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Biomedical subjects

S Mezzano

Publications and source records attributed to S Mezzano.

50 records · Page 3Linked to original sources
PubMed1986

Immune thrombocytopenic purpura associated with hepatitis A.

A 23-year-old man developed thrombocytopenic purpura at the end of the second week of the clinical evolution of hepatitis A confirmed by viral markers. The bone marrow of this patient showed megakaryocytic hyperplasia. Circulating in his serum immune complexes were demonstrated by solid phase conglutinin enzymo-immunoassay. Platelet-reactive serum factors were also detected by an indirect immunofluorescence test using fresh donor platelets as targets. The evolution of both the hepatitis and the purpura were benign with no therapy other than bedrest. Platelet count normalized within five weeks of the onset of purpura, and IgM antibodies against hepatitis A virus as well as circulating immune complexes dropped to normal levels. It is postulated that the thrombocytopenia of this case was caused by nonspecific deposition of immune complexes at the platelet surface.

Adult↗
PubMed1986

Incidence of circulating immune complexes in patients with acute poststreptococcal glomerulonephritis and in patients with streptococcal impetigo.

In an attempt to further study the possible contribution of circulating immune complexes (CIC) in the pathogenesis of acute poststreptococcal glomerulonephritis, 61 patients with APSGN were studied during the first three weeks of the disease, and 13 patients with noncomplicated streptococcal impetigo as a control group. C1q solid phase ELISA and Conglutinin (K) solid phase ELISA were used to measure the levels of immune complexes. The incidence of CIC in a single serum sample from patients with APSGN was 48%. Elevated levels of immune complexes were found in 46% of the patients with streptococcal impetigo. The absolute levels of CIC were comparable in both groups of patients. No correlation was found among the presence of CIC and the clinical, immunoserological or pathological findings of the disease. Our results do not support the hypothesis that trapping of the circulating immune complexes play an important role on the renal injury poststreptococcal infection. Instead, we suggest that CIC are an epiphenomena present in APSGN, and may represent rather a systemic inflammatory immune response in patients with group A streptococcal infection.

Acute Disease↗
PubMed1984

Analysis of humoral and cellular factors that contribute to impaired immune responsiveness in experimental uremia.

An experimental model in rats was developed to define the nature of humoral and cellular factors that contribute to impaired immune responsiveness in chronic renal failure. Addition of uremic rat serum to both normal and uremic lymphocytes significantly suppressed cellular responses, the suppression being more pronounced with uremic lymphocytes. Lymphocytes from uremic rats were only marginally less responsive than normal lymphocytes to concanavalin A stimulation when normal rat serum was added to the cultures, indicating that the cellular factors in impairment were less important than humoral ones. Antibody formation in rat splenocyte cultures to bovine serum albumin was suppressed by addition of uremic serum, but the response to sheep erythrocytes was unaffected. Thus the effect on antibody response in uremic animals is dependent upon the antigen tested.

Animals↗
PubMed1982

Antibody production and antigenic specific suppression to bovine serum albumin in uremic rats.

Antibody response and antigen specific suppression to bovine serum albumin (BSA) in uremic rats have been investigated. Primary immune response was found to be significantly reduced independent of the route of administration or adjuvant while secondary response was affected only in animals in which a weak adjuvant such as Al(OH)3 was used. Antigen specific suppression of uremic rats was achieved by intravenous pretreatment with BSA or a C terminal fragment (505-582) of BSA. Secondary response in sham operated controls was suppressed by BSA but not by the fragment. There was about five-fold greater retention of the fragments in the uremic rats than in sham-operated controls at a 6 hr or later after i.v. administration.

Animals↗