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Biomedical subjects

A Gattoni

Publications and source records attributed to A Gattoni.

At least 19 recordsLinked to original sources
PubMed1997

Eosinophilia triggered by beta-interferon therapy for chronic hepatitis C.

The authors describe a case of eosinophilia occurring in an atopic patient suffering from chronic active hepatitis C following a 2-week course with beta-interferon. Since the most common causes of eosinophilia were ruled out by laboratory and instrumental investigations, the authors suggest a possible role of beta-interferon in triggering eosinophilia, in light of current beliefs about the factors modulating eosinophil growth, differentiation and survival. In particular, it has been supposed that the inhibitory effect of beta-interferon on gamma-interferon production could have triggered a preferential expansion of Th2 type T-helper cells whose particular profile of cytokine secretion has been shown to play a crucial role in the development of eosinophilia. To the authors' knowledge, this is the first report of eosinophilia induced by beta-interferon therapy for chronic hepatitis C.

Chronic Disease↗
PubMed1997

[Hepatitis C and systemic diseases].

In 1989 HCV was demonstrated to be the leading cause of non-A, non-B hepatitis. Not only HCV is able to determine chronic hepatitis in most patients, often leading to hepatocellular carcinoma, but it has also been shown to be strictly associated with a number of immunologically-mediated diseases. This review focuses on the reported associations between HCV and other diseases and the role that HCV might play in their pathogenesis.

Hepacivirus↗
PubMed1997

Serum levels of soluble intercellular adhesion molecule 1 (sICAM-1) as a potential marker of disease activity and remission in patients with chronic hepatitis C.

AIM: To assess whether serum levels of sICAM-1 can be correlated with clinical parameters associated with liver inflammation in chronic hepatitis C patients before and after IFN-alpha treatment and whether in patients who respond to this treatment sICAM-1 levels correlate with relapse or sustained response. METHODS: 34 patients diagnosed with chronic active hepatitis C were administered IFN-alpha at a dose of 9 mU per week for 12 months. In all patients sICAM-1 levels were measured by ELISA before treatment and after 6 and 12 months of therapy. In addition, sICAM-1 levels were measured in all patients who responded to IFN-alpha at 6-month intervals after stopping treatment, for a total 2-year follow-up. RESULTS: In all patients, a significant correlation between sICAM-1 levels and the degree of hepatic involvement at biopsy was observed before starting the treatment. sICAM-1 levels remained elevated throughout the study in all patients who did not respond to IFN-alpha therapy, whereas they showed a significant decrease in all patients exhibiting normal ALT levels following IFN-alpha administration. Moreover, a slow but steady decrease in sICAM-1 serum concentrations to values overlapping those of control subjects was observed in sustained responders after a 2-year follow-up; in contrast, all the patients who relapsed showed a further increase in sICAM-1 levels. CONCLUSIONS: These observations suggest that measurement of sICAM-1 serum levels in chronic hepatitis C patients may be useful for monitoring liver inflammation, especially considering that ALT values may only reflect hepatocellular necrosis while invasive procedures, such as follow-up-liver biopsies, are often not well accepted by patients. Further studies will be necessary to assess whether sICAM-1 levels may be used in helping decide the optimal dose and duration of IFN-alpha treatment.

Adult↗
PubMed1996

Case report of a monoclonal gammopathy in a patient with chronic hepatitis: effects of beta-IFN treatment.

A sixty-one-year-old woman, with cirrhosis, presented with a monoclonal gammopathy of uncertain significance (MGSU). Often in a condition of cirrhosis is present a benign M component hypergammaglobulinemia. The electrophoresis and the immunophoresis showed a dense papraprotein in the gamma-region, an IgG with K light chain, an uncertain Bence-Jones proteinuria, a medullary plasmacytosis (9%), and a following growth of paraprotein were present. Lymphoblastic plasma cell were absent. Treatment with beta-IFN 6 MU for a period of six months and 3 MU for a further period of three months proved ineffective for hepatic disease, but produced a quantitative reduction in gamma-G globulin, the Bence-Jones proteinuria was absent, a reduction in M component and in medullary plasmacytosis. Electrophoresis showed a polyclonal evolution of the gammopathy. Suspension of treatment was followed by de novo rise of monoclonal immunoglobulin. The authors report the use of beta-IFN in the therapy of multiple myeloma.

Antiviral Agents↗
PubMed1996

[Hepatitis C].

HCV carriers are supposed to me 100,000,000 worldwide. 5-15% of subjects are infected via haemotransfusion and another significant amount via intravenous drugs; nevertheless in the major part of subjects the via of transmission remains unclear. HCV causes long-term infectious in the host because of its high frequency of mutations. Mutations origin multiple mutants, called quasi-species, who have distinct immunological features and can so easily escape host immune response. Chronic HCV infection leads to cirrhosis in 5-10 years and to a possible hepatocarcinoma in 15-20 years. Nevertheless, it remains unclear why some patients undergo a slight clinical course, while others experience an aggressive one (exitus in less than 5 years). Alpha-interferon (alpha-IFN) is at date the only drug of proven efficacy in HCV chronic hepatitis, even if HCV eradication is a rare event. The goal to obtain is to standardize doses and duration of the treatment.

Adult↗
PubMed1995

Behavior of soluble intercellular adhesion molecule-1 and endothelial-leukocyte adhesion molecule-1 concentrations in patients with Graves' disease with or without ophthalmopathy and in patients with toxic adenoma.

