ACTA ENDOCRINOLOGICA (BUC)

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: Pseudo-primary hyperaldosteronism of pregnancy was previously reported by our group during correction in twin-to-twin transfusion syndrome (TTTS). Aim: Focus on plasma volume changes and renin-angiotensin (RAS) and aldosterone response in 45 TTTS patients requiring amnioreductions above 1000 ml for severe hydramnios. Methods: 45 patients necessitating placental surgery and amnioreduction >1000ml for severe TTTS, under local anesthesia, as previously described. Assesment of plasma volume variations (%ΔPV) and simultaneous assays of aldosterone, renin, angiotensin II and ANP performed by standard kits prior to, 6 hours after and 12-24 hours after procedure. Statistical results expressed as median and interquartile ranges for non-parametric data, after correction of post-op levels with %ΔPV. Results: Depletion of 1600 ml (1000-3700) amniotic fluid (extravascular depletion) unexpectedly increased the intravascular plasma volume by 20,38% and dramatically changed the hormonal picture of primary hyperaldosteronism. Aldosterone decreased from a median of 730 pg/ml (T0) to 553 pg/ml (T6) to 515,9 pg/ml (T24). ANP increased from 8,95 pg/ml (T0) to 14,51pg/ml (T6) to 19,9 pg/ml (T24) pg/ml (ANOVA p=0,0036), while renin and angiotenin II stayed unchanged (ANOVA p=0,91). Conclusion: Depletion of extracelular fluid (amnioreduction) is indicated for the correction of hyperaldosteronism in pregnancies with severe hydramnios, to reduce to normal the aldosteron levels without the interference of the renin-angiotensin system, while natriuretic activity increases through ANP and, possibly, other less known natriuretic factors .

Introduction. Obesity was considered to protect against osteoporosis. Recent studies indicate the opposite.\r\nThe study aimed to see if adipose tissue has a protective effect on bone mass and if adipocytokines can explain the\r\nrelationship between obesity and osteoporosis.\r\nSubjects and methods We designed a study enrolling 83\r\npostmenopausal women, aged over 60, without diagnosed or treated osteoporosis and no secondary osteoporosis. We formed 3 groups- group 1- osteoporosis and metabolic syndrome (MetSyn), group 2- osteoporosis, group 3- MetSyn.\r\nWe evaluated the hematological, biochemical profile, bone turnover markers and adipocytokines. DXA of the spine and\r\nthe hip (left) was performed on all the enrolled women. Insulin resistance was appreciated using HOMA index. Metsyn\r\nwas defined using the International Diabetes Federation?s criteria.Results were statistically analyzed using SPSS program, version 15.\r\nResults. All groups were vitamin D insufficient with lower vitamin D, osteocalcin and adiponectin levels in the\r\ngroups with MetSyn and higher leptin levels. BMI correlated positively with spine BMD, while leptin correlated positively with hip BMD, pointing out to the protective effect of obesity against osteoporosis due to leptin?s involvement.\r\nConclusion. Obesity seems to have a protective effect against osteoporosis, probably due to leptin.

Context. Nonalcoholic fatty liver disease (NAFLD) includes simple steatosis, steatohepatitis (NASH) which can evolve with progressive fibrosis, cirrhosis and hepatocellular carcinoma. As liver biopsy cannot be used as a screening method, noninvasive markers are needed. Objective. The aim of this study was to test if there is a significant association between vitamin D deficit and the severity of NAFLD. Design. The patients were divided into two groups (vitamin D insufficiency/deficiency) and statistical analyses were performed on the correlation of clinical and biochemical characteristics with histopathological hepatic changes. Subjects and methods. We prospectively studied 64 obese patients referred for bariatric surgery between 2014 and 2016 to our Surgical Unit. Anthropometric, clinical measurements, general and specific biological balance were noted. NAFLD diagnosis and activity score (NAS) were evaluated on liver biopsies. Results. Increased serum fibrinogen was correlated with NASH (p=0.005) and higher NAS grade. T2DM was positively correlated with liver fibrosis (p=0.002). 84.37% of the patients had vitamin D deficit and 15.62% were vitamin D insufficient. Lobular inflammation correlated with vitamin D deficit (p=0.040). Fibrosis (p=0.050) and steatohepatitis (p=0.032) were independent predictors of low vitamin D concentration. Conclusions. Vitamin D status in conjunction with other parameters - such as T2DM - or serum biomarkers – namely fibrinogen level and PCR level - may point out the aggressive forms of NAFLD and the need for liver biopsy for appropriate management.

Turner syndrome is one of the genetic disorders studied on their association with celiac disease. We present a 27 year old female with an association of Turner syndrome and celiac disease. Gluten intolerance presenting with atypical extraintestinal symptoms (recurrent aphthous stomatitis, iron-deficient anemia, short-stature) was confirmed by intestinal biopsy showing flat small bowel mucosa (Marsh IIIc lesion) and a peripheral lymphocyte karyotype analysis revealed a Turner syndrome determined by isochromosome 46,X,i (Xq) structural abnormality. Our patient fits perfect into this variant of Turner’s Syndrome presenting at least one autoimmune disorder (celiac disease) and hearing loss. Her clinical, biological and immunological disturbances caused by two irreversible disorders have a poor outcome in the absence of gluten-free diet associated with adequate endocrinologic treatment and need sustained long-term follow - up for a good quality of life.

