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ACTA ENDOCRINOLOGICA (BUC)
The International Journal of Romanian Society of Endocrinology / Registered in 1938in Web of Science Master Journal List
Acta Endocrinologica(Bucharest) is live in PubMed Central
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Endocrine Care
Matei VP, Mihailescu A, Paraschiv G, Al-Bataineh R, Purnichi T
Weight Gain and Antipsychotics. Data from EUFEST StudyActa Endo (Buc) 2016 12(2): 177-184 doi: 10.4183/aeb.2016.177
AbstractContext. Schizophrenia is a chronic disease most frequently necessitating lifelong antipsychotic treatment. Selecting which antipsychotic is to be prescribed in an individual schizophrenia patient represents an important clinical decision that need to take into account efficacy and side effects. Objective. Evaluating weight gain related with one year antipsychotic treatment in antipsychotic naive firstepisode schizophrenia patients. Design. This study is an analysis of weight gain associated with typical or atypical antipsychotics used in European First Episode Schizophrenia Trial (EUFEST) study. Subjects and Methods. 113 first episode naïve antipsychotic schizophrenia patients included in EUFEST - Romanian cohort, who were randomized to one of the 5 treatment arms. Weight was obtained at baseline, 3, 6, 9 and 12 months for the 5 antipsychotics (typical-Haloperidol; atypical-Olanzapine, Amisulpride, Ziprasidone, Quetiapine). Results. There are no statistically significant differences between groups treated with typical or atypical antipsychotics or between any individual antipsychotics concerning weight gain during the study. Weight gain was the highest in the first 3 months (57.49%) for all the studied neuroleptics. At the end of the study, the less increase was observed with ziprasidone (3.87 kg) and the highest with olanzapine (9.83 kg). Conclusion. Increase in weight has taken place for each individual neuroleptic, but also as a group (all neuroleptics) in the first three months (57.49%). Therefore, we should address the issue of weight gain with great care, especially in first period of antipsychotic administration, in order to fast deploy intervention tailored to maintain pretreatment weight. -
General Endocrinology
Cobilinschi C, Tincu RC, Baetu AE, Deaconu CO, Totan A, Rusu A, Neagu PT, Grintescu IM
Endocrine Disturbances Induced by Low-Dose Organophosphate Exposure in Male Wistar RatsActa Endo (Buc) 2021 17(2): 177-185 doi: 10.4183/aeb.2021.177
AbstractBackground. Organophosphate exposure induces many endocrine effects. Aim. In this study we observed the effects of acute stress induced by cholinesterase inhibition on the main hormonal axes. Materials and Methods. We included thirteen weanling Wistar rats that were subjected to organophosphate exposure. They were first tested for baseline levels of butyrylcholinesterase, cortisol, free triiodothyronine, thyroxine, thyroid-stimulating hormone and prolactin. Secondly, chlorpyrifos was administered. Next samples were taken to determine the level of all the above-mentioned parameters. Results. Butyrylcholinesterase was significantly decreased after exposure (p<0.001). Cortisol levels were significantly higher after clorpyrifos administration (358.75±43 vs. 241.2±35 nmoL/L)(p<0.01). Although prolactin had a growing trend (450.25±24.65 vs. 423±43.4 uI/mL), the results were not statistically significant. Both free triiodothyronine and thyroxine were significantly higher after exposure. Surprisingly, thyroid-stimulating hormone level almost doubled after exposure with high statistical significance (p<0.001), suggesting a central stimulation of thyroid axis. Butyrylcholinesterase level was proportional with thyroid-stimulating hormone level (p=0.02) and thyroxine level was inversely correlated to the cortisol level (p=0.01). Acute cholinesterase inhibition may induce high levels of cortisol, free triiodothyronine, thyroxine and thyroid-stimulating hormone. From our knowledge this is the first study dedicated to the assessment of acute changes of hormonal status in weanling animals after low-dose organophosphate exposure. Conclusion. Acute cholinesterase inhibition may cause acute phase hormonal disturbances specific to shocked patients. -
