Effects of weight intervention-induced changes in pathological fat mass of patients with extreme obesity and anorexia nervosa on adipokines and visceral adipocyte functions: a prospective, comparative, observational study.

OBJECTIVE: Adipose tissue is the largest endocrine organ in the human body, and as its mass changes, the serum levels of the molecules it secretes also change. Visceral adipose tissue index (VAI) is a simple surrogate marker of visceral adipose tissue dysfunction. This study evaluated the effects of changes in fat mass on adipocytokine behavior and VAI in patients with anorexia nervosa (AN) and extreme obesity (EO). PATIENTS AND METHODS: The study group consisted of three subgroups: Group 1, patients with EO who were candidates for obesity surgery with BMI≥50 kg/m2 (n=20). Group 2, newly diagnosed patients with AN (n=12). Group 3 controls with BMI 20-25 kg/m2 (n=20). The AN and EO groups were followed until at least a 10% weight change before and after the intervention. RESULTS: Prior to the intervention, EO patients exhibited the lowest levels of apelin, omentin, and adiponectin, while AN patients demonstrated the highest levels of these markers. Leptin and IL-6 were elevated in EO and reduced in AN patients. After treatment, all adipokines and VAI increased in AN patients, and omentin, adiponectin, and IL-6 increased in EO patients, while apelin, leptin, and VAI decreased. The change in each adipocytokine (∆) was positively correlated with the other adipocytokines (p<0.050) and negatively correlated with metabolic and VAI changes (p<0.050). The regression analysis determined that the following variables were associated with the change in adipose tissue mass: Δapelin (OR: 1.061; p=0.028) and Δadiponectin (OR: 1.057; p=0.036). CONCLUSIONS: In individuals with pathological adipocyte mass, the change in adipocytokine levels in response to weight change is not as expected. The fact that these changes are not seen in the early period of the weight intervention treatment indicates that these patients have compensatory physiological mechanisms to protect them. In addition, using VAI instead of BMI, whose reliability is increasingly questioned because it does not reflect body fat mass, can be considered an alternative. However, there may be modeling errors in the early stages of weight change and in AN and EO patients where metabolic parameters reach extreme values. Therefore, it should be tested in studies where larger patient groups are followed for a more extended period.

Massive Upper Gastrointestinal Bleeding Caused by Diffuse Large B-Cell Lymphoma.

Massive upper gastrointestinal bleeding is a life-threatening emergency which needs urgent intervention. Hematological malignancies are very rare causes of this type of bleeding and they usually originate from duodenum. In this case we present a gastric diffuse large B-cell lymphoma (DLBCL) causing massive upper gastrointestinal system bleeding. A 77-year-old male patient was admitted to emergency clinic with hematemesis and hematochezia. In physical examination patient was pale and sweaty; his vitals were unstable with a heart rate of 110 per minute and a blood pressure of 90/50 mmHg. His hemoglobin level was found 7.5 g/dL and he was transfused with one unit of packed red blood cells. After his vitals were normalized, gastroscopy was performed showing mosaic pattern in corpus and antrum mucosa and multiple ulcers in various sizes, largest being approximately 2 cm in diameter, higher than mucosa covered with exude mostly on corpus and large curvature. Biopsy results were reported as DLBCL. Gastric mucosa is involved in most of the DLBCL cases. Although not listed as a common cause of massive gastrointestinal bleeding DLBCL can cause life-threatening situations mostly because of its malignant nature.

NEUROPATHY ASSOCIATED WITH HYPERTRIGLYCERIDEMIA IN PATIENTS WITH METABOLIC SYNDROME.

CONTEXT: With more studies investigating effects of high serum lipid levels, new findings are emerging regarding the damage these biomolecules may cause. AIM: In this study we aimed to find a relation between neuropathy and hypertriglyceridemia in patients with metabolic syndrome (MS). MATERIAL AND METHODS: One hundred and twenty subjects (Ninety subjects with metabolic syndrome and 30 healthy controls) were included in the study. Subjects with MS were divided into three groups. HbA1C levels of the subjects were < 5.7% in group A, ≥ 5.7% - < 6.5% in group B, and ≥ 6.5% - < 8.0% in group C. Pin-Prick test and Semmes- Weinstein Monofilament were used for neurological examination. Electromyography was performed to patients with neuropathy to support the diagnosis. RESULTS: Neuropathy prevalence was found to be higher in the subjects with metabolic syndrome compared to control group. (9.9 %; 16.65 %; 23.31 % vs. 3.3%; in group A, group B, group C vs. healthy control group respectively) (p=0.003 for group A, p=0.0002 for group B, p=0.0002 for group C). There was an association between triglyceride levels and neuropathy in group C. CONCLUSION: Patients with MS may have more neuropathy risk than we estimate.