Membranoproliferative glomerulonephritis associated with hepatitis C virus infection responsive to interferon-α

Yamabe, Hideaki; Johnson, Richard J.; Gretch, David R.; Osawa, Hiroshi; Inuma, Hiroshi; Sasaki, Takashi; Kaizuka, Mitsuaki; Tamura, Naoyuki; Tsunoda, Satoru; Fujita, Yoshiko; Sato, Atsushi; Onodera, Kenji

doi:10.1016/0272-6386(95)90628-2

Cited by 54 publications

(25 citation statements)

References 7 publications

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“…Two major extrahepatic manifestations of HCV (mixed cryoglobulinemia and membranoproliferative gloumerulonephritis) – which are immune by nature, may respond to treatment with interferon-α [24, 25, 26]. The response is accompanied by the disappearance of the HCV viremia, but a relapse of both the viremia and the extrahepatic manifestation is the rule [24, 26].…”

Section: Discussionmentioning

confidence: 99%

Pure Red Cell Aplasia Responsive to Interferon-α in a Patient with Hepatitis C Virus Infection

Davidovitz

Halpern²,

Vardi³

et al. 1998

Acta Haematol

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A 51-year-old man presented with severe anemia, mild splenomegaly and elevated serum aspartate aminotransferase and serum alanine aminotransferase levels. The bone marrow findings were consistent with pure red cell aplasia (PRCA) with a ‘maturation arrest’ at the level of pronormoblast. The patient has been transfusion-dependent for 8 months. Following diagnosis of chronic active hepatitis due to hepatitis C virus (HCV), therapy with interferon-α was initiated. Two weeks later, the hemoglobin level stabilized, and he has not required any transfusion ever since. In spite of ongoing HCV viremia, cessation of interferon therapy, and deterioration of the liver function tests, the patient, followed for 2 years, maintains a high-normal hemoglobin level. To the best of our knowledge, this is the first report of prolonged PRCA corrected by interferon-α therapy, with or without an ongoing HCV infection. We speculate that the ‘maturation arrest’ of the erythroid lineage seen in the bone marrow was the result of an immune mechanism, possibly induced by the HCV, and that the elimination of this mechanism, rather than the elimination of the HCV, provided the opportunity for regeneration of erythropoiesis.

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Section: Discussionmentioning

confidence: 99%

Pure Red Cell Aplasia Responsive to Interferon-α in a Patient with Hepatitis C Virus Infection

Davidovitz

Halpern²,

Vardi³

et al. 1998

Acta Haematol

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“…Interferon alpha has been approved for use in the treatment of chronic HCV infection. Many investigators have reported that interferon alpha lowers urinary protein concomitant with the disappearance of HCV RNA in HCVassociated glomerulonephritis (2,3). These reports suggest that HCV is very important as an antigen.…”

Section: Introductionmentioning

confidence: 99%

Clinicopathological Study on Hepatitis C Virus-associated Glomerulonephritis without Hepatitis C Virus in the Blood

et al. 2010

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Purpose Patients with hepatitis C virus (HCV)-associated glomerulonephritis in whom HCV RNA was not detected in the blood have been reported. We attempted to uncover the differences between HCV RNAnegative and HCV RNA-positive cases. Methods The clinical and pathological findings for 5 patients with HCV-associated glomerulonephritis without HCV in the blood were compared with those for 23 patients with HCV RNA-positive HCVassociated glomerulonephritis. Results The HCV RNA-negative cases were characterized by advanced age, female dominance, no cryoglobulinemia and no glomerular deposition of IgG compared with the HCV RNA-positive cases, although no differences were observed in amount of urinary protein, frequency of nephrotic syndrome, serum levels of total protein, creatinine level, presence of hypocomplementemia and rheumatoid factor. The prognosis was similar for both groups. Conclusion These cases point to the need for further study of the pathogenesis of this disease.

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“…HCV enhances pulmonary fibrosis 5881 cutanea tarda [9] , membranoproliferative glomerulonep hritis [12,13] , autoimmune thyroiditis [14][15][16] , sialadenitis [17] , and cardiomyopathy [18] . A few previous studies have presented conflicting results, with some suggesting that an incidence of anti-HCV antibody positivity in patients with idiopathic pulmonary fibrosis (IPF) is significantly higher than that in patients without IPF both in Italy and Japan [19,20] .…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus enhances incidence of idiopathic pulmonary fibrosis

Arase¹,

Suzuki²,

Suzuki³

et al. 2008

WJG

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AIM: To investigate the cumulative development incidence and predictive factors for idiopathic pulmonary fibrosis in hepatitis C virus (HCV) positive patients. METHODS: We studied 6150 HCV infected patients who were between 40-70 years old (HCV-group). Another 2050 patients with hepatitis B virus (HBV) were selected as control (HBV-group). The mean observation period was 8.0 ± 5.9 years in HCV-group and 6.3 ± 5.5 years in HBV-group. The primary goal is the development of idiopathic pulmonary fibrosis (IPF) in both groups. The cumulative appearance rate of IPF and independent factors associated with the incidence rate of IPF were calculated using the KaplanMeier method and the Cox proportional hazard model. All of the studies were performed retrospectively by collecting and analyzing data from the patient records in our hospital. RESULTS: Fifteen patients in HCV-group developed IPF. On the other hand, none of the patients developed IPF in HBV-group. In HCV-group, the cumulative rates of IPF development were 0.3% at 10th year and 0.9% at 20th year. The IPF development rate in HCV-group was higher than that in HBV-group (P = 0.021). The IPF development rate in patients with HCV or HBV was high with statistical significance in the following cases:(1) patients ≥ 55 years (P < 0.001); (2) patients who had smoking index (package per day × year) of ≥ 20 (P = 0.002); (3) patients with liver cirrhosis (P = 0.042). CONCLUSION: Our results indicate that age, smoking and liver cirrhosis enhance the development of IPF in HCV positive patients.

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Membranoproliferative glomerulonephritis associated with hepatitis C virus infection responsive to interferon-α

Cited by 54 publications

References 7 publications

Pure Red Cell Aplasia Responsive to Interferon-α in a Patient with Hepatitis C Virus Infection

Pure Red Cell Aplasia Responsive to Interferon-α in a Patient with Hepatitis C Virus Infection

Clinicopathological Study on Hepatitis C Virus-associated Glomerulonephritis without Hepatitis C Virus in the Blood

Hepatitis C virus enhances incidence of idiopathic pulmonary fibrosis

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