General Endocrinology
Sedighi M, Seidi H, Asadi F, Biranvand H, Banaei P, Torkashvand M, Nazari A, Rafieian-Kopaei M, Hashemzadeh P, Kiani AA, Ghorbanzadeh V
Cardioprotective Effect of Dichloromethane Valerian (Valeriana Officinalis) Extract on Ischemia-Reperfusion-Induced Cardiac Injuries in RatsActa Endo (Buc) 2023 19(2): 178-186 doi: 10.4183/aeb.2023.178
AbstractBackground. Valepotriate is an active ingredient of valerian (Valeriana officinalis) with strong antioxidant activity that is effective for numerous cardiovascular diseases. Objective. The aim of this study was to investigate the effect of an active ingredient of V. officinalis extract on ischemia-reperfusion-induced cardiac injuries in male rats. Methods. Thirty-two male rats were subjected to ischemia for 40 minutes and reperfusion for five days. The rats were divided into 4 groups of 8 each; group 1 (control) was given normal saline, and groups 2-4 were gavaged with 0.2, 0.1, 0.05 mg/kg of valepotriate extract, respectively, and received extract (0.2 mg/kg ip) two weeks before ischemia induction. Results. Dichloromethane V. officinalis (valepotriate) extract exerted a protective effect against ischemia-reperfusion-induced injuries. So that infarct size and number of ventricular arrhythmia and ventricular escape beats decreased compared to the control group. Moreover, ST segment amplitude, QTC interval, and heart rate decreased in the injured hearts and serum levels of antioxidant enzymes glutathione peroxidase, catalase, and superoxide dismutase increased. Biochemical markers malondialdehyde and lactate dehydrogenase also decreased on day 5 after the onset of reperfusion. Conclusion. V. officinalis extract may have a protective effect against myocardial ischemia-reperfusion by producing antioxidant effects. -
Endocrine Care
Atalay K, Gezer Savur F, Kirgiz A, Erdogan Kaldirim H, Zengi O
Serum Vitamin D Levels in Different Morphologic Forms of Age Related CataractActa Endo (Buc) 2020 16(2): 178-182 doi: 10.4183/aeb.2020.178
AbstractPurpose. Vitamin D insufficiency and age related cataract (ARC) are public health problems. We evaluated serum vitamin D levels in ARC patients. Method. A prospective hospital-based crosssectional study was designed to measure the vitamin D status of patients with ARC. Patients have grouped either presence of any type of posterior subcapsular cataract (PSC) (group 1) or ARC without the PSC component (Group 2). After full ophthalmologic consideration, patients over 40 years of age with no history of ocular trauma, multivitamin supplement ingestion, chronic renal failure, thyroidectomy, parathyroidectomy, skin cancer, and cigarette smoking were included in the study. Results. Totally, 79 subjects of which 26 (32.9%) subjects in group 1 and 53 (67.1%) subjects in group 2 were included in the study. Group 1 had mean vitamin D levels of 17.31±13.30 ng/mL. Vitamin D levels in Group 2 were 13.34±7.87 ng/mL. Group 1 did not show vitamin D insufficiency (P = 0.31; one-sample t-test). However, Group 2 showed a statistically significantly lower vitamin D level compared to the insufficiency level of 20ng/mL (P= 0.00; one-sample t-test). Conclusion. Vitamin D may have an important function in lens metabolism. Vitamin D deficiency and cataract development need further extensive researches. -
Endocrine Care
Pelinescu-Onciul D, Albu D
Intrauterine progestin and estradiol subdermic implant as hormonal replacement therapy for the patients with metrorrhagia in preclimaxActa Endo (Buc) 2007 3(2): 179-187 doi: 10.4183/aeb.2007.179
