Visceral Fat Thickness, Serum Adiponectin, and Metabolic Syndrome in Patients with Colorectal Adenomas.

BACKGROUND/OBJECTIVES: Most cases of colorectal cancer (CRC) arise from adenomatous polyps. Identifying risk factors for colorectal adenoma (CRA) is critical for CRC prevention. Emerging evidence suggests a link between metabolic syndrome (MetS) and an elevated risk of CRA and CRC, potentially mediated by visceral obesity and adiponectin (APN). We aimed to evaluate the association between different markers of visceral obesity, serum APN, MetS, and the presence of CRA. METHODS: A cross-sectional study was conducted at the University Clinical Center of Vojvodina, involving 120 patients, aged 40-75 years, who underwent colonoscopy between January 2022 and January 2023. Sixty patients with CRA were compared to 60 controls with normal colonoscopy findings. Visceral fat thickness (VFT) was measured using ultrasound (US), and bioelectrical impedance analysis (BIA) was used to assess visceral fat area (VFA). Serum APN levels, anthropometric measures, and MetS components were also evaluated. RESULTS: Patients with CRA had significantly higher VFT measured by US (p < 0.05), but no significant differences were found in VFA measured by BIA, waist circumference (WC), or waist-to-hip ratio (WHR). MetS was significantly more prevalent in the CRA group (55% vs. 31.6%, p < 0.05), and logistic regression confirmed MetS as a significant predictor of CRA presence (OR = 2.6). Serum APN levels were inversely correlated with visceral fat measurements and MetS (p < 0.01), but no significant difference in APN levels was observed between patients with and without CRA. CONCLUSIONS: This study highlights the importance of VFT measured by US and the presence of MetS as significant factors associated with CRA.

Vitamin D supplementation in patients with alcoholic liver cirrhosis: a prospective study.

BACKGROUND: The liver is involved in the metabolism of vitamin D. The prevalence of osteopenia in alcoholic liver disease (ALD) patients is 34-48%, and the prevalence of osteoporosis is 11-36%. Advanced liver disease is considered a risk factor for the development of osteoporosis. The aim of this study was to establish the relationship between vitamin D level and Child-Pugh score in patients with alcoholic liver cirrhosis (ALC), and to evaluate the effects of oral vitamin D supplementation. METHODS: Seventy male ALC patients in the absence of active alcohol intake were enrolled and their clinical and laboratory data were recorded. A supplementation of cholecalciferol 1000 IU/day was administered. The vitamin D status was analyzed during the study, in patients stratified by Child-Pugh score. RESULTS: The study was completed by fifty patients. At the enrollment, the mean level of vitamin D was 60.73±28.02, 50.53±39.52 and 26.71±12.81 nmol/L, respectively for Child-Pugh score class A, B and C. During vitamin D supplementation it was found in all the patients a significant increase of its levels during the first six months (P<0.05). However, in class C the improvement was consistent also after year (P<0.05). At the end of the study, two of seven patients initially in class C changed in class A, four from class C to B, and one remained in class C (P=0.012). Out of seventeen patients initially in class B, eleven changed to class A, and six remained in class B. CONCLUSIONS: In patients with ALC, higher level of vitamin D level is related with lower Child-Pugh score. The supplementation of 1000 IU/day of vitamin D in these patients was optimal for a period of at least six months. A decrease in the Child-Pugh score was also found, with a redistribution of the patients in different classes.

An enigma of eosinophilic esophagitis.

Introduction: Eosinophilic esophagitis is a chronic immunogenic-antigen mediated disease of the esophagus, characterized by symptoms related to esophagus dysfunction, histologically defined by over 15 eosinophil counts seen in high-power microscopic field, without gastroesophageal reflux disease. In adults, the most common clinical manifestations are dysphagia, reflux, chest pain, regurgitation and bolus impaction. Case report: We presented the case of a female patient, hospitalized for a serious form of pancreatitis with complications, which required artificial ventilation and enteral feeding, after the initial esophagoscopy verified reflux esophagitis. Further treatment cured the primary illness, and peroral feeding was reintroduced. However, dysphagia with regurgitation occurred, and endoscopic and radiological tests verified esophagus stenosis, which histopathologically corresponded to erosive esophagitis. Two months of treatment by a double dosage of proton pump inhibitors led to no regression of disorders, and the repeated biopsies from the stenotic segments resulted in over 30 eosinophil counts in the high-power microscopic field, which histologically corresponds to eosinophilic esophagitis. Subsequent therapy included fluticasone 880 µg/day orally for a period of eight weeks, which led to complete regression of disorders, and endoscopic and histopathologic remission. Conclusion: In case of irresponsiveness to the conventional therapy by proton pump inhibitors, repeated esophagoscopy and histopathological analyses of esophagus mucosa biopsy can point to the diagnosis of eosinophilic esophagitis, and a good therapeutic response to topical corticosteroids can be regarded as the clinical confirmation of the diagnosis.

