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[This corrects the article DOI: 10.1016/j.aed.2025.03.011.].
Demographic data clearly demonstrate that the percentage of the population in the older age group is increasing. Androgen deficiency in the aging male has become a topic of increasing interest and debate throughout the world. Cross-sectional and longitudinal data indicate that testosterone falls progressively with age and that a significant percentage of men over the age of 60 years have serum testosterone levels that are below the lower limits of young adult (age, 20–30 years) men (Gray et al, 1991; Harman et al, 2001; Araujo et al, 2007; Wu et al, 2008). The principal questions raised by these observations are whether older hypogonadal men will benefit from testosterone treatment and what will be the risks associated with such intervention. The past decade has brought evidence of benefit of androgen treatment of hypogonadal men on multiple target organs, and recent studies show short-term beneficial effects of testosterone in older men that are similar to those in younger men. This has been comprehensively reviewed and summarized by the Institute of Medicine in Testosterone and Aging: Clinical Research Directions (Liverman and Blazer, 2004). Long-term data on the effects of testosterone treatment in the older population are limited mainly to effects on body composition and bone mass (Snyder et al, 1999a,b; Amory et al, 2004; Isidori et al, 2005a,b; Page et al, 2005). Key questions of the effects of testosterone on patient reported outcomes and functional benefits that may retard physical or mental frailty of the elderly or improve the quality of life are not yet available. Specific risk data on the prostate and cardiovascular systems are needed. Recent guidelines for the testosterone treatment of younger hypogonadal men are available from professional societies (AACE Hypogonadism Task Force, 2002; The Practice Committee of the American Society for Reproductive Medicine, 2004; Bhasin et al, 2006). Recommendations on the diagnosis, treatment, and monitoring of late-onset hypogonadism was published by the International Society for the Study of Aging Male (ISSAM) in 2002 (Morales and Lunenfeld, 2002). In 2005, a writing committee formed by the International Society of Andrology (ISA), the ISSAM, and the European Association of Urology (EAU) prepared a set of recommendations specifically on the “investigation, treatment, and monitoring of late onset hypogonadism.” In order to reach a large audience, these recommendations were published in the International Journal of Andrology, the Journal of Andrology, the Aging Male, and European Urology (Nieschlag et al, 2005a,b,c, 2006). In view of the growing interest from practitioners on the treatment of older men with testosterone, the ISA, ISSAM, EAU, European Academy of Andrology (EAA), and American Society of Andrology (ASA) convened meetings of the writing group with expert representatives from each of the societies. The writing group membership from 2005 was expanded to include additional urologists. Members of the writing group met in Berlin in 2007, Toronto in 2007, and Tampa in 2008 to revise these recommendations. There was no corporate funding or support for the development of these recommendations. The revised recommendations are supported by a selection of appropriate references and categorized by the level of evidence and grade of recommendation according to the US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research (1992:115–127; Table). To ensure broad outreach to multidisciplinary audiences, these recommendations are published in the European Journal of Endocrinology, European Urology, the International Journal of Andrology, the International Journal of Impotence Research, the Journal of Andrology, and The Aging Male simultaneously. Late-onset hypogonadism (LOH, also referred to as age-associated testosterone deficiency syndrome [TDS]) is a clinical and biochemical syndrome associated with advancing age and characterized by symptoms and a deficiency in serum testosterone levels (below the young healthy adult male reference range; Morales et al, 2006; Nieschlag et al, 2005a,b,c, 2006). This condition may result in significant detriment in the quality of life and adversely affect the function of multiple organ systems. At present, the diagnosis of treatable hypogonadism requires the presence of symptoms and signs suggestive of testosterone deficiency (level 3, grade A; Bhasin et al, 2006; Nieschlag et al, 2005a,b,c, 2006). The symptom most associated with hypogonadism is low libido (level 3, grade A; Schiavi et al, 1991; Travison et al, 2006). Other manifestations of hypogonadism include: erectile dysfunction (ED), decreased muscle mass and strength, increased body fat, decreased bone mineral density and osteoporosis, decreased vitality, and depressed mood. None of these symptoms are specific to the low-androgen state, but may raise suspicion of testosterone deficiency. One or more of these symptoms must be corroborated with a low serum testosterone level (level 3, grade A; Kelleher et al, 2004; Zitzmann et al, 2006; Araujo et al, 2007; Morales et al, 2007). Questionnaires such as Aging Male Symptom Score (AMS; Heinemann et al, 2004; Moore et al, 2004) and Androgen Deficiency in Aging Men (ADAM; Morley et al, 2000) are not recommended for the diagnosis of hypogonadism because of low specificity (level 3, grade B; Tancredi et al, 2004; Beutel et al, 2005; Morales et al, 2007). In patients at risk or who are suspected of hypogonadism, a thorough physical and biochemical work-up is necessary (level 4, grade A). Transient decreases of serum testosterone levels, such as due to acute illnesses, should be excluded by careful clinical evaluations and repeated hormone measurement. Hypogonadism (primary or secondary) can occur at all ages, including in elderly men. Risk factors for hypogonadism in older men may include chronic illnesses (including diabetes mellitus, chronic obstructive lung disease, and inflammatory arthritic, renal, and HIV-related diseases), obesity, metabolic syndrome, and hemachromatosis (Bhasin et al, 2006). Such chronic diseases should be investigated and treated (level 4, grade A). A serum sample for total testosterone determination should be obtained between 0700 and 1100 hours (level 2a, grade A; Diver et al, 2003). The most widely accepted parameter to establish the presence of hypogonadism is the measurement of serum total testosterone. There are no generally accepted lower limits of normal. There is, however, general agreement that total testosterone level above 12 nmol/L (350 ng/dL) does not require substitution. Similarly, based on the data of younger men, there is consensus that patients with serum total testosterone levels below 8 nmol/L (230 ng/dL) will