AbstractObjectives. To determine whether levonorgestrel releasing intrauterine device (LNGIUD) in association with oestradiol subdermic implant is an efficient and safe therapy for neurovegetative disturbances in climacterium, for the patients who had previous metrorrhagia in preclimax.\r\nPatients and method. We performed a prospective study on 18 menopausal patients (group A) with a mean age of 50.2 ? 1.5 years with LNG-IUD, inserted in preclimacterium for dysfunctional uterine bleeding (biopsy showed us simple endometrial hyperplasia) and 20 menopausal women with neurovegetative symptoms that refused hormonal replacement therapy (HRT) as control group B. In group A, patients had amenorrhea after 6.8 ? 1.7 months from IUD insertion. Our criteria for selection were: presence of neurovegetative disturbances, FSH >25 UI/L, no contraindication for hormonal replacement therapy. Group A patients had a subdermic implant with estradiol 25 mg every six months. All patients were regularly followed: first visit after one month, the next visits every three months for three years. At each visit we observed neurovegetative symptoms, uterine bleeding, endometrial thickness assessed by transvaginal ultrasonography. The Kupperman test of menopausal distress index was calculated at each visit.\r\nResults. All patients reported the absence of neurovegetative symptoms after 4.5 ? 1.8 months of therapy. Fifteen of them (83.33%) had no vaginal bleeding during the study, three patients presented minor uterine bleeding during the first six months of follow-up. Transvaginal ultrasonography showed endometrial thickness < 5mm in all our subjects. Four patients presented breast discomfort for a short period.\r\nConclusion. LNG-IUD in association with estradiol subdermic implant proved to be an efficient therapy in climacterium. The capacity of LNG-IUD to determine endometrial atrophy contributes to local safety of this hormonal replacement therapy. -
Endocrine Care
Ince S, Buldanli M, Cinar A, Hancerliogullari O, Okuyucu K
Evaluation and Management of Parathyroid Incidentalomas Detected by Routine Neck Ultrasonography with a Multidisciplinary Clinical ApproachActa Endo (Buc) 2024 20(2): 179-185 doi: 10.4183/aeb.2024.179
AbstractContext. Detection of parathyroid incidentalomas (PTIs) by ultrasonography (US) generally depends on clinical experience and it can be usually confused with perithyroidal lymph nodes. Objective. We aimed to evaluate the role of US for the detection of PTIs and define clinicopathologic features of PTIs detected during routine neck US. Design. In this retrospective study, we studied PTIs in a multidisciplinary clinical approach of nuclear medicine and general surgery clinics. Subjects and Methods. US indications and reports of 41275 were reviewed retrospectively. Of these patients, PTI was suspected in 66 (0.16%) patients. Those with a pathology-confirmed diagnosis after surgery formed Group PCD and those without a pathology-confirmed diagnosis and operation Group NPCD. These groups were compared statistically according to demographic data, laboratory tests, imaging results and postoperative findings. Results. The diagnosis of PTI was confirmed pathologically in 31 operated patients. Other pathologies rather than PTI on US were multinodular goiter, thyroiditis, thyroid nodule and perithyroidal lymph node. PTH and calcium levels were significantly higher in PCD Group;anti- TPO and anti-TG levels were significantly higher in NPCD Group. Conclusions. Lesions suspected of PTI on US should be followed-up with further evaluation by laboratory tests and imaging methods and a multidisciplinary working environment should be established. -
Endocrine Care
Zimmermann A, Grigorescu-Sido P, Rossmann H, Lackner KJ, Drugan C, Khzouz CAl, Bucerzan S, Nascu I, Popp RA, Zimmermann T, Weber MM
A Prospective Study of Insulin Resistance in Gaucher Disease Type 1 Patients with Normal Weight, under Enzyme Replacement TherapyActa Endo (Buc) 2015 11(2): 180-188 doi: 10.4183/aeb.2015.180