The study comments unusual associations between thyroid and cutaneous autoimmunity: Graves-Basedow disease (GBD), vitiligo and alopecia areata (AA) starting from two cases. In the first case, a woman with systemic lupus erythematosus (SLE), data were recorded from 38 to 49 years as follows: vitiligo (at 38 ys), alopecia areata (4-6 months afterwards), SLE (after 2 ys) and then GBD (after 8 ys). After 3 years, hyperthyroidism has spontaneously vanished, but vitiligo, AA, leucothrichia, SLE, goiter and ophthalmopathy persisted. In the second case, a man, data were recorded from 26 to 70 years and the disease was associated with psoriasis. The sequence of diseases was: vitiligo (at 26 ys), AA and GBD (after 8 ys), followed by iatrogenic 131I hypothyroidism, and psoriasis (after 33 ys). Vitiligo and AA have spontaneously vanished before GBD began. These multiple immune syndrome associations bring up the question: ?Are these diseases multiple associations or a unique immune disease?? A possible point of view, related to immune network, suggests that these multiple associations represent in fact only one process, therefore they represent not many diseases, but different expressions in time (sequence) and space (organ-lesion) of the disease of the immune network.

Background. Atypical antipsychotics proved efficacy in monotherapy and more so in\r\nassociation with mood stabilizers, but choosing the atypical antipsychotic requires special\r\ncautions due to metabolic adverse effects. The aim: to verify if Quetiapine-valproate\r\ncombination improves rapidly acute depressive symptoms and has a good endocrinemetabolic\r\ntolerability. Case presentation. A 49 years male, bipolar patient, admitted for a\r\nmajor depressive episode. The patient also has type 2 DM for which he takes oral antidiabetics.\r\nWhen inpatient, he had persistent hyperglycemia (>250mg/dL). DM&#8217;s\r\ncomplications (poly-neuropathy, retinopathy and right bundle-branch block). Diabetic status\r\noriented us to choose quetiapine (600 mg/day) for both antidepressive effect and its safe\r\nmetabolic profile associated with valproate (1000 mg/day). Antidiabetic medication was\r\nadjusted following the clinical outcome. Instruments. for depression we used Montgomery-\r\nAsberg Rating Scale (MARS), for mania Young Mania Rating Scale (YMRS), Clinical\r\nGlobal Impression for Bipolar Disorder (CGI-BP), for diabetes (glycemia, HbA1c,\r\nglycosuria, body weight, adverse events and relapse were followed-up for 6 months. The\r\nevaluations were performed weekly during hospitalization (6 weeks) and then monthly, for\r\n6 months quetiapine together with valproate therapy led to remission of depressive\r\nsymptoms (MADRS <50% vs. baseline). At the same time DM was compensated with\r\nglimpirid and metformin (glycemia < 120mg/dL). These results maintained till the end of\r\nthe follow-up period. Conclusion. Quetiapine associated to valproate in acute and chronic\r\nmanagement of bipolar depression proved to be efficient and well tolerated, along 6 months,\r\nin patient with type 2 diabetes.

Diabetes mellitus is a complex disorder of the energy metabolism of the human body. In the last WHO/ADA classification, the main forms of this disease are Type 1 (T1DM) and Type 2 (T2DM) diabetes mellitus. According to the same classification, the pathogenesis of T2DM is considered to include a progressive insulin secretory defect on the background of insulin resistance. Recently, controversies surround the concept of peripheral insulin\r\nresistance emerging in the 70's as an attempt to explain the differences from the T1DM phenotype whose autoimmune nature was as that time revealed. The insulin resistance\r\nhypothesis was based on the supposition that high plasma insulin levels are the result of a primary molecular defect against which the normal beta cells will react with an increased insulin secretion. This hypothesis has been\r\nused to explain both the pathogenesis of T2DM and the metabolic syndrome, named also for a short period of time "the insulin resistance syndrome". We will try to argue\r\nthat what it is attributed to peripheral insulin\r\nresistance belongs in fact to obesity. Special emphasis is put on the role of the adipocytes, including the secretion of different adipokines with the secondary lipotoxicity, oxidative stress and pro-inflammatory reaction, explaining the complex relationship between obesity and diabetes.

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Aims. To investigate the historical changes in survival with diabetes in patients treated with insulin from diagnosis.\r\nMethods. We analyzed 2811 deaths, 51.5% males, registered at ?I. Pavel? Bucharest Diabetes Centre, aged 40-64 years and deceased between 1943 and 2009. We split the analysis in three time periods according to year of death: 1943-1965,\r\n1966-1988 and 1989-2009.\r\nResults. The mean age at diabetes onset was 51.4?6.8 years, with mean disease duration at death of 17.7?11.6 years\r\nand mean age at death of 69.1?11.2 years. The mean survival after diabetes onset was 13.9?9.8 years in 1943-1965, and rose to 17.3?9.6 years (p<0.001) in 1989-2009. There was a significant increase for coronary heart diseases and cancer and a significant decrease for infections and endstage\r\nrenal disease as causes of death.\r\nConclusions. We found no significant changes in age at onset, which combined with an increase in survival with diabetes lead to a significant increase in age at death.\r\nMajor historical events have a strong impact over survival after the onset of diabetes.