Endocrine Practice最新文献

Objective: To review the pathophysiology, risk factors, clinical implications, monitoring strategies, and therapeutic approaches for glucocorticoid-induced hyperglycemia (GCIH), with a focus on patients with cancer.

Methods: This narrative review integrates findings from clinical studies, expert guidelines, and recent advances in glucose monitoring and pharmacologic therapy, particularly in oncologic settings where glucocorticoid use is common.

Results: GCIH is a frequent and often underrecognized complication, even in individuals without preexisting diabetes. In patients with cancer, GCIH is associated with increased risk of infections, chemotherapy delays, longer hospital stays, and higher mortality. Key mechanisms include enhanced insulin resistance, increased hepatic gluconeogenesis, and β-cell dysfunction. Afternoon and postprandial hyperglycemia are typical due to the pharmacodynamics of once-daily morning glucocorticoids. Self-monitoring of blood glucose (SMBG) and continuous glucose monitoring (CGM) are essential tools. HbA1c may assist in baseline assessment, but fructosamine better reflects short-term glycemic changes. Insulin is the treatment of choice for moderate to severe GCIH, with basal-bolus regimens, especially using NPH insulin aligned with glucocorticoid timing, providing effective control. Selected non-insulin agents may be considered in stable outpatients with mild hyperglycemia. However, standardized definitions, evidence-based algorithms, and randomized trials remain limited.

Conclusion: Optimal GCIH management requires proactive monitoring and individualized treatment strategies tailored to glucocorticoid type, dose, and clinical setting. Further research should aim to refine diagnostic criteria, validate therapeutic protocols, and assess emerging technologies such as automated insulin delivery systems and selective glucocorticoid receptor modulators.

Objectives: The optimal blood pressure (BP) target for stroke prevention in patients with primary aldosteronism (PA) remains to be determined. This cohort study examined the association between mean BP levels during follow-up and stroke incidence in this population.

Methods: The study retrospectively enrolled patients with PA aged ≥30 years who were hospitalized at our hypertension center between January 2008 and December 2019. The exposure variable was the mean BP from ≥3 follow-up visits per patient. The primary outcome was incident stroke during follow-up. The association of mean follow-up BP with risk of stroke was assessed using Cox proportional hazard models and restricted cubic splines.

Results: The cohort comprised 3138 patients with PA (median age 49 years, 55% male). During a median follow-up of 6 years, 101 patients experienced incident stroke (ischemic, n=79; hemorrhagic, n=22). After adjusting for age, sex,pretreatment BP, and other relevant confounders, the mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) during follow-up showed significant positive associations with the risk of incident stroke (HR 1.04, 95% CI 1.02-1.06, P<0.001 and HR 1.05, 95% CI 1.01-1.08, P=0.005, respectively). In multivariable survival analysis, compared with the SBP ≥140 mmHg group, the risk of stroke was decreased by 54% in the SBP <130 mmHg group (HR 0.46, 95% CI 0.26-0.80, P=0.006) and by 47% in the SBP 130-139 mmHg group (HR 0.53, 95% CI 0.33-0.84, P=0.007). No association was observed when DBP was analyzed categorically. When variables were modeled using restricted cubic splines, the risk of stroke increased linearly with SBP and DBP. The risk of stroke began to increase rapidly at a BP of around 133/83 mmHg. In subgroup and sensitivity analyses, the association between mean follow-up SBP and stroke incidence remained consistent.

Conclusions: A target BP of <130/80 mmHg might be associated with a reduced risk of stroke in patients with primary aldosteronism. Nevertheless, additional validation remains necessary through prospective, randomized controlled trials.