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Fibroblast growth factor 21 (FGF21) is a novel hepatokine involved in regulating glucose and lipid metabolism, and has been linked to the prediction, treatment, and improvement of prognosis in multiple cardiovascular diseases (CVDs). The aim of this study is to explore the relationship between FGF21 levels and vascular diseases (VDs) including carotid atherosclerosis (CAS) and hypertension (HP) in patients with T2DM.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>Baseline serum FGF21 was determined in a cross-sectional study of 701 patients with T2DM and 258 healthy control.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>The morbidity of CAS was increased in T2DM patients with HP as compared with those without (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001). The average serum FGF21 level of healthy was [123.9 (67.2-219.3)]. Baseline FGF21 was significantly higher in those who developed CAS or HP than in those who did not [305.9 (177.2-508.4) vs. 197.2 (129.7-308.3) pg\u002FmL, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001]. In addition, an elevated serum FGF21 was observed in T2DM patients with HP and CAS than that of T2DM patients with CAS or HP [550.5 (312.6-711.3) vs. 305.9 pg\u002FmL, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001]. Serum FGF21 levels were positively correlated with body mass index and carotid intima media thicknes (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05), the association remained significant after adjusting for age and T2DM duration. Furthermore, the multinomial logistic regression showed that serum FGF21 was independently associated with CAS and HP in patients with T2DM after adjustment for demographic and traditional VDs risk factors (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001).\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n                \u003Cjats:p>Baseline FGF21 is elevated in VDs during diabetes, changes of serum FGF21 levels were appropriately matched to metabolic stress. FGF21can be used as an independent predictor for diagnosing VDs and predicting prognosis.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":143},"Increased circulating FGF21 level predicts the burden of metabolic demands and risk of vascular diseases in adults with type 2 diabetes",{"VOID":145},"38057786",{"VOID":147},"10.1186\u002Fs12902-023-01523-y","PUBLICATION","VERIFIED","Auto 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Metabolic stress and Cardiovascular Disease in Diabetes Mellitus: the role of protein O-GlcNAc modification. Arterioscler Thromb Vasc Biol. 2019;39(10):1911–24. https:\u002F\u002Fdoi.org\u002F10.1161\u002FATVBAHA.119.312192.",{"doi":390},"10.1161\u002FATVBAHA.119.312192",{"id":20,"text":392,"url":20,"identifiers":393},"Gonzalez LL, Garrie K, Turner MD. Type 2 Diabetes - an autoinflammatory Disease driven by metabolic stress. Biochim Biophys Acta Mol Basis Dis. 2018;1864(11):3805–23. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbadis.2018.08.034.",{"doi":394},"10.1016\u002Fj.bbadis.2018.08.034",{"id":20,"text":396,"url":20,"identifiers":397},"Vinciguerra F, Baratta R, Farina MG, Tita P, Padova G, Vigneri R, et al. Very severely obese patients have a high prevalence of type 2 Diabetes Mellitus and Cardiovascular Disease. 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Cell Metab. 2018;27(6):1323–1337e5. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cmet.2018.04.002.",{"doi":418},"10.1016\u002Fj.cmet.2018.04.002",{"id":20,"text":420,"url":20,"identifiers":421},"Lin Z, Pan X, Wu F, Ye D, Zhang Y, Wang Y, et al. Fibroblast growth factor 21 prevents Atherosclerosis by suppression of hepatic sterol regulatory element-binding protein-2 and induction of adiponectin in mice. Circulation. 2015;131(21):1861–71. https:\u002F\u002Fdoi.org\u002F10.1161\u002FCIRCULATIONAHA.115.015308.",{"doi":422},"10.1161\u002FCIRCULATIONAHA.115.015308",{"id":20,"text":424,"url":20,"identifiers":425},"Xiao Y, Liu L, Xu A, Zhou P, Long Z, Tu Y, et al. Serum fibroblast growth factor 21 levels are related to subclinical Atherosclerosis in patients with type 2 Diabetes. Cardiovasc Diabetol. 2015;14:72. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12933-015-0229-9.",{"doi":426},"10.1186\u002Fs12933-015-0229-9",{"id":20,"text":428,"url":20,"identifiers":429},"Tan H, Yue T, Chen Z, Wu W, Xu S, Weng J. Targeting FGF21 in cardiovascular and metabolic Diseases: from mechanism to medicine. Int J Biol Sci. 2023;19(1):66–88. https:\u002F\u002Fdoi.org\u002F10.7150\u002Fijbs.73936.",{"doi":430},"10.7150\u002Fijbs.73936",{"id":20,"text":432,"url":20,"identifiers":433},"Lin ZF, Pan XB, Wu F, Zhang Y, Wang C. Application of FGF21 in the preparation of Drugs for the treatment of HP and\u002For vascular injury caused by angiotensin II. People’s Republic of China, CN108379555. 2018.08.10. No doi or PMID.",{},{"id":20,"text":435,"url":20,"identifiers":436},"Silveira Rossi JL, Barbalho SM, Reverete de Araujo R, Bechara MD, Sloan KP, Sloan LA. Metabolic syndrome and Cardiovascular Diseases: going beyond traditional risk factors. Diabetes Metab Res Rev. 2022;38(3):e3502. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fdmrr.3502.",{"doi":437},"10.1002\u002Fdmrr.3502",{"id":20,"text":439,"url":20,"identifiers":440},"Sun P, Dwyer KM, Merz CN, Sun W, Johnson CA, Shircore AM, et al. Blood pressure, LDL cholesterol, and intima-media thickness: a test of the response to injury hypothesis of Atherosclerosis. Arterioscler Thromb Vasc Biol. 2000;20(8):2005–10. https:\u002F\u002Fdoi.org\u002F10.1161\u002F01.atv.20.8.2005.",{"doi":441},"10.1161\u002F01.atv.20.8.2005",{"id":20,"text":443,"url":20,"identifiers":444},"Lonardo A, Nascimbeni F, Mantovani A, Targher G. Hypertension, Diabetes, Atherosclerosis and NASH: cause or consequence? J Hepatol. 2018;68(2):335–52. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jhep.2017.09.021.",{"doi":445},"10.1016\u002Fj.jhep.2017.09.021",{"id":20,"text":447,"url":20,"identifiers":448},"Grimaldi A, Heurtier A. Diagnostic criteria for type 2 Diabetes. Rev Prat. 1999;49(1):16–21. No doi or PMID.",{},{"id":20,"text":450,"url":20,"identifiers":451},"Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604–12. https:\u002F\u002Fdoi.org\u002F10.7326\u002F0003-4819-150-9-200905050-00006.",{"doi":452},"10.7326\u002F0003-4819-150-9-200905050-00006",{"id":20,"text":454,"url":20,"identifiers":455},"Nonterah EA, Crowther NJ, Klipstein-Grobusch K, Oduro AR, Kavousi M, Agongo G, et al. Racial and Ethnic Differences in the Association between Classical Cardiovascular Risk Factors and common carotid intima-media thickness: an Individual Participant Data Meta-Analysis. J Am Heart Assoc. 2022;11(15):e023704. https:\u002F\u002Fdoi.org\u002F10.1161\u002FJAHA.121.023704.",{"doi":456},"10.1161\u002FJAHA.121.023704",{"id":20,"text":458,"url":20,"identifiers":459},"Crouse JR, Harpold GH, Kahl FR, Toole JF, McKinney WM. Evaluation of a scoring system for extracranial carotid Atherosclerosis extent with B-mode ultrasound. Stroke. 1986;17(2):270–5. https:\u002F\u002Fdoi.org\u002F10.1161\u002F01.str.17.2.270.",{"doi":460},"10.1161\u002F01.str.17.2.270",{"id":20,"text":462,"url":20,"identifiers":463},"An SY, Lee MS, Yi SA, Ha ES, Han SJ, Kim HJ, et al. Serum fibroblast growth factor 21 was elevated in subjects with type 2 Diabetes Mellitus and was associated with the presence of carotid artery plaques. Diabetes Res Clin Pract. 2012;96(2):196–203. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.diabres.2012.01.004.",{"doi":464},"10.1016\u002Fj.diabres.2012.01.004",{"id":20,"text":466,"url":20,"identifiers":467},"Kaihara T, Hoshide S, Tomitani N, Kanegae H, Kario K. Maximum home systolic blood pressure is a marker of carotid Atherosclerosis. Clin Exp Hypertens. 2019;41(8):774–8. https:\u002F\u002Fdoi.org\u002F10.1080\u002F10641963.2018.1557678.",{"doi":468},"10.1080\u002F10641963.2018.1557678",{"id":20,"text":470,"url":20,"identifiers":471},"Lin Z, Tian H, Lam KS, Lin S, Hoo RC, Konishi M, et al. Adiponectin mediates the metabolic effects of FGF21 on glucose homeostasis and insulin sensitivity in mice. Cell Metab. 2013;17(5):779–89. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cmet.2013.04.005.",{"doi":472},"10.1016\u002Fj.cmet.2013.04.005",{"id":20,"text":474,"url":20,"identifiers":475},"Liu X, Zhang Y, Ma C, Lin J, Du J. Alternate-day fasting alleviates high fat diet induced non-alcoholic fatty Liver Disease through controlling PPARα\u002FFgf21 signaling. Mol Biol Rep. 2022;49(4):3113–22. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11033-022-07142-5.",{"doi":476},"10.1007\u002Fs11033-022-07142-5",{"id":20,"text":478,"url":20,"identifiers":479},"Lin Z, Wu Z, Yin X, Liu Y, Yan X, Lin S, et al. Serum levels of FGF-21 are increased in coronary Heart Disease patients and are independently associated with adverse lipid profile. PLoS ONE. 2010;5(12):e15534. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0015534.",{"doi":480},"10.1371\u002Fjournal.pone.0015534",{"id":20,"text":482,"url":20,"identifiers":483},"Yafei S, Elsewy F, Youssef E, Ayman M, El-Shafei M. Fibroblast growth factor 21 association with subclinical Atherosclerosis and arterial stiffness in type 2 Diabetes. Diabetes Metab Syndr. 2019;13(1):882–8. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.dsx.2018.12.007.",{"doi":484},"10.1016\u002Fj.dsx.2018.12.007",{"id":20,"text":486,"url":20,"identifiers":487},"Chow WS, Xu A, Woo YC, Tso AW, Cheung SC, Fong CH, et al. Serum fibroblast growth factor-21 levels are associated with carotid Atherosclerosis Independent of established cardiovascular risk factors. Arterioscler Thromb Vasc Biol. 2013;33(10):2454–9. https:\u002F\u002Fdoi.org\u002F10.1161\u002FATVBAHA.113.301599.",{"doi":488},"10.1161\u002FATVBAHA.113.301599",{"id":20,"text":490,"url":20,"identifiers":491},"Kaur N, Gare SR, Shen J, Raja R, Fonseka O, Liu W. Multi-organ FGF21-FGFR1 signaling in metabolic health and Disease. Front Cardiovasc Med. 2022;9:962561. