Obstructive jaundice secondary to tuberculosis (TB) is extremely rare. It can be caused by TB enlargement of the head of the pancreas, TB lymphadenitis, TB stricture of the biliary tree, or a TB mass of the retroperitoneum.A 29-year-old man with no previous history of TB presented with abdominal pain, obstructive jaundice, malaise and weight loss. Ultrasonography (US), computer tomography (CT) scan and endoscopic retrograde cholangiopancreatography (ERCP) were suggestive of a stenosis of the distal common bile duct (CBD) caused by a mass in the posterior head of the pancreas. Tumor markers, CEA and CA19-9 were within normal limits. At operation, an enlarged, centrally caseous lymph node of the posterior head of the pancreas was found, causing inflammatory stenosis and a fistula with the distal CBD. The lymph node was removed and the bile duct resected and anastomosed with the Roux-en Y jejunal limb. Histology and PCR based-assay confirmed t u b e rc u l o u s l y m p h a d e n i t i s . A f t e r a n u n e ve n t fu l postoperative recovery, the patient was treated with anti-tuberculous medication and remained well 2.5 years later. Though obstructive jaundice secondary to tuberculous lymphadenitis is rare, abdominal TB should be considered as a differential diagnosis in immunocompromised patients and in TB endemic areas. Any stenosis or fistulation into the CBD should also be taken into consideration, and biliary bypass surgery be performed to both relieve jaundice and prevent further stricture.
Malignant fibrous histiocytoma (MFH) is a distinct and pleomorphic form of sarcoma, which usually occurs in soft tissues but can be found in bones, kidney, larynx, lung, heart, and even aorta. Since the first description of MFH of the spleen by Govoni et al. in 1982, only 10 cases have been reported in the literature worldwide. We report on a 45-yr-old female with MFH of the spleen and liver, with special emphasizes on immunohistochemical findings.
Immunosuppressive therapy is one of the standard therapy protocols for aplastic anemia (AA). However, immunosuppressive therapy and androgenic steroids can promote development of solid tumors such as squamous carcinoma, head and neck tumors, adenocarcinoma of the stomach, hepatocarcinoma and breast carcinoma in long surviving patients with aplastic anemia. We present here a rare case of a 56-year-old woman in whom bilateral adenocarcinoma of the breast developed 11 years after the start of immunosuppressive and androgenic steroid therapy for aplastic anemia. Histological examination showed invasive ductal carcinoma with intense nuclear staining for estrogen receptors. HeR2 immunohistochemistry was positive for 80% of stained cells, and chromogenic in situ hybridization showed a high level of HER2 gene amplification. This case indicated that a new therapy option is needed for estimation and evaluation to avoid the consequence of cancer occurrence.
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