ACTA ENDOCRINOLOGICA (BUC)

Context. Although, many studies have been made on the clinical course of autoimmune thyroiditis, this study focused on women and the factors effecting the natural course such as Selenium. Objective. The study aimed to determine Hashimoto’s thyroiditis (HT) clinical course in adults and the factors that could affect it. Design. The study was in a retrospective manner between 2010-2018. Subjects and Methods. 101 patients with HT were followed for 60.7±32.7 months. Biochemical and ultrasonographic data were collected. We investigated whether the age at diagnosis, family history, smoking habits, levothyroxine replacement therapy, and serum selenium (Se) levels influenced the disease course. Results. No relationship was observed between age and thyroid functions, thyroid volumes (TV), and autoantibody (Ab) levels at diagnosis. Ab levels were irrelevant with TV, echogenicity, and nodularity at diagnosis. However, initial TSH levels were significantly associated with anti-TPO levels (p=0.028, r=0.218). In the untreated group, thyroid functions seemed to be stable. TV decreased significantly in both treated and untreated patients (p<0.001). The decrease in TV was significantly higher in the treatment group (p=0.002). In euthyroid and subclinical hypothyroid patients, levothyroxine therapy did not affect the decrease in TV. Ab levels remained stable in untreated patients, but anti-TPO levels significantly decreased in treated patients (p<0.001). Smoking seemed to increase only anti-Tg levels (p=0.009). Family history was not associated with any of the studied parameters. Serum Se level was negatively correlated only with thyroid echostructure and only in treated patients. TV showed a “Gaussian distribution” in all patients at the diagnosis and at the end, independent of levothyroxine treatment. Conclusions. Most euthyroid patients remained euthyroid during five years of follow-up. The decrease in TV was significantly prominent with LT4 treatment. Importantly, TV followed a normal distribution instead of the bimodal distribution that is classically described.

kidney disease (CKD), a growing public health issue, than in general population. The key issue in management of fragility fracture in CKD patients is determining whether fractures have occurred as a result of qualitative abnormalities (consequences of renal osteodystrophy or CKD-mineral and bone disorder), a reduced bone mineral density (osteoporosis) or a combination of both. In CKD patients bone histomorphometry is the gold standard for evaluating bone quality and strength, but the routine use of this method is not practical. Fracture risk can be assessed in this population by DEXA (Dual-Energy X-Ray Absorptiometry), but biochemical markers, like intact PTH and bone-specific alkaline phosphatase may be helpful. The new and emerging high resolution imaging tools need more studies for a correct evaluation of their utility in predicting fracture risk. Pharmacological therapies for fragility fracture based on current understanding of the metabolic disturbances in CKD will be reviewed. Antiresorptive and anabolic agents used in the treatment of osteoporosis are discussed with special focus on CKD population.

Objective. This study aims to determine the prevalence of neuropathy in the prediabetic period. Design, Subjects and Method. Informed consent was attained from the patients who volunteered to participate in the study after ethics committee approval was obtained. Patients under the age of 18, having vitamin B12 or folic acid deficiency, history of collagen tissue-rheumatological disease, chronic kidney failure, cirrhosis, ethylism, thyroid disease, autoimmune disease, malignancy, tuberculosis, type 1 or 2 diabetes mellitus and pregnant women were excluded from the study. Patients diagnosed with prediabetes were evaluated by the DN4 neuropathy complaint questionnaire. Neuropathy was diagnosed in patients having a score of four or more. For the statistical analyses Student t-test, Pearson chi-square test, and Fisher's exact test were performed using the NCSS program. Results. A total of 224 volunteers, 167 women and 57 men, were included in the study. The mean age of the participants was 51 and the mean level of hemoglobin A1C was 5.9. Neuropathy was detected in 45% of the cases. Especially in women, there was a significant increase in the frequency of neuropathy compared to men. The most common complaints found in our study were burning sensation and numbness in the extremities. Conclusions. Similar to diabetic patients, prediabetic patients also have a high rate of neuropathy. For the early diagnosis of neuropathy and to be treated promptly, screening tests such as DN4 should be performed for all prediabetic patients. According to the test results, advanced examinations such as EMG or biopsy should be performed earlier.

Context. Parental history of osteoporosis is associated with an increased risk of fracture. However, there are not many data on the mechanism of action. Our objective was to determine if heredity influences fracture rate: independently or through the bone mineral density; to identify also the strongest independent risk factors of osteoporotic fractures among our study population. Methods. We processed data of 541 women outpatients with an average age of 55 years, participating in an osteoporosis screening program. Our results confirm that the presence of family history significantly increases fracture prevalence, (37% vs. 17%, p<0.001, OR 2.853, p=0.001) and decreases BMD scores. Fractures occur at higher (better) T and Z-scores. The risk of having T values in the range of (0- -1) and Z values in (-1--2) is much higher in the positive group. The logistic regression analysis confirms the BMD-independent influence of heredity on fracture risk. Conclusions. Parental history of osteoporosis negatively affects bone density and significantly increases the incidence of fractures. The latter happens also independently of the bone density values. Timely intervention in these easy-to-detect cases may be the most effective prevention of osteoporotic fractures.