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffcvm.2022.962561.",{"doi":492},"10.3389\u002Ffcvm.2022.962561",{"id":20,"text":494,"url":20,"identifiers":495},"Ding X, Boney-Montoya J, Owen BM, Bookout AL, Coate KC, Mangelsdorf DJ. at al. βKlotho is required for fibroblast growth factor 21 effects on growth and metabolism. Cell Metab. (2012) 16(3):387 – 93. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cmet.2012.08.002.",{"doi":496},"10.1016\u002Fj.cmet.2012.08.002",{"id":20,"text":498,"url":20,"identifiers":499},"Huang Z, Xu A, Cheung BMY. The potential role of fibroblast growth factor 21 in lipid metabolism and Hypertension. Curr Hypertens Rep. 2017;19(4):28. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11906-017-0730-5.",{"doi":500},"10.1007\u002Fs11906-017-0730-5",{"id":20,"text":502,"url":20,"identifiers":503},"Gaich G, Chien JY, Fu H, Glass LC, Deeg MA, Holland WL, et al. The effects of LY2405319, an FGF21 analog, in obese human subjects with type 2 Diabetes. Cell Metab. 2013;18(3):333–40. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cmet.2013.08.005.",{"doi":504},"10.1016\u002Fj.cmet.2013.08.005",{"id":20,"text":506,"url":20,"identifiers":507},"Shang W, Yu X, Wang H, Chen T, Fang Y, Yang X, et al. Fibroblast growth factor 21 enhances cholesterol efflux in THP-1 macrophage-derived foam cells. Mol Med Rep. 2015;11(1):503–8. https:\u002F\u002Fdoi.org\u002F10.3892\u002Fmmr.2014.2731.",{"doi":508},"10.3892\u002Fmmr.2014.2731",{"id":20,"text":510,"url":20,"identifiers":511},"Kim WJ, Kim SS, Lee HC, Song SH, Bae MJ, Yi YS, et al. Association between Serum Fibroblast Growth Factor 21 and coronary artery Disease in patients with type 2 Diabetes. J Korean Med Sci. 2015;30(5):586–90. https:\u002F\u002Fdoi.org\u002F10.3346\u002Fjkms.2015.30.5.58.",{"doi":512},"10.3346\u002Fjkms.2015.30.5.58",false,{"id":515,"createTime":516,"updateTime":517,"relativeEntities":518,"slug":519,"properties":520,"entityType":148,"verifyStatus":149,"verifyTime":517,"verifyNote":150,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":529,"fullTextUrl":20,"authors":530,"publicationType":349,"publisherRelationship":765,"citationCount":20,"citationInfo":20,"publishDate":799,"publishYear":800,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":513},"b27401a4-3b1d-4b11-a6d4-014e8a650721","2024-01-08T16:40:22.103+00:00","2025-02-02T23:57:58.806+00:00",[],"Diagnosis-and-treatment-of-primary-central-nervous-system-lymphoma-with-the-primary-lesion-in-the-hypothalamus-a-case-report",{"references":521,"abstract":523,"title":525,"doi":527},{"VOID":522},"Grommes C, DeAngelis LM. Primary CNS lymphoma. J Clin Oncol. 2017;35(21):2410–8.\nBrain Tumor Registry of Japan (2005–2008). Neurol Med Chir (Tokyo). 2017;57(Suppl 1):9–102.\nDeWitt JC, Mock A, Louis DN. The 2016 WHO classification of central nervous system tumors: what neurologists need to know. Curr Opin Neurol. 2017;30(6):643–9.\nBrandsma D, Bromberg JEC. Primary CNS lymphoma in HIV infection. Handb Clin Neurol. 2018;152:177–86.\nLi L, Rong JH, Feng J. Neuroradiological features of lymphomatosis cerebri: a systematic review of the English literature with a new case report. Oncol Lett. 2018;16(2):1463–74.\nTanki HN, Malik KN, Makhdoomi R, Feroz S, Ramzan AU. Primary hypothalamic lymphoma in an adult male: a case report and literature review. Oman Med J. 2018;33(4):346–51.\nKuker W, Nagele T, Korfel A, Heckl S, Thiel E, et al. Primary central nervous system lymphomas (PCNSL): MRI features at presentation in 100 patients. J Neuro-Oncol. 2005;72(2):169–77.\nGiustina A, Gola M, Doga M, Rosei EA. Clinical review 136: primary lymphoma of the pituitary: an emerging clinical entity. J Clin Endocrinol Metab. 2001;86(10):4567–75.\nVillano JL, Koshy M, Shaikh H, Dolecek TA, McCarthy BJ. Age, gender, and racial differences in incidence and survival in primary CNS lymphoma. Br J Cancer. 2011;105(9):1414–8.\nSu L, Ding M, Chen L, Li C, Lao M. Primary central nervous system lymphoma in a patient with systemic lupus erythematosus mimicking high-grade glioma: a case report and review of literature. Medicine (Baltimore). 2018;97(23):e11072.\nTsang M, Cleveland J, Rubenstein JL. On point in primary CNS lymphoma. Hematol Oncol. 2000;38(5):640–7.",{"EN":524},"Primary central nervous system lymphoma is a rare extra-nodal lymphoma of the central nervous system. Primary central nervous system lymphoma lesions usually appear in the vicinity of the ventricle, and there are few reports of primary central nervous system lymphoma with hypothalamic-pituitary lesions. We treated a 56-year-old male with primary central nervous system lymphoma with the primary lesion in the hypothalamus, which was found by magnetic resonance imaging after sudden onset of endocrinological abnormalities. Initially, he was hospitalized to our department for hyponatremia. Endocrinological examination in conjunction with head magnetic resonance imaging and endoscopic biopsy revealed hypothalamic hypopituitarism and tertiary hypoadrenocorticism caused by a rapidly growing, diffuse large B-cell lymphoma in the hypothalamus. Remission of the tumor was achieved by high-dose methotrexate with whole brain radiotherapy, and some of the hormone responses were normalized. While primary central nervous system lymphoma is rare, it is important to note that hypopituitarism can result and that the endocrinological abnormalities can be partially restored by its remission.",{"EN":526},"Diagnosis and treatment of primary central nervous system lymphoma with the primary lesion in the hypothalamus: a case 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ID. IDF Diabetes Atlas 2019 [Cited 2019]. Available from: http:\u002F\u002Fwww.diabetesatlas.org.\nKaiser AB, Zhang N, Van Der Pluijm W. Global prevalence of type 2 diabetes over the next ten years (2018-2028). Am Diabetes Assoc. 2018. https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdb18-202-LB.\nAamir AH, Ul-Haq Z, Mahar SA, Qureshi FM, Ahmad I, Jawa A, et al. Diabetes prevalence survey of Pakistan (DPS-PAK): prevalence of type 2 diabetes mellitus and prediabetes using HbA1c: a population-based survey from Pakistan. BMJ Open. 2019;9(2):e025300.\nNeeland IJ, Salahuddin U, McGuire DK. A safety evaluation of empagliflozin for the treatment of type 2 diabetes. Expert Opin Drug Saf. 2016;15(3):393–402.\nAamir AH, Raja UY, Asghar A, Mahar SA, Ghaffar T, Ahmed I, et al. Asymptomatic urinary tract infections and associated risk factors in Pakistani Muslim type 2 diabetic patients. BMC Infect Dis. 2021;21(1):1–6.\nKalra S, Ghosh S, Aamir A, Ahmed MT, Amin MF, Bajaj S, et al. Safe and pragmatic use of sodium–glucose co-transporter 2 inhibitors in type 2 diabetes mellitus: south Asian Federation of Endocrine Societies consensus statement. Indian J Endocrinol Metab. 2017;21(1):210.\nProfessional practice committee: standards of medical Care in Diabetes—2021. Diabetes Care. 2021;44(Supplement_1):S3. https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdc21-Sppc.\nJan A, Weir CB. BMI Classification Percentile and Cut Off Points. Treasure Island: StatPearls; 2021.\nVasilakou D, Karagiannis T, Athanasiadou E, Mainou M, Liakos A, Bekiari E, et al. Sodium–glucose cotransporter 2 inhibitors for type 2 diabetes: a systematic review and meta-analysis. Ann Intern Med. 2013;159(4):262–74.\nBurroughs TE, Desikan R, Waterman BM, Gilin D, McGill J. Development and validation of the diabetes quality of life brief clinical inventory. Diabetes Spectr. 2004;17(1):41–9.\nDevi R, Mali G, Chakraborty I, Unnikrishnan MK, Abdulsalim S. Efficacy and safety of empagliflozin in type 2 diabetes mellitus: a meta-analysis of randomized controlled trials. Postgrad Med. 2017;129(3):382–92.\nFigueiredo IR, Rose SCP, Freire NB, Patrocínio MS, Pierdoná N, Bittencourt RJ. Use of sodium-glucose cotransporter-2 inhibitors and urinary tract infections in type 2 diabetes patients: a systematic review. AMB Rev Assoc Med Bras. 2019;65(2):246–52.\nZinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2015;373(22):2117–28.\nZinman B, Lachin JM, Inzucchi SE. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2016;374(11):1094. https:\u002F\u002Fdoi.org\u002F10.1056\u002FNEJMc1600827.\nRoden M, Merker L, Christiansen AV, Roux F, Salsali A, Kim G, et al. Safety, tolerability and effects on cardiometabolic risk factors of empagliflozin monotherapy in drug-naïve patients with type 2 diabetes: a double-blind extension of a phase III randomized controlled trial. Cardiovasc Diabetol. 2015;14(1):1–11.\nKumar N, Garg A, Bhatt DL, Sabongui S, Gupta N, Chaudhry S, et al. Empagliflozin improves cardiorespiratory fitness in type 2 diabetes: translational implications. Can J Physiol Pharmacol. 2018;96(11):1184–7.\nFerdinand KC, Izzo JL, Lee J, Meng L, George J, Salsali A, et al. Antihyperglycemic and blood pressure effects of empagliflozin in black patients with type 2 diabetes mellitus and hypertension. Circulation. 2019;139(18):2098–109.\nAnsary TM, Nakano D, Nishiyama A. Diuretic effects of sodium glucose cotransporter 2 inhibitors and their influence on the renin-angiotensin system. Int J Mol Sci. 2019;20(3):629.\nSohail E, Ahsan T, Ghaus S, Aijaz W. SGLT 2 inhibitors; glycemic control, weight loss and safety profile in patients with type 2 diabetes, at Medicell institute (MIDEM). Pak J Med Sci. 2021;37(1):87–92.\nZhang Y-J, Han S-L, Sun X-F, Wang S-X, Wang H-Y, Liu X, et al. Efficacy and safety of empagliflozin for type 2 diabetes mellitus: meta-analysis of randomized controlled trials. Medicine. 