ACTA ENDOCRINOLOGICA (BUC)

Introduction. Even if the last decade brings new information about the existence of the local pulmonary renin-angiotensin system (RAS), published results about its involvement in the progression of various pulmonary diseases remain contradictory. Methods. Using an experimental model of pulmonary allergic disease induced by ovalbumin (OVA) sensitization we studied effects of intratracheal (i.t.) administrated AT1 receptor blocker losartan (LOS) on inflammatory processes supposed to be mediated by pulmonary RAS. Alterations in bronchoalveolar lavage fluid (BALF) cellularity and variations of airway reactivity from OVA sensitized and challenged rats after LOS or vehicle i.t. instillation were comparatively assessed. Results. Blocking of RAS decreased the total BALF cellularity and polymorphonuclear cell count. LOS instillation also reduced the increases in specific airway resistance (sRaw) induced by inhalation of allergen (with 20%) or acetylcholine (with at least 15%). Conclusions. Our data suggest that expressly blocking of local RAS by i.t. administration of LOS have inhibitory effects on allergen - induced lung inflammation and sustain the participation of pulmonary RAS, activated by local or systemic factors, in lung diseases.

Context. Persistent inflammation and impaired neovascularization are important contributors to the development of diabetic retinopathy (DR). Gene polymorphisms of adiponectin (APN) were demonstrated to have an important role on the plasma level and activity of adiponectin. APN has anti-inflammatory, anti-diabetic and anti-atherogenic properties. Toll-Like Receptor 4 (TLR4) is a critical mediator of innate immunity. Polymorphisms in TLR-4 gene were shown to be associated with impaired inflammatory response in diabetes. Objective. The aim of the study was to analyze the association of +276G>T variant of APN gene and Asp299Gly and Thr399Ile of TLR-4 gene variants in relationship with T2DM and DR in an Eastern European population group. Design. The distribution of the mutant alleles in 198 T2DM patients with DR and 200 non-T2DM controls was examined. Genomic DNA from T2DM patients and healthy controls genotyped through the use of PCR-RFPL assay. Results. Genotype and allele frequencies of the Asp299Gly and Thr399Ile polymorphisms differed between T2DM patients and non diabetic subjects (P<0.001). Moreover, the presence of the minor alleles of these polymorphisms were significantly identified as protective factors against T2DM, under a dominant model of Fisher’s exact test (χ2=4.988, phi=0.745, OR=0.767, 95% CI=0.602-0.867, P<0.001; respectively χ2=5.254, phi=0.820, OR=0.487, 95% CI=0.211- 0.648, P<0.001). Genotype analysis for the adiponectin 276G>T gene polymorphism yielded no significant association with T2DM, but revealed a borderline significance for the association with DR (χ2=5.632, phi=0.423, OR =1.101, 95% CI=0.887-1.203, P=0.009). Conclusions. We found an association between the TLR4 Asp299Gly and Thr399Ile polymorphisms and protection for DR. The APN genetic polymorphism is not associated with T2DM.

