Hepatitis C virus (HCV) infection is a major public health concern worldwide, raising important medical and economic issues. HCV-related end-stage liver disease is one of the most common indications for hepatic transplantation. Chronic hepatitis C is also assimilated to a systemic disease because of multiple extrahepatic manifestations, including lymphoproliferative disorders. The revolution of HCV treatment with the advent of direct-acting antivirals has significantly improved the management with high antiviral efficacy and good safety profile compared with old regimens, thus allowing good outcomes on hepatic and extrahepatic symptoms. However, with the widespread use of these new agents, controversial concerns about unexpected increasing cases of hepatocellular carcinoma were reported. We now report the case of a patient presenting with HCV-related cirrhosis, treated with direct-antiviral therapy and diagnosed with primary hepatic lymphoma shortly after the end of the treatment.
Background:
Background: Patients with Cohn’s disease (CD) treated with thiopurines are at an increased risk of developing cancer. Leukemias are less frequent than other hematopoietic tumors and development of Chronic myeloid leukemia (CML) after immunosuppression has not been proven.
Case Report:
We describe the case of a 61-year-old female who developed a CML after 8 years of treatment with azathioprine (AZA) for ileal Crohn’s disease associated to a duodenal localization. We reviewed the current evidence on the interactions between CD, CML and AZA as well as the potential underlying mechanisms of leukemia in AZA-treated patients.
Conclusion:
We concluded that the pathogenesis of CML is multifactorial in CD. The nature of the association between AZA and CML in CD patients warrants further investigation.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
H syndrome is an extremely rare autosomal recessive affection caused by biallelic mutations in the SLC29A3 gene encoding the human equilibrative nucleoside transporter hENT3. The hallmark signs are cutaneous consisting of hyperpigmentation and hypertrichosis patches. Besides, associated systemic manifestations are highly various reflecting phenotypic pleiotropism. Herein, we report a first case of pseudo-Meigs’ syndrome occurring in a young Tunisian H syndrome diagnosed patient with a novel homozygous frameshift mutation in exon 2 of the SLC29A3 gene: p.S15Pfs*86 inducing a premature stop codon. The patient developed ascites associated with left ovarian mass and she underwent surgery. After tumor resection, ascites disappeared rapidly. Histological examination showed serous cystadenoma of the ovary orienting the diagnosis towards pseudo-Meigs’ syndrome.
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