2018;97(43):e12843. https:\u002F\u002Fdoi.org\u002F10.1097\u002FMD.0000000000012843.",{"EN":811},"Sodium-Glucose-Co-Transporter 2 (SGLT2) inhibitor (Empagliflozin) is an effective drug in controlling blood glucose through predominantly glycosuria. Glycosuria increases the risk of genitourinary infections in diabetes. This study was aimed to establish the safety and efficacy of Empagliflozin (Group-A) versus standard care (Group-B) in Pakistani Muslim individuals with type 2 diabetes. A multicenter, randomized clinical trial was conducted in five cities across Pakistan from July 2019 to August 2020. Patients of both genders aged 18–75 years, body mass index (BMI) ≤ 45 kg\u002Fm2, glycosylated hemoglobin (HbA1c) 7–10% (53 mmol\u002Fmol to 86 mmol\u002Fmol) and treatment-naive to Empagliflozin were included. Treatment was given for 24 weeks, and allocation was done through randomization. Out of 745 screened patients, 333 met the eligibility criteria, and a total of 244 (73.3%) patients were enrolled. More hypoglycemic events were reported in the standard care group, whereas positive urine culture, fungal infection, dehydration, and hypotension occurrence were comparable between the two groups. The 6 months mean HbA1c reduction was significant in both groups; (Group-A: 0.91 ± 0.15; p \u003C 0.001 vs. Group-B2: 0.79 ± 0.14; p \u003C 0.001). Efficacy comparison at 6 months revealed a significant reduction in weight and systolic blood pressure (SBP) in Group A only (Group-A: 1.4 ± 0.4 kg; p \u003C 0.002 vs. Group-B: 0.01 ± 0.5 kg; p \u003C 1.00), (Group-A: 5.1 ± 1.7 mmHg; p \u003C 0.012 vs. Group-B: 2.3 ± 1.7 mmHg; p \u003C 0.526). Empagliflozin was a safe drug compared to standard care in Pakistani Muslim patients with diabetes. It was as effective as standard care in the clinical setting but achieved glycemic control by reducing weight and SBP in type 2 diabetes patients. This study was registered in the NIH US National Library of Medicine clinical trials registry at Clinicaltrials.gov with the registration number: NCT04665284 on 11\u002F12\u002F2020.",{"EN":813},"Safety and efficacy of Empagliflozin in Pakistani Muslim patients with type 2 diabetes (SAFE-PAK); a randomized clinical 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RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005;365(9468):1415–28.\nGrundy SM. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 2008;28(4):629–36.\nGrundy SM. Metabolic syndrome: connecting and reconciling cardiovascular and diabetes worlds. J Am Coll Cardiol. 2006;47(6):1093–100.\nMottillo S, Filion KB, Genest J, Joseph L, Pilote L, Poirier P, Rinfret S, Schiffrin EL, Eisenberg MJ. The metabolic syndrome and cardiovascular risk a systematic review and meta-analysis. J Am Coll Cardiol. 2010;56(14):1113–32.\nWu SH, Liu Z, Ho SC. Metabolic syndrome and all-cause mortality: a meta-analysis of prospective cohort studies. Eur J Epidemiol. 2010;25(6):375–84.\nO'Neill S, O'Driscoll L. Metabolic syndrome: a closer look at the growing epidemic and its associated pathologies. Obesity reviews : an official journal of the International Association for the Study of Obesity. 2015;16(1):1–12.\nCai H, Huang J, Xu G, Yang Z, Liu M, Mi Y, Liu W, Wang H, Qian D. Prevalence and determinants of metabolic syndrome among women in Chinese rural areas. PLoS One. 2012;7(5):e36936.\nSong P, Yu J, Chang X, Wang M, An L: Prevalence and Correlates of Metabolic Syndrome in Chinese Children: The China Health and Nutrition Survey. Nutrients 2017, 9(1).\nMozumdar A, Liguori G. Persistent increase of prevalence of metabolic syndrome among U.S. adults: NHANES III to NHANES. Diabetes care 2011. 1999-2006;34(1):216–9.\nXi B, He D, Hu Y, Zhou D. Prevalence of metabolic syndrome and its influencing factors among the Chinese adults: the China health and nutrition survey in 2009. Prev Med. 2013;57(6):867–71.\nHan TS, Williams K, Sattar N, Hunt KJ, Lean MEJ, Haffner SM. Analysis of obesity and Hyperinsulinemia in the development of metabolic syndrome: San Antonio heart study. Obes Res. 2002;10(9):923–31.\nYong-Woo Park M. PhD, Shankuan Zhu, MD, PhD, Latha Palaniappan, MD, Stanley, Heshka, PhD, Mercedes R. Carnethon, PhD, and Steven B. Heymsfield, MD: the metabolic syndrome: prevalence and associated risk factor findings in the US population from the third National Health and nutrition examination survey, 1988-1994. Arch Intern Med. 2003;24:427–36.\nAgredo-Zuniga RA, Aguilar-de Plata C, Suarez-Ortegon MF. Waist:height ratio, waist circumference and metabolic syndrome abnormalities in Colombian schooled adolescents: a multivariate analysis considering located adiposity. Br J Nutr. 2015;114(5):700–5.\nBeydoun MA, Kuczmarski MT, Wang Y, Mason MA, Evans MK, Zonderman AB. Receiver-operating characteristics of adiposity for metabolic syndrome: the healthy aging in neighborhoods of diversity across the life span (HANDLS) study. Public Health Nutr. 2011;14(1):77–92.\nSakurai M, Takamura T, Miura K, Kaneko S, Nakagawa H. BMI may be better than waist circumference for defining metabolic syndrome in Japanese women. Diabetes Care. 2008;31(3):e12.\nRodea-Montero ER, Evia-Viscarra ML, Apolinar-Jimenez E. Waist-to-height ratio is a better anthropometric index than waist circumference and BMI in predicting metabolic syndrome among obese Mexican adolescents. Int J Endocrinol. 2014;2014:195407.\nNascimento-Ferreira MV, Rendo-Urteaga T, Vilanova-Campelo RC, Carvalho HB, da Paz OG, Paes Landim MB, Torres-Leal FL. The lipid accumulation product is a powerful tool to predict metabolic syndrome in undiagnosed Brazilian adults. Clin Nutr. 2017;36(6):1693–700.\nYang F, Lv JH, Lei SF, Chen XD, Liu MY, Jian WX, Xu H, Tan LJ, Deng FY, Yang YJ, et al. Receiver-operating characteristic analyses of body mass index, waist circumference and waist-to-hip ratio for obesity: screening in young adults in central south of China. Clin Nutr. 2006;25(6):1030–9.\nGuo SX, Zhang XH, Zhang JY, He J, Yan YZ, Ma JL, Ma RL, Guo H, Mu LT, Li SG, et al. Visceral adiposity and anthropometric indicators as screening tools of metabolic syndrome among low income rural adults in Xinjiang. Sci Rep. 2016;6:36091.\nZhang ZQ, Deng J, He LP, Ling WH, Su YX, Chen YM. Comparison of various anthropometric and body fat indices in identifying cardiometabolic disturbances in Chinese men and women. PLoS One. 2013;8(8):e70893.\nZeng Q, He Y, Dong S, Zhao X, Chen Z, Song Z, Chang G, Yang F, Wang Y. Optimal cut-off values of BMI, waist circumference and waist:height ratio for defining obesity in Chinese adults. Br J Nutr. 2014;112(10):1735–44.\nZhang XH, Zhang M, He J, Yan YZ, Ma JL, Wang K, Ma RL, Guo H, Mu LT, Ding YS, et al. Comparison of anthropometric and Atherogenic indices as screening tools of metabolic syndrome in the Kazakh adult population in Xinjiang. Int J Environ Res Public Health. 2016;13(4):428.\nKahn HS. The \"lipid accumulation product\" performs better than the body mass index for recognizing cardiovascular risk: a population-based comparison. BMC Cardiovasc Disord. 2005;5:26.\nAlberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC Jr, et al. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; National Heart, Lung, and Blood Institute; American Heart Association; world heart federation; international atherosclerosis society; and International Association for the Study of obesity. Circulation. 2009;120(16):1640–5.\nWildman RP, Muntner P, Reynolds K, McGinn AP, Rajpathak S, Wylie-Rosett J, Sowers MR. The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999-2004). Arch Intern Med. 2008;168(15):1617–24.\nCraig CL, Marshall AL, Sjostrom M, Bauman AE, Booth ML, Ainsworth BE, Pratt M, Ekelund U, Yngve A, Sallis JF, et al. International physical activity questionnaire: 12-country reliability and validity. Med Sci Sports Exerc. 2003;35(8):1381–95.\nUlla Uusitalo AC, Liisa Palonen, Milorad Toša Zikic, et al.: Geographical variation in the major risk factors of coronary heart disease in men and women aged 35–64 years. Wld hlth statist quan 1988, 41:115–140.\nDoak CM, Hoffman DJ, Norris SA, Campos Ponce M, Polman K, Griffiths PL. Is body mass index an appropriate proxy for body fat in children? Global Food Security. 2013;2(2):65–71.\nWang CJ, Li YQ, Wang L, Li LL, Guo YR, Zhang LY, Zhang MX, Bie RH. Development and evaluation of a simple and effective prediction approach for identifying those at high risk of dyslipidemia in rural adult residents. PLoS One. 2012;7(8):e43834.\nPerloff D, Grim C, Flack J, Frohlich ED, Hill M, Mcdonald M, Morgenstern BZ. Human blood-pressure determination by Sphygmomanometry. Circulation. 1993;88(5):2460–70.\nBairaktari E, Hatzidimou K, Tzallas C, Vini M, Katsaraki A, Tselepis A, Elisaf M, Tsolas O. Estimation of LDL cholesterol based on the Friedewald formula and on apo B levels. Clin Biochem. 2000;33(7):549–55.\nLiu Y, Tong G, Tong W, Lu L, Qin X. Can body mass index, waist circumference, waist-hip ratio and waist-height ratio predict the presence of multiple metabolic risk factors in Chinese subjects? BMC Public Health. 2011;11:35.\nde Oliveira CC, Roriz AK, Ramos LB, Gomes Neto M. Indicators of adiposity predictors of metabolic syndrome in the elderly. Annals of nutrition & metabolism. 2017;70(1):9–15.\nYu J, Tao Y, Tao Y, Yang S, Yu Y, Li B, Jin L. Optimal cut-off of obesity indices to predict cardiovascular disease risk factors and metabolic syndrome among adults in Northeast China. BMC Public Health. 2016;16(1):1079.\nMotamed N, Razmjou S, Hemmasi G, Maadi M, Zamani F. Lipid accumulation product and metabolic syndrome: a population-based study in northern Iran, Amol. J Endocrinol Investig. 2016;39(4):375–82.\nKo KP, Oh DK, Min H, Kim CS, Park JK, Kim Y, Kim SS. Prospective study of optimal obesity index cutoffs for predicting development of multiple metabolic risk factors: the Korean genome and epidemiology study. J Epidemiol. 2012;22(5):433–9.\nSaito I. Epidemiological evidence of type 2 diabetes mellitus, metabolic syndrome, and cardiovascular disease in Japan. Circulation journal : official journal of the Japanese Circulation Society. 2012;76(5):1066–73.\nShao J, Yu L, Shen X, Li D, Wang K. Waist-to-height ratio, an optimal predictor for obesity and metabolic syndrome in Chinese adults. J Nutr Health Aging. 2010;14(9):782–5.\nJanes H, Pepe MS. Adjusting for covariates in studies of diagnostic, screening, or prognostic markers: an old concept in a new setting. Am J Epidemiol. 2008;168(1):89–97.\nChiang JK, Koo M. Lipid accumulation product: a simple and accurate index for predicting metabolic syndrome in Taiwanese people aged 50 and over. BMC Cardiovasc Disord. 2012;12:78.\nTellechea ML, Aranguren F, Martinez-Larrad MT, Serrano-Rios M, Taverna MJ, Frechtel GD. Ability of lipid accumulation product to identify metabolic syndrome in healthy men from Buenos Aires. Diabetes Care. 2009;32(7):e85.