usually benefit from testosterone treatment. If the serum total testosterone level is between 8 and 12 nmol/L, repeating the measurement of total testosterone with sex hormone—binding globulin (SHBG) to calculate free testosterone or free testosterone by equilibrium dialysis may be helpful (see 3.5 and 3.7 below; level 2b, grade A). Measurements of serum luteinizing hormone will assist in differentiating between primary and secondary hypogonadism, and serum prolactin is indicated when the serum testosterone is lower than 5.2 nmol/L (150 ng/dL; Citron et al, 1996; Buvat and Lemaire, 1997; Bunch et al, 2002; Rhoden et al, 2003) or when secondary hypogonadism is suspected (level 3, grade B; Araujo et al, 2004; Vermeulen, 2005; Bhasin et al, 2006). Since there are known variations between assay methods, it is imperative that the practitioners utilize reliable laboratories and are acquainted with the reference ranges for testosterone from their local laboratory (level 2b, grade A; Taieb et al, 2003; Wang et al, 2004; Sikaris et al, 2005; Rosner et al, 2007). Current immunometric methods for measurement of testosterone can distinguish between hypogonadism and normal adult men. However, methods based on mass spectrometry (MS) are more accurate and precise (level 2b, grade A; Taieb et al, 2003; Wang et al, 2004; Sikaris et al, 2005) and are increasingly recognized as the method of choice for serum testosterone measurement. Measurement of free or bioavailable testosterone should be considered when the serum total testosterone concentration is not diagnostic of hypogonadism, particularly in obese men. There are no generally accepted lower limits of normal for free testosterone for the diagnosis of hypogonadism. However, a free testosterone level below 225 pmol/L (65 pg/mL) can provide supportive evidence for testosterone treatment (level 3, grade C; Vermeulen et al, 1999, 2005; Rosner et al, 2007). Threshold values for bioavailable testosterone depend on the method used and are not generally available (Rosner et al, 2007). Equilibrium dialysis is the gold standard for free testosterone measurement. Free testosterone assays based on analog displacement immunoassays are widely available but do not give an accurate measurement of free testosterone; thus, they should not be used (Rosner 1997; Swerdloff and Wang, 2008). Alternately, measuring serum SHBG levels together with reliable serum total testosterone levels provides the data necessary for calculating free testosterone levels (level 2b, grade A). Calculated free testosterone correlates well with free testosterone by equilibrium dialysis (Vermeulen et al, 1999; Rosner et al, 2007). 7) Efforts to create standardization of testosterone assays, agreement on standards for testosterone measurement and accurate reference ranges for testosterone by liquid chromatography-MS/MS are being developed. International reference standards, characterization of methodology, and population-based reference ranges for free testosterone by equilibrium dialysis are needed. Consensus on the equilibrium constants for testoseterone binding to SHBG and albumin will allow improved calculation of free testosterone (Rosner et al, 2007). Salivary testosterone has also been shown to be a reliable substitute for free testosterone measurements, but cannot be recommended for general use at this time since the methodology has not been standardized and adult male ranges are not available in most hospital or reference laboratories (level 3, grade B; Wang et al, 1981). Alterations in other endocrine systems occur in association with aging (ie, estradiol, growth hormone [GH], and dehydroepiandrosterone [DHEA]), but the significance of these changes is not well understood. Determinations of estradiol, thyroid hormones, cortisol, DHEA, dehydroepiandrosterone sulfate (DHEA-S), melatonin, GH, and insulinlike growth factor 1 are not indicated unless other endocrine disorders are suspected based on the clinical signs and symptoms of the patient (level 2, grade A; Bhasin et al, 2006). Improvement in signs and symptoms of testosterone deficiency should be sought. Failure to benefit clinical manifestations within a reasonable time interval (3 to 6 months is adequate for libido and sexual function, muscle function, and improved body fat; improvement in bone mineral density requires a longer interval to show improvement) should result in discontinuation of treatment. Further investigation for other causes of symptoms is then mandatory (level 1b, grade A). In men with hypogonadal values of testosterone, testosterone administration improves body composition (decrease of fat mass, increase of lean body mass; level 1b, grade A; Snyder et al, 1999b; Liverman and Blazer, 2004; Isidori et al, 2005b; Page et al, 2005; Allan et al, 2008). Secondary benefits of these changes of body composition on strength, muscle function, and metabolic and cardiovascular dysfunction are suggested by available data but require confirmation by large-scale studies. Osteopenia, osteoporosis, and fracture prevalence rates are greater in hypogonadal younger and older men (Meier et al, 2008). Bone density in hypogonadal men of all ages increases under testosterone substitution (level 1b, grade A; Snyder et al, 1999a; Kenny et al, 2000; Amory et al, 2004). Fracture data are not yet available, and thus the long-term benefit of testosterone requires further investigation. Assessment of bone density at 2-year intervals is advisable in hypogonadal men, and serum testosterone measurements should be obtained in all men with osteopenia (Schousboe et al, 2007; Freitas et al, 2008). The initial assessment of all men with ED and/or diminished libido should include determination of serum testosterone. These dysfunctions, with or without a testosterone deficiency, might be related to comorbidities (ie, diabetes mellitus, hyperprolactinemia, the metabolic syndrome, bladder outlet obstruction, peripheral vascular disease, or medications; level 2a, grade A; Morales et al, 2004). Men with ED and/or diminished libido and documented testosterone deficiency are candidates for testosterone therapy (level 2a, grade A). An inadequate response to testosterone treatment requires reassessment of the causal mechanisms responsible for the ED (see 7.4 below). In the presence of a clinical picture of testosterone deficiency and borderline serum testosterone levels, a short (eg, 3 months) therapeutic trial may be justified. An absence of response calls for discontinuation of testosterone administration. A satisfactory response might be placebo generated so that continued assessment is advisable before long-term treatment is recommended (level 2a, grade B; Black et al, 2004). There is evidence suggesting therapeutic synergism with combined use of testosterone and phosphodiesterase-5 inhibitors in hypogonadal or