritoneal effluent were always negative for HCV RNA. In addition, 13 patients tested positive for HCV antibodies and 19 out of 32 patients sharing the dialysis monitors with 17 PCR-positive individuals remained negative. From these findings, we conclude that the dialysis ultrafiltrate or peritoneal fluid seems to be an improbable source of HCV dissemination in the dialysis setting. Moreover, a significant group of patients remained HCV-antibody-negative although they shared the same dialysis machine with positive patients. Therefore, the importance of other sources of HCV transmission, namely blood-contaminated material, should be emphasized.
The present study correlated histopathology and diagnostic tests in hemodialysis patients with serologic markers for hepatitis C virus (HCV). Hepatitis C virus infection was found in 65 of 163 patients, as assessed by anti-c100-3 (ELISA 1), anti-c22-3, c33C (ELISA 2), and RIBA 2. Several histopathologic patterns were found in 33 liver samples from HCV-positive individuals: cirrhosis (n = 3), chronic active hepatitis (n = 14), chronic persistent hepatitis (n = 2), isolated hemosiderosis (n = 5), reactive hepatitis (n = 6), and others (n = 3). There was a positive correlation between time from the first aminotransferase peak and histologic damage (P = 0.015). However, the severity of liver disease did not correlate with the intensity of RIBA 2 positivity, mean levels or pattern of aminotransferases elevation, or markers of past hepatitis B virus infection. Moreover, aminotransferases were persistently normal in three patients with severe liver disease and were elevated in 10 patients with only mild changes. In 19 biopsied patients, the presence of plasma HCV RNA was examined by the polymerase chain reaction (PCR), which was positive in 15 of the 19 biopsy specimens. The ability of PCR positivity to predict the histologic severity of the disease was insufficient: four patients with minor liver damage had positive PCR and two patients with significant liver damage had negative PCR. No further correlations of PCR positivity were found with the other biochemical or immunologic markers of HCV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
Three cases of calciphylaxis in patients with terminal renal insufficiency are discussed. The existence of metastatic calcifications, mainly vascular, in patients with chronic renal insufficiency is frequent. However calciphylaxis is a process which is rarely found in these patients. This entity is characterized by the obliteration of small vessels with ischemia and necrosis. The exceptionality of the disease, its difficult treatment and poor evolution make calciphylaxis a bad prognostic complication which should be considered in the differential diagnosis of cutaneous lesions in patients with chronic renal insufficiency.
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