\nTaverna MJ, Martinez-Larrad MT, Frechtel GD, Serrano-Rios M. Lipid accumulation product: a powerful marker of metabolic syndrome in healthy population. Eur J Endocrinol. 2011;164(4):559–67.\nYuji M. Metabolic syndrome-definition and diagnostic criteria in Japan. J Atheroscler Thromb. 2005;12(6):301.\nYuji M. Metabolic syndrome-definition and diagnostic criteria in Japan. J Jpn Soc Intern Med. 2005;94:188–203.",{"EN":1087},"To compare the accuracy of different obesity indexes, including waist circumference (WC), weight-to-height ratio (WHtR), body mass index (BMI), and lipid accumulation product (LAP), in predicting metabolic syndrome (MetS) and to estimate the optimal cutoffs of these indexes in a rural Chinese adult population. This prospective cohort involved 8468 participants who were followed up for 6 years. MetS was defined by the International Diabetes Federation, American Heart Association, and National Heart, Lung, and Blood Institute criteria. The power of the 4 indexes for predicting MetS was estimated by receiver operating characteristic (ROC) curve analysis and optimal cutoffs were determined by the maximum of Youden’s index. As compared with WHtR, BMI, and LAP, WC had the largest area under the ROC curve (AUC) for predicting MetS after adjusting for age, smoking, drinking, physical activity, and education level. The AUCs (95% CIs) for WC, WHtR, BMI, and LAP for men and women were 0.862 (0.851–0.873) and 0.806 (0.794–0.817), 0.832 (0.820–0.843) and 0.789 (0.777–0.801), 0.824 (0.812–0.835) and 0.790 (0.778–0.802), and 0.798 (0.785–0.810) and 0.771 (0.759–0.784), respectively. The optimal cutoffs of WC for men and women were 83.30 and 76.80 cm. Those of WHtR, BMI, and LAP were approximately 0.51 and 0.50, 23.90 and 23.00 kg\u002Fm2, and 19.23 and 20.48 cm.mmol\u002FL, respectively. WC as a preferred index over WHtR, BMI, and LAP for predicting MetS in rural Chinese adults of both genders; the optimal cutoffs for men and women were 83.30 and 76.80 cm.",{"EN":1089},"Identification of an obesity index for predicting metabolic syndrome by gender: the rural Chinese cohort 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S, Rocha VM, Taylor R. Artefactual inflation of type 2 diabetes prevalence in WHO STEP surveys. Tropical Med Int Health. 2019;24(4):477–83.\nGLOBAL REPORT ON DIABETES.\nIDF Diabetes Atlas IDF Diabetes Atlas. 2021.\nSun H, Saeedi P, Karuranga S, Pinkepank M, Ogurtsova K, Duncan BB, et al. IDF diabetes atlas: global, regional and country-level diabetes prevalence estimates for 2021 and projections for 2045. Diabetes Res Clin Pract. 2022;183:109119. Available from. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.diabres.2021.109119.\nChiwanga FS, Njelekela MA, Diamond MB, Bajunirwe F, Guwatudde D, Nankya-Mutyoba J, et al. Urban and rural prevalence of diabetes and pre-diabetes and risk factors associated with diabetes in Tanzania and Uganda. Glob Health Action. 2016;9(1):1–6.\nMary M, Gibson K. Tanzania steps survey report ministry of health and social nationalinstitute for medical in collaboration with world health. Tanzania J Heal Reasearch-NIMR Tanzania. 2013;22(8):28–39.\nCervin C, Lyssenko V, Bakhtadze E, Lindholm E, Nilsson P, Tuomi T, et al. Diabetes in Adults , Type 1 Diabetes , and Type 2 Diabetes Genetics of LADA. Diabetes Res Clin Pract. 2008;57(5):1433–7.\nGroop LC, Niskanen LEOK, Karjalainen J. GAD Antibodies in Non Insulin Dependant diabetes Melitus. Diabetes Care. 1995;18(12):1557–65.\nKumar A, de Leiva A. Latent autoimmune diabetes in adults (LADA) in Asian and European populations. Diabetes Metab Res Rev. 2017;33(5):5–19.\nNaik RG, Brooks-Worrell BM, Palmer JP. Latent autoimmune diabetes in adults. J Clin Endocrinol Metab. 2009;94(12):4635–44.\nVan Deutekom AW, Heine RJ, Simsek S. The islet autoantibody titres: their clinical relevance in latent autoimmune diabetes in adults (LADA) and the classification of diabetes mellitus. Diabet Med. 2008;25(2):117–25.\nTowns R, Pietropaolo M. GAD65 autoantibodies and its role as biomarker of type 1 diabetes and latent autoimmune diabetes in adults (LADA). NIH Public Access. 2012;36(11):1–14.\nBu DF, Tobin AJ. The exon-intron organization of the genes (gad1 and gad2) encoding two human glutamate decarboxylases (gad67 and gad65) suggests that they derive from a common ancestral gad. Genomics. 1994;21(1):222–8.\nCernea S, Buzzetti R, Pozzilli P. Beta-cell protection and therapy for latent autoimmune diabetes in adults. Diabetes Care. 2009;32 suppl 2(11):S246–9.\nAdeleye OO, Ogbera AO, Fasanmade O, Ogunleye OO, Dada AO, Ale AO, et al. Latent autoimmune diabetes mellitus in adults (LADA) and its characteristics in a subset of Nigerians initially managed for type 2 diabetes. Int Arch Med. 2012;5(1):1–5.\nOgurtsova K, Rocha JD, Huang Y, Linnenkamp U, Guariguata L. IDF diabetes atlas : global estimates for the prevalence of diabetes for 2015 and 2040. Diabetes Res Clin Pract. 2017;128(12):40–50.\nBrahmkshatriya PP, Mehta AA, Saboo BD, Goyal RK. Characteristics and prevalence of latent autoimmune diabetes in adults (LADA). ISRN Pharmacol. 2012;2012(1):1–8.\nGrant SFA, Thorleifsson G, Reynisdottir I, Benediktsson R, Manolescu A, Sainz J, et al. Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes. Nat Genet. 2006;38(3):320–3.\nTakeda H, Kawasaki E, Shimizu I, Konoue E, Fujiyama M, Murao S, et al. Clinical, autoimmune, and genetic characteristics of adult-onset diabetic patients with GAD autoantibodies in Japan (Ehime study). Diabetes Care. 2002;25(6):995–1001.\nPozzilli P, Pieralice S. Latent autoimmune diabetes in adults: current status and new horizons. Endocrinol Metab. 2018;33(2):147–59.\nFourlanos S, Dotta F, Greenbaum CJ, Palmer JP, Rolandsson O, Colman PG, et al. Latent autoimmune diabetes in adults (LADA) should be less latent. Diabetologia. 2005;48(11):2206–12.\nSchiel R, Müller UA. GAD autoantibodies in a selection-free population of insulin-treated diabetic patients: Indicator of a high prevalence of LADA? Diabetes Res Clin Pract. 2000;49(1):33–40.\nLundgren VM, Isomaa B, Lyssenko V, Laurila E, Korhonen P, Groop LC, et al. GAD antibody positivity predicts type 2 diabetes in an adult population. Diabetes. 2010;59(2):416–22.\nFourlanos S, Perry C, Stein MS, Stankovich J, Harrison LC, Colman PG. A clinical screening tool identifies autoimmune diabetes in adults. Diabetes Care. 2006;29(5):970–5.\nZimmet P, Tuomi T, Mackay IR, Rowley MJ, Knowles W, Cohen M, et al. Latent autoimmune diabetes mellitus in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency. Diabet Med. 1994;11(3):299–303.\nHealth T Ministry of. National Infection Prevention and Control Guidelines for Healthcare Services in Tanzania. 2004;2(12):29–119.\nTuomi T, Groop LC, Zimmet PZ, Rowley MJ, Knowles W, Mackay IR. Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin-dependent onset of disease. Diabetes. 1993;42(2):359–62.\nNaik RG, Palmer JP. Latent autoimmune diabetes in adults. Type 1 Diabetes Adults Princ Pract. 2007;54(December):17–32.\nSachan A, Zaidi G, Sahu RP, Agrawal S, Colman PG, Bhatia E. Low prevalence of latent autoimmune diabetes in adults in northern India. Diabet Med. 2015;32(6):810–3.\nTurner R, Stratton I, Horton V, Manley S, Zimmet P, Mackay IR, et al. Early report UKPDS 25 : autoantibodies to islet-cell cytoplasm and glutamic acid decarboxylase for prediction of insulin requirement in type 2 diabetes. Lancet. 1997;350(11):1288–93.\nJuneja R, Hirsch IB, Naik RG, Brooks-Worrell BM, Greenbaum CJ, Palmer JP. Islet cell antibodies and glutamic acid decarboxylase antibodies, but not the clinical phenotype, help to identify type 1 1\u002F2 diabetes in patients presenting with type 2 diabetes. Metabolism. 2001;50(9):1008–13.\nZimmet PZ, Shaten BJ, Kuller LH, Rowley MJ, Knowles WJ, Mackay IR. Antibodies to glutamic acid decarboxylase and diabetes mellitus in the multiple risk factor intervention trial. Am J Epidemiol. 1994;140(8):683–90.\nLutale JJK, Thordarson H, Holm PI, Eide GE, Vetvik K. Islet cell autoantibodies in African patients with type 1 and type 2 diabetes in Dar Es Salaam Tanzania: a cross sectional study. J Autoimmune Dis. 2007;4:1–7.\nZinman B, Kahn SE, Haffner SH, O’Neill MC, Heise MA, Freed MI. Phenotypic characteristics of GAD antibody-positive recently diagnosed patients with type 2 diabetes in North America and Europe. Diabetes. 2004;53(12):3193–200.\nHawa MI, Buchan AP, Ola T, Wun CC, DeMicco DA, Bao W, et al. LADA and CARDS: a prospective study of clinical outcome in established adult-onset autoimmune diabetes. Diabetes Care. 2014;37(6):1643–9.\nCarlsson S, Midthjell K, Tesfamarian MY, Grill V. Age, overweight and physical inactivity increase the risk of latent autoimmune diabetes in adults: results from the Nord-Trøndelag health study. Diabetologia. 2007;50(1):55–8.\nHorton V, Stratton I, Bottazzo GF, Shattock M, Mackay I, Zimmet P, et al. Genetic heterogeneity of autoimmune diabetes: age of presentation in adults is influenced by HLA DRB1 and DQB1 genotypes (UKPDS 43). Diabetologia. 1999;42(5):608–16.\nQi X, Sun J, Wang J, Wang PP, Xu Z, Murphy M, et al. Prevalence and correlates of latent autoimmune diabetes in adults in Tianjin, China: a population-based cross-sectional study. Diabetes Care. 2011;34(1):66–70.\nHwangbo Y, Kim JT, Kim EK, Khang AR, Oh TJ, Jang HC, et al. Prevalence and clinical characteristics of recently diagnosed type 2 diabetes patients with positive anti-glutamic acid decarboxylase antibody. Diabetes Metab J. 2012;36(2):136–43.\nDiabetes UKP, Group S. Perspectives in diabetes U.K. prospective diabetes study 16 overview of 6 years’ therapy of type II diabetes: a progressive disease. Diabetes. 1998;44(5):1249–58.\nBalducci S, Massimo S, Jonida H, Giorgio O, Valeria D’E, Sara F, et al. Physical Exercise as therapy for type II diabetes. Diabetes Metab Res Rev. 2014;32(30):13–23.\nBrophy S, Davies H, Mannan S, Brunt H, Williams R. Interventions for latent autoimmune diabetes (LADA) in adults. Cochrane Database Syst Rev. 2011;2017(12).\nHawa MI, Thivolet C, Mauricio D, Alemanno I, Cipponeri E, Collier D, et al. Metabolic syndrome and autoimmune diabetes: action LADA 3. Diabetes Care. 2009;32(1):160–4.