borderline eugonadal men (level 1b, grade B; Shabsigh et al, 2004; Greenstein et al, 2005). These observations are still preliminary and require additional study. However, the combination treatment should be considered in hypogonadal patients with ED failing to respond to either treatment alone. It is unclear whether men with hypogonadism and ED should be treated initially with phosphodiesterase-5-inhibitor, testosterone, or the combination of the two. Many of the components of the metabolic syndrome (obesity, hypertension, dyslipidemia, impaired glucose regulation, and insulin resistance) are also present in hypogonadal men. Numerous epidemiologic studies have established a close relationship between obesity and low serum testosterone levels in healthy men (Allen et al, 2002). Twenty percent to 64% of obese men have a low serum total or free testosterone levels (Kalyani and Dobs, 2007). The metabolic syndrome and type 2 diabetes mellitus are associated with low plasma testosterone (Allen et al, 2002; Laaksonen et al, 2004; Derby et al, 2006; Kupelian et al, 2006; Zitzmann et al, 2006; Kapoor et al, 2007; Rodriguez et al, 2007; Selvin et al, 2007). Serum testosterone should be measured in men with type 2 diabetes mellitus with symptoms suggestive of testosterone deficiency (level 2b, grade A). The effects of testosterone administration on glycemic control of men with diabetes mellitus are much less certain (Corrales et al, 2004; Kapoor et al, 2006; Basu et al, 2007). It is premature to recommend testosterone treatment for the metabolic syndrome or diabetes mellitus in the absence of laboratory and other clinical evidence of hypogonadism. In men with hypogonadism and diabetes and/or the metabolic syndrome, testosterone treatment for traditional hypogonadal symptoms may have other unproven benefits on their metabolic status (level 2a, grade B). At the present time, there is no conclusive evidence that testosterone therapy increases the risk of prostate cancer or benign prostatic hyperplasia (Carpenter et al, 2008; Roddam et al, 2008). There is also no evidence that testosterone treatment will convert subclinical prostate cancer to clinically detectable prostate cancer (level 4, grade C). However, there is unequivocal evidence that testosterone can stimulate growth and aggravate symptoms in men with locally advanced and metastatic prostate cancer (level 2a, grade A; Fowler and Whitmore, 1982; McConnell, 1995). Currently, adequately powered and optimally designed long-term prostate disease data are not available to determine whether there is any additional risk from testosterone replacement. Hypogonadal older (>45 years) men should be counseled on the potential risks and benefits of testosterone replacement before treatment and carefully monitored for prostate safety during treatment (level 3, grade A). Prior to therapy with testosterone, a man's risk of prostate cancer must be assessed using, as a minimum, digital rectal examination (DRE) and determination of serum prostate-specific antigen (PSA). However, the pretreatment assessment can be improved by incorporating other risk predictors such as age, family history, and ethnicity/race. Several tools have been developed to assist the clinician in assessing prostate cancer risk (eg, on-line prostate cancer risk calculator Parekh et al, 2006; Thompson et al, 2006a). These tools have not been validated for patients with LOH (TDS). If the patient and physician feel that the risk is sufficiently high, further assessment may be desirable (level 2a, grade B; Thompson et al, 2006a,b). However, pretreatment prostate ultrasound examinations or biopsies are not recommended as routine requirements. After initiation of testosterone treatment, patients should be monitored for prostate disease at 3 to 6 months, 12 months, and at least annually thereafter (level 3, grade C). Should the patient's prostate cancer risk be sufficiently high (suspicious finding on DRE, increased PSA, or as calculated using a combination of risk factors as noted above) transrectal ultrasound-guided biopsies of the prostate are indicated (level 2b, grade A; Meikle et al, 1997; Bhasin et al, 2003; Rhoden and Morgentaler, 2004; Marks et al, 2006). Severe symptoms of lower urinary tract symptoms (LUTS) evident by a high (>21) International Prostate Symptom Score due to benign prostate hyperplasia represent a relative contraindication (although there are no compelling data to suggest that testosterone treatment causes exacerbation of LUTS or promotes acute urinary retention [level 3, grade C]. After successful treatment of lower urinary tract obstruction, this contraindication is no longer applicable (level 4, grade C) Men successfully treated for prostate cancer and suffering from confirmed symptomatic hypogonadism are potential candidates for testosterone substitution after a prudent interval if there is no clinical or laboratory evidence of residual cancer (Kaufman and Graydon, 2004; Agarwal and Oefelein, 2005; Khera and Lipshultz, 2007; Sarosdy, 2007). As long-term outcome data are not available, clinicians must exercise good clinical judgment together with adequate knowledge of advantages and drawbacks of testosterone therapy in this situation (level 2b, grade C; Nieschlag and Behre, 2004; Nieschlag, 2006). The risk and benefits must be clearly discussed with and understood by the patient, and the follow-up must be particularly careful. Preparations of natural testosterone should be used for substitution therapy. Currently available intramuscular, subdermal, and of testosterone are and (level 1b, grade A). The physician should have knowledge and adequate of the as well as of the advantages and drawbacks of each The selection of the should be a of an patient and physician et al, 2005). Since the development of an during treatment or prostate et al, 2005) requires discontinuation of testosterone may be over in the initial treatment of patients with LOH (level 4, grade C). data are available to determine the serum testosterone level for and the present time, to lower young adult male serum testosterone levels appropriate as the therapeutic and Nieschlag, 2007). levels should be evidence for or the to the of serum testosterone levels (level 3, grade B). men are more to effects (level 2b, grade B; et al, 2005; Zitzmann and Nieschlag, 2007). The androgen such as testosterone, are because of their potential and should no longer be (level 2b, grade A). There is not evidence to recommend substitution of in aging other androgen such as DHEA, or are not recommended (level 1b, grade A). Human testosterone of at a lower in older than in younger men. Since the therapeutic and effects of treatment in older men and this treatment cannot be recommended in LOH when is an (level 1b, grade B). and inhibitors have been shown to increase testosterone levels (level 2b, grade B). evidence does not to recommend their androgen are under but are not yet clinically available. Many of these are and the risks of long-term use are Testosterone treatment is in men with prostate or cancer (level 3, grade A). Testosterone treatment is in men at high risk of prostate It is unclear whether 7) prostate cancer a relative or contraindication for treatment. for more level 4, C; et al, 2005; et al, 2006; Men with significant level 3, grade obstructive (level 3, grade (level 3, grade should not be on treatment with testosterone without of the condition et al, 2005; et al, 1995). can during testosterone treatment, in older men treated by testosterone assessment is indicated (ie, before treatment, then 3 to and 12 months in the of treatment, and annually it is not yet what is and/or may be necessary to below to (level 3, grade A; Bhasin et al, 2006; et al, 2005; Nieschlag, 2006). is not a contraindication to testosterone treatment. assessment of comorbidities causes of and potential risks benefits of testosterone treatment is particularly in elderly men (level 2a, grade A). The diagnosis of late-onset testosterone deficiency is based on the presence of symptoms or signs and low serum testosterone The benefits and risks of testosterone therapy must be clearly discussed with the patient and assessment of prostate and other risk factors considered before testosterone treatment. to testosterone treatment should be If there is no improvement of symptoms and treatment should be and the patient investigated for other causes of the clinical
Laparoscopic sleeve gastrectomy/duodenojejunal bypass (LSG/DJB) aids weight loss and improves type 2 diabetes mellitus (T2DM) in patients with obesity. Herein, we present a 1-year longitudinal evaluation using continuous glucose monitoring (CGM), bioelectrical impedance analysis (BIA), and computed tomography (CT) fat scans after LSG/DJB in a patient with obesity and T2DM. Our patient was a 33-year-old female with obesity and T2DM who had been treated with intensive insulin therapy (50 units/d) before LSG/DJB. Preoperatively, the patient had uncontrolled diabetes, with a fasting blood glucose level of 252 mg/dL and HbA1c of 10.0%. Moreover, the CGM showed 1%, 99%, and 0% time-in range (TIR), time-above range, and time-below range, respectively. LSG/DJB significantly increased the 3-, 6-, and 12-month TIR to 96%, 93%, and 89%, respectively, and decreased the time-above range to 4%, 7%, and 11%, respectively, indicating high-dose insulin withdrawal and complete diabetes remission. Twelve months post-LSG/DJB, effective abdominal fat mass loss was observed on CT. Furthermore, both FM and the percentage of fat mass were reduced, and muscle mass was maintained according to the BIA. Effective weight loss, abdominal FM loss, and complete diabetes remission were observed after LSG/DJB, according to BIA and CT. The significant increase in TIR suggests that this therapeutic approach may improve the prognosis of patients with T2DM and obesity. CGM, BIA, and CT fat scans are highly useful for the long-term management of obesity and diabetes after LSG/DJB surgery.
Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is a rare congenital anomaly characterized by agenesis or hypoplasia of the uterus and upper vagina in phenotypically normal females. Although patients with MRKH syndrome typically exhibit normal secondary sexual development, associations with extragenital anomalies and metabolic conditions such as diabetes mellitus have been increasingly reported. A female patient initially presented at the age of 15 (currently 19 year old) with primary amenorrhea and absence of secondary sexual characteristics. Initial laboratory evaluation showed elevated follicle-stimulating hormone (FSH) and thyroid-stimulating hormone (TSH) levels, while thyroid antibodies and prolactin were within normal limits. Pelvic magnetic resonance imaging revealed poorly visualized ovaries, a hypoplastic or absent uterus and upper vagina, and urinary tract anomalies including a duplicated right ureter. One year later, she developed symptoms suggestive of diabetes mellitus and was found to have elevated random and fasting blood glucose levels. Her mother had been diagnosed with type 2 diabetes mellitus prior to conception. The patient was referred to endocrinology to evaluate the possibility of monogenic diabetes. The constellation of uterovaginal aplasia, renal anomalies, and endocrine dysfunction raises clinical suspicion of an expanded phenotypic spectrum or a potential overlap syndrome, such as Müllerian duct aplasia, renal dysplasia, and cervicothoracic somite anomalies (Reference ranges: FSH: 3-10 mIU/mL in follicular phase; TSH: 0.4-4.0 μIU/mL). This case highlights the importance of comprehensive systemic evaluation in patients with MRKH syndrome, especially when extragenital anomalies or metabolic abnormalities such as diabetes mellitus coexist. Early recognition and multidisciplinary management are essential for optimal care and may provide valuable insights into potentially shared developmental and genetic pathways.
Diabetes mellitus (DM) arises from insufficiencies in insulin secretion and action. The pancreatic α-amylase enzyme is involved in starch metabolism and influences glycated hemoglobin (HbA1c) level. The current study examines relationships between blood glucose level, α-amylase activity, HbA1c, and several trace elements (Cu, Zn, and Mg). Eighteen healthy control subjects and 31 patients with type 2 diabetes from both genders were recruited for this study. The enzymatic colorimetric method was used to assess serum glucose levels and α-amylase activity. The boronate affinity method and atomic absorption spectroscopy were used to measure HbA1c and trace elements, respectively. In comparison to the control group, the diabetes groups' mean levels of α-amylase were slightly higher. The Cu level was significantly increased (P < 0.05) in the patient group, whereas Zn and Mg levels did not change significantly. HbA1c demonstrated a significant negative correlation (r = -0.394, P < 0.05) with α-amylase in patients with diabetes. The α-amylase also exhibited a negative correlation with glucose level in these patients. Cu level increased in hyperglycemia, and α-amylase negatively correlated with Cu. The diabetes group's HbA1c and Zn levels were inversely correlated, which suggests that uncontrolled DM causes a reduction in Zn levels. Cu and Mg correlated positively with HbA1c in healthy people but not in people with diabetes. As the enzyme α-amylase correlated with HbA1c and glucose levels, it may serve as a supplementary marker of pancreatic exocrine involvement in patients with diabetes, but its predictive or diagnostic utility remains unproven. The pathophysiology of DM is complicated by altered trace element levels.
