Cases reported "Recurrence"

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1/271. liver transplantation for endstage hepatitis c cirrhosis in a patient with primary hypogammaglobulinaemia.

    liver transplantation was performed in a patient with primary hypogammaglobulinaemia, chronic hepatitis c and hepatic failure. The immediate posttransplant period was uncomplicated. Owing to a stricture of the choledochojejunostomy the patient was reoperated with construction of a hepaticojejunostomy 11 months posttransplant. The patient remained hepatitis c virus (HCV) rna-positive, with high and increasing levels of HCV. Liver biopsies demonstrated the recurrence of HCV. 14 months after the transplantation the patient developed severe diarrhoea caused by cryptosporidium parvum. The infection did not respond to available therapeutic measures. He deteriorated with development of liver failure and died 18 months after the transplantation. The present case report illustrates the difficulties associated with organ transplantation in patients with primary hypogammaglobulinaemia.
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2/271. Autologous bone marrow transplantation for recurrent malignant lymphoma after liver transplantation.

    BACKGROUND: Cancer chemotherapy in chronic carriers of hepatitis b virus is known to promote viral replication, and, when immunosuppressive treatment is stopped, the return of immune competence can be followed by a fulminant hepatitis. liver transplantation may be required and has been successfully performed for this condition. However, malignancy recurrence after transplantation has not been reported yet. methods AND RESULTS: We here report the case of an asymptomatic hepatitis B surface antigen carrier who developed a malignant lymphoma, which was treated by chemotherapy. After cessation of chemotherapy, he developed a fulminant hepatitis, requiring liver transplantation. Three years later, he developed a recurrent malignant lymphoma, which was treated successfully by autologous bone marrow transplantation. In order to prevent viral replication, lamivudine and intermittent administration of fresh-frozen plasma highly concentrated in anti-HBs immunoglobulin was initiated before the bone marrow transplantation. The patient remains well 12 and 56 months after autologous bone marrow and liver transplantation, respectively. CONCLUSIONS: This experience suggests that all hepatitis B surface antigen-positive patients for whom chemotherapy is indicated would benefit from prophylactic antiviral hepatitis b virus therapy. Furthermore, successful autologous bone marrow transplantation is possible after liver transplantation.
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3/271. Abdominal ultrasound findings in children with hemophagocytic lymphohistiocytosis.

    Hemophagocytic lymphohistiocytosis, a variant of histiocytosis, is characterized by an uncontrolled activation of the cellular immune system, including hepatic mononuclear phagocytic cells. Abdominal ultrasound findings in children are evaluated in this disease. We present six pediatric cases, two with familial and four with sporadic hemophagocytic lymphohistiocytosis, examined by abdominal sonography. Three signs were frequently observed: thickening of the gallbladder wall (all cases), increased periportal echogenicity (four cases), and enlarged lymph nodes in the porta hepatis (four cases). hepatomegaly, splenomegaly, and ascitic fluid may also be found. These imaging findings are not specific and may be seen in viral hepatitis. However, once hepatitis is excluded, they may suggest the diagnosis of hemophagocytic lymphohistiocytosis in a critically ill child. A bone smear must be done to establish the diagnosis.
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4/271. sarcoidosis with selective involvement of a second liver allograft: report of a case and review of the literature.

    A case of sarcoidosis recurrent in a patient's second liver allograft is described. There was no granulomatous disease seen in the patient's first liver allograft. After the second orthotopic liver transplantation (OLT), the patient was successfully treated for acute rejection, aspergillus infection, and cytomegalovirus viremia. Approximately 2 months after the second OLT, the patient was treated with long-term interferon-alpha for recurrent hepatitis c. Five years after the operation, he experienced liver failure secondary to recurrent hepatitis and underwent a third OLT. This is only the second reported case of sarcoidosis recurrent in the liver parenchyma of a transplanted organ and the first in which interferon-alpha might have played a role.
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5/271. Secondary hyperparathyroidism exacerbation: a rare side-effect of interferon-alpha?

    Recombinant human interferon alpha (alpha IFN) is the only treatment with proven benefit for chronic hepatitis c virus (HCV) infection. Nevertheless its use in some susceptible individuals has led to the development or aggravation of different autoimmune conditions. We report the case of a 20 year old woman on peritoneal dialysis with chronic lobular hepatitis secondary to HCV infection who developed de novo psoriasis 9 months after starting treatment with alpha-IFN. In addition to psoriasis, alpha-IFN prescription was also concurrent with an unexpected and refractory secondary hyperparathyroidism exacerbation initially characterized by a marked reduction of serum calcium levels and a consequential increase of PTH. Both complications disappeared after drug withdrawal. The clinical sequence makes an alpha-IFN-induced autoimmune side effect the most plausible hypothesis. The case is discussed and some possible etiopathogenic factors are briefly reviewed.
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6/271. Long-term administration of cyclosporin A to HCV-antibody-positive patients with dermatologic diseases.

    BACKGROUND: cyclosporine A (CYA) is an immunosuppressive agent which is being used in the treatment of an increasingly wide range of dermatologic diseases, but its use has been avoided in carriers of hepatitis c virus (HCV). methods: We administered small doses of CYA (maximum, 3 mg/kg/day) for a long time to treat dermatologic diseases in one HCV-antibody-positive patient with no HCV-rna in the blood, one patient with a small amount of HCV-rna in the blood, and two patients with large amounts of HCV-rna in the blood. RESULTS: skin lesions improved in all patients, but recurred upon complete or partial withdrawal of CYA. In the absence of HCV-rna in the blood, or when only a small quantity of HCV-rna was present in the blood, HCV-rna load showed no apparent change. In one patient with a large blood HCV-rna load, CYA dosage reduction was followed by increases in alanine aminotransferase (ALT) levels and decreases in blood HCV-rna. Aggravation of hepatitis due to immunologic reactivation was suspected in this patient. CONCLUSIONS: The reduction of CYA dosage is a key element in the use of this agent for cutaneous diseases.
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7/271. Antiviral treatment for human immunodeficiency virus patients co-infected with hepatitis b virus: combined effect for both infections, an obtainable goal?

