Background: Transgender individuals often require gender-affirming interventions, such as endogenous sex hormone inhibition or gender-affirming hormone therapy (HT), while there is discordance between their body and gender identity. However, a recent study found that the incidence of cardiovascular events is higher in transgender patients receiving cross-sex HT. The aim of this study was to investigate the metabolic effects of an altered sex hormone profile. Methods: This retrospective study, conducted in a referral center in Northern Taiwan, analyzed metabolic changes over time in 65 trans masculine and 45 trans feminine persons. The transgender individuals were examined at 4 time points: before the gender affirming HT, as well as 3, 6, and 12 months following treatment. Results: Compared with baseline measurements, the trans masculine patients showed significant increases in body mass index (BMI) (22.6 ± 0.3 vs 23.3 ± 0.4 kg/m2; p < 0.001; t = 3M), low-density lipoprotein cholesterol (124.3 ± 3.7 vs 131.3 ± 3.9 mg/dL; p = 0.03; t = 12M), creatinine (0.75 ± 0.01 vs 0.83 ± 0.14 mg/dL; p < 0.001; t = 12M), and hemoglobin (13.5 ± 0.7 vs 15.2 ± 0.2 g/dL; p < 0.001; t = 12M), as well as decreased high-density lipoprotein cholesterol (57 ± 2.1 vs 51 ± 2.0 mg/dL; p < 0.001; t = 12M). The trans feminine patients had reduced low-density lipoprotein cholesterol (104.2 ± 3.2 vs 100.8 ± 3.5 mg/dL; p = 0.05; t = 3M), hemoglobin (14.0 ± 0.1 vs 13.5 ± 0.1 g/dL; p = 0.008; t = 12M), and creatinine (0.82 ± 0.01 vs 0.79 ± 0.14 mg/dL; p < 0.001; t = 3M) compared with baseline data. In addition, most of these metabolic effects persisted during the follow-up period. Conclusion: This observational, retrospective study revealed that gender-affirming HT increased the relative cardiovascular risk in trans masculine individuals.

Diabetic dyslipidemia is characterized by elevated levels of triglycerides (TGs) and small dense low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C). 1 The atherogenic lipid profile contributes to the excess risk of cardiovascular disease (CVD) in people with type 2 diabetes mellitus (DM). 2 Current consensus for the management of diabetic dyslipidemia recommends that the primary lipid goal of treatment is LDL-C <2.6 mmol/L, and a non-HDL-C goal of <3.4 mmol/L is a secondary target for primary CVD prevention. 3,4 Extensive evidence supports these recommendations and suggests to preferably use a statin (3-hydroxy-3-methylgluatryl coenzyme A reductase inhibitor), along with lifestyle intervention, to control diabetic dyslipidemia. 4,5 For example, in the Collaborative Atorvastatin Diabetes Study (CARDS), lowering LDL-C by 40% to a mean level of 2.1 mmol/L and lowering non-HDL-C by 36% to a mean level of 2.9 mmol/L with atorvastatin monotherapy led to a 37% reduction in the relative CVD risk compared with the placebo. 6 However, statins differ in multiple characteristics, including bioavailability, potency, liver and renal metabolism, and effects on serum lipid components. 7 Head-to-head comparisons between different statins are essential for effectively managing lipid disorders, especially in specific populations with a distinct lipid profile, such as patients with DM. 7 Simvastatin, a long-established statin, is now available in generic forms. The results from the Heart Protection Study clearly demonstrated the beneficial effects of simvastatin on cardiovascular outcomes in patients with DM after 5 years of daily treatment with 40 mg simvastatin. 8 Rosuvastatin, a synthetic statin, has high potency for lowering LDL-C levels on a milligram-equivalent basis. 9 Several studies have compared the effects of rosuvastatin with those of other statins on lipid goal attainment in patients with DM. [10][11][12][13] Moreover, in a recent primary prevention study, 20 mg of rosuvastatin significantly reduced the incidence of major cardiovascular events in individuals with elevated C-reactive protein levels. 14 However, the

Background In this study, we investigated whether serum levels of advanced glycation end products (AGEs) independently correlated with relative muscle strength after adjustment for clinical variables including diabetic peripheral neuropathy in patients with type 2 diabetes. Relative muscle strength was defined as muscle strength (in decinewtons, dN) divided by total muscle mass (in kg). Methods We enrolled 152 ambulatory patients with type 2 diabetes. Each participant underwent measurements of muscle strength and total muscle mass. Serum levels of AGEs were determined. The Michigan Neuropathy Screening Instrument Physical Examination (MNSI-PE) was performed to assess diabetic peripheral neuropathy. Results The participants were divided into three groups on the basis of tertiles of serum AGEs levels. Significant differences were observed among the three groups in relative handgrip strength (71.03 ± 18.22, 63.17 ± 13.82, and 61.47 ± 13.95 dN/kg in the low-tertile, mid-tertile, and high-tertile groups, respectively, P = 0.005). The relative muscle strength of the ankle plantar flexors was higher in the low-tertile group than in the mid-tertile and high-tertile groups (107.60 ± 26.53, 94.97 ± 19.72, and 94.18 ± 16.09 dN/kg in the low-tertile, mid-tertile, and high-tertile groups, respectively, P = 0.002). After adjustment for MNSI-PE score and other clinical variables in partial correlation analysis, the correlations between serum levels of AGEs and the relative muscle strength of handgrip, ankle dorsiflexor, and ankle plantar flexor remained significant. Serum AGEs level was the only variable that remained significantly related to the relative muscle strength of handgrip, ankle dorsiflexor, and ankle plantar flexor when AGEs level, fasting plasma glucose, and glycated hemoglobin (HbA1c) were entered into multiple regression models simultaneously. Conclusions After adjustment for multiple factors including diabetic peripheral neuropathy, this study demonstrated that increased serum levels of AGEs were independently associated with decreased relative muscle strength in patients with type 2 diabetes. Compared with fasting plasma glucose and HbA1c, serum level of AGEs is more strongly associated with relative muscle strength.

Background Chronic low-grade inflammation is considered one of the major mechanisms for the progression of diabetic kidney disease. We investigated the prognostic value of circulating soluble tumor necrosis factor receptor 2 (sTNFR2) for early nephropathy in patients with type 2 diabetes. Materials and methods A total of 364 patients with type 2 diabetes and an estimated glomerular filtration rate (eGFR) ≥30 mL/min/1.73m2 were followed up for a median of 4 years. Renal outcomes were defined as a composite of either or both a >30% decline in the eGFR and/or albuminuria stage progression determined with consecutive tests. Results Seventy-three patients developed renal composite events. Serum concentrations of sTNFR2 were strongly associated with the risk of renal function decline and progressive changes in albuminuria. Through a receiver operating characteristic curve analysis, a serum sTNFR2 level of 1.608 ng/mL was adopted as the discriminator value for predicting renal outcomes (area under the curve 0.63, 95% confidence interval 0.57–0.70, p < 0.001), yielding a sensitivity of 75.3% and a specificity of 51.2%. The association of sTNFR2 levels ≥1.608 ng/mL to renal outcomes was significant after adjusting for relevant variables (hazard ratio 2.27, 95% confidence interval 1.23–4.20, p = 0.009) and remained consistent across subgroups stratified by age, sex, systolic blood pressure, eGFR, albuminuria, and the use of renin-angiotensin system blockers. Conclusions Higher circulating levels of sTNFR2 are independently associated with an eGFR decline and progressive albuminuria in patients with type 2 diabetes.