Early-onset type 2 diabetes (T2D) is an emerging public health concern. Despite its rising burden, national data on the prevalence and risk factors in Bangladesh remain scarce. This study aimed to estimate the prevalence of early-onset T2D and identify risk factors among young people in Bangladesh. This nationwide, population-based survey encompassed 2,300 young people-adolescents (10-18 years) and young adults (19-34 years)-from rural and urban sites across 8 divisions of Bangladesh using multistage random sampling in 2024. Glycemic status (by oral glucose tolerance test except in pre-existing diabetes mellitus), fasting lipid profile, sociodemographics, lifestyle, anthropometry, and blood pressure were assessed. Glucose was measured by the glucose-oxidase method, and lipids by the enzymatic method. Prevalence of early-onset T2D and prediabetes was 4.5% (104/2,300) and 18.4% (423/2,300), respectively. Among those with diabetes, 66.3% (69/104) were newly diagnosed. Diabetes prevalence was higher in young adults (89/1,182; 7.5%) than in adolescents (15/1,118; 1.3%), and in urban residents (65/1,079; 6.0%) than in rural residents (39/1,221; 3.2%) (P < .05 for both). Higher odds for diabetes were linked with suboptimal physical activity (odds ratio [OR] 2.0, 95% CI: 1.1-4.0), smokeless tobacco use (OR 2.6, 95% CI: 1.4-4.9), central obesity (OR 2.0, 95% CI: 1.3-3.3), hypertension (OR 3.3, 95% CI: 1.6-6.7), and hypertriglyceridemia (OR 2.9, 95% CI: 1.8-4.5). Early-onset T2D affects 4.5% of young people in Bangladesh, whereas 18.4% have prediabetes. Prevalence is higher in young adults and urban residents. Suboptimal physical activity, smokeless tobacco use, central obesity, hypertension, and hypertriglyceridemia are key risk factors.
Nonadherence to insulin therapy remains a major challenge to achieving optimal glycemic control, leading to complications and increased health care costs. Despite accessible insulin therapy in tertiary hospitals, barriers such as injection fear, complex regimens, inadequate storage, stigma, and limited health literacy contribute to poor adherence. Evidence on determinants of insulin nonadherence in tertiary care settings in India remains limited. This study aimed to determine the prevalence and predictors of insulin nonadherence among adults with diabetes mellitus. A cross-sectional survey was conducted from February to July 2025 among adults (≥18 years) with type 1 or type 2 diabetes mellitus receiving insulin therapy for at least 6 months, selected using a consecutive sampling technique. The 8-item Morisky Medication Adherence Scale assessed adherence; scores <6 indicated nonadherence. Data were analyzed using SPSS version 29, and binary logistic regression identified independent predictors. Of 402 participants, 36.8% were nonadherent. Independent predictors of nonadherence included upper-middle socioeconomic status (adjusted odds ratio [AOR] 2.11; 95% CI 1.07-4.15; P = 0.031), type 2 diabetes (AOR 2.23; 95% CI 1.20-4.14; P = 0.011), lack of insulin storage (AOR 4.72; 95% CI 2.28-9.76; P < 0.001), polypharmacy (AOR 4.00; 95% CI 0.99-16.14; P = 0.046), and poor lifestyle adherence (AOR 1.62; 95% CI 0.95-2.77; P = 0.047). Primary education was associated with lower odds of nonadherence (AOR 0.26; 95% CI 0.08-0.83; P = 0.023). Over one-third of patients were nonadherent to insulin therapy. Findings highlight the need for focused educational support, behavioral counseling, and structural solutions such as improved storage provisions to enhance adherence and metabolic outcomes.
To investigate the remission rate and metabolic outcomes under the Diabetes Reversal Clinic with multidisciplinary management. Patients with type 2 diabetes who visited the Diabetes Reversal Clinic from April 2022 to December 2024 were enrolled. Baseline characteristics and metabolic indicators were recorded. Participants received comprehensive multidisciplinary management including personalized treatment plans, structured lifestyle modification, continuous glucose monitoring, and traditional Chinese medicine as adjunctive therapy. After 6 months, the remission rate, the rate of target glycated hemoglobin A1c < 53 mmol/mol (7.0%), and changes of metabolic indicators in patients were analyzed. Our major results found that, among 171 patients with type 2 diabetes who were followed for more than 6 months, 50 (29.24%) patients achieved remission and 149 (87.13%) patients achieved the target of glycated hemoglobin A1c < 53 mmol/mol (7.0%). At the end of 2022, 2023, and 2024, the annual diabetes remission rate reached 6.12% (6/98), 16.78% (25/149), and 16.24% (19/117), respectively. The multidisciplinary management significantly decreased body mass index, waist circumference, waist-to-height ratio, fasting blood glucose, glycated hemoglobin A1c, and homeostasis model assessment of insulin resistance, while significantly increasing high-density lipoprotein cholesterol (all P < 0.05). A diabetes remission rate of 29.24% and a target rate of 87.13% were obtained after 6 months of multidisciplinary management among patients with type 2 diabetes in the Diabetes Reversal Clinic. Our findings suggest that the multidisciplinary management model employed in the Diabetes Reversal Clinic is superior to conventional management in general outpatient clinics for promoting diabetes remission and metabolic reversal.
