ACTA ENDOCRINOLOGICA (BUC)

Context. Recent evidence has stressed that many proinflammatory factors are particularly conducive to the progression of diabetic nephropathy, but the mechanisms underlying the changes are poorly understood. Objective. The purpose of this study was to investigate if up-regulated expression of both phospholipase A2 (PLA2) and cyclooxygenase-2 (COX-2) is involved in renal damage and micro-inflammatory state in streptozotocin-induced diabetic rats. Animals and methods. Sixteen Sprague Dawley rats were randomly divided into 2 groups: control group and diabetes group. Animals in diabetes group were treated with intraperitoneal injection of streptozotocin. Eight weeks later, rat renal tissue was studied with light and transmission electron microscopes, and PLA2 and COX-2 and their mRNA expression were examined by immunohistochemistry and reverse transcription polymerase chain reaction, respectively. Results. The renal pathological lesions in diabetes group were obvious, including increased amounts of mesangial matrix, thickening of the glomerular and tubular basement membranes and fusion and effacement of the adjacent podocyte foot processes. Infiltrating inflammatory cells were observed in the tubules. Compared with control group, the expression of cytosolic PLA2 and COX-2 was significantly increased in diabetes group. Conclusions. It uncovers that the PLA2-COX-2 pathway may lead to renal inflammation associated with renal damage in streptozotocin- induced diabetic rats.

Introduction. With the introduction of iodized salt, more and more people are exposed to iodine sufficiency in some regions. The purpose of this study was to investigate the prevalence of nontoxic nodular goiter (NTNG) in the littoral region with high iodine supply after a nearly twodecade universal salt iodization. Subjects and Methods. Eight hundred and thirtyfive participants (from 25~65 years; males 421 and females 414) were invited for the study from Huan-cui District of Weihai City, Shandong Province from January 2013 to September 2014. All participants were inspected and diagnosed by endocrinologists according to the thyroid function tests and the thyroid gland imaging. After the normal diet of three days, the urine samples of the participants were collected between 8:00AM and 9:00AM and the urinary iodine (UI) concentrations were analyzed using Urinary Iodide Test Kit. Results. The overall prevalence of NTNG in the region was 40.1%, and different prevalence occurred in the different age ranges (p<0.01). The prevalence of NTNG was 32.51%, 37.44%, 49.70%, 58.57 and 74.77% in the age group of ≤ 30, 31-40, 41-50, 51-60 and >60 years, respectively. Meanwhile, the prevalence of NTNG in women (42.08%) was higher than that in men (34.29%, p<0.05). The median of UI concentrations were 139.4μg/L and 101.5μg/L for the group with NTNG and without NTNG, respectively (p<0.01). However, there was no significant difference in UI concentrations among the groups with different age ranges (p>0.05), and statistical difference was not observed for UI concentrations between women and men (p>0.05). Intriguingly, higher UI concentrations were found in the group with larger thyroid size (p<0.01). Conclusion. The iodine excess can lead to the high occurrence of nodular goiter in the littoral region, and individual UI concentration detection is recommended for the iodine nutritional status analysis among normal people when Universal Salt Iodization (USI) continues to be implemented in the region.

Aim. The aim of our study was to investigate the effect of pioglitazone on glycemic and blood pressure control, on inflammation markers in diabetic patients.\r\nPatients and methods. Forty-nine diabetic patients who had been followed up as outpatients for 2.7 years and HbA1c was >7% were included in the study. The patients had never received thiazolidinedione therapy before. Clinical, metabolic variables, high-sensitive Creactive protein (hsCRP), homocysteine (HCY) and asymmetric dimethylarginine (ADMA) levels were measured. 30 mg pioglitazone were administered. The patients were followed up for six months and all the measurements were re-evaluated for comparison.\r\nResults. Body mass index (BMI) significantly increased after treatment. Fasting glucose, HbA1c and HsCRP were decreased. Insulin resistance was improved and HOMA-IR index was decreased after pioglitazone treatment [8 (?6.5) vs 4(?3.1); p<0.0001]. Pioglitazone improved lipid metabolism. Mean total cholesterol and LDL cholesterol levels were decreased and HDL cholesterol was increased after treatment. The decrease in triglyceride and homocysteine levels did not reach significance. Mean ADMA level did not change after therapy [0.62 (?0.39) vs 0.61 (?0.44); p=0.85].\r\nConclusion. Pioglitazone treatment in type 2 DM produced significant improvements in measures of glycemic control, plasma lipids, blood pressure and homocysteine levels. Pioglitazone had no influence on ADMA levels.