Context. Non-psychogenic polydipsia-induced hyponatremia is a rare clinical finding. The effects of severe hyponatremia on the electrical activity of the heart in this setting are far from clear. Case report. Resting ECG and 24-h ambulatory ECG monitoring performed in an 80-year-old hypertensive female accusing nonspecific symptoms of confusion, lethargy, disorientation, nausea, and palpitations, demonstrated significant intraatrial and atrioventricular conduction disorders and numerous atrial tachyarrhythmia episodes. Laboratory analysis revealed severe hyponatremia (108 mEq/L) as only significant disorder. Extensive endocrine, neurological, cardiology, and pulmonary examinations excluded the most common causes of hyponatremia, including the inappropriate antidiuretic hormone secretion syndrome. Careful history revealed excessive voluntary water intake of up to 6 L/day and low sodium intake, associated with long-term thiazidelike diuretic treatment. Correction of sodium levels was associated with complete resolution of both atrial arrhythmias and conduction disorders. Conclusions. This report presents the first case of severe hyponatremia caused by combined non-psychogenic polydipsia and thiazide-like diuretic use complicated with reversible cardiac conduction disorders and atrial arrhythmias. The close temporal relationship between the fully reversible cardiac electric abnormalities and severe hyponatremia strongly indicates hyponatremia as key feature in the pathogenesis of these electric abnormalities.

Prader-Willi syndrome (PWS) is commonly caused by the absence of the paternal contribution for imprinted genes in chromosomes 15q11.\r\nWe present a case of a 16 years-old girl with hypotonia, feeding difficulties, failure to thrive and strabismus during infancy followed by hyperphagia, early-onset obesity with insulin-dependent diabetes mellitus and necrobiosis lipoidica diabeticorum, short stature, hypogonadotropic hypogonadism and some of the facial characteristics of individuals with PWS. Routine Giemsa banded chromosomes were obtained from peripheral blood lymphocytes. Karyotype analysis showed a mosaic triple X (46,XX/47,XXX). Using\r\nmethylation studies of the PWS critical region (SNRPN locus) and by polymorphic microsatellite analysis, the existence of microdeletion of the critical area on paternal\r\nchromosome 15 was shown in white blood cells. Mosaicism for triple-X was observed in other three reported patients with PWS but in all of these reported cases an uniparental maternal heterodisomy for chromosome 15 was described. The X chromosome mosaicism in our case is presumed to have arisen postzygotically. The findings in our patient provide evidence that these two chromosomal anomalies are not related and had occurred together coincidentally. Genetic counseling for this family should consider these two conditions separately and provide separate recurrence\r\nrisks for each.

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Context. Hepatitis C and diabetes represent important health problems globally. The new-onset diabetes after transplantation is a particular entity that appears due to the use of immunosuppression among transplanted patients. Objective. We aim to describe the clinical and biological aspects of severe hyperglycemia in a kidney transplant recipient undergoing Interferon-free therapy for chronic hepatitis C, discussing the interference of different factors with the glucose metabolism. Design. The occurrence of diabetes in a patient with history of renal transplantation and Interferon-free treated hepatitis C was studied from both clinical and paraclinical points of view. Subjects and methods. When presenting to the hospital, extensive blood tests were performed on the patient, revealing significant hyperglycemia and an elevated level of blood tacrolimus. Creatinine clearance was calculated. ECG presented T-wave alterations. Intensive insulin protocol was applied, the case being managed in a multidisciplinary approach. Results. Blood glucose and tacrolimus were slowly normalized, under therapy. The antiviral treatment was continued, with the achievement of sustained virologic response. Conclusions. Diabetes mellitus can have many causes, hepatitis C and transplantation both having an impact on glucose metabolism. The association of the three entities should be carefully managed, due to its enhancing effect on morbidity and mortality.

Context. Chronic idiopathic urticaria (CIU) is often associated with autoimmune thyroiditis (AT). Objective. The aim of this study was to analyze the clinical particularities of patients with CIU associated with AT and to evaluate the efficacy of dapsone in such patients. Design. We performed an observational study of patients hospitalized in our clinic between January 2010 - December 2013 for moderate/severe chronic urticaria (CU). Subjects and Methods. Data regarding medical history, clinical, paraclinical findings, coexistence of AT and response to treatment were compared between patients with CU and AT and those without AT. Patients continued oral H1 antihistamines. Severe flares required systemic corticotherapy. 11 patients with refractory CIU associated with AT received dapsone treatment. Levothyroxine was administered in patients with hypothyroidism. Results. Among the 210 patients admitted for CU, 39 (92% female) were diagnosed with CIU associated with AT. Patients with CIU associated with AT had a slightly longer disease duration, a higher prevalence of angioedema (25.6% vs. 16.7%) and a more frequent need of systemic corticotherapy for urticaria exacerbations (46.2% vs. 30.4%). All 39 patients achieved significant clinical improvement after a mean period of 4 weeks based on urticaria activity score (UAS) 7 (p<0.0001). Conclusions. Assays for thyroid autoantibodies and thyroid function should be part of the workup in patients with CU, enabling the diagnosis of autoimmune urticaria. Without correction of the underlying autoimmune mechanisms, CU may persist regardless of conventional treatment. Dapsone represents a therapeutic option in autoimmune CU.