\nThe low prevalence of Immunogenetic. 1996;19(3):241–245.\nLindholm E, Hallengrem B, Agardh CD. Gender differences in GAD antibody - positive diabetes mellitus in relation to age at onset, C-peptide and other endocrine autoimmune diseases. Diabetes Metab Res Rev. 2004;20(2):158–64.\nMyhill P, Davis WA, Bruce DG, MacKay IR, Zimmet P, Davis TME. Chronic complications and mortality in community-based patients with latent autoimmune diabetes in adults: the Fremantle diabetes study. Diabet Med. 2008;25(10):1245–50.",{"EN":1460},"The Latent Autoimmune Diabetes in Adults (LADA) is a slowly progressive Type 1 diabetes subgroup with onset during middle age. Studies report that about 10% of adults initially diagnosed with clinical Type 2 diabetes (T2D) have LADA. Inappropriate diagnosis and mismanagement of the LADA can increase the risk of diabetic complications, which affect the quality of life and is the cause of increased mortality. In low-income countries setting, data regarding the magnitude of LADA is limited. We carried out this study to estimate the burden of misdiagnosed LADA among T2D patients in selected health facilities in Dar es Salaam and to bring awareness to the use of Glutamic Acid Decarboxylase (GAD) autoantibody in screening for LADA. We enrolled 186 phenotypically T2D patients in this cross-sectional study, through a standardized data collection tool we obtained participants’ demographic and clinical information. For testing GAD levels, we used a double-antibody Enzyme-Linked Immunosorbent Assay (ELISA). The Fisher’s Exact and student t-tests were used to test the significance of the statistical associations of the glycaemic control and diabetes complications between T2D and LADA. Out of 186 patients, 156 gave conclusive GAD Ab ELISA reading with LADA accounting for 5.1% (95% CI: 2.5 - 10.0). The mean age of subjects was 54.3 years (Range: 33-85 years). The parameters such as mean age, family history of diabetes mellitus status, Fasting Blood Glucose, clinical characteristics, and complications did not show significant statistical differences between patients with LADA and Type 2 diabetes. However, all LADA- Human Immunodeficiency Virus (HIV) comorbid patients had retinopathy, which was statistically insignificant in 20 (87%) T2D-HIV comorbid patients (p = 0.669). Neither neuropathy, nephropathy, nor Diabetic Mellitus (D.M.) foot syndrome was observed among LADA-HIV comorbid patients. Nevertheless, 22 (95.7%), 3 (13%), and 2 (8.7%) of T2D-HIV comorbidity had neuropathy, nephropathy, or D.M. foot syndrome, respectively. The study established a LADA prevalence of 5.1% among T2D patients and has shown the role of GAD autoantibody in the screening for LADA. The study calls for a well- designed larger longitudinal study to generate strong evidence on the association of risk factors and complications associated with the LADA. This will develop robust evidence on the association of risk factors and complications associated with the LADA and T2D.",{"EN":1462},"Prevalence and factors associated with latent autoimmune diabetes in adults (LADA): a cross-sectional study",{"VOID":1464},"10.1186\u002Fs12902-022-01089-1","https:\u002F\u002Fbmcendocrdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12902-022-01089-1",[1467,1492,1504,1531],{"id":1468,"sortIndex":21,"researcher":20,"roles":1469,"affiliations":1470,"properties":1489},"6ec2df13-1253-4608-a36b-ec910489f6ea",[534],[1471,1481],{"id":1472,"sortIndex":106,"affiliation":1473,"properties":1480},"785b2a26-5531-4adc-8fe3-7e26455beb8f",{"id":1474,"createTime":1475,"updateTime":1475,"relativeEntities":1476,"slug":20,"properties":1477,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"8da460e5-6c11-42cf-adcd-91e610d20542","2024-01-18T07:41:07.283+00:00",[],{"title":1478},{"VI":1479},"Department of Biochemistry and Physiology, Mwanza University, Mwanza, Tanzania",{},{"id":20,"sortIndex":21,"affiliation":1482,"properties":20},{"id":1483,"createTime":1484,"updateTime":1484,"relativeEntities":1485,"slug":20,"properties":1486,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"20ab39f1-aff9-480b-91e2-d9478fd1751c","2024-01-18T07:41:07.180+00:00",[],{"title":1487},{"VI":1488},"Department Biochemistry, School of Medicine, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania",{"title":1490},{"VI":1491},"Anselmo M. 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pre-publication history for this paper can be accessed here:http:\u002F\u002Fwww.biomedcentral.com\u002F1472-6823\u002F13\u002F6\u002Fprepub",{"EN":1597},"The editors of BMC Endocrine Disorders would like to thank all our reviewers who have contributed to the journal in Volume 12 (2012).",{"EN":1599},"Reviewer acknowledgement 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DS, Wiseman SM. Fusion imaging for parathyroid localization in primary hyperparathyroidism. Expert Rev Anticancer Ther. 2010;10(3):353–63.\nPark HS, Lee YH, Hong N, Won D, Rhee Y. Germline mutations related to primary hyperparathyroidism identified by Next-Generation sequencing. Front Endocrinol (Lausanne). 2022;13:853171.\nAlagaratnam S, Kurzawinski TR. Aetiology, diagnosis and surgical treatment of primary hyperparathyroidism in children: new trends. Horm Res Paediatr. 2015;83(6):365–75.\nVan der Tuin K, Tops CM, Adank MA, Cobben JM, Hamdy NA, Jongmans MC, et al. CDC73-related disorders: clinical manifestations and case detection in primary hyperparathyroidism. J Clin Endocrinol Metab. 2017;102(12):4534–40.\nZhu CY, Sturgeon C, Yeh MW. Diagnosis and management of primary hyperparathyroidism. JAMA. 2020;24(12):1186–7.\nDuan K, Gomez Hernandez K, Mete O. Clinicopathological correlates of hyperparathyroidism. J Clin Pathol. 2015;68(10):771–87.\nZheng HC, Xue H, Zhang CY. The roles of the tumor suppressor parafibromin in cancer. Front Cell Dev Biol. 2022;10:1006400.\nIacobone M, Carnaille B, Palazzo FF, Vriens M. Hereditary hyperparathyroidism–a consensus report of the European Society of Endocrine Surgeons (ESES). Langenbecks Arch Surg. 2015;400(8):867–86.\nDiacinti D, Cipriani C, Biamonte F, et al. Imaging technologies in the differential diagnosis and follow-up of brown tumor in primary hyperparathyroidism: case report and review of the literature. Bone Rep. 2020;14:100745.\nMinisola S, Arnold A, Belaya Z, et al. Epidemiology, pathophysiology, and Genetics of primary hyperparathyroidism. J Bone Miner Res. 2022;37(11):2315–29.\nNewey PJ, Bowl MR, Cranston T, Thakker RV. Cell division cycle protein 73 homolog (CDC73) mutations in the hyperparathyroidism-jaw tumor syndrome (HPT-JT) and parathyroid tumors. Hum Mutat. 2010;31(3):295–307.\nIijima Y, Ishikawa M, Iwai S, et al. Robotic resection of ectopic mediastinal parathyroid adenoma with intraoperative parathyroid hormone monitoring: a case report. J Cardiothorac Surg. 2022;17(1):195.\nWang X, Wang M, Zhang J, et al. Humeral brown tumor as first presentation of primary hyperparathyroidism caused by ectopic parathyroid adenomas: report of two cases and review of literature. Int J Clin Exp Pathol. 2014;7(10):7094–9.\nDhiwakar M, Damodharan S, Rajeshwari KM, Mehta S. Ectopic parathyroid adenoma presenting as facial expansile growths. B-ENT. 2016;12(1):73–6.\nHaber RS, Kim CK, Inabnet WB. Ultrasonography for preoperative localization of enlarged parathyroid glands in primary hyperparathyroidism: comparison with (99m)technetium sestamibi scintigraphy. Clin Endocrinol (Oxf). 2002;57(2):241–9.\nTaterra D, Wong LM, Vikse J, et al. The prevalence and anatomy of parathyroid glands: a meta-analysis with implications for parathyroid surgery. Langenbecks Arch Surg. 2019;404(1):63–70.\nCallender GG, Grubbs EG, Vu T, et al. The fallen one: the inferior parathyroid gland that descends into the mediastinum. J Am Coll Surg. 2009;208(5):887–93. discussion 893-5.\nWakamatsu H, Noguchi S, Yamashita H, et al. Technetium-99m tetrofosmin for parathyroid scintigraphy: a direct comparison with (99m)Tc-MIBI, (201)tl, MRI and US. Eur J Nucl Med. 2001;28(12):1817–27.\nMachado NN, Wilhelm SM. Diagnosis and evaluation of primary hyperparathyroidism. Surg Clin North Am. 2019;99(4):649–66.\nLoh KC, Duh QY, Shoback D, Gee L, Siperstein A, Clark OH. Clinical profile of primary hyperparathyroidism in adolescents and young adults. Clin Endocrinol (Oxf). 1998;48(4):435–43.\nMacfarlane DP, Yu N, Leese GP. Subclinical and asymptomatic parathyroid disease: implications of emerging data. Lancet Diabetes Endocrinol. 2013;1(4):329–40.\nNilsson IL, Norenstedt S, Zedenius J, Pernow Y, Bränström R. Primary hyperparathyroidism, hypercalciuria, and bone recovery after parathyroidectomy. Surgery. 2017;162(2):429–36.\nMehrabibahar M, Mousavi Z, Sadeghi R, Layegh P, Nouri M, Asadi M. Feasibility and safety of minimally invasive radioguided parathyroidectomy using very low intraoperative dose of Tc-99m MIBI. Int J Surg. 2017;39:229–33.\nReséndiz-Colosia JA, Rodríguez-Cuevas SA, Flores-Díaz R, et al. Evolution of maxillofacial brown tumors after parathyroidectomy in primary hyperparathyroidism. Head Neck. 2008;30(11):1497–504.\nCasteràs A, Darder L, Zafon C et al. Brown tumor of the jaw after pregnancy and lactation in a MEN patient. Endocrinol Diabetes Metab Case Rep. 2016;2016:16–0111.