Background. Alcohol ingestion can induce either a hypoglycemia or a hyperglycemia,\r\nin patients with acute and chronic ethanol poisoning, unknown with diabetes mellitus.\r\nAim. The aim of this study was to evaluate whether 5 hours prolonged oral glucose\r\ntolerance test (5h-OGTT) is useful in evaluating the abnormalities of glucose metabolism in\r\nacute and chronic ethanol poisoning, in comparison with standard methods (fasting blood\r\nglucose - FBG, and/or 2h-OGTT).\r\nMethods. 497 consecutive patients were enrolled in a 34 months cross sectional study.\r\nIn all cases, glucose tolerance was assessed by a 75-g oral glucose tolerance, OGTT 2 hours,\r\nprolonged to 5 hours. The relationship between clinical and biochemical variables of ethanol\r\npoisoning (liver status, lipid profile, metabolic syndrome) and glucose tolerance was\r\ninvestigated. Risk factors for hypoglycemia in ethanol poisoning were identified.\r\nResults. 349 subjects presented acute ethanol poisoning, and 148 subjects had chronic\r\nethanol poisoning. 254 patients (51.10%) had documented alcoholic liver disease (ALD -\r\nclinical, biochemical and imagistic criteria). Glucose metabolism abnormalities were\r\nrecorded in 143 subjects with chronic ethanol poisoning and ALD (96.63%), and in 207\r\ncases with acute alcohol poisoning (59.31%). 371 patients (74.65%) showed normal FBG,\r\ndiabetes mellitus (DM) was diagnosed in 54 subjects (10.86%), impaired glucose tolerance\r\n(IGT) in 43 subjects (8.65%), delayed hypoglycemia in 172 subjects (34.60%) and normal\r\nglucose tolerance (NGT) in 147 subjects (29.57%) using OGTT and ADA diagnosis criteria.\r\nHypoglycemia was recorded in more than two thirds of acutely poisoned patients, when alcohol\r\nlevel was 0.5-1.5 g/L. Impaired glucose tolerance (IGT) were recorded in half of patients with\r\nblood ethanol levels > 2.5 g/L.\r\nConclusions. OGTT 2 hours and OGTT 5 hours revealed the same number of patients\r\nwith diabetes mellitus. Frequent co morbidities in patients with ethanol poisoning influence\r\nthe prolonged OGTT and revealed .especially delayed hypoglycemia, and IGT, as an indicator\r\nof alcoholic liver disease (ALD).

Introduction. In the community, hypoglycemic coma is commonly caused by therapies for diabetes mellitus, or excessive alcohol consumption. Little information is available on the causes and outcome of hypoglycemic coma in non-diabetic patients. Patients and Methods. We retrospectively surveyed adult patients admitted to a regional emergency hospital with hypoglycemic coma in a 18-years period, identifying 80 admissions of 79 patients. 72 cases (91.14%) presented hypoglycemic coma induced by anti-diabetic medications in attempted suicide. The others had hypoglycemic coma induced by deliberate selfpoisoning with other drugs influencing glucose metabolism, sometimes associated with excessive consumption of alcohol. Results. A history of psychiatric illness was present in 15 patients (19%), and 2 cases (2.53%) had chronic alcoholism. Neurological manifestations of hypoglycemia were the principal reason for admission, observed in all patients, and 15 patients (19%) had precipitated convulsions. Although some patients received treatment for hypoglycemia before admission, hypoglycemia recurred in 12 cases (15.19%) in hospital. Morbidity included ventricular arrhythmias (8.86%), non-cardiogenic acute pulmonary edema (1.26%), and transient neurological disturbances, in 2 elderly patients. Two cases died following admission, but death was not the direct result of hypoglycemia. Therapeutic measures consisted in antidote therapy, toxin removal, and supportive therapy. Conclusion. Though drug-induced hypoglycemic coma is rarely encountered in medical practice (2.44% in our study), management of these patients represents a challenging task in every practitioner.

Aim. The goal was to study immunostaining with Inhibin alpha, Melan- A and MNF 116 in tumors located in the adrenals (benign adrenocortical tumors and metastatic lesions in the adrenal gland) because sometimes pathology cannot distinguish between the two. Patients and Methods. We included 35 patients with benign adrenal tumors and 15 patients with adrenal metastases from nonadrenal tumors submitted to laparoscopic (n=40) or classical (n=10) surgery. In our study we have explored immunostaining with inhibin α-subunit, melan-A, MNF 116 in adrenocortical tumors and metastatic lesions in the adrenal gland in order to make the distinction between primary adrenal cortical lesions and metastatic lesions. Results. All nonsecreting adrenocortical adenomas were stained with inhibin α-subunit and melan-A, but did not stain with MNF 116. All adrenal metastases stained with MNF 116 but were negative for inhibin α-subunit and melan-A with the exception of the 2 melanomas, which stained for melan-A. Conclusion. Inhibin α-subunit and melan-A were sensitive for benign adrenocortical tumors, while MNF 116 was sensitive for metastases from extraadrenal tumors.