In addition to the hypoglycemia and weight gain associated with many treatments for type 2 diabetes, alpha-glucosidase inhibitors, thiazolidinediones, metformin, sulfonylureas, and the glinides do not address all of the multiple defects existing in the pathophysiology of the disease. Cumulatively, these oral agents address the influx of glucose from the gastrointestinal tract, impaired insulin activity, and acute beta-cell dysfunction in type 2 diabetes; however, until recently, there were no means to deal with the inappropriate hyperglucagonemia or chronic beta-cell-decline characteristic of the disease. The recently introduced incretin-based therapies serve to address some of the challenges associated with traditionally available oral antidiabetic agents. In addition to improving beta-cell function, stimulating insulin secretion, and inhibiting glucagon secretion, these agents reduce appetite, thereby stabilizing weight and/or promoting weight loss in patients with type 2 diabetes. Of the incretin-based therapies, both the dipeptidyl peptidase-4 (DPP-4) inhibitors and the glucagon-like peptide-1 (GLP-1) receptor agonists stimulate insulin secretion and inhibit glucagon secretion. The subsequent review outlines evidence from selected clinical trials of the currently available GLP-1 receptor agonists, exenatide and liraglutide, and DPP-4 inhibitors, sitagliptin and saxagliptin. Earlier and more frequent use of these incretin-based therapies is recommended in the treatment of type 2 diabetes, based on their overall safety and ability to achieve the glycosylated hemoglobin level goal. As such, both the American Diabetes Association and the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE) treatment algorithms recommend the use of incretin-based therapy in both treatment-naive and previously treated patients. The AACE/ACE guidelines clearly state that these agents should not be limited to third- or fourth-line therapy.
To compare glycemic control and metabolic outcomes between multiple daily injections (MDIs) and continuous subcutaneous insulin infusion (CSII) in pediatric type 1 diabetes mellitus. Searches were conducted in PubMed MEDLINE, Web of Science, Scopus, CNKI, CINAHL, Cochrane, and EMBASE on 02/2025. A systematic review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Outcomes included HbA1c levels, total daily dose, diabetic ketoacidosis, hypoglycemia events, body mass index change, and adverse events. Statistical analysis was performed using R version 3.4.3. Eighteen randomized controlled trials (1229 participants) were analyzed. CSII compared to MDI significantly reduced HbA1c (MD = -0.37%; 95% CI: -0.62 to -0.12; P < 0.01; I2 = 86.6%), adverse events (relative risk [RR]: 1.45; 95% CI: 1.10 to 1.90; P < 0.01; I2 = 0.0%), and increased body mass index (MD = 0.43; 95% CI: 0.31 to 0.55; P < 0.01; I2 = 0.0%). No significant differences were found for insulin requirement (MD = -0.08 U/kg/d; P = 0.14), severe hypoglycemia (RR = 1.09; P = 0.73), or diabetic ketoacidosis (RR = 1.40; P = 0.43). Trial sequential analysis for HbA1c reduction indicated conclusive evidence, while for insulin requirements, it remains inconclusive due to insufficient sample size. Our meta-analysis confirms CSII achieves superior HbA1c reduction versus MDI in pediatric type 1 diabetes, as supported by trial sequential analysis. However, evidence for insulin requirements remains inconclusive, highlighting the need for larger trials and personalized treatment considering patient preferences and accessibility.
The management of hypothyroidism has evolved over time as the development of new guidelines and formulations of thyroid hormone have become available. A survey of American Association of Clinical Endocrinology members in the United States examining the treatment of hypothyroidism, including questions about initial choice of therapy, use of liothyronine (LT3)-containing regimens, and use of thyroid hormones in hypothyroid and non-hypothyroid patients. Survey links were opened by 387 of 4000 potential respondents and completed by 299 (7%). Respondents unanimously cited levothyroxine (LT4) as the initial treatment choice for hypothyroidism. Forty-seven percent indicated they would use thyroid hormones in patients with euthyroidism with infertility and elevated thyroid antibodies, with smaller numbers for goiter, depression, hypercholesterolemia, fatigue, and obesity. About 60% would consider combination LT4/LT3 in a patient with euthyroidism who does not feel well on treatment or has persistent symptoms. In contrast, a much smaller minority (16% for LT4/LT3 and 5% for desiccated thyroid extract) used such regimens to manage their own hypothyroidism. Persistent symptoms in treated patients with a normal TSH were most often attributed to psychosocial factors, unrealistic patient expectations, and comorbidities. Significant associations were identified between respondent demographics and treatment choices, most notably age, practice setting, and volume of patients with hypothyroidism. LT4 monotherapy is overwhelmingly employed as first line therapy for hypothyroidism by U.S. clinicians. However, the high usage of thyroid hormones for patients whose symptoms were considered to be unrelated to hypothyroidism is at odds with current international guidelines for the management of hypothyroidism.
Recent observational studies report conflicting evidence on whether semaglutide use is associated with non-arteritic anterior ischemic optic neuropathy (NAION). This systematic review synthesizes available evidence and critically evaluates bias and confounding. PubMed, Embase, and the Cochrane Library were searched through December 2025 for observational studies assessing semaglutide and NAION. Two reviewers independently screened records, extracted data, and assessed study quality using the Newcastle-Ottawa Scale. Owing to substantial clinical and methodological heterogeneity, results were synthesized narratively. Nine large retrospective cohort studies, encompassing more than 3 million patients, and one major regulatory review were included. Findings were sharply divided. Four studies reported statistically significant increased risk, with hazard ratios ranging from 1.76 to 4.28. Four studies found no significant association, while one suggested a protective effect (odds ratio 0.36). All studies were of moderate quality and exhibited high risk of bias in cohort comparability. Notably, studies using broad or untreated comparators consistently reported elevated risk, whereas studies employing active comparators with similar metabolic risk profiles generally found no association. Current evidence does not support a causal relationship between semaglutide and NAION. The divergent findings are most plausibly explained by confounding by indication: patients prescribed semaglutide tend to have more severe diabetes, obesity, and cardiovascular disease, all independent risk factors for NAION. Even under the highest reported relative risk estimates, the absolute risk remains very low and is outweighed by well-established cardiovascular and renal benefits of semaglutide. Definitive clarification will require prospective studies with standardized ophthalmologic adjudication and measurement.