    A large percentage of human immunodeficiency virus (hiv) patients have serological evidence of a past or present hepatitis b virus infection (HBV). Long-term survival is increasing for hiv patients because of highly active antiretroviral therapy. Therefore, the chronic hepatitis B infection may become an important determinant of disease outcome in these co-infected patients. We describe two hiv/HBV co-infected patients who were treated with extended antiviral therapy, initially indicated for the hiv infection. lamivudine, a suppressor of viral replication in both infections, was one of these antiviral drugs. One patient showed a severe rebound of the HBV after withdrawal of lamivudine, the other patient developed a mutant hepatitis b virus after 18 months of treatment. This mutation was exclusively induced by lamivudine. These patients show that, with improved hiv-related survival, the HBV infection should be monitored carefully, thereby enabling the physician to interfere with therapy when necessary.
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keywords = hepatitis
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8/271. Recurring fibro-obliterative venopathy in liver allografts.

    Recurrent diseases in liver allografts are not uncommon. These occur most frequently in those transplanted for viral hepatitis B and C. We report an unusual case of recurrent process in two consecutive liver allografts received by a 37-year-old woman, who previously had an unremarkable past medical history but developed a rapidly progressive cholestatic liver failure. Histopathologic examination of the native liver showed fibroocclusive lesions of both terminal hepatic venules and portal vein branches. The exuberant fibroobliterative process created dense fibrosis with whorled appearance, and broad fibrous septa connecting adjacent central areas, and sometimes bridging portal to central areas. Dense portal fibrosis resulted in compression atrophy and loss of bile ducts. The first allograft, which failed within 3 months, showed histopathologic findings similar to that of the native liver. A liver biopsy that was performed 20 months after the second liver transplant again showed similar histopathology. The histopathologic features and clinical presentation of this patient suggest an unusual form of recurring progressive fibroobliterative venopathy causing liver failure.
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keywords = hepatitis
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9/271. Selection of hepatitis B surface "escape" mutants during passive immune prophylaxis following liver transplantation: potential impact of genetic changes on polymerase protein function.

    CASE REPORT: A patient is described who developed hepatitis b virus (HBV) reinfection five months following liver transplantation. Failure of hepatitis B immunoglobulin prophylaxis was associated with the emergence of mutations. HBV gene sequencing identified nucleotide substitutions associated with amino acid changes, one within the major hydrophilic region (MHR) of the HBV surface antigen at amino acid position 144 and one outside the MHR. Because of the overlapping reading frames of surface and polymerase genes, the latter surface antigen change was associated with an amino acid change in the polymerase protein. The patient developed significant allograft hepatitis and was treated with lamivudine (3TC) 100 mg daily. Rapid decline of serum HBV dna was observed with loss of HBV e antigen and HBV surface antigen from serum. There was normalisation of liver biochemistry, and liver immunohistochemistry showed a reduction in HBV core and disappearance of HBs antigen staining. CONCLUSION: Surface antigen encoding gene mutations associated with HBIg escape may be associated with alteration of the polymerase protein. The polymerase changes may affect sensitivity to antiviral treatment. Selection pressure on one HBV reading frame (for example, HBIg pressure on HBsAg, or nucleoside analogue pressure on polymerase protein) may alter the gene product of the overlapping frame. Such interactions are relevant to strategies employing passive immune prophylaxis and antiviral treatment.
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keywords = hepatitis
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10/271. association of lamivudine resistance in recurrent hepatitis B after liver transplantation with advanced hepatic fibrosis.

    BACKGROUND: Orthotopic liver transplantation (OLT) in patients with hepatitis b virus (HBV) infection is known to be associated with a high recurrence rate and poor prognosis. lamivudine, a nucleoside analogue, is a potent inhibitor of HBV replication, but it is associated with a 14-39% rate of resistance. methods: We report on four patients who underwent OLT for HBV infection. In all cases, the HBV infection recurred in the grafted liver and was treated with lamivudine (100 mg daily) on a compassionate-use basis. The patients were monitored closely for serum liver enzymes, hepatitis B surface antigen and HBV dna (by hybridization). Liver biopsy was performed before and after lamivudine therapy. HBV dna was amplified from serum for each patient and sequenced through a conserved polymerase domain, the tyrosine-methionine-aspartate-aspartate (YMDD) locus. RESULTS: All four patients exhibited lamivudine resistance 9-20 months after initiation of the drug. In all patients with a clinically mild disease, liver histology findings (12-24 months after lamivudine therapy) showed progressive fibrosis as compared to biopsies performed before lamivudine therapy, with a significant increase (> or =2 points) in the Knodell score in three patients. Moreover, two patients exhibited worsening of the necroinflammatory process. A mutation at the YMDD motif of the HBV polymerase gene was detected in all cases. CONCLUSIONS: lamivudine resistance frequently occurs in patients with recurrent HBV infection after OLT and is associated with advanced hepatic fibrosis and necroinflammatory process. A combination of antiviral therapies may be necessary.
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