ABSTRACT
Upper gastrointestinal bleeding as a result of gastrointestinal metastases from lung cancer is extremely rare. We report two cases of patients with duodenal metastases from lung adenocarcinoma presented with recurrent melena. Histopathological examination and immunohistochemical staining of the duodenal biopsies supported the diagnosis of metastatic lung adenocarcinoma.
ABSTRACT
BACKGROUNDS: The aim of this study was to appraise the relationship between serum fragmented cytokeratin-18(CK-18), controlled attenuation parameter (CAP), and liver steatosis assessed by ultrasound (US) in nonalcoholic fatty liver disease (NAFLD) patients. METHODS: Patients who underwent abdominal US were recruited, followed with measurement of CAP using Fibroscan® and serum fragmented CK-18 using enzyme-linked immunosorbent assay. The degree of liver steatosis assessed by US was categorized into mild (S1), moderate (S2), and severe (S3). RESULTS: A total of 109 patients were included in our study. CAP and fragmented CK-18 level were significantly correlated with liver steatosis grade with rs = 0.56 and 0.68, p=0.001, respectively. NAFLD Fibrosis Score was poorly correlated with liver steatosis grade (rs=-0.096, p=0.318). Using fragmented CK-18 level, area under receiver operating characteristic (AUROC) curves for S≥2 and S≥3 were excellent (0.82 and 0.84, respectively). Using CAP, AUROC curves for detection of S≥2 and S≥3 were good (0.76, 0.77, respectively). We also proposed cut-off value of CAP to detect S≥2 and S≥3 to be 263 and 319db/m, respectively, and fragmented CK-18 level to detect S≥2 and S≥3 (194 and 294 U/L, respectively). CONCLUSIONS: Both the fragmented CK-18 level and the CAP, but not NAFLD Fibrosis Score, were well correlated with hepatic steatosis grade as assessed by US.
ABSTRACT
A 59-year-old man presented with proximal myopathy, myalgia, and weight loss, with the initial markedly elevated serum creatine kinase at 11,000 U/L. Due to his refusal for muscle biopsy, he was initially treated as inflammatory myositis and responded well with the corticosteroids. However, he subsequently had a relapse of the symptoms with more extensive systemic involvement, i.e., hypercalcemia, lymphadenopathy and subcutaneous nodules. Finally, a biopsy of the thigh and subcutaneous nodule revealed non-caseating granulomatous inflammation, consistent with sarcoidosis. He responded well to the corticosteroids, and finally, azathioprine was added as a steroid-sparing agent. Including our series, there are 103 cases of symptomatic muscle involvement in sarcoidosis patients published in the English literature to date. Further pool analysis of the cases will be reported in this review.