The COVID-19 infection impacts endocrine tissues, and various thyroid disorders have been reported in affected patients. Subacute thyroiditis (SAT), a self-limited inflammatory thyroid condition, is associated with viral respiratory tract infections. Studies have suggested a link between COVID-19 and SAT. Our study expands on this by examining differences in SAT severity before and after COVID-19. A retrospective cohort study analyzed SAT cases at an outpatient Ontario endocrinology clinic. Cases were identified as pre-Covid (December 2015 - April 2019) or post-Covid (December 2019 - April 2023). Patient charts were screened for diagnostic characteristics of SAT and relevant lab data, including thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3). From 436 pre-Covid and 629 post-Covid cases, 32 and 37 met the inclusion criteria. Our study showed no difference between incidence of SAT cases post-Covid versus pre-Covid. However, post-Covid, more patients had severe SAT, defined as values of FT4 and FT3 >30% above their upper normal range and TSH >10, (FT4 37.8 ∓ 6.7 vs 50.9 ∓ 23.5 [P = 0.05]; FT3 9.6 ∓ 2.2 vs 18.6 ∓ 10.9 [P = 0.02]). No significant differences were identified in median TSH levels during hyperthyroid phase (P = 0.12). In the hypothyroid phase, median TSH values were significantly higher post-Covid (P = 0.0046). Low FT4 values also showed significance (P = 0.001). Our study shows SAT incidence was similar pre- and post-COVID-19. Severity of the SAT disease course was amplified after the onset of the COVID-19 pandemic, with a significant elevation in FT4 and FT3 levels during hyperthyroidism and higher TSH during hypothyroidism in the post-Covid cohort.
We assessed the impact of adding subcutaneous basal insulin to hybrid closed-loop insulin pump therapy on diabetic ketoacidosis (DKA) rates and glycemic outcomes in adults with type 1 diabetes (T1D) and recurrent DKA. We conducted a retrospective review of electronic health records from adults with T1D and recurrent DKA who received concurrent treatment with subcutaneous basal insulin and hybrid closed-loop insulin pump therapy at an academic health system in the United States. We performed an as-treated analysis using descriptive statistics. Our cohort included 5 adults (3 women, 2 men; mean age 39.4 ± 10.8 years) with T1D and recurrent DKA. Due to elevated DKA risk, all 5 adults were initiated on once-daily subcutaneous basal insulin (degludec or glargine, mean dose 0.14 units/kg/d, range 0.07-0.22 units/kg/d) in addition to insulin pump therapy (Omnipod 5 with automated insulin delivery). Mean HbA1c decreased from 9.3% (79 mmol/mol) (days -360 to -1) to 8.2% (66 mmol/mol) (days 0 to 360) following the intervention. The frequency of DKA-related hospitalizations decreased from a mean of 2.0 events per person (days -360 to -1) to 0.75 events per person (days 0 to 360). One individual discontinued subcutaneous basal insulin due to recurrent level 1 hypoglycemia. Adding once-daily subcutaneous basal insulin to hybrid closed-loop therapy may have the potential to reduce DKA-related hospitalizations and improve glycemic outcomes in adults with T1D and recurrent DKA. However, given this was a retrospective study with a small cohort, further research is needed to rigorously evaluate this approach.
Maturity Onset Diabetes in the Young (MODY) is the most common form of monogenic diabetes caused by various single gene mutations. We present a patient with presumed type 2 diabetes mellitus (T2DM), ultimately diagnosed with MODY due to heterozygous Wolfram Syndrome 1 (WFS1) gene mutation. Our patient was diagnosed with T2DM at age 22 and treated with oral medications and lifestyle modifications. At age 45, patient's HbA1c was 11.4% (reference <5.7%) on metformin XR 1000 mg twice daily. Additional testing (serum glucose 216 mg/dL [reference: 70-125 mg/dL], C-peptide level 2.18 ng/mL [reference 0.78-5.19 ng/mL], undetectable glutamic acid decarboxylase antibody 65 [GAD-65] [reference: 0.0-5.0 IU/mL], undetectable IgG Islet Cell cytoplasmic antibody [reference: <1:4]) ruled out type 1 diabetes mellitus (T1DM). Due to family history of diabetes and normal body mass index (BMI) 23.2 kg/m2, MODY testing was done. This revealed one variant of uncertain significance in the WFS1 gene (NM_006005.3:c.2026C > T; p.Arg676Cys; heterozygous) not previously described in literature. MODY is a known but uncommon cause of diabetes in young adults. While mutations in HNF1A, GCK, and HNF4A are commonly associated with MODY, rare mutations such as the WFS1 gene mutation should be considered. Our patient's WFS1 mutation (NM_006005.3:c.2026C > T; p.Arg676Cys; heterozygous) has not been reported in literature. Young adults with family history of diabetes and normal BMI should be evaluated for MODY when diagnosed with diabetes. A complete mutation panel for MODY should be done to evaluate for lesser-known mutations such as the WFS1 gene mutation.
Severe pediatric hypothyroidism may cause growth failure and pituitary hyperplasia mimicking adenoma. Although thyroid nodules are rare in children, their malignancy risk is higher than in adults. We report a boy with severe hypothyroidism, growth failure, pituitary hyperplasia, and oncocytic thyroid carcinoma, underscoring the need for comprehensive evaluation. A 10-year-old boy presented with growth delay, height 105 cm (<1st percentile, -6.7 SD), and weight 21.2 kg (third percentile, -2.03 SD). Examination revealed pallor, dry skin, alopecia, Tanner stage I/I, and bitemporal hemianopsia. Laboratory results showed thyroid stimulating hormone >500 mIU/ml (reference 0.45-4.50 mIU/L), free thyroxine <0.30 ng/dl (reference 0.93-1.60 ng/dl), prolactin 102 ng/ml (reference 5-20 ng/ml), and insulin-like growth factor 1 of 8 ng/ml (reference 123-497 ng/ml). Pituitary magnetic resonance imaging demonstrated a homogeneous, isointense sellar lesion with optic chiasma displacement. Thyroid ultrasound showed a 43.9 mm hypoechoic nodule, and fine-needle aspiration classified it as Bethesda category IV. Total thyroidectomy confirmed encapsulated angioinvasive oncocytic carcinoma, followed by radioactive iodine therapy. With levothyroxine and growth hormone treatment, pituitary hyperplasia regressed, and height increased by 15 cm in 1 year. Pituitary hyperplasia secondary to hypothyroidism is reversible with levothyroxine and must be differentiated from adenomas to avoid unnecessary surgery. Oncocytic thyroid carcinoma is rare in children, and its coexistence with hypothyroidism is unusual. This case emphasizes the importance of thyroid function testing in children with growth failure and sellar lesions, and vigilance in evaluating pediatric thyroid nodules given their elevated risk of malignancy.