AbstractA certain degree of insulin resistance in patients with Gaucher disease type 1 (GD) under enzyme replacement therapy (ERT) was reported. Data on insulin sensitivity in treatment naïve patients are inconsistent. Objective. To analyse prospectively changes in parameters of insulin resistance under ERT and to estimate when they occur. Design. prospective, controlled study; three years follow-up. Patients and methods. 12 treatment naïve patients with GD type 1 (M/W 8/4), 29.5±12.9 years, without overweight, diagnosed enzymatically and by genotyping, without previous diabetes mellitus. Patients were evaluated before and every 6 months up to 3 years under ERT and compared at baseline and after 3 years with matched healthy controls. Fasting-glucose (FG), - insulin (FI), C-peptide, HOMA-IR, IRI, HOMA-B, blood count, hepatic and splenic volume, chitotriosidase, severity score index di Rocco (SSI) were assessed. Results. Baseline glycemic parameters did not differ from controls. FG increased from baseline after two years of ERT (+16.4%,p<0.010), FI (+40.3%,p=0.030), HOMA-IR (+61.2%,p=0.007) and IRI (+9.1%,p=0.010) after 18 months, HOMA-B after 2.5 years (+51%, p=0.015. After 3 years of ERT patients were more insulin resistant compared to controls (p<0.001): FG (96.0±6.2 vs. 73.2±6.4 mg/dL), FI (11.2±2.4 vs. 5.6±1.3 μU/L), HOMA-IR (2.7±0.6 vs. 1.0+0.3), IRI (3.02±0.10 vs. 2.62±0.13). FG, FI, HOMAIR, IRI, HOMA-B correlated with disease severity markers. Conclusions. This is the first controlled study which evaluates prospectively insulin resistance in GD patients, finding significant differences compared to baseline starting with 18 months ERT. -
Endocrine Care
Alzoubi A, Mahdi H, Bashir S. Al, Halalsheh O, Ebbini M Al, Alzarir M, Al-Ahmar K, Alfaqih M, Al-Hadidi AH
Normalization of Serum Vitamin D Improves Semen Motility Parameters in Patients with Idiopathic Male InfertilityActa Endo (Buc) 2017 13(2): 180-187 doi: 10.4183/aeb.2017.180
AbstractContext. Idiopathic male infertility is evident in half of infertile males. Vitamin D receptors are expressed throughout male reproductive tract, including spermatozoa, promoting motility. Epidemiological studies revealed the positive association between serum vitamin D and semen quality. However, there are no clinical studies examining the differential role of vitamin D in idiopathic male infertility. Objectives. 1) To investigate the association between vitamin D deficiency and idiopathic male infertility, and 2) To determine whether vitamin D deficient males would show restoration of semen quality parameters upon supplementation with vitamin D. Design. This was a year-long case-control study from November 2015 to November 2016. A therapeutic intervention cohort for 2 months was also performed. Subjects and Methods. 117 Jordanian males were enrolled. Following a clinical evaluation by a urologist, baseline serum vitamin D and semen fluid analyses were collected. Participants were stratified into 3 groups: controls (n=30), idiopathic infertility (n=67), and secondary infertility (n=20). Idiopathic infertility patients with low vitamin D (n= 45) were supplemented with oral vitamin D, 5000 IU, once daily for two months. Thereafter, serum vitamin D and semen fluid analyses were reassessed (n= 34; 11 patients were lost to follow up). Results. Vitamin D was significantly lower in patients with idiopathic infertility than in both controls and men with secondary infertility. Significant improvement of progressive and total sperm motility was observed after vitamin D treatment. Vitamin D correlated significantly with semen quality in the study population. However, no correlation was found between vitamin D and any of the semen quality parameters in the idiopathic infertility group. Conclusions. Vitamin D supplementation improves sperm motility in idiopathic male infertility patients with low vitamin D. Larger and longer clinical trials are warranted to validate the use of vitamin D in these cases. -
Endocrine Care
Mircescu G, Capusa C, Andreiana I
The management of secondary hyperparathyroidism in chronic kidney diseaseActa Endo (Buc) 2005 1(2): 181-200 doi: 10.4183/aeb.2005.181