Context. The effects of COVID-19 on the adrenocortical system and its hormones are not well known. Objectives. We studied serum cortisol, serum adrenocorticotropic hormone (ACTH), and their ratio in hospitalized non-critically ill COVID-19 patients. Design. A prospective case-control study. Methods. The study participants were divided into 2 groups. Group 1 consisted of 74 COVID-19 patients. The second group consisted of 33 healthy persons. Early admission above hormones levels was determined and compared between the study groups. Besides that, COVID-19 patients were grouped according to their Glasgow Coma Score (GCS), CURB-65 score, and intensive care unit (ICU) requirement, and further sub-analyses were performed. Results. There were no significant differences in the mean age or gender distribution in both groups. In the patients’ group, the serum ACTH concentration was lower than in the healthy group (p<0.05). On the other hand, the serum cortisol levels and cortisol/ACTH ratio of the patients’ group were significantly higher than of the healthy controls (p<0.05, all). Further analyses showed that, although serum cortisol and ACTH levels were not high, the cortisol/ACTH ratio was higher in COVID-19 patients with low GCS (<15) than patients with normal GCS (=15) (p<0.05). In COVID-19 in patients with different CURB-65 scores, the cortisol/ACTH ratio was significantly different (p<0.05), while serum cortisol and ACTH were not different in groups (p>0.05). Serum cortisol levels and cortisol/ACTH ratio were higher but ACTH level was lower in the ICU needed COVID-19 patients than in patients who do not need ICU (p<0.05). Conclusion. Our pilot study results showed that the cortisol/ACTH ratio would be more useful than serum cortisol and/or ACTH levels alone in evaluating the adrenocortical system of COVID-19 patients. Still, further detailed studies are needed to confirm these.

Background. Bilateral adrenal hemorrhage is a serious condition that can result in adrenal insufficiency, shock, acute adrenal crisis, and mortality if it is not managed with adequate treatment. We report a rare case of idiopathic bilateral adrenal hemorrhage. C ase presentation. A 50-year-old woman visited our hospital with complaints of right upper abdominal pain. A computed tomography (CT) revealed unilateral left adrenal gland hemorrhage. However, the results of rapid adrenocorticotropic hormone (ACTH) stimulation test and adrenomedullary hormone function test were normal. Since the patient did not show signs of adrenal insufficiency, corticosteroid therapy was postponed and only supportive management therapy was started. After 1 week, a followup CT showed a previously unseen adrenal hemorrhage on the right adrenal gland, but the rapid ACTH stimulation test result was normal. One year later, no hemorrhagic signs were observed on the follow-up CT. Conclusion. In most cases of idiopathic bilateral adrenal hemorrhage, patients are treated with steroid replacement therapy due to adrenal insufficiency. In some other cases, patients are treated with steroids despite the absence of adrenal insufficiency. Here we reported a very rare case of idiopathic bilateral adrenal hemorrhage sequentially to emphasize that before initiation of adrenal hormone replacement therapy, it is important to determine whether adrenal insufficiency is present. If there is no evidence of adrenal insufficiency, adrenal replacement therapy should be postponed until the presence of adrenal insufficiency is confirmed.

Introduction. Fahr’s syndrome is an infrequent disorder characterized by bilateral symmetrical calcification of basal ganglia and the cerebral cortex. It can be seen genetic, idiopathic, or secondary to endocrine diseases. This disease is related to different metabolic disorders particularly with diseases of the parathyroid gland. Case 1. A 63-year-old female patient applied to our clinic due to having hypoparathyroidism with bilateral basal ganglia calcification in head computed tomography(CT). She had subtotal thyroidectomy 25 years ago. In the neurological examination, mild symmetrical parkinsonism was determined. In laboratory examination Ca:8 mg/dL (8.6- 10.2), P:5.1 mg/dL (2.3-4.5), PTH:9.53 pg/mL (15-65) were detected. Calcitriol 0.25 μ/day was added to her treatment. Her parkinsonism disappeared after the treatment. Case 2. A 49-year-old male patient was consulted when he was admitted to the department of neurology in our hospital. The physical examination demonstrated the characteristics of Albright’s hereditary osteodystrophy. The neurological examination shows bilateral symmetrical bradykinesia, dysphagia, and moderate dysarthria. In the laboratory examination PTH: 46.5 ng/L(15-65), Ca:8.6 mg/dL (8.6-10.2), P:2.7 mg/dL (2.3-4.5) were detected and were all within the normal ranges. Consequently, pseudopseudohypoparathyroidism was decided as a diagnosis. G protein alpha subunit mutation (Gsα) was not detected due to technical limitations. Conclusion. When a patient is diagnosed as Fahr’s syndrome, we should keep in mind parathyroid disorders. Fahr’s syndrome must be evaluated in patients showing intracranial calcification accompanied by parathyroid diseases.

