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Anargiros Mariolis

Publications and source records attributed to Anargiros Mariolis.

10 recordsLinked to original sources
PubMed2006

Elevated serum triglycerides is the strongest single indicator for the presence of metabolic syndrome in patients with type 2 diabetes.

BACKGROUND: Patients with diabetes already fulfill one diagnostic criterion for MS according to the existing classifications. Our aim was to identify one single clinical parameter, which could effectively predict the presence of MS in patients with type 2 diabetes. METHODS: We studied all patients with type 2 diabetes who attended our Diabetes Outpatient Clinic during a three-month period. Waist circumference, blood pressure and serum lipids were measured. Establishment of MS diagnosis was based a) on National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria and b) on International Diabetes Federation (IDF) criteria. Receiver operating characteristic (ROC) analysis was applied in order to identify the clinical parameter with the highest predictive capability for MS. Among the 500 participating patients (231 males, 269 females), MS was diagnosed in 364 patients (72.8%) according to the NCEP ATP III criteria and in 408 patients (81.6%) according to the IDF criteria. RESULTS: For the NCEP ATP III classification, serum triglycerides (in the overall population), waist and HDL (in female population) demonstrated the highest predictive capability for MS (AUCs:0.786, 0.805 and 0.801, respectively). For the IDF classification, no single parameter reached an AUC > 0.800 in the overall population. In females, HDL displayed a satisfactory predictive capability for MS with an AUC which was significantly higher than the one in males (0.785 vs. 0.676, respectively, p < 0.05). CONCLUSION: Elevated serum triglycerides strongly indicate the presence of MS in patients with type 2 diabetes. In female patients with type 2 diabetes, central obesity was the second stronger predictor of MS besides hypertriglyceridemia.

Aged↗
PubMed2006

Associations among benign prostate hypertrophy, atypical adenomatous hyperplasia and latent carcinoma of the prostate.

AIM: To investigate the frequency of atypical adenomatous hyperplasia (AAH) and its associations with benign prostate hypertrophy (BPH) and latent histological carcinoma of the prostate (LPC) in autopsy material. METHODS: Two hundred and twelve prostate specimens obtained from autopsy material were subjected to whole mount analysis in an attempt to investigate the associations among BPH, AAH and LPC. RESULTS: Most histological carcinomas and AAH lesions were found in enlarged prostates with intense hypertrophy. No statistically significant relation was found between BPH and the main characteristics of LPC, such as tumor volume, histological differentiation and biological behavior. Our data regarding multi-focal tumors showed a tendency for multi-focal carcinomas to develop in larger prostates, and a tendency of AAH lesions to develop in larger prostates. No statistically significant relation was found between AAH and LPC. CONCLUSION: There seems not any causative aetiopathogenetical or topographical relation between AAH lesions and prostate adenocarcinoma. AAH lesion seems to be a well-defined mimicker of prostatic adenocarcinoma, and the reported association of AAH with prostatic carcinoma could probably be an epiphenomenon.

Adenocarcinoma↗
PubMed2005

Serological profile of HBV infection and liver histopathology among injecting drug users with chronic HCV infection in Greece.

BACKGROUND: The aim of this study was to evaluate the serological status of HBV infection and liver histology in chronic HCV-infected injecting drug users (IDUs) and to correlate them with the possible time of infection and the principal HCV genotype. METHODS: Some 130 prior IDUs with chronic HCV infection were consecutively evaluated for the serological status of HBV infection. Fifty-eight (44.62%) reported intravenous drug use beginning before 1992 (group A) and 72 (55.38%) after 1992 (group B). HCV genotyping was available in 86 patients (PCR). Liver biopsy was performed in 48 patients (Ishak scoring system). There was no available data about alcohol consumption in the study population. Statistical analysis was based on the t-test and the chi(2) test (p<0.05). RESULTS: Some 82.8% of group A patients had previous HBV infection, whereas only 22.2% of group B patients did (p<0.001). Among group A patients, 10.3% were HBV-seronegative whereas 61.1% of group B patients were (p<0.001). Only 3.4% of group A patients were HBV-vaccinated compared to 16.7% in group B (p=0.016). HCV genotype was not associated with HBV serological status. No significant differences were detected in age, sex, possible time of infection, HBV serological status, or HCV genotype among those with higher vs. lower total grading scores. Seventy-five percent of patients had mild or no detectable fibrosis unrelated to the possible period of infection, the HBV serological status, and the HCV genotype. CONCLUSIONS: The serological profile of HBV infection is changing among Greek chronic HCV-infected IDUs, while the percentages of successfully HBV-vaccinated IDUs are relatively low. Severe liver disease is an uncommon finding in these patients, irrespective of the possible time of infection, the HBV serological status, and the HCV genotype.

Journal Article↗
PubMed2004

Tamoxifen induced hepatotoxicity in breast cancer patients with pre-existing liver steatosis: the role of glucose intolerance.

OBJECTIVE: Tamoxifen induced hepatotoxicity has not been investigated in breast cancer patients with pre-existing liver steatosis. The aim of our study was to investigate the most common predisposing factors for non-alcoholic fatty liver disease in breast cancer patients with liver steatosis, treated with adjuvant tamoxifen therapy, in order to evaluate their role in the appearance of tamoxifen induced hepatotoxicity. METHODS: Clinical and laboratory evaluation, including an oral glucose tolerance test, was done in 60 women with breast cancer and liver steatosis before the beginning of adjuvant tamoxifen treatment and every 6 months during treatment. Tamoxifen induced hepatotoxicity was defined as abnormal liver function tests during tamoxifen treatment whereas these test results were below the normal range at baseline control. Statistical evaluation of data was performed using parametric methodology (the chi-squared test, and Student's t-test, P < 0.05). RESULTS: Twenty-six patients (43.3%) exhibited tamoxifen induced hepatotoxicity (group A) whereas 34 (56.7%) did not (group B). The mean overall follow-up period for the whole group was 37.5 months (SD 27.8, range 6-120 months) and did not differ between the two groups (P = 0.055). There was significant statistical difference in body mass index (BMI) and baseline fasting glucose, cholesterol and triglyceride levels between the two groups. Eighteen of 26 patients (69.2%) from group A had impaired glucose tolerance compared with only 8/34 patients (23.5%) from group B (P < 0.001), a finding observed even in BMI matched patients from the two groups (62.5% vs 12.5%, P = 0.002). CONCLUSIONS: Tamoxifen induced hepatotoxicity is observed in a great proportion of breast cancer patients with pre-existing liver steatosis, especially those with higher BMI and higher glucose and lipid levels at baseline control. Glucose intolerance before the beginning of tamoxifen treatment seems to be a predictor of the hepatotoxicity, unrelated to baseline BMI.

Adult↗