[Hereditary coproporphyria from clinician's point of view--a case report].

INTRODUCTION: Acute hepatic porphyrias can mimic a range of unrelated diseases and conditions that may occur independently of porphyria and trigger their initial manifestations and further attacks. CASE REPORT: A 46-year-old female patient was subjected to cholecystectomy for biliary colic. Histopathological analysis revealed acute purulent exacerbation of chronic cholecystitis. On the 8th day post surgery, the patient was rehospitalized for nausea, abdominal pain, weakness and faintness, poor general condition, hypertension, tachycardia, apathy and profuse sweating. Laboratory findings revealed hyponatremia, hypokalemia, and metabolic alkalosis. Exploratory laparotomy did not detect a pathomorphological substrate. The patient was transferred to surgery department of the tertiary care institution. Due to metabolic imbalance, she was transferred to the Department of Endocrinology with signs of paleness, profuse sweating, tachycardia, and tachydyspnoea. The cardiologist performed echocardiography. The patient was diagnosed to have acute left ventricular failure and sub-acute myocardial infarction and transferred to the Department of Cardiology. Coronarography findings were normal. Cramps and pain in the legs with sensory loss, general weakness, apathy and mental confusion suggested acute hepatic porphyria. Thus, hereditary coproporphyria was diagnosed in the second month of illness. The treatment was continued at the Department of Gastroenterology. Clinical manifestations included polyneuropathy, flaccid paraparesis and acute brain syndrome, precordial oppressions and tachycardia. Haem arginate and hypertonic glucose were applied. The condition of the patient gradually improved. CONCLUSION: Porphyrias should always be taken into consideration in doubtful, frequently dramatic clinical pictures characterized by neurovisceral symptoms and precipitating factors of acute porphyria attacks must never be neglected.

[Experience in the treatment of some complications of portal hypertension in alcoholic liver cirrhosis].

BACKGROUND/AIM: Portal hypertension (PH) is hemodynamical abnormality associated with the most serious complications of alcoholic liver cirrhosis (ALC): ascites, varices and variceal bleeding. The aim of this study was to determine characteristics of portal hypertension, especially of upper gastrointestinal bleedings in patients with alcoholic liver cirrhosis (ALC). METHODS: A total of 237 patients with ALC were observed in a 3-year period. RESULTS: A total of 161 patients (68%) were hospitalized because of PH elements: 86 (36.3%) had upper gastrointestinal bleeding, 75 (31.7%) were decompensated. Only 76 (32%) of the patients had icterus. General mortality was 85 (36%). According to the source of bleeding, 61 (71%) patients bled from varices, and 25 (29%) from other sources with existing varices but non-incriminated for bleeding in 16 (64%) of those patients. Active bleeding or stigmata of recent bleeding were found in 63 (73%) cases. Endoscopic treatment of variceal bleeding along with octreotide applied in 20 (32.78%) patients, just octreotide in 32 (52.46%), and octreotid plus balloon tamponade in 9 (14.75%). According to Child-Pugh classification, 25 (29%) of the bleeding patients were in class A, score 5.4; 43 (50%) in class B, score 7.8; and 18 (21%) in class C, score 10.9. Average hemoglobin level was 93 g/L, hematocrit 0.27, AST 71.52 U/L (normal to 37 U/L), ALT 37.74 U/L (normal to 40 U/L). Until this bleeding episode, 41 (47%) of the patients already bled. In the decompensated patients 3 (4%) were in Child Pugh class A, score 6; 42 (56%) in class B, score 8.3; and 30 (40%) in class C, score 10.6. Until this decompensation episode, 7 (9.3%) patients already bled. CONCLUSION: Patients with ALC need early detection of varices, primary and secondary profilaxis of variceal bleeding and adequate therapy of ascites. When bleeding occurs, patients need urgent upper endoscopy and intensive treatment.