About 250 patients with acquired partial lipodystrophy (Barraquer-Simons) syndrome have been reported so far. It is characterized by the loss of adipose tissue from the face and upper extremities, and accumulated fat in the rest of the body. The disease usually starts in females during childhood or adolescence, and usually after a febrile illness. Fat loss often comes into view in months or years. We present a 23-year-old female patient with acquired partial lipodystrophy , which is rarely seen.

Context. The expression of TSHR-C on the serum tetraiodothyronine (T4) and TSH receptor antibody (TRAb) levels are rarely studied. Objective. The effect of TSHR-c on T4 and TRAb levels and concomitant thyroid histological changes in mice was investigated. Design. Animal experimental study. Subjects and methods. Female BALB/c mice at 6-8 weeks of age were immunized with the thyroid stimulating hormone receptor antigen C-terminus (TSHR-C), and randomly divided into control group (treated with the corresponding concentrations of normal saline) and four experimental subgroups: TSHR-c1 subgroup (4 μg), TSHR-c2 subgroup (6 μg), TSHR-c3 subgroup (8 μg) and TSHR-c4 subgroup (10 μg). Serum T4 and TRAb levels were determined. Results. The serum T4 level decreased significantly in the experimental mice as the concentration increased. All the experimental mice were positive for serum TRAb (experimental groups: 40 positive/40, 100% vs. control group: 3 positive/10, 30%) compared to the control group (P =0.000). HE staining showed that the follicles in the control mice were composed of small to medium-sized round follicles, whereas the follicles in the experimental mice were irregularly enlarged under light microscope. Conclusions. TSHR-c immunization resulted in thyroid hormone changes like those observed in hypothyroidism, probably due to the induction of TRAb generation.

Purpose. We aimed to assess the relationship between the regional body fat distribution and insulin resistance and pancreas volume (PV) in type-2 diabetes (DM) patients. Methods. Fifty-three consecutive type-2 diabetic and 51 non-diabetic patients matched by age, gender and body mass index (BMI) were enrolled. Subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), waist circumference, and PV were measured with computed tomography. Insulin resistance was assessed by the homeostasis model assessment of insulin resistance (HOMA-IR). Results. Patients with type-2 DM had significantly lower PV than non-diabetic individuals. HOMA-IR ranged from 0.74 to 6.24; and from 0.37 to 3.26, in type-2 DM patients and non-diabetics, respectively. VAT was positively correlated with HOMA-IR in two groups. There were inverse correlations between PV and VAT and VAT/SAT but only in diabetics. Conclusions. The VAT/SAT ratio may reflect the possible role of VAT to better understand the pathogenesis of obesity-related disorders in patients with type-2 DM.

Background. 21-hydroxylase deficiency (21 OHD) is the most common form of congenital adrenal hyperplasia (CAH) and it has been widely described in the literature. Adrenocortical incidentalomas are unfrequently the presenting manifestations of CAH, especially in nonclassical form of 21 OHD (NC 21 OHD). Myelolipoma has previously been reported more frequently than other adrenal adenomas associated with CAH. Case. We report a 40-year old male case of NC 21 OHD with hypoadrenocorticism after unilateral adrenalectomy of the right side because of a large solid incidentaloma (5×4×4cm3) at the age of 31. This patient began to suffer from obvious symptoms of adrenal insufficiency after 9 years from the surgery. He was reviewed and a very low-density adrenal mass (4.1×3.9cm) was found on computed tomography of the abdomen. After he was admitted to our hospital, this patient was confirmed with NC 21 OHD and presented low level cortisol, striking elevated ACTH, aldosterone insufficiency, increased 17-hydroxyprogesterone, progesterone, decreasing androgens and azoospermatism. Conclusion. Patients with 21 OHD could be on risk not only for adrenal hyperplasia, but also to develop adrenal adenomas, particularly if the disease was poorly controlled.