\nSzabo Yamashita T, Gudmundsdottir H, Foster TR, et al. Pediatric primary hyperparathyroidism: Surgical pathology and long-term outcomes in sporadic and familial cases. Am J Surg. 2023;225(4):699–702.",{"EN":1664},"Primary hyperparathyroidism (PHPT) is an uncommon disorder characterised by hypercalcemia with an increased parathyroid hormone level. We reported a PHPT familial case with two subjects, a father and a daughter, and both of them had suffered from the brown tumor. The proband, a 43-year-old patient, developed parathyroid adenomas at the age of 15; a histologically confirmed right parathyroid adenoma was removed by parathyroidectomy; and after six months follow-up, the serum calcium level was normalised. At the age of thirty-three, a CT scan of his head and neck revealed a mass in the right maxilla, as well as PHPT (i.e., left inferior parathyroid adenoma). Then, he underwent a biopsy of an exophytic lesion in the right maxilla and was diagnosed by pathology as a brown tumor, with the serum calcium and PTH levels at 2.78 mmol\u002FL and 221 pg\u002FmL, respectively. Subsequently, the patient took a left inferior parathyroid microwave ablation with ultrasound guidance. After three months of follow-up, the serum calcium and PTH levels returned to normal, and the brown tumor was resolved. After three years, it mineralised as revealed in a CT scan. By the time he was 43 years old, during the 28-year follow-up period, the serum calcium and PTH levels were still within the normal range, and there was no discomfort reported. He has consistently taken calcium supplements throughout the 28 years. Since the initial diagnosis, his blood indicators of kidney function have been normal, and ultrasound showed renal calculus in the right kidney and a normal left kidney. The proband’s daughter, a 15-year-old girl, experienced left upper extremity pain for ten months. CT scan revealed a mass in the distal left radius, and a giant cell tumor was suspected. A surgical internal fixation was performed, and the pathology showed a brown tumor. Laboratory tests revealed a serum parathyroid hormone (PTH) level of 1554pg\u002FmL, calcium level of 3.14 mmol\u002FL, phosphorus level of 0.72 mmol\u002FL, and alkaline phosphatase level of 1892 U\u002FL. Given the osteitic changes and elevated levels of calcium and PTH, ultrasonography was performed, after which a mass was detected measuring 19 × 9 × 7 mm mixed with solid components and cystic fluid in the right thyroid gland. The results of 99mTc-MIBI scintigraphy confirmed the abnormal accumulation of 99mTc-MIBI in the right thyroid gland but not seen in the bilateral parathyroid glands. The patient underwent thyroidectomy, and the postoperative pathology report indicated an intra-thyroid ectopic parathyroid adenoma. The serum calcium and PTH levels became normal at 4 h after surgery. One to three months after operation, the serum calcium level was low, while the serum PTH level was high. Then, the patient was advised to take calcium supplements. Until the sixth month after the operation, the serum calcium level and serum PTH level returned to normal, and the bone pain was relieved. The patient’s blood tests for kidney function remained normal. There was no evidence of bilateral kidney disease (such as nephrolithiasis or nephrocalcinosis) detected by ultrasound scan. There were several similarities in the state of illness between these two subjects. Both the father and the daughter developed parathyroid adenomas at the age of 15, and there was no lesion in other endocrine glands. And genetic testing revealed mutations in the CDC73 genes in both father and daughter. On the other hand, there were also a few differences. The father’s first signs of brown tumor were in the right maxilla, while the daughter’s appeared in the distal left radius. The father presented pathological changes in the left and right parathyroid glands, whereas the daughter presented with an ectopic parathyroid adenoma in the right thyroid gland. We report a familial case in which father and daughter were diagnosed to have brown tumors due to parathyroid adenoma and ectopic parathyroid adenoma, and genetic testing revealed CDC73 gene mutations in both. Therefore, in the diagnostic and differential process of young patients having bone disease, clinicians should not only focus on the clinical manifestations of the skeleton, but also implement a comprehensive analysis of systemic symptoms, considering the possibility that the patient has familial PHPT.",{"EN":1666},"Brown tumor due to primary hyperparathyroidism in a familial case: a case 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J Am Coll Cardiol. 2004;43(3):423–8.",{"doi":2111},"10.1016\u002Fj.jacc.2003.08.042",{"id":20,"text":2113,"url":20,"identifiers":2114},"Yang Z, Xia WH, Zhang YY, Xu SY, Liu X, Zhang XY, et al. Shear stress-induced activation of Tie2-dependent signaling pathway enhances in vivo reendothelialization capacity of human endothelial progenitor cells. J Mol Cell Cardiol. 2012;52:1155–63.",{"doi":2115},"10.1016\u002Fj.yjmcc.2012.01.019",{"id":20,"text":2117,"url":20,"identifiers":2118},"James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311:507–20.",{"doi":2119},"10.1001\u002Fjama.2013.284427",{"id":20,"text":2121,"url":20,"identifiers":2122},"The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997;20:1183–97.",{"doi":2123},"10.2337\u002Fdiacare.20.7.1183",{"id":20,"text":2125,"url":20,"identifiers":2126},"Yang Z, Xia WH, Su C, Wu F, Zhang YY, Xu SY, et al. Regular exercise-induced upregulation of circulating endothelial progenitor cells attenuated age-related decline in arterial elasticity in healthy men. Int J Cardiol. 2013;165:247–54.",{"doi":2127},"10.1016\u002Fj.ijcard.2011.08.055",{"id":20,"text":2129,"url":20,"identifiers":2130},"Corretti MC, Anderson TJ, Benjamin EJ, Celermajer D, Charbonneau F, Creager MA, et al. Guidelines for the ultrasound assessment of endothelial-dependent flowmediated vasodilation of the brachial artery: a report of the International Brachial Artery Reactivity Task Force. J Am Coll Cardiol. 2002;39:257–65.",{"doi":2131},"10.1016\u002FS0735-1097(01)01746-6",{"id":20,"text":2133,"url":20,"identifiers":2134},"Sibal L, Aldibbiat A, Agarwal SC, Mitchell G, Oates C, Razvi S, et al. Circulating endothelial progenitor cells, endothelial function, carotid intima–media thickness and circulating markers of endothelial dysfunction in people with type 1 diabetes without macrovascular disease or microalbuminuria. Diabetologia. 2009;52:1464–73.",{"doi":2135},"10.1007\u002Fs00125-009-1401-0",{"id":20,"text":2137,"url":20,"identifiers":2138},"Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, et al. Circulating Endothelial Progenitor Cells, Vascular Function, and Cardiovascular Risk. N Engl J Med. 2003;348(7):593–00.",{"doi":2139},"10.1056\u002FNEJMoa022287",{"id":20,"text":2141,"url":20,"identifiers":2142},"Avogaro A, Toffolo G, Kiwanuka E, de Kreutzenberg SV, Tessari P, Cobelli C. L-Arginine-nitric oxide kinetics in normal and type 2 diabetic subjects: a stable-labelled 15 N arginine approach. Diabetes. 2003;52:795–02.",{"doi":2143},"10.2337\u002Fdiabetes.52.3.795",{"id":20,"text":2145,"url":20,"identifiers":2146},"Shyu K-G. Enhancement of new vessel formation by Angiopoieti n-2\u002FTie2 signaling in endothelial progenitor cells: a new hope for future therapy? Cardiovasc Res. 2006;72(3):359–60.",{"doi":2147},"10.1016\u002Fj.cardiores.2006.09.017",{"id":20,"text":2149,"url":20,"identifiers":2150},"Hildbrand P, Cirulli V, Prinsen RC, Smith KA, Torbett BE, Salomon DR, et al. The role of angiopoietins in the development of endothelial cells from cord blood CD34 + progenitors. Blood. 2004;104(7):2010–9.",{"doi":2151},"10.1182\u002Fblood-2003-12-4219",{"id":20,"text":2153,"url":20,"identifiers":2154},"Morello F, Perino A, Hirsch E. Phosphoinositide 3-kinase signalling in the vascular system. Cardiovasc Res. 2009;82:261–71.",{"doi":2155},"10.1093\u002Fcvr\u002Fcvn325",{"id":20,"text":2157,"url":20,"identifiers":2158},"Fulton D, Gratton JP, McCabe TJ, Fontana J, Fujio Y, Walsh K, et al. Regulation of endothelium-derived nitric oxide production by the protein kinase Akt. Nature. 1999;399:597–01.",{"doi":2159},"10.1038\u002F21218",{"id":20,"text":2161,"url":20,"identifiers":2162},"Thum T, Fraccarollo D, Schultheiss M, Froese S, Galuppo P, Widder JD, et al. Endothelial nitric oxide synthase uncoupling impairs endothelial progenitor cell mobilization and function in diabetes. Diabetes. 2007;56:666–74.",{"doi":2163},"10.2337\u002Fdb06-0699",{"id":2165,"createTime":2166,"updateTime":2167,"relativeEntities":2168,"slug":2169,"properties":2170,"entityType":148,"verifyStatus":149,"verifyTime":2167,"verifyNote":150,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":106,"primaryUrl":2179,"fullTextUrl":20,"authors":2180,"publicationType":349,"publisherRelationship":2276,"citationCount":20,"citationInfo":20,"publishDate":2309,"publishYear":1449,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":513},"5e076168-c411-41ca-85dd-2474e3695dfb","2023-12-26T14:55:40.968+00:00","2024-12-09T23:51:28.801+00:00",[],"Hyperglycemia-related-central-pontine-demyelinization-after-a-binge-eating-attack-in-a-patient-with-type-2-diabetes-a-case-report",{"references":2171,"abstract":2173,"title":2175,"doi":2177},{"VOID":2172},"Laureno R. Central pontine myelinolysis following rapid correction of hyponatremia. Ann Neurol. 1983;13:232–42.\nAshrafian H, Davey P. A review of the causes of central pontine myelinosis: yet another apoptotic illness? Eur J Neurol. 2001;8:103–9.\nBurns JD, Kosa SC, Wijdicks EF. Central pontine myelinolysis in a patient with hyperosmolar hyperglycemia and consistently normal serum sodium. Neurocrit Care. 2009;11:251–4.\nSaini M, Mamauag MJ, Singh R. Central pontine myelinolysis: a rare presentation secondary to hyperglycaemia. Singap Med J. 2015;56:e71–3.\nSharma C, Kumawat BL, Panchal M, et al. Osmotic demyelination syndrome in type 1 diabetes in the absence of dyselectrolytaemia: an overlooked complication? BMJ Case Rep. 2017. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fbcr-2016-219148.\nTajitsu M, Yamada T, Cao X, Fukui A, Nagai J, Yambe Y, et al. Osmotic demyelination syndrome complicating diabetes with anti-glutamic acid decarboxylase antibodies and Graves’ disease: a case report. J Diabetes Investig. 2016;7:130–1.\nLevey AS, Eckardt KU, Tsukamoto Y, Levin A, Coresh J, Rossert J, et al. Definition and classification of chronic kidney disease: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int. 2005;67:2089–100.\nGayoso-Diz P, Otero-Gonzalez A, Rodriguez-Alvarez MX, Gude F, Garcia F, De FA, et al. Insulin resistance (HOMA-IR) cut-off values and the metabolic syndrome in a general adult population: effect of gender and age: EPIRCE cross-sectional study. BMC Endocr Disord. 2013;13:47.\nMartin RJ. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry. 2004;75(Suppl III):iii22–i2.\nOscar-Berman M. Function and dysfunction of prefrontal brain circuitry in alcoholic Korsakoff’s syndrome. Neuropsychol Rev. 2012;22:154–69.