Publications by authors named "Misiani R"

The Mailing List SociSIN (ML-SIN) is beginning to develop, beside more experienced organisational topics, there is also some discussion on clinical topics. During the month of May, some messages requesting the opinion of experienced Colleagues on the use of plasma exchange in the cryoglobulinaemia correlated with HCV have risen an interesting debate on this argument. This issue of the review dedicated to the ML-SIN presents a short introduction dedicated to the definition, the main characteristics and the therapeutic bases of the cryoglobulinaemia associated to HCV.

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Background: Renal involvement in patients with hepatitis C virus (HCV) infection commonly manifests as cryoglobulinemic glomerulonephritis (CGN). The combination of interferon-alpha (IFN-alpha) and ribavirin, which is currently considered the standard antiviral therapy in chronic hepatitis C, could be difficult to carry out in cryoglobulinemic patients who are frequently anemic, even in the absence of renal failure. Clinical and histologic long-term results of this therapeutic regimen have not been so far reported in patients with CGN.

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Background: Hepatitis C virus (HCV) infection is present in most but not all patients with type II mixed cryoglobulinemia.

Objective: To investigate the role of GB virus C (GBV-C) in type II mixed cryoglobulinemia.

Design: Retrospective study of serum and cryoprecipitate samples.

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We report a case of renin-producing leiomyosarcoma associated with the hyponatremic hypertensive syndrome and nephrotic-range proteinuria. Extremely high levels of active renin and, to a greater extent, of prorenin were found in plasma and tumor tissue. Immunohistochemical and in situ hybridization studies demonstrated that the neoplastic cells were the source of renin production.

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Background: Essential mixed cryoglobulinemia is frequently associated with hepatitis C virus (HCV) infection. A beneficial effect of interferon alfa therapy has been reported, but we do not know whether the antiviral activity of the drug affects the clinical and biochemical manifestations of disease.

Methods: In a prospective randomized, controlled trial, we studied 53 patients with HCV-associated type II cryoglobulinemia.

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Objective: To study the association between hepatitis C virus (HCV) infection and essential mixed cryoglobulinemia.

Setting: Wards and clinics of the Ospedali Riuniti di Bergamo and Ospedale di Treviglio e Caravaggio, Italy.

Patients: Fifty-one patients with essential mixed cryoglobulinemia associated with glomerulonephritis and 45 controls with noncryoglobulinemic glomerulopathies.

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We measured the urinary excretion of albumin in 67 healthy primigravidae, at monthly intervals, from 16 to 36 weeks of gestation and 12 weeks postpartum. Of the 67 primigravidae, 55 completed a normal pregnancy and 12 developed pregnancy-induced hypertension. In the latter group, an additional measurement of urinary albumin excretion was performed at 24 weeks postpartum.

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This report describes the course of 23 patients with multiple myeloma and severe renal failure treated with a combination of plasmapheresis, chemotherapy, and supportive measures. Eight of ten patients with acute renal failure (ARF) obtained recovery of renal function, and in five of them serum creatinine concentration returned to normal. The remaining two patients died before the effect of treatment could be evaluated.

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The therapeutic effect of plasma infusion was evaluated in 10 children and seven adults with haemolytic uraemic syndrome. All but one patient responded to this treatment with rapid disappearance of haematological abnormalities. The patient who apparently failed to respond to plasma infusion obtained complete remission of the disease after plasmapheresis.

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Activity of prostacyclin-stimulating factor was measured in six normal, non-pregnant women, six women in early normal pregnancy, six in late normal pregnancy, and six in late pregnancy complicated by severe pre-eclampsia. The activity was lower in the women in late pregnancy than in those in early pregnancy and the controls but was about normal in those with severe pre-eclampsia. These results may be relevant to the physiology of pregnancy and the pathogenesis of pre-eclampsia.

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Prostacyclin production was significantly depressed in foetal and placental vascular tissues from five patients with severe pre-eclampsia in comparison to vascular tissues from women with uncomplicated pregnancy. Such an abnormality may be responsible for a reduced blood flow and defective fetal nutrition thus playing a major role in the pathogenesis of this syndrome.

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Haemolytic uraemic syndrome (HUS) is a severe clinical condition characterised by thrombocytopenia, microangiopathic haemolytic anaemia and renal impairment [1]. At histological examination hyaline microthrombi occluding terminal arterioles and capillaries are generally found. Other syndromes share major clinical and histological diagnostic criteria with HUS.

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Two patients with the hemolytic uremic syndrome were treated with plasma exchange an infusion: in both cases, the reduced platelet count reverted to normal values and the microangiopathic anemia ceased within a few days. Systemic blood pressure and requirement for antihypertensive drug therapy were also markedly reduced following treatment with plasma. Venousprostacyclin (antiplatelet aggregating) activity was undetectable in both patients before but was restored after treatment with plasma.

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Tissues from human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels from normal adults. High prostacyclin generation could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation in which blood pressure is low despite very high cardiac output.

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Three patients with multiple myeloma and severe acute renal failure were treated by repeated plasmapheresis. Recovery of renal function was observed in all. The pathogenetic role of light chains and the possible mechanisms responsible for renal damage are discussed.

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It is suggested that patients with the haemolytic-uraemic syndrome and related disorders (such as thrombotic thrombocytopenic purpura) lack a plasma factor which stimulates prostacyclin (P.G.I2) activity.

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