Evaluation of Cardiovascular Risk With Arterial Stiffness in Patients With Nonfunctioning Pituitary Adenoma

Çağır, Yavuz; Altay, Mustafa; Çağır, Büşra Betül; Çakal, Erman; Akkan, Tolga; Yıldız, Canan; Ünsal, Yasemin Aydoğan; Dağdeviren, Murat; Beyan, Eśin

doi:10.4158/ep-2018-0122

Cited by 3 publications

(1 citation statement)

References 18 publications

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“…Due to the benign nature of PAs, however, cardiovascular disease is the leading cause of death in PA patients, accounting for 40% of all deaths ( 14 ). While most notable in cases of acromegaly and Cushing disease, both patients with functional and nonfunctional pituitary adenomas have been shown to carry an increased risk for cardiovascular disease comorbidity and mortality ( 15 – 17 ).…”

Section: Introductionmentioning

confidence: 99%

Pituitary adenomas and cerebrovascular disease: A review on pathophysiology, prevalence, and treatment

Osorio

Choudhary

et al. 2022

Front. Endocrinol.

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Pituitary adenomas (PAs) have been shown to cause excess cardiovascular disease comorbidity and mortality. Cerebrovascular disease (CeVD) is a small subset of cardiovascular disease with high morbidity, and its risk in patients with pituitary adenomas has been sparingly explored. In this review, we examine what is known about the prevalence of cerebrovascular disease in patients with PAs, from its initial discovery in 1970 to present. An abundance of literature describes increased cerebrovascular mortality in patients with acromegaly, while research on other PA subtypes is less frequent but shows a similarly elevated CeVD mortality relative to healthy populations. We also review how cerebrovascular risk changes after PAs are treated, with PA treatment appearing to prevent further accumulation of cerebrovascular risk without reversing prior elevations. While acromegaly-associated CeVD appears to be caused by elevated growth hormone (GH) levels and Cushing disease’s elevated glucocorticoids similarly cause durable alterations in cerebrovascular structure and function, less is known about the mechanisms behind CeVD in other PA subpopulations. Proposed pathophysiologies include growth hormone deficiency inducing vessel wall damage or other hormone deficits causing increased atherosclerotic disease. Early diagnosis and treatment of PAs may be the key to minimizing lifetime CeVD risk elevations. More research is needed to better understand the mechanisms behind the increased CeVD seen in patients with PAs. Physicians caring for PA patients must remain vigilant for signs and symptoms of cerebrovascular disease in this patient population.

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Section: Introductionmentioning

confidence: 99%

Pituitary adenomas and cerebrovascular disease: A review on pathophysiology, prevalence, and treatment

Osorio

Choudhary

et al. 2022

Front. Endocrinol.

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Meta-Analysis of Randomized Clinical Trials on the Speed of Pulse Wave Propagation

Gharamyan

2023

BIOPHYSICS

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Central and peripheral blood pressures and arterial stiffness increase in hypoparathyroidism

Pamuk¹,

Akkan²,

Dağdeviren³

et al. 2020

Archives of Endocrinology and Metabolism

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Objective:The aim of the present study was to evaluate whether arterial stiffness is affected in the patients with hypoparathyroidism through pulse wave analysis (PWA). Subjects and methods: Sixty-three patients diagnosed with hypoparathyroidism and sixty volunteers were evaluated for the study. When 21 patients were excluded in the hypoparathyroidism group due to exclusion criteria, the research continued with 42 patients and 60 volunteers who are similar to the patients in terms of age, gender and body mass index (BMI). Fasting plasma glucose after 10 hours of fasting, creatinine, thyroid stimulating hormone (TSH), free thyroxine (fT4), albumin, calcium, phosphorus, magnesium, 25-OH vitamin D, parathormone (PTH) and urine calcium results in 24-hour urine for the patients in the hypoparathyroidism group were recorded. Evaluation of arterial stiffness was performed by Mobil-O-Graph 24h PWA device. Results: Systolic blood pressure (SBP) (p = 0.01), diastolic blood pressure (DBP) (p = 0.005), mean blood pressure (p = 0.009), central SBP (p = 0.004), central DBP (p = 0.01) and pulse wave velocity (PWV) (p = 0.02) were found higher in the hypoparathyroidism group. A positive correlation was detected between phosphorus level and SBP [(p = 0.03. r = 0.327)], central SBP [(p = 0.04, r = 0.324)] and PWV [(p = 0.003, r = 0.449)]. We detected that age and serum phosphorus levels were independent predictor variables for PWV (B = 0.014, p < 0.001 and B = 0.035, p < 0.001, respectively). Conclusion: We detected that hypoparathyroidism causes an increase in blood pressure and arterial stiffness. The most significant determinant factors were detected as advanced age and hyperphosphatemia. The patients diagnosed with hypoparathyroidism should be closely monitored and treatment planning should include to prevent the patients from hyperphosphatemia.

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Evaluation of Cardiovascular Risk With Arterial Stiffness in Patients With Nonfunctioning Pituitary Adenoma

Cited by 3 publications

References 18 publications

Pituitary adenomas and cerebrovascular disease: A review on pathophysiology, prevalence, and treatment

Pituitary adenomas and cerebrovascular disease: A review on pathophysiology, prevalence, and treatment

Meta-Analysis of Randomized Clinical Trials on the Speed of Pulse Wave Propagation

Central and peripheral blood pressures and arterial stiffness increase in hypoparathyroidism

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