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Biomedical subjects

L E Muñoz

Publications and source records attributed to L E Muñoz.

6 recordsLinked to original sources
PubMed2006

Further description of early clinically silent lupus nephritis.

Thirty silent lupus nephritis (SLN) patients were compared to 16 individuals bearing overt lupus nephritis (OLN). Results included: years of systemic lupus erythematosus (SLE) diagnosis were significantly earlier (4.6 +/- 2.8 years) in SLN than in OLN (7.18 +/- 3.61) (P < 0.05). Neurological compromise, hypertension, normocitic anemia and lymphopenia were significantly prevalent in OLN than in SLN (P < 0.05). Beside normal urinary sediment and renal function tests, the SLN group showed a moderate increase of both activity (AI) and chronicity (CI) renal pathology index when compared to highly increased AI and CI in OLN (P < 0.05). Seventy percent of SLN patients were ISN/RPS Classes I (6.6%) and II (63.3%) while 81% of OLN cases were Classes III, IV (37.5%) and V. IgG, IgA, IgM, lambda chain, C3 and fibrinogen immune deposits were found in 90% or over in both SLN and OLN individuals while in 60% or over, both groups also showed kappa chain, Clq and C4 deposits. While prevalence of ANA, anti-dsDNA and anti-C1q antibodies were similar in both groups, anti-histone, anti-RNP, CIC and CH50 serum levels were significantly different in OLN versus SLN (P < 0.05). We strongly suggest that indeed SLN is the earliest stage in the natural history of lupus nephritis.

Adult↗
PubMed2001

Expression of inducible nitric oxide synthase in the liver of bile duct-ligated Wistar rats with modulation by lymphomononuclear cells.

BACKGROUND: The current study evaluated whether biliary tract obstruction stimulates inducible nitric oxide synthase (iNOS) protein expression in the liver and analyzed the implication of lymphomononuclear cells and interleukin-4 (IL-4). METHODS: Male Wistar rats were used. Bile flow interruption was achieved by a complete division of the extrapancreatic common bile duct. iNOS expression was determined by both the Western blot technique and immunohistochemistry. RESULTS: iNOS protein was markedly expressed in the liver 7 days after bile duct obstruction. Treatment with thymostimulin (TP-1), a partially purified thymic extract, reduced the intensity of the expression of iNOS protein in the liver after bile duct ligation. Recent data have suggested that IL-4 attenuates iNOS protein expression. We then analyzed the involvement of this anti-inflammatory cytokine on the modulation of iNOS expression in the liver. The liver from rats that underwent bile duct ligation (BDL) showed a lower content of IL-4 than that of sham-operated (SO) rats. TP-1 treatment increased the content of IL-4 in the liver. Liver slices incubated in vitro with Escherichia coli lipopolysaccharide (LPS, 10 microg/mL) stimulated the expression of iNOS protein. The level of LPS-induced iNOS expression was reduced by lymphomononuclear cells obtained from sham-operated animals. However, lymphomononuclear cells isolated from BDL rats potentiated the induction of iNOS expression by LPS-stimulated liver. However, lymphomononuclear cells from TP-1-treated BDL rats failed to modify LPS-stimulated iNOS expression. The different effect of lymphomononuclear cells on the modulation of iNOS expression in the liver was associated with their ability to generate IL-4. CONCLUSIONS: The liver of jaundiced rats markedly expressed iNOS protein, which was associated to modifications in the content of IL-4 in the liver. Furthermore, lymphomononuclear cells modulate iNOS protein expression in the liver by a mechanism in which IL-4 is involved.

Animals↗
PubMed1992

Early detection of complications in amebic liver abscess.

A retrospective analysis of 140 cases with amebic liver abscess (ALA) seen at the AUNL University Hospital was done to see if patients with complications can be identified earlier in order to decrease morbidity and mortality. Sixteen patients (11.4%) presented complications and six patients died (4.2%). Patients with complications presented jaundice, large or multiple abscesses, acute abdomen, liver failure and sepsis more often than patients without complications. Hemoglobin, hematocrit, prothrombin time, total proteins, albumin, LDH, and BUN were more altered in patients who presented complications. The titer of antibodies against E. histolytica was higher in this group of patients. The six patients who died had been operated on. The causes of death were septic shock in two, sepsis in one, peritonitis in one, liver failure in one and colon perforation in one patient. Pleural effusion, jaundice and acute abdomen were seen in three patients, respectively (50%), two cases had multiple abscesses (33.3%), one patient had a ruptured abscess (16.7%). Patients who died exhibited more alterations in six laboratory examinations at admission: partial prothrombin time, total bilirubin, albumin, BUN, LDH, and leukocytes. Clinical data together with the severe alterations in laboratory examinations at admission for patients with ALA should alert the clinician to suspect complications earlier in order to decrease morbidity and mortality.

Abdomen, Acute↗
PubMed1987

Complement activation in patients with amebic liver abscess.

Serum or plasma concentrations of components of the classical (C1q, C4) and alternative (C3, factor B) pathways, regulatory protein factor H, and one of the C3 products of degradation, C3d, were determined in 19 patients with amebic liver abscess (ALA). Patients were divided into two groups. Thirteen patients that recovered under medical treatment who had a significantly shorter clinical course on admission (P less than 0.05) (group 1) exhibited either normal (C1q; C4; factor B; C3d) or increased levels of these components (C3, P less than 0.001; factor B, P less than 0.01). On the other hand, 16 patients that recovered after medical treatment and abscess drainage (group 2) exhibited significantly diminished serum levels of C1q (P less than 0.05), C3 (P less than 0.001), factor B (P less than 0.01) and factor H (P less than 0.05), and normal levels of C4, and C3d as compared to the control group. The relationships among the complement components studied were suggestive of activation of the complement system through the classical pathway in patients within group 1 and through both pathways in group 2. Sera of 3 out of the 5 patients who initially exhibited low plasma levels of C3d showed an increase during convalescence. Plasma levels of C3d were demonstrated to show a direct correlation with serum albumin and SGOT in this group of patients. Possible implications of the complement system in the immunopathogenesis of ALA are discussed.

Complement Activating Enzymes↗
PubMedDate not supplied

[The clinical laboratory in the diagnosis of autoimmune liver diseases].

The mechanism of production of autoimmune diseases is a loss of tolerance to autoantigens, which in turn produces a destruction of target organs. We review two autoimmune liver diseases which are non-organ specific: autoimmune chronic active hepatitis and primary biliary cirrhosis. The former is classified in three types according to its' profile of autoantibodies: type 1, in which anti smooth muscle and antinuclear autoantibodies are found in high titers; type 2, is characterized by the presence in serum of anti liver/kidney and anti cytosolic 1 autoantibodies; in type 3 anti soluble liver antigen antibody is present, results in this last type of autoimmune hepatitis await confirmation. In primary biliary cirrhosis the most important advance in the serologic diagnosis has been in the classification of anti mitochondrial antibodies. Up to now 9 different types of these antibodies are known, 4 of which are found in this disease: anti M2, anti M4, anti M8 and anti M9. Anti M2 and/or anti M9 are associated with a benign course of the disease, whereas anti M2, anti M8 and anti M8 are associated with a progressive course.

Autoantibodies↗