High-magnification chromoscopic pouchoscopy: a novel in vivo technique for surveillance of the anal transition zone and columnar cuff following ileal pouch-anal anastomosis

Abstract Background Persistence of underlying disease in the residual rectal mucosa and anal transition zone (ATZ) following ileal pouch-anal anastomosis (IPAA) for ulcerative colitis and familial adenomatous polyposis provides a site for potential malignancy. For this reason endoscopic surveillance is performed, although conventional assessment may be unreliable. We hypothesized that the novel technique of high-magnification chromoscopic pouchoscopy (HMCP) may permit accurate anatomical localization of this high risk zone in vivo and permit improved biopsy accuracy. Patients and methods We studied 132 patients with IPAA using HMCP. Three distinct zones were defined using magnification endoscopy: ATZ, appearing as a linear cellular marix; columnar cuff, identifiable by a type I crypt pattern; and ileal pouch body, appearing as villous projections. Quadrantic biopsies of these zones were taken in addition to biopsies of any other lesions noted. Results A total of 1586 biopsies were taken from zones 1–3 (median, 12; range, 5–16 per patient). Overall biopsy-targeting accuracies using magnification guidance as compared with histopathology were 82%, 73% and 91% for the ATZ, cuff and pouch body, respectively. No dysplasia was identified in the quadrantic surveillance biopsies. Histologically confirmed columnar metaplasia was visualized in vivo using magnification chromoscopy. Patients with IPAA >3 years duration were more likely to have pouch reservoir columnar metaplasia as compared to those <3 years (p<0.01). Pouch reservoir metaplasia was associated with a pre-morbid diagnosis of high-grade dysplasia or carcinoma within the premorbid colectomy specimen (p<0.001). Conclusions This is the first study to evaluate this novel application of high magnification chromoscopy. Magnification pouchoscopy is a valid predictor of ATZ and cuff anatomy, permitting accurate biopsy targeting. Further randomized studies validating this technique with an emphasis on dysplasia detection in larger cohorts are required.     

Mood and metabolic consequences of sleep deprivation as a potential endophenotype’ in bipolar disorder

It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression–dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression–dejection and anger–hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression–dejection, anger–hostility, and confusion–bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first-degree relatives of patients with bipolar disorder.     

Tuberculosis in Austria 1995-99: geographical distribution and trends

A descriptive analysis of routine surveillance data on tuberculosis (TB) from 1995 to 1999 was performed in Austria. The federal states of Vienna and Upper Austria showed the highest yearly incidences for all five years. In general, however, a decrease of the yearly incidence was observed for all federal states except for Carinthia (where there was a small increase of 3.2 %). In the cities of Vienna, Linz, Wels, Salzburg, Klagenfurt and St-P?lten, as well as in the regions of Eastern Tyrol, Southern Carinthia, and Southern Burgenland, the incidence was above average (>19 cases/100,000 for each). The number of cases per year and per district reported by the statutory reporting system were clearly in excess of those reported by hospitals. The comparison of the two datasets, however, showed a highly significant regional correlation of age standardised morbidity rates at district level. The findings are prone to reporting bias and might not reflect the real TB situation. The responsible health authorities should therefore consider the results as a 'working hypothesis in order to review the reporting behaviour at district level.     

Bone mineral density evaluation of patients with type 2 diabetes mellitus

[Purpose] Diabetes mellitus is a metabolic disorder resulting from a defect in insulin secretion, insulin action, or both. A consequence of this is chronic hyperglycemia with disturbances in carbohydrate, fat and protein metabolism. We investigated whether there is any difference among DM patients and a control group in terms of lumbar and femur BMD (bone mineral density), and standard deviation scores (Z score and T score). [Subjects and Methods] This randomized, prospective, controlled, single-blind study was conducted in the Physical Medicine and Rehabilitation Department Faculty of Medicine, Bezm-i Alem Vakıf University. Patients with type 2 diabetes mellitus were included in the patient groups. Healthy individuals were included in the control group. [Results] A total of 126 patients completed the study (63 in the study group, 63 in the control group). There was no significant difference in the results of the laboratory examinations of the cases. The bone mineral densities of the cases were found to be significantly low in terms of the lumbar (L1–4) T scores in the type 2 diabetes group. [Conclusion] Although osteoporosis is one of the potential complications of type 1 diabetes, its effect on bone mineral density in type 2 DM is controversial. In different studies, the bone mineral density values have increased, decreased or remained normal. With the exception of the lumbar (L1–4) T score, similar results were obtained in this study.Key words: pan class="kwd-text">Type 2 diabetes mellitus, Osteoporosis, Bone mineral densitypan>     

S6K1 controls pancreatic β cell size independently of intrauterine growth restriction

Type 2 diabetes mellitus (T2DM) is a worldwide heath problem that is characterized by insulin resistance and the eventual loss of β cell function. As recent studies have shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivity, S6K1 inhibitors are being pursued as potential agents for improving insulin resistance. Here we found that S6K1 deficiency in mice also leads to decreased β cell growth, intrauterine growth restriction (IUGR), and impaired placental development. IUGR is a common complication of human pregnancy that limits the supply of oxygen and nutrients to the developing fetus, leading to diminished embryonic β cell growth and the onset of T2DM later in life. However, restoration of placental development and the rescue of IUGR by tetraploid embryo complementation did not restore β cell size or insulin levels in S6K1p>–/–p> embryos, suggesting that loss of S6K1 leads to an intrinsic β cell lesion. Consistent with this hypothesis, reexpression of S6K1 in β cells of S6K1p>–/–p> mice restored embryonic β cell size, insulin levels, glucose tolerance, and RPS6 phosphorylation, without rescuing IUGR. Together, these data suggest that a nutrient-mediated reduction in intrinsic β cell S6K1 signaling, rather than IUGR, during fetal development may underlie reduced β cell growth and eventual development of T2DM later in life.