\nGuideline. Sugars intake for adults and children. Geneva: World Health Organization; 2015.",{"EN":2174},"Here, we report a case of central pontine demyelinization in a type-2 diabetes patient with hyperglycemia after a binge-eating attack in the absence of a relevant hyponatremia. A 55-year-old, male type-2 diabetic patient with liver cirrhosis stage Child-Pugh B was admitted due to dysmetria of his right arm, gait disturbance, dizziness, vertigo, and polyuria, polydipsia after a binge-eating attack of sweets (a whole fruit cake and 2 Liters of soft drinks). A recently initiated insulin therapy had been discontinued for 8 months. A serum glucose measurement obtained 5 days prior to hospitalisation was 38.5 mmol\u002Fl (694 mg\u002Fdl). The patient graved for sweets since stopping alcohol consumption 8 months earlier. On admission, venous-blood glucose was 29.1 mmol\u002Fl (523.8 mg\u002Fdl), glycated hemoglobin was 168.0 mmol\u002Fmol or 17.6%. No supplementation of sodium chloride was reported. Laboratory exams revealed an elevated serum ammonia level (127.1 μmol\u002Fl), rendering a hepatic encephalopathy very likely. After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from 133 on admission to 144 mmol\u002Fl during the hospital stay. In retrospect, the mild hyponatremia on admission was classified as pseudohyponatremia due to hyperglycemia. The patient had an insulin resistance (HOMA-IR 7.8 (normal range \u003C 2.5)). A T2-weighted magnetic resonance imaging (MRI) of the head and a cranial computed tomography scan were obtained demonstrating a symmetric central pontine demyelinization. After 26 days in hospital, the patient was discharged with an inkretin-mimetic therapy (dulaglutide SC, 1.5 mg\u002Fweek) and an intensified conventional insulin therapy (insulin aspart: 14 units\u002Fd in euglycemia, insulin glargin 20 units\u002Fd). Central pontine and\u002For cerebellar myelinolysis can be caused by sudden, severe, and sustained hyperglycemia, especially when another risk factor (in this case, liver cirrhosis) is present. Functional neurological deficits in the context of hyperglycemia should prompt for the consideration of this differential diagnosis in all diabetes patients.",{"EN":2176},"Hyperglycemia-related central pontine demyelinization after a binge-eating attack in a patient with type-2 diabetes: a case report",{"VOID":2178},"10.1186\u002Fs12902-018-0245-3","https:\u002F\u002Fbmcendocrdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12902-018-0245-3",[2181,2196,2208,2220,2232,2247,2259],{"id":2182,"sortIndex":333,"researcher":20,"roles":2183,"affiliations":2184,"properties":2193},"656808e2-bcf4-4b6d-972f-01b16d476cf8",[534],[2185],{"id":20,"sortIndex":21,"affiliation":2186,"properties":20},{"id":2187,"createTime":2188,"updateTime":2188,"relativeEntities":2189,"slug":20,"properties":2190,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"860674f8-d0c9-4f5a-855b-f2746349aa7e","2024-02-13T18:08:19.382+00:00",[],{"title":2191},{"VI":2192},"Department of Internal Medicine II, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany",{"title":2194},{"VI":2195},"Alexandra Schreiber",{"id":2197,"sortIndex":178,"researcher":20,"roles":2198,"affiliations":2199,"properties":2205},"82c8b16f-8eec-4154-9642-33eb32ea1b8b",[534],[2200],{"id":20,"sortIndex":21,"affiliation":2201,"properties":20},{"id":2187,"createTime":2188,"updateTime":2188,"relativeEntities":2202,"slug":20,"properties":2203,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":2204},{"VI":2192},{"title":2206},{"VI":2207},"Matthias Girndt",{"id":2209,"sortIndex":21,"researcher":20,"roles":2210,"affiliations":2211,"properties":2217},"b18ca0d6-ff7b-49a9-83db-d9bdbbdf54d7",[534],[2212],{"id":20,"sortIndex":21,"affiliation":2213,"properties":20},{"id":2187,"createTime":2188,"updateTime":2188,"relativeEntities":2214,"slug":20,"properties":2215,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":2216},{"VI":2192},{"title":2218},{"VI":2219},"Rainer U. Pliquett",{"id":2221,"sortIndex":285,"researcher":20,"roles":2222,"affiliations":2223,"properties":2229},"69e42f0d-e06c-49f1-8346-3207d2de0627",[534],[2224],{"id":20,"sortIndex":21,"affiliation":2225,"properties":20},{"id":2187,"createTime":2188,"updateTime":2188,"relativeEntities":2226,"slug":20,"properties":2227,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":2228},{"VI":2192},{"title":2230},{"VI":2231},"Charlotte Ackmann",{"id":2233,"sortIndex":106,"researcher":20,"roles":2234,"affiliations":2235,"properties":2244},"679b5641-b6e6-469e-9373-e75701ededc0",[534],[2236],{"id":20,"sortIndex":21,"affiliation":2237,"properties":20},{"id":2238,"createTime":2239,"updateTime":2239,"relativeEntities":2240,"slug":20,"properties":2241,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"ac3b7ea5-a562-42a4-b5ae-cf2d8fb5df5c","2023-12-26T14:55:41.000+00:00",[],{"title":2242},{"VI":2243},"Department of Radiology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany",{"title":2245},{"VI":2246},"Arno Noll",{"id":2248,"sortIndex":109,"researcher":20,"roles":2249,"affiliations":2250,"properties":2256},"b48dad8b-83da-48a2-a8c0-61a6f73e11ed",[534],[2251],{"id":20,"sortIndex":21,"affiliation":2252,"properties":20},{"id":2187,"createTime":2188,"updateTime":2188,"relativeEntities":2253,"slug":20,"properties":2254,"entityType":48,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":2255},{"VI":2192},{"title":2257},{"VI":2258},"Alexandra 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Ibe",{"url":2179,"publisher":2277,"properties":2305},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2278,"slug":10,"properties":2279,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2283,"manageAffiliations":2284,"indexDatabases":2285,"url":20,"thumbnailPath":20,"statistic":2300,"gsStatistic":20,"type":125,"analyzePriority":20},[],{"issn":2280,"title":2281,"url":2282},{"VOID":13},{"EN":15},{"VOID":17},[],[],[2286,2293],{"id":84,"indexDatabase":2287,"url":99,"indexYears":20,"academicFieldIds":2292,"indexDatabaseRanking":20},{"id":86,"createTime":87,"updateTime":88,"relativeEntities":2288,"label":2289,"description":2290,"key":95,"publicationTags":2291,"standard":20},[],{"EN":91,"VI":91},{"VI":93,"EN":94},[97,98],[101],{"id":64,"indexDatabase":2294,"url":77,"indexYears":78,"academicFieldIds":2299,"indexDatabaseRanking":82},{"id":66,"createTime":67,"updateTime":68,"relativeEntities":2295,"label":2296,"description":2297,"key":74,"publicationTags":2298,"standard":20},[],{"EN":71,"VI":71},{"EN":71,"VI":73},[76],[80,81],{"impactFactor":21,"impactFactorByYear":2301,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":104,"totalPublicationByYear":2302,"totalCitation":21,"totalCitationByYear":2303,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":2304,"hindexLast5Year":21,"hindex":21},{},{"2001":106,"2002":107,"2003":106,"2004":106,"2005":108,"2006":109,"2007":109,"2008":60,"2009":108,"2010":49,"2011":110,"2012":111,"2013":112,"2014":113,"2015":114,"2016":115,"2017":114,"2018":116,"2019":117,"2020":118,"2021":119,"2022":120,"2023":121,"2024":122},{},{},{"volume":2306,"pages":2307},{"VOID":1445},{"VOID":2308},"1-5","2018-03-12",{"id":2311,"createTime":2312,"updateTime":2313,"relativeEntities":2314,"slug":2315,"properties":2316,"entityType":148,"verifyStatus":149,"verifyTime":2325,"verifyNote":150,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2326,"fullTextUrl":20,"authors":2327,"publicationType":349,"publisherRelationship":2500,"citationCount":20,"citationInfo":20,"publishDate":2532,"publishYear":1788,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":513},"94cf794d-fd5b-4fb8-895a-52fbb9073a71","2024-01-05T12:35:19.241+00:00","2024-12-15T23:49:38.382+00:00",[],"Magnitude-of-erectile-dysfunction-and-associated-factors-among-adult-diabetic-men-on-follow-up-at-Goba-and-Robe-hospitals-Bale-Zone-South-East-Ethiopia-hospital-based-cross-sectional-study",{"references":2317,"abstract":2319,"title":2321,"doi":2323},{"VOID":2318},"Research NI. .o.H.O.o.M.A.o., NIH Consensus Statement. 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J., Harrison’s Principles of Internal Medicine, 20e 2018. ISBN 978-1-259-64404-7; MHID 1-259-64404-9.\nBlair M. Diabetes Mellitus review. Urol Nurs, 2016. 36(1).\nRew KT, Heidelbaugh JJ. Erectile dysfunction. Am Family Phys. 2016;94(10):820–7.\nAl-Hunayan A, Kehinde A-MM, Thalib EO, Al-Ghorory L. M, he prevalence and predictors of erectile dysfunction in men with newly diagnosed with type 2 diabetes mellitus BJU international, 2007. 99(1):130–134.\nThorve VS, et al. Diabetes-induced erectile dysfunction: epidemiology, pathophysiology and management. J Diabetes Complicat. 2011;25(2):129–36.\nGoldstein I, et al. The association of erectile dysfunction with productivity and absenteeism in eight countries globally. Int J Clin Pract. 2019;73(11):e13384.\nBurnett AL, et al. Erectile dysfunction: AUA guideline. J Urol. 2018;200(3):633–41.\nJannini EA, et al. Health-related characteristics and unmet needs of men with Erectile Dysfunction: a Survey in five E uropean countries. J Sex Med. 2014;11(1):40–50.\nFrost M, et al. Chronic Diseases in elderly men: underreporting and underdiagnosis. Age Ageing. 2012;41(2):177–83.\nGoldstein I, et al. Real-world observational results from a database of 48 million men in the United States: relationship of Cardiovascular Disease, Diabetes Mellitus and depression with age and erectile dysfunction. Int J Clin Pract. 2018;72(4):e13078.\nWeldesenbet AB, Kebede SA, B.S.J.J.o.I MR, Tusa. Prevalence of erectile dysfunction and its associated factors among patients with diabetes in Ethiopia: a systematic review and meta-analysis 2021. 49(2): p. 0300060521993318.\nAl-Shaiji TF. Breaking the ice of Erectile Dysfunction Taboo: a focus on clinician–patient communication. J Patient Experience. 2022;9:23743735221077512.\nGoonewardene SS, Pietrzak P, Albala D. Diagnosis and management of ED, in Basic Urological Management. Springer; 2019. pp. 305–5.\nAntonio L, et al. Erectile dysfunction predicts mortality in middle-aged and older men Independent of their sex steroid status. Age Ageing. 2022;51(4):afac094.