Expression of intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1) on endothelium can be considered a critical early step for leukocyte migration from blood to tissues during inflammatory processes. Increased circulating soluble ICAM-1 (sICAM-1) levels have been found in sera from patients with Graves' disease (GD) with or without ophthalmopathy. Serum soluble ELAM-1 (sELAM-1) levels have not been measured in these patients. The aim of this study was to clarify the behavior of sICAM-1 and sELAM-1 levels in patients with hyperthyroidism due to GD with or with or without ophthalmopathy and in hyperthyroid patients with toxic thyroid adenoma. We studied sICAM-1 and sELAM-1 levels in 130 subjects (age 23-54 yr), grouped as follows: group 1, 30 untreated hyperthyroid GD patients (21 females and 9 males) with active ophthalmopathy; group 2, 26 euthyroid GD patients (16 females and 10 males) with active ophthalmopathy; group 3, 33 hyperthyroid GD patients (22 females and 11 males) without ophthalmopathy; group 4, 11 untreated hyperthyroid patients (7 females and 4 males) with single toxic adenoma; and a control group of 30 healthy subjects (21 females and 9 males). sICAM-1 and sELAM-1 concentrations were measured by a sandwich enzyme linked immunosorbent assay (ELISA) method. Groups 1, 2, and 3 (P < 0.001 for all 3 groups) but not group 4 showed increased sICAM-1 levels compared with the control group. However, groups 1 and 2 (P < 0.001 for both) showed higher values of sICAM-1 than group 3, and group 1 showed higher sICAM-1 levels than group 2 (P < 0.002). Groups 1 and 2 (P < 0.001 for both) but not groups 3 and 4 showed sELAM-1 levels significantly higher than the control group and positively correlated to the severity score of Graves' ophthalmopathy (GO) (P < 0.002 for group 1 and < 0.01 for group 2). Our results confirm that increased sICAM levels in GD patients with or without ophthalmopathy (with higher levels in patients with GO) but not in hyperthyroid nonautoimmune patients may be the consequence of orbital and thyroid inflammation, and they also suggest that sICAM concentrations could reflect the degree of inflammatory activity. Increased sELAM-1 concentrations only, in patients with ophthalmopathy with or without hyperthyroidism significantly correlated to severity score of GO, suggest the measurement of sELAM-1 levels as a specific marker of endothelium activation in GO.

Adenoma↗
PubMed1992

CD11B lymphocytes in type 1 diabetes mellitus of recent onset.

To evaluate the behaviour of CD8+ cells (suppressor/cytotoxic T lymphocytes) and CD8+Leu15+ cells (CD11B, suppressor T lymphocytes) in type 1 diabetes mellitus, 27 newly diagnosed diabetic patients and 47 normal controls were studied. CD8 cells were significantly increased in 6 patients, decreased in 9 and unchanged in 12. In all diabetic patients was present a lack of CD8+ Leu15+ cells. These results show that in newly diagnosed type 1 diabetes mellitus, suppressor T lymphocytes are reduced independently from the number of CD8 cells.

Adolescent↗
PubMed1989

[Biological tumor markers].

The classification of tumor markers can at present be only provisional since in this field new acquisitions are reported daily. Nevertheless, during the last few years, a number of monographs and chapters in oncology texts have become available for students and physicians in which certain parameters (sensitivity, specificity, predictive value of individual markers) are illustrated, thus allowing for a more accurate evaluation of their diagnostic efficacy and offering indications as to which of these markers are most useful in relation to the site of the tumor. Although tumor markers are present throughout the organism, the above review is limited to those found in blood. Clinical results obtained to far have already lead to the conclusion that tumor markers are useful above all for the diagnostic and therapeutic follow-up of patients rather than for the diagnosis of tumors. The present tendency is for the association of several markers since a higher percentage of positive results is achieved both for diagnostic purposes and for the detection of residual foci after apparently successful treatments and for the precocious detection of recurrences, as well as for the evaluation of the efficacy of ongoing therapies.

Adult↗
PubMed1989

Differential roles of splanchnic and peripheral tissues in determining diurnal fluctuation of glucose tolerance.

To identify the mechanisms and the sites of the diurnal fluctuation in glucose tolerance in humans, we selectively quantitated the components of net splanchnic glucose balance, i.e., splanchnic glucose uptake and hepatic glucose output, as well as peripheral glucose uptake, by combining tritiated glucose infusion with hepatic and femoral venous catheterization. The studies were carried out in 11 healthy volunteers at 8:00 A.M. and at 6:00 P.M. on different days after 12 h of fasting. After intravenous glucose infusion (6.5 mg.kg-1.min-1 for 120 min) blood glucose rose twofold at 8:00 A.M. and threefold at 6:00 P.M. (P less than 0.01). Insulin levels did not differ significantly between the two series of tests. Splanchnic glucose balance switched from the net output of the basal state to a net uptake in both morning and afternoon studies. However, this effect was more marked at 6:00 P.M. than at 8:00 A.M. (at 60-120 min, P less than 0.05). The different pattern of splanchnic glucose balance was entirely accounted for by a greater rise in splanchnic glucose uptake in the afternoon, as the suppression of endogenous glucose output by the glucose load was practically complete in both series of studies. In contrast, glucose uptake by leg tissues increased less at 6:00 P.M. than at 8:00 A.M. (at 30-60 min, P less than 0.05; at 75 and 90 min, P less than 0.01; at 105 and 120 min, P less than 0.005). These data indicate that the mechanism responsible for the reduced glucose tolerance later in the day resides in the peripheral tissues whose ability to dispose of a glucose load is drastically decreased.

Adult↗
PubMed1979

Further suggestions for cerebral CT-localization.

A method of obtaining lateral diagrams of brain lesions or structures from CT-scan pictures has been described and tested for accuracy with satisfactory results. Possible sources of error are discussed.

Brain Diseases↗