High-resolution magnified endoscopy combined with flexible spectral imagining colour enhancement techniques in the diagnosis of Helicobacter pylori disease.

AIM: To evaluate the efficiency of the flexible spectral imaging colour enhancement (FICE) procedure added to high-resolution magnified endoscopy (HRME) for the evaluation of structural changes in gastric mucosa infected with Helicobacter pylori (H. pylori). MATERIAL AND METHODS: A total of 104 patients were included in the study. First HRME and then HRME + FICE methods were used for the evaluation of the gastric mucosal structure, and examined areas were studied histopathologically. Mucosal appearance was evaluated with the modified Yagi classification. Images were shown to five endoscopists in order to examine inter- and intra-observer variability in image assessment. RESULTS: Sensitivity and specificity of the image pattern noted with HRME in the antrum in the detection of H. pylori were 67.9% and 84.6%, respectively, while these were 93.5% and 92.3%, respectively, with HRME + FICE. Type 5 pattern in the antrum, which we thought to be associated with intestinal metaplasia, was not observed in any patient with HRME. Sensitivity and specificity values of type 5 pattern noted with HRME + FICE technique for intestinal metaplasia were 50% and 98.8%, respectively. CONCLUSIONS: The results show that HRME + FICE as a digital chromoendoscopic method provided an additional diagnostic contribution to HRME for showing the presence of H. pylori and intestinal metaplasia and is a method with higher sensitivity and specificity. The "patchy appearance" (type 5) observed in the antrum not previously described in the evaluations with FICE can be a guiding sign especially for the diagnosis of intestinal metaplasia.

A new type of familial partial lipodystrophy: distinctive fat distribution and proteinuria.

PURPOSE: To describe an interesting subtype of familial partial lipodystrophy (FPLD). METHODS: The phenotype of this distinctive FPLD subtype was studied in three Turkish female siblings. RESULTS: Mutation testing was negative for the genes associated with lipodystrophy syndromes. In MRI studies, fat loss was prominent in the posterior aspects of the proximal lower limbs, whilst some fat was preserved in the anterior, medial and lateral aspects. Remarkably, fat tissue was preserved in the distal part of the limbs. Local fat accumulation was observed in the mons pubis area. Asymmetrical fat loss was also remarkable in the upper extremities. All three patients had severe insulin resistance associated with diabetes mellitus, acanthosis nigricans, hypertriglyceridemia and hepatic steatosis. Abnormal amounts of proteinuria were detected in all three subjects. Renal biopsy showed mild tubular atrophy, interstitial fibrosis, irregular thickening and wrinkling of glomerular basal membranes, small areas of segmental sclerosis and pedicel effacement. CONCLUSIONS: We reported a form of FPLD characterized by a striking pattern of highly selective partial fat loss and proteinuria.

Renal complications of lipodystrophy: A closer look at the natural history of kidney disease.

OBJECTIVES: Lipodystrophy syndromes are a group of heterogeneous disorders characterized by adipose tissue loss. Proteinuria is a remarkable finding in previous reports. STUDY DESIGN: In this multicentre study, prospective follow-up data were collected from 103 subjects with non-HIV-associated lipodystrophy registered in the Turkish Lipodystrophy Study Group database to study renal complications in treatment naïve patients with lipodystrophy. METHODS: Main outcome measures included ascertainment of chronic kidney disease (CKD) by studying the level of proteinuria and the estimated glomerular filtration rate (eGFR). Kidney volume was measured. Percutaneous renal biopsies were performed in 9 patients. RESULTS: Seventeen of 37 patients with generalized and 29 of 66 patients with partial lipodystrophy had CKD characterized by proteinuria, of those 12 progressed to renal failure subsequently. The onset of renal complications was significantly earlier in patients with generalized lipodystrophy. Patients with CKD were older and more insulin resistant and had worse metabolic control. Increased kidney volume was associated with poor metabolic control and suppressed leptin levels. Renal biopsies revealed thickening of glomerular basal membranes, mesangial matrix abnormalities, podocyte injury, focal segmental sclerosis, ischaemic changes and tubular abnormalities at various levels. Lipid vacuoles were visualized in electron microscopy images. CONCLUSIONS: CKD is conspicuously frequent in patients with lipodystrophy which has an early onset. Renal involvement appears multifactorial. While poorly controlled diabetes caused by severe insulin resistance may drive the disease in some cases, inherent underlying genetic defects may also lead to cell autonomous mechanisms contributory to the pathogenesis of kidney disease.