Wang Ling, Sun Yushi, Zhang Meng, He Hairong, Wang Jingya, Xu Huayang, Hao Yang, Zhang Wenqiang, Wang Yawen, Chong Kelvin K L, Guo Hui, Shi Bingyin, Wang Yue
Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Center of Investigator Initiated Trials, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Front Endocrinol (Lausanne). 2025 Apr 11;16:1548953. doi: 10.3389/fendo.2025.1548953. eCollection 2025.
Hypertension is a common adverse event after systemic glucocorticoid therapy. Previous studies have suggested that blood pressure (BP) regulation is related to serum calcium. However, whether serum calcium affects the risk of glucocorticoid-induced hypertension remains understudied.
We used data from thyroid-associated ophthalmopathy (TAO) patients who completed a course of intravenous methylprednisolone (IVMP). Patients with high BP at baseline, a history of hypertension, and missing data were excluded. Glucocorticoid-induced hypertension was defined as systolic BP (SBP) ≥ 140 mmHg or diastolic BP (DBP) ≥ 90 mmHg during follow-up. Multivariate logistic regression and generalized additive models were used to investigate the associations between serum calcium and glucocorticoid-induced hypertension. Bar charts were used to compare the SBP and DBP fluctuations between patients with and without hypocalcemia. After accounting for missing data, all analyses were repeated in the imputed cohort.
Serum calcium was negatively correlated with glucocorticoid-induced hypertension after adjusting for covariates with p-value < 0.1 (including age, body mass index, SBP, and DBP). For each 0.1 mmol/L increase in serum calcium, the OR (95% CI) was 0.61 (0.39, 0.95). Furthermore, a nonlinear relationship was observed, with an inflection point at 2.10 mmol/L. After the serum calcium level was converted into a categorical variable, hypocalcemia was positively associated with glucocorticoid-induced hypertension (OR = 3.26, 95% CI = 1.11-9.53). Patients with hypocalcemia exhibited significantly greater SBP fluctuations than patients without hypocalcemia (p < 0.05). These results were stable when adjusting for confounders and in the analyses of the imputed cohort.
Hypocalcemia was associated with glucocorticoid-induced hypertension in TAO patients. Further research is needed to confirm these findings in larger populations and to investigate whether calcium supplementation before glucocorticoid therapy may reduce such risk.
高血压是全身糖皮质激素治疗后常见的不良事件。既往研究提示血压调节与血清钙有关。然而,血清钙是否影响糖皮质激素诱导的高血压风险仍研究不足。
我们使用了完成静脉注射甲泼尼龙(IVMP)疗程的甲状腺相关性眼病(TAO)患者的数据。排除基线时血压高、有高血压病史及数据缺失的患者。糖皮质激素诱导的高血压定义为随访期间收缩压(SBP)≥140 mmHg或舒张压(DBP)≥90 mmHg。采用多因素逻辑回归和广义相加模型研究血清钙与糖皮质激素诱导的高血压之间的关联。使用柱状图比较有和无低钙血症患者的SBP和DBP波动情况。在考虑数据缺失后,在插补队列中重复所有分析。
在校正协变量(p值<0.1,包括年龄、体重指数、SBP和DBP)后,血清钙与糖皮质激素诱导的高血压呈负相关。血清钙每增加0.1 mmol/L,比值比(OR,95%置信区间)为0.61(0.39,0.95)。此外,观察到一种非线性关系,拐点为2.10 mmol/L。将血清钙水平转换为分类变量后,低钙血症与糖皮质激素诱导的高血压呈正相关(OR = 3.26,95%置信区间 = 1.11 - 9.53)。低钙血症患者的SBP波动明显大于无低钙血症患者(p < 0.05)。在校正混杂因素时以及在插补队列分析中,这些结果是稳定的。
低钙血症与TAO患者糖皮质激素诱导的高血压有关。需要进一步研究在更大人群中证实这些发现,并研究糖皮质激素治疗前补钙是否可降低此类风险。