Biomedical subjects
Publications and source records attributed to G Pasero.
A case of recurrent, superficial phlebitis in the lower extremities, with raised blood uric acid levels, responsive to colchicine and to urate pool depletion, but unassociated with articular complaint is reported. The possibility that such a phlebitis may represent an isolated, critical manifestation of acute gout is stressed.
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Since a striking association between hepatitis C virus (HCV) infection and mixed cryoglobulinemia has been demonstrated, the aim of this study is to investigate the effect of alpha-interferon (alpha-IFN) on HCV viraemia and clinico-serological manifestations of 15 patients (ten female and five male, mean [+/- SD] age 53 +/- 7 years). In 14/15 patients pre-study steroid dosage remained unchanged during treatment. alpha-IFN was administered at a dose of 2 x 10(6) IU daily for a month, then every other day for five months. On the whole, a statistically significant improvement of purpura (p < 0.001), serum transaminases (p < 0.001), and cryocrit (p < 0.01) was observed after alpha-IFN treatment. HCV viraemia was detected by polymerase chain reaction technique in 13/15 patients with mixed cryoglobulinemia and anti-GOR antibodies, expression of HCV-related autoimmunity, were present in 8/15. After alpha-IFN treatment, HCV RNA levels showed a clear-cut reduction in five persons and disappeared in another, while anti-HCV antibodies (Chiron ELISA and RIBA II) did not change after the six-month period of therapy. These data further support the possible etiopathogenetic role of HCV in patients with mixed cryoglobulinemia and suggest that alpha-IFN may be regarded as the elective treatment in this disease.
The prevalence of antibodies against hepatitis C virus (anti-HCV) in an unselected series of 45 mixed cryoglobulinemia patients was assessed by an enzyme linked immunosorbent assay (Chiron ELISA HCV, Second Generation). The anti-HCV specificity was evaluated by a recombinant based immunoblot assay (Chiron RIBA HCV, Second Generation Assay). HBV-related markers and HIVAb were detected in the same samples. The prevalence of anti-HCV observed in mixed cryoglobulinemia was compared with 80 patients with other immunological systemic diseases. Anti-HCV were found in 91% of mixed cryoglobulinemia patients, and confirmed by RIBA in all cases; on the other hand, anti-HCV were practically absent in other control diseases. HBV markers were recorded in 49% of mixed cryoglobulinemia subjects; while HIVAb were constantly absent. These data give us new insights into the etiopathogenesis of mixed cryoglobulinemia.
Twenty-one of 30 patients with essential mixed cryoglobulinemia (EMC) had evidence of liver involvement. The liver disease was characterized by the absence of clinical symptoms, hepatosplenomegaly, mild elevation of enzymes, abnormal BSP retention and low albumin levels. Histology, available in 12 patients, showed either chronic persistent or chronic active hepatitis or liver cirrhosis; 44% of the patients had HBsAg or HBsAb in sera and/or cryoglobulins, confirming the high frequency of exposure to hepatitis B virus (HBV) infection in EMC. However, liver lesions were similar in all patients, regardless of HBV exposure. Since other factors usually associated with chronic liver diseases were absent or apparently irrelevant, it is temptative to speculate that a 'cryoglobulinemic hepatitis' may exist as a distinct syndrome. The characteristic complement profile of the patients with EMC (low CH50 and C4, normal C3PA), not related to albumin levels, can help to differentiate this disease from chronic liver disease without cryoglobulins.
The authors review the role, clinico-serological correlations and the putative pathogenetic relevance of a number of immunological parameters in essential mixed cryoglobulinemia. On the whole, in spite of the fact that levels of cryoglobulins, immune complexes, complement as well as reticuloendothelial splenic function are frequently abnormal in this condition, they are generally poorly correlated with clinical features. Therefore, it is postulated that this apparent discrepancy may either be due to the contemporary presence in the same serum of many types of immune complexes with different toxicity, or to the influence of rheumatoid factor on the nature of circulating immune complexes.