Abstract ReferencesSecondary hyperparathyroidism, i.e. increased synthesis and secretion of parathyroid hormone and gland hyperplasia, is commonly found in chronic kidney disease. Although it is, at first, an adaptive response to the loss of renal functions in order to maintain the calcium/phosphate homeostasis and normal bone turnover, it is also an important cause of increased morbidity in this clinical setting by leading to renal osteodystrophy and cardiovascular complications. Recent advances in the knowledge on the pathogenesis of parathyroid-related complications in renal failure allowed for new therapeutic approaches. However, many problems remain to be solved in the future. This paper briefly presents the current understanding of pathogenic mechanisms of hyperparathyroidism, bone disease and vascular calcification during chronic kidney disease. In addition, it summarizes the main therapeutic methods available today for controlling secondary hyperparathyroidism and the challenges of practitioners concerning this issue. Finally, the current status of secondary hyperparathyroidism management is analyzed, with emphasis on the Romanian experience.1. K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. Am J Kidney Dis, 42(4, suppl 3):S1-S201, 2003. [CrossRef]2. Hsu C-Y, Chertow GM. Chronic renal confusion: Insufficiency, failure, dysfunction, or disease. Am J Kidney Dis, 36(2):415-418, 2000. [CrossRef]3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification, Am J Kidney Dis, 39(suppl 1):S1-S92, 2002.4. Mircescu G, Capusa C. Chronic kidney disease: A useful concept for integrated approach of chronic renal failure (Part I). Medicina Interna, 1(4):17-28, 2004.5. Fournier A, Oprisiu R, Hottelart C et al. Renal osteodystrophy in dialysis patients: Diagnosis and treatment. Artif Org, 22(7):530-557, 1998. [CrossRef]6. Elder J. Pathogenesis and management of hyperparathyroidism in end-stage renal disease and after renal transplantation. Nephrology, 6:155-160, 2001. [CrossRef]7. Cozzolino M, Brancaccio D, Gallieni M, Galasi A, Slatopolsky E, Dusso A. Pathogenesis of parathyroid hyperplasia in renal failure. J Nephrol, 18(1):5-8, 2005.8. Dusso AS, Thadhani R, Slatopolsky E. Vitamin D receptor and analogs. Sem Nephrol, 24(1):10-16, 2004. [CrossRef]9. Dusso AS. Vitamin D receptor: Mechanisms for vitamin D resistance in renal failure. Kidney Int, 63(suppl 85):S6-S9, 2003. [CrossRef]10. Urena P, Frazao JM. Calcimimetic agents: Review and perspectives. Kidney Int, 63(suppl 85): S91- S96, 2003. [CrossRef]11. Slatopolsky E, Dusso A, Brown AJ. Control of uremic bone disease: Role of vitamin D analogs. Kidney Int, 61(suppl 80):S143-S148, 2002. [CrossRef]12. Fatica RA, Dennis VW. Cardiovascular mortality in chronic renal failure: hyperphosphatemia, coronary calcification, and the role of phosphate binders. Cleve Clinic J Med, 69(suppl 3):S21-S27, 2002. [CrossRef]13. Hruska KA, Saab G, Chaudhary LR, Quinn CO, Lund RJ, Surendran K. Kidney-bone, bone-kidney, and cell-cell communications in renal osteodystrophy. Semin Nephrol, 24(1):25-38, 2004. [CrossRef]14. Hercz G. Regulation of bone remodeling: Impact of novel therapies. Semin Dialysis, 14(1):55-60, 2001. [CrossRef]15. Malluche HH, Langub MC, Monier-Faugere M-C. The role of bone biopsy in clinical practice and research. Kidney Int, 56(suppl 73): S20-S25, 1999. [CrossRef]16. Couttenye MM, D?Haese PC, Verschoren WJ, Behets GJ, Schrooten I, De Broe ME. Low bone turnover in patients with renal failure. Kidney Int, 56(suppl 73): S70-S76, 1999. [CrossRef]17. Ganesh SK, Stack AG, Levin NW, Hulbert-Shearon TE, Port FK. Association of elevated serum PO4, Ca ? PO4 product and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol, 12(10):2131-2138, 2001.18. Giachelli CM, Jono S, Shioi A, Nishizawa Y, Mori K, Morii H. Vascular calcification and inorganic phosphate. Am J Kidney Dis, 38(suppl 1):S34-S37, 2001. [CrossRef]19. Wilmer WA, Magro CM. Calciphylaxis: Emerging concepts in prevention, diagnosis, and treatment. Semin Dialysis, 15(3):172-186, 2002. [CrossRef]20. Shanahan C. Bone turnover and extraosseous calcifications: Is there a relationship? Presentation at the ASN Renal Week, San Diego, Nov 2003, www.hdcn.com/symp/03asn/07/sha/sha.htm.21. Block G, Port FH. Calcium phosphate metabolism and cardiovascular disease in patients with chronic kidney