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Biomedical subjects

E Muñoz de Bustillo

Publications and source records attributed to E Muñoz de Bustillo.

10 recordsLinked to original sources

Fibrosing cholestatic hepatitis-like syndrome in hepatitis B virus-negative and hepatitis C virus-negative renal transplant recipients.

Cholestatic hepatitis and diffuse liver fibrosis have been described in immunosuppressed patients with hepatitis B virus or hepatitis C virus infection as fibrosing cholestatic hepatitis (FCH). FCH is characterized by cholestasis, with only a modest increase in aminotransferase levels. The pathologic picture typically shows periportal and perisinusoidal fibrosis, scarce mixed infiltrates, hepatocellular ballooning, and histologic cholestasis. We report two patients with diffuse fibrosis and cholestasis quite similar to the histologic picture of FCH, but in whom neither hepatitis B virus nor hepatitis C virus infection could be shown, highlighting the potential contribution of cytomegalovirus infection and azathioprine toxicity in the development of this severe complication of solid-organ transplantation.

Adult↗

Hepatitis C virus-related fibrosing cholestatic hepatitis after cardiac transplantation: is azathioprine a contributory factor?

We report a patient who acquired hepatitis C virus (HCV) infection at cardiac transplantation, developing fibrosing cholestatic hepatitis (FCH) with early liver failure and a fatal outcome. FCH is a recently described clinicopathological entity characterized by a cholestatic pattern of serum liver enzyme abnormalities, a progressive course leading to liver failure, and a pathological picture defined by periportal fibrosis, neutrophilic infiltrates and signs of histological cholestasis. Although it was initially described secondary to hepatitis B virus infection, it has also been recently related to HCV infection. Some histopathological features consistent with azathioprine hepatotoxicity like cholestasis, perisinusoidal fibrosis, veno-subocclusive lesions and nodular regenerative hyperplasia were also observed in this case. Therefore, a direct cytopathic effect of HCV and the concurrent pathogenic role of azathioprine hepatotoxicity may be involved in the development of this complication of transplantation.

Azathioprine↗

Eradication and follow-up of Helicobacter pylori infection in hemodialysis patients.

It is currently accepted that Helicobacter pylori (Hp) infection is crucial in the pathogenesis of peptic ulcer. Therefore, we developed a prospective study to assess the prevalence of Hp infection by the 13C Urea Breath Test (13C UBT) in 52 hemodialysis patients, and we evaluated the efficacy of two consecutive eradication regimens in 23 positive patients with dyspepsia and/or on a transplantation list. The correlation between anti-Hp serology and 13C UBT results was also analyzed in 34 patients who were followed up during 18 months. The Hp prevalence by 13C UBT was 63.5% (33/52). The eradication rate after the first cycle of therapy (amoxicillin 500 mg/8 h and omeprazole 20 mg/12 h, 14 days) was 60.8% (14/23). After the second cycle (clarithromycin 500 mg/12 h plus omeprazole 20 mg/12 h, 14 days), the eradication rate reached 82.6% (19/23). The serological procedure showed a good correlation with 13C UBT (about 80% sensitive and specific) when very restrictive diagnostic and eradication criteria were adopted. We conclude that an eradication rate higher than 80% can be reached after two consecutive cycles of dual therapy in hemodialysis patients. Anti-Hp serological tests must be cautiously interpreted in these patients.

Aged↗

Recurrent type III membranoproliferative glomerulonephritis after kidney transplantation.

The first well-documented case of recurrent type III membranoproliferative glomerulonephritis after kidney transplantation is reported in this article. A 48-year-old man was admitted to the hospital because of nephrotic syndrome and moderate renal failure. The renal biopsy showed double-contour images at light microscopy. Electron microscopy revealed electron-dense deposits in the mesangium and in both the subepithelial and subendothelial sides of the basement membrane. Subepithelial deposits were sometimes hump-like and produced an irregular disruption of the lamina densa. A diagnosis of type III membranoproliferative glomerulonephritis was suggested. The patient had a rapid decrease in renal function and received dialysis in 3 months. Three years later, he received a cadaveric kidney transplant, and subsequently recovered normal renal function. Proteinuria appeared after 13 months, and a biopsy of the graft demonstrated recurrence of the original disease. Seven years after transplantation, he returned to hemodialysis.

Biopsy↗