\nFeldman HA, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994;151(1):54–61.\nHackett G, et al. The British Society for Sexual Medicine guidelines on male adult testosterone deficiency, with statements for practice. The World Journal of Men’s Health; 2023. p. 41.\nO’Donnell AB, Araujo AB, McKinlay JB. The health of normally aging men: the Massachusetts Male Aging Study (1987–2004). Exp Gerontol. 2004;39(7):975–84.\nCalzo JP et al. Erectile dysfunction in a sample of sexually active young adult men from a us cohort: demographic, metabolic and mental health correlates 2021. 205(2): p. 539–544.\nNutalapati S et al. Association of erectile dysfunction and type II Diabetes Mellitus at a tertiary care centre of south India. 2020. 14(4): p. 649–53.\nZeleke M, Hailu D. J.B.e.d. Daka, Erectile dysfunction and associated factors among diabetic patients at. Hawassa South Ethiopia. 2021;21(1):1–9.\nYafi FA, et al. Erectile dysfunction. Nat Reviews Disease Primers. 2016;2(1):1–20.\nForoutan SK, Jadid M, Milani. The prevalence of sexual dysfunction among divorce requested. Daneshvar Med. 2008;15(5):39–44.\nSaeed R, et al. Prevalence of erectile dysfunction and associated factors among males visiting family medicine clinics in a Tertiary Care Hospital in Karachi. Pakistan. 2021;10(3):1294.\nMehiret G, Dersie B, J.J.o.D L. Magnitude and factors contributing to Erectile Dysfunction among Diabetic Men Attending the Diabetic Clinic at Debre Tabor Comprehensive and Specialized, Hospital in North West, Ethiopia 2020, institutional based cross-sectional study. 2021. 11(3): p. 69–82.\nShiferaw WS, Akalu TY. and Y.A.J.I.j.o.e. Aynalem, Prevalence of erectile dysfunction in patients with diabetes mellitus and its association with body mass index and Glycated hemoglobin in Africa: a systematic review and meta-analysis 2020. 2020.\nKB N et al. Prevalence and factors associated with erectile dysfunction among adult men in Moshi municipal, Tanzania: community-based study 2020.\nAsaduzzaman M, et al. Frequency and risk factors of Erectile Dysfunction among Bangladeshi adult men with type 2. Diabetes Mellitus. 2020;29(1):66–72.\nAsefa A, et al. Prevalence of sexual dysfunction and related factors among Diabetes Mellitus patients. Southwest Ethiopia. 2019;19(1):1–8.\nMcMahon CG. Current diagnosis and management of erectile dysfunction. Med J Aust. 2019;210(10):469–76.\nBeckman N, Ostling WM, Sundh S, Skoog V. Determinants of sexual activity in four birth cohorts of Swedish 70-year-olds examined 1971–2001. J Sex Med. 2014;11:401–10.\nHurisa AD, G.Z.J.T.O.P HJ, Negera. Erectile Dysfunct among Diabet Patients Tert Hosp Southwest Ethiopia 2020. 13(1).\nXu Y et al. Prevalence and correlates of erectile dysfunction in type 2 diabetic men: a population-based cross-sectional study in Chinese men. 2019. 31(1): p. 9–14.\nWalle B et al. Prevalence of erectile dysfunction and associated factors among diabetic men attending the diabetic clinic at Felege Hiwot Referral Hospital, Bahir Dar, North West Ethiopia, 2016. 2018. 11(1): p. 1–5.\nRosen RC, et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. Urology. 1997;49(6):822–30.\nPelluri R, et al. The role of body mass index or metabolic syndrome components causing depression in women: an observation from weight reduction clinical trial. J Clin Pharm Ther. 2021;46(6):1757–63.\nArroll B, et al. Validation of PHQ-2 and PHQ-9 to screen for major depression in the primary care population. The Annals of Family Medicine. 2010;8(4):348–53.\nManea L, Gilbody S, McMillan D. A diagnostic meta-analysis of the Patient Health Questionnaire-9 (PHQ-9) algorithm scoring method as a screen for depression. Gen Hosp Psychiatry. 2015;37(1):67–75.\nLee PH, et al. Validity of the international physical activity questionnaire short form (IPAQ-SF): a systematic review. Int J Behav Nutr Phys Activity. 2011;8(1):1–11.\nJensen MD et al. 2013 AHA\u002FACC\u002FTOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology\u002FAmerican Heart Association Task Force on Practice Guidelines and The Obesity Society Journal of the American college of cardiology, 2014. 63(25 Part B): p. 2985–3023.\nBao X, et al. Proteomic profiles of body Mass Index and Waist-to-hip ratio and their role in incidence of Diabetes. The Journal of Clinical Endocrinology & Metabolism; 2022.\nSeftel AD. J.T.J.o.u., re: Prevalence of Erectile Dysfunction and Associated Factors among Diabetic Men Attending Diabetic Clinic at Muhimbili National Hospital in Dar-Es-Salaam. Tanzania. 2015;193(4):1325–6.\nMutagaywa RK et al. Prevalence of erectile dysfunction and associated factors among diabetic men attending diabetic clinic at Muhimbili National Hospital in Dar-Es-Salaam, Tanzania 2014. 17.\nNisahan B et al. Erectile dysfunction and associated factors among men with Diabetes Mellitus from a tertiary diabetic center in Northern Sri Lanka. 2019. 12(1): p. 1–6.\nSerwaa D, et al. Prevalence and determinant of erectile dysfunction in type II Diabetes Mellitus and healthy men. SciMedicine J. 2021;3(1):23–34.\nTridiantari DK, Saraswati LD, Udiyono AJMJoI. Epidemiology of erectile dysfunction in men with Diabetes Mellitus: a study. Prim Health care Cent Indonesia. 2020;29(1):82–7.\nAbeway S et al. Erectile Dysfunction and Correlates Among Diabetic Men at Dessie Referral Hospital: North Central Ethiopia, 2020 2020. 13: p. 4201.\nSeid A et al. Prevalence and determinants of erectile dysfunction among diabetic patients attending in hospitals of central and northwestern zone of Tigray, northern Ethiopia: a cross-sectional study. 2017. 17(1): p. 1–7.\nDegavi G, et al. Determinants and prevalence of Impotence among Diabetic patients in Northwestern hospitals of Nefasit. Eretria. 2021;14:1177.\nShiferaw WS et al. Risk factors of erectile dysfunction among diabetes patients in Africa: a systematic review and meta-analysis 2020: p. 100232.\nCorona G et al. Sexual dysfunction in type 2 Diabetes at diagnosis: progression over time and drug and non-drug correlated factors. 2016. 11(10): p. e0157915.\nKouidrat Y et al. High prevalence of erectile dysfunction in Diabetes: a systematic review and meta-analysis of 145 studies. 2017. 34(9): p. 1185–92.\nMahbub M et al. Frequency and predictors of Erectile Dysfunction in Bangladeshi men with type 2 Diabetes Mellitus: experience from a Tertiary Center. 2019. 28(1): p. 137–43.\nTamrakar D, et al. Association between Erectile Dysfunction and Type 2 Diabetes Mellitus. 2021;19(2):378–83.\nPakpahan C et al. Stem cell therapy and diabetic erectile dysfunction: a critical review. 2021. 13(10): p. 1549.\nAhsaini M et al. Prevalence and severity of erectile dysfunction in patients with type 2 diabetes in the Department of Urology at the University Hospital Center Hassan II, Fez, Morocco: a cross-sectional study of 96 cases 2020. 37: p. 205–205.\nUgwumba FO, et al. Prevalence of, and risk factors for erectile dysfunction in male type 2 diabetic outpatient attendees in Enugu. South East Nigeria. 2018;17(4):215.\nShiferawa WS, Akalub TY, Petruckac PM, Habtamu Abera YAA, Arerid. Risk factors of erectile dysfunction among diabetes patients in Africa: A systematic review and meta-analysis, in elsivier. 2020. p. 9.\nNguyen CP, et al. Testosterone and age-related hypogonadism—FDA concerns. N Engl J Med. 2015;373(8):689.\nDuca Y, et al. Erectile dysfunction, physical activity and physical exercise: recommendations for clinical practice. Andrologia. 2019;51(5):e13264.\nOwiredu WK, et al. Determinants of sexual dysfunction among clinically diagnosed diabetic patients. Reproductive Biology and Endocrinology. 2011;9(1):1–11.\nTekalegn Y. Determinants of overweight or obesity among men aged 20–59 years: A case-control study based on the 2016 Ethiopian demographic and health survey Journal of Obesity, 2021. 2021.\nAbrha S, Shiferaw S, Ahmed KY. Overweight and obesity and its socio-demographic correlates among urban Ethiopian women: evidence from the 2011 EDHS. BMC Public Health. 2016;16:1–7.\nDarebo T, Mesfin A, Gebremedhin S. Prevalence and factors associated with overweight and obesity among adults in Hawassa City, southern Ethiopia: a community based cross-sectional study. BMC Obes. 2019;6:1–10.",{"EN":2320},"Erectile dysfunction is defined as the inability to achieve and\u002For maintain an erection of sufficient rigidity and duration to permit satisfactory sexual performance. The purpose of this study is to assess the prevalence of erectile dysfunction and associated factors among adult diabetic men on follow-up at Goba and Robe hospitals, Bale Zone, South East Ethiopia,2022. Hospital-based cross-sectional study design was used among 420 adult diabetic men from March 1 to April 30 using a systematic random sampling technique. An international index of erectile function questionnaire containing five questions was used to assess the outcome variable. The data were entered, edited, and coded using Epidata version 4.6 and analyzed using SPSS version 26. Bivariable and multivariable binary logistic regression analysis were performed to identify factors associated with erectile dysfunction. Adjusted odds ratios with their corresponding 95% confidence interval were computed to estimate the strength of association. Statistical significance was declared at p-value \u003C 0.05. The prevalence of erectile dysfunction was found to be 354 (84.3%). Multivariable logistic regression revealed that erectile dysfunction is significantly associated with old age (AOR = 12.39, 95% CI:5.10–30.08), inadequate physical activity (AOR = 4.15, 95% CI:1.33–12.97), and being rich (AOR = 2.62, 95% CI = 1.21–5.66). The prevalence of erectile dysfunction in this study population is nearly nine out of ten. Age, inadequate physical activity, and wealth index were independent predictors of erectile dysfunction. Assessment and management of erectile dysfunction in diabetic clinics should be routine medical care.",{"EN":2322},"Magnitude of erectile dysfunction and associated factors among adult diabetic men on follow-up at Goba and Robe hospitals, Bale Zone, South East Ethiopia: hospital-based cross-sectional 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