Adrenal insufficiency (AI) is characterized by glucocorticoid deficiency, with symptoms such as fatigue and hypoglycemia. Since AI presents with various severities in actual clinical settings, its evaluation using endocrine stress tests also requires a graded and comprehensive interpretation. We aimed to classify AI severity in patients who underwent endocrine stress tests and analyze their clinical characteristics using real-world medical data. This cross-sectional study was conducted at Tokyo Rosai Hospital. Inpatients who underwent endocrine stress tests, including the insulin tolerance test, corticotropin-releasing hormone stimulation test, and standard-dose and low-dose corticotropin stimulation tests. Patients were classified into 3 groups based on hormone responses: overt AI, suspected early-stage AI, and normal adrenal function. Clinical characteristics, laboratory findings, and treatment interventions were analyzed across groups. The 104 patients (mean age: 46.4 ± 13.5 years, 18.9% male, body mass index: 24.3 ± 6.7) exhibited low cortisol levels and fatigue. Among 90 patients completing severity-classifying tests, 19 (21.1%) had overt AI, 38 (42.2%) had suspected early-stage AI, and 33 (36.7%) had normal adrenal function. Corticotropin-releasing hormone stimulation test results indicated varying pituitary-adrenal axis function based on AI severity. In routine care, a pragmatic classification combining stress tests can help stratify suspected cases. These findings underscore the importance of flexible and comprehensive interpretation of dynamic endocrine stress tests to detect diverse and subtle dysfunctions of the hypothalamic-pituitary-adrenal axis.
Endocrine emergencies, although uncommon, are potentially life-threatening and require prompt diagnosis and timely intervention. Although diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are well described, data on nondiabetic endocrine emergencies remain limited, particularly from low-resource settings. This study aimed to evaluate spectrum, clinical characteristics, and outcomes of endocrine emergencies presenting to a tertiary care hospital in North India. A prospective observational study was conducted over 18 months at a tertiary care academic hospital in North India. Patients aged ≥12 years presenting to the emergency department with endocrine emergencies were included. Clinical details, biochemical parameters, and outcomes were systematically recorded and analyzed. A total of 212 patients were enrolled, with an incidence of 1.82 per 1000 emergency visits annually. DKA was the most frequent diagnosis (69.3%), followed by hypercalcemia (11.3%) and hypoglycemia (7.1%). HHS accounted for 3.8% of cases and had the highest mortality (50%). All patients with thyroid storm (n = 3) succumbed. Myxedema coma had a mortality rate of 33.3%. In DKA, older age, reduced estimated glomerular filtration rate, and higher plasma osmolality were associated with poor outcomes. In HHS, nonsurvivors had significantly higher osmolality (P = .029). DKA is common and treatable, whereas HHS and thyroid storm carry high mortality, warranting early recognition and aggressive management.
Gender-affirming hormone therapy (GAHT) improves psychological well-being in transfeminine individuals but may cause endocrine alterations, including hyperprolactinemia and, rarely, pituitary adenomas. We report the youngest known case of galactorrhea and pituitary microadenoma associated with unsupervised GAHT, highlighting multifactorial contributing factors. An 18-year-old transfeminine youth presented with galactorrhea while taking self-administered GAHT without medical supervision. Laboratory testing showed elevated prolactin, and magnetic resonance imaging revealed a pituitary microadenoma. Contributing factors included high-dose estradiol, cyproterone acetate, concomitant antiretroviral and antidepressant therapy, and frequent breast massage. This case highlights the endocrine vulnerability of adolescents using unsupervised GAHT. The combined effects of estrogen excess, antiandrogen therapy, serotonergic and dopaminergic modulation, and mechanical breast stimulation likely contributed to hyperprolactinemia. Limited pediatric data and lack of structured hormonal monitoring delayed diagnosis and optimal management. Multidisciplinary care integrating endocrine follow-up and mental health support is essential to ensure treatment safety. Unsupervised GAHT in adolescents can lead to significant endocrine complications through multifactorial mechanisms. Early recognition, structured monitoring, and coordinated multidisciplinary care are crucial to balance gender-affirming goals with patient safety.
Internal carotid artery aneurysms are rare and can lead to hypopituitarism due to their mass effect. Hypopituitarism triggered by aneurysmal compression may persist, and postsurgical restoration of pituitary function is challenging, often necessitating long-term hormone replacement therapy. We herein report a case of hypopituitarism caused by intrasellar aneurysm. A 77-year-old female with history of left eye blindness, Hashimoto's thyroiditis, and chronic kidney disease presented with nausea, vomiting, malaise, and altered mental status. Physical examination was unremarkable with no visual field or neurologic deficits except for blindness in left eye. The patient was noted to have hyponatremia which prompted checking serum cortisol level and endocrinology consultation. Workup demonstrated secondary adrenal insufficiency with low cortisol and low adrenocorticotropic hormone, central hypogonadism, and secondary hypothyroidism with low serum thyroid-stimulating hormone and low free thyroxine level. Prolactin was mildly elevated, likely due to stalk effect. Imaging revealed 2.3 × 3.1 × 2.3 cm right cavernous carotid aneurysm in the sella extending into the suprasellar cistern. Hydrocortisone therapy was started, and levothyroxine dose was adjusted which improved her mental status. Subsequently, the patient underwent stent-assisted coil embolization after unsuccessful placement of a flow diversion device by neurosurgery. The patient continues to be on hormone replacement therapy. Close monitoring of pituitary hormones is required in the context of giant intrasellar aneurysms, given their potential to induce pituitary dysfunction through mass effect. Timely diagnosis and intervention are paramount to prevent fatal outcomes.