Prolonged plasma-exchange without addition of cytotoxic agents was employed in 16 patients with mixed cryoglobulinemia and kidney, liver or neurologic involvement. Patients with rapidly progressive renal failure or active and reversible lesions generally improved after plasma-exchange, as well as those with a recently occurring sensory-motor peripheral neuropathy. In 4 out of 6 patients with mixed cryoglobulinemia and chronic active hepatitis, plasma-exchange was followed by either normalization or significant reduction of liver enzymes and bromosulfophthalein retention. In all cases responding to plasma-exchange the beneficial effects were evident after the first 2-3 weeks of treatment, while symptoms did not generally recur when the procedures were either slowly tapered or discontinued. Although the pathogenetic mechanism(s) of action of plasma-exchange remains largely unknown, preliminary data indicate that these procedures induce quantitative as well as qualitative changes in the immune system.
Pathological abnormality (neuroma) related to the painful foot condition commonly called "Morton's metatarsalgia" was first observed in 1835 by Filippo Civinini (1805-1844) of Pistoia, in course of a cadaverous dissection, and clearly described in the anatomic letter entitled "Su un nervoso gangliare rigonfiamento alla pianta del piede" ("On the neural ganglion swelling of the foot sole"). In this study a brief review on the history of Morton's metatarsalgia is carried out, and the importance of Civinini in the discovery of the neuroma of the III intermetatarsal web is underlined.
OBJECTIVE: To investigate the prevalence of human parvovirus B19 (B19) infection in the bone marrow of systemic sclerosis (SSc) patients. METHODS: Twenty-one consecutive SSc patients and 15 sex- and age-matched subjects without immunological rheumatic diseases were studied for: (i) the presence of circulating anti-B19 antibodies (anti-B19 IgG and IgM type and anti-B19 NS1 IgG) detected by means of standard methodologies, and (ii) B19 genomic sequences in sera and bone marrow biopsy specimens using a nested-PCR technique. RESULTS: The presence of B19 DNA was demonstrated in a significant percentage of bone marrow biopsies from SSc patients (12/21; 57%) and was never detected in the control group (p < 0.01). In no case was the B19 viremia observed, while serum anti-B19 NS1 antibodies, possible markers of B19 persistent infection, were more frequently detected in SSc patients than in controls (33% vs 13%). SSc patients with bone marrow B19 infection showed a shorter mean disease duration than B19-negative patients (5.6 +/- 4.2 vs 12.7 +/- 7.8 yrs; p < 0.01). CONCLUSIONS: This is the first demonstration of bone marrow B19 infection in a significant percentage of SSc patients. The possible etiopathogenetic role of B19 should be verified in a larger patients series and further investigated by means of molecular biology studies.
OBJECTIVE: To assess vertebral bone mineral density (BMD) changes in rheumatoid arthritis (RA) patients taking low-dose methotrexate (MTX). METHODS: We evaluated in a 2-year, longitudinal study female RA patients, who had recently started a disease-modifying antirheumatic drug (DMARD), divided into two groups: group A, receiving MTX, and group B, receiving other DMARDs. Lumbar spine BMD was assessed at baseline and every year; RA activity was assessed every 3 months. RESULTS: Sixty-two patients were enrolled in the study; 40 completed the follow-up period: 22 of group A, and 18 of group B. The results after 2 years showed that both groups lost bone significantly vs baseline (p < 0.001) in a comparable fashion: group A (mean +/- SD) -3.9 +/- 4.9% vs group B -3.0 +/- 3.7% (p = NS). The patients who showed active disease lost significantly (p < 0.05) more bone (-5.5 +/- 3.8%) than those with less active disease (-1.1 +/- 3.6%), independently of their DMARD. CONCLUSION: Low-dose MTX in RA does not seem to exert relevant effects on trabecular bone.