disease. Semin Dialysis, 16(2):140-147, 2003. [CrossRef]22. Elder GJ. Targets for phosphate control in chronic kidney disease. Nephrology, 9:2-6, 2004. [CrossRef]23. Block GA, Martin KJ, de Francisco AM et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med, 350:1516-1525, 2004. [CrossRef]24. De Francisco AM, Ellis HA, Owen JP et al. Parathyroidectomy in chronic renal failure. Q J Med, 55(218):289-315, 1985.25. Malberti F, Marcelli D, Conte F, Limido A, Spotti D, Locatelli F. Parathyroidectomy in patients on renal replacement therapy: An epidemiologic study. J Am Soc Nephrol, 12:1242-1248, 2001.26. TominagaY, Uchida K, Haba T et al. More than 1000 cases of total parathyroidectomy with forearm autograft for renal hyperparathyroidism. Am J Kidney Dis, 38(4, suppl 1):S168-S171, 2001. [CrossRef]27. Mircescu G, C?pu?? C. Guidelines for surgical management of secondary hyperparathyroidism in dialysis patients. Nefrologia, 9(23-24):51-56, 2004.28. De Francisco AM, Fresnedo GF, Rodrigo E, Pinera C, Amado JA, Arias M. Parathyroidectomy in dialysis patients. Kidney Int, 61(suppl 80): S161-S166, 2002. [CrossRef]29. The CARI Guidelines (Caring for Australians with Renal Impairment) for bone disease, calcium, phosphate and parathyroid hormone. /www.kidney.org.au/cari/drafts/bone_management. Australian Kidney Foundation and Australia New Zealand Society of Nephrology30. Mircescu G et al, on behalf of the Romanian Society of Nephrology. Guidelines for best medical practice: Secondary hyperparathyroidism in chronic kidney disease, Ed. InfoMedica, Bucharest, 2005.31. Kim J, Pisoni RL, Danese MD et al. Achievement of proposed NKF-K/DOQI bone metabolism and disease guidelines : Results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Abstract for ASN Annual Meeting - San Diego, J Am Soc Nephrol (Nov), 1 -
Endocrine Care
Kacso IM, Lenghel A, Rusu CC, Rahaian R, Nita C, Craciun M, Luculescu N, Negru D, Hancu N, Bondor CI, Gherman Caprioara M
Determinants of plasma adiponectin levels in patients with type 2 diabetes mellitus and microalbuminuria or low grade proteinuriaActa Endo (Buc) 2010 6(2): 181-189 doi: 10.4183/aeb.2010.181
AbstractBackground. Recent experimental data show that increased plasma adiponectin in chronic kidney disease could be a response to inflammation.\r\nObjective. To identify factors influencing adiponectinemia in patients with type 2 diabetes (T2DM) and microalbuminuria or low grade proteinuria.\r\nDesign. 32 patients with urinary albumin excretion rate (UAER)> 30 mg/g creatinine but without significant proteinuria (< trace COMBUR) were included and compared to 59 normalbuminuric T2DM controls. History, anthropometric measurements, laboratory analysis, total plasma adiponectin were obtained.\r\nResults. In our patients with UAER of 273.51?57.26 mg/g creatinine and estimated glomerular filtration rate (eGFR) 64.92?4.56 mL/min, in simple regression, adiponectinemia\r\ncorrelates inversely to eGFR (p=0.02, r= -0.38), triglyceridemia (p=0.03, r=-0.37) and hemoglobin\r\n(Hb -p= 0.01, r=-0.45) and positively to HDL cholesterol (p=0.001, r=0.54) and UAER (p<0.0001, r=0.71); the two latter parameters remain significant in multiple regression. In controls, adiponectinemia correlates inversely to age (p=0.04, r=-0.26) and BMI (p=0.04, r=-0.24); these and UAER predict adiponectinemia in multiple regression. 11 patients have UAE superior to 300 mg/g creatinine and 21 are strictly microalbuminuric (mean UAER 653.16?97.02 and 83.68?10.28mg albumin/g creatinine respectively). In microalbuminuric patients serum C reactive protein (CRP) correlates positively (p=0.0008, r=0.68) and Hb negatively (p=0.04, r=-0.41) to adiponectinemia; in multiple regression adiponectinemia only depends on CRP. In proteinuric patients CRP and\r\nglycated Hb correlate to adiponectinemia in stepwise multiple regression.\r\nConclusion. Adiponectinemia is mainly predicted by UAER in our cohort whereas it depends on age and BMI in normalbuminuric T2DM controls; in strictly microalbuminuric\r\npatients CRP is a major predictor of adiponectinemia.