Glucocorticoid replacement therapy and fibrinolysis in patients with hypopituitarism

Peacey, Steven R.; Wright, Dianne; Aye, Mo; Moisey, Robert

doi:10.1111/j.1365-2265.2011.04314.x

Cited by 5 publications

(2 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peacey et al (115) found that an increased dose of HCT for 2 weeks did not significantly affect PAI1, tPA or FBR levels in patients with hypopituitarism.…”

Section: Secondary Aimentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

107

View full text Add to dashboard Cite

Glucocorticoids (GCs) target several components of the integrated system that preserves vascular integrity and free blood flow. Cohort studies on Cushing's syndrome (CS) have revealed increased thromboembolism, but the pathogenesis remains unclear. Lessons from epidemiological data and post-treatment normalisation time suggest a bimodal action with a rapid and reversible effect on coagulation factors and an indirect sustained effect on the vessel wall. The redundancy of the steps that are potentially involved requires a systematic comparison of data from patients with endogenous or exogenous hypercortisolism in the context of either inflammatory or non-inflammatory disorders. A predominant alteration in the intrinsic pathway that includes a remarkable rise in factor VIII and von Willebrand factor (vWF) levels and a reduction in activated partial thromboplastin time appears in the majority of studies on endogenous CS. There may also be a rise in platelets, thromboxane B2, thrombin-antithrombin complexes and fibrinogen (FBG) levels and, above all, impaired fibrinolytic capacity. The increased activation of coagulation inhibitors seems to be compensatory in order to counteract disseminated coagulation, but there remains a net change towards an increased risk of venous thromboembolism (VTE). Conversely, GC administered in the presence of inflammation lowers vWF and FBG, but fibrinolytic activity is also reduced. As a result, the overall risk of VTE is increased in long-term users. Finally, no studies have assessed haemostatic abnormalities in patients with Addison's disease, although these may present as a consequence of bilateral adrenal haemorrhage, especially in the presence of antiphospholipid antibodies or anticoagulant treatments. The present review aimed to provide a comprehensive overview of the complex alterations produced by GCs in order to develop better screening and prevention strategies against bleeding and thrombosis.

show abstract

“…Peacey et al (115) found that an increased dose of HCT for 2 weeks did not significantly affect PAI1, tPA or FBR levels in patients with hypopituitarism.…”

Section: Secondary Aimentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Isidori

Minnetti

Sbardella

et al. 2015

European Journal of Endocrinology

107

View full text Add to dashboard Cite

show abstract

“…[ 39 ] Furthermore, glucocorticoid (GC) over-replacement and a lack of sex steroids contribute to impaired metabolic parameters and atherogenesis in patients with hypopituitarism. [ 40 41 ]…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risk Factors in Sheehan’s Syndrome: A Case-Control Study

Agrawal,

Yadav,

Singh

et al. 2024

Indian Journal of Endocrinology and Metabolism

View full text Add to dashboard Cite

Introduction: Obesity, dyslipidaemia and insulin resistance are associated with hypopituitarism. The association between these conditions and Sheehan’s syndrome (SS) caused by post-partum pituitary gland necrosis is poorly understood. This study aimed to assess cardiovascular risk surrogate markers in SS patients, and we compared clinical, biochemical and radiological testing with healthy controls. Methods: In this cross-sectional study, we studied 45 patients with SS on standard replacement therapy and compared them with healthy controls. All subjects underwent anthropometric, inflammatory marker and hormonal measurement (adrenocorticotropic hormone (ACTH), stimulated cortisol, insulin-like growth factor-1 (IGF-1), thyroxine (T4), follicle-stimulating hormone (FSH), luteinising hormone (LH), oestradiol (E2), prolactin (Prl), insulin, interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP)). Carotid intima-media thickness (CIMT), flow-mediated dilation (FMD) and echocardiography were also performed. Results: The mean age and body mass index (BMI) of SS patients were 48.1 ± 10.0 years and 24.3 ± 4.3 kg/m2, respectively, while those of controls were 44.6 ± 12.0 years and 24.6 ± 3.2 kg/m2, respectively. Systolic blood pressure was significantly higher in SS (124.6 ± 20.8 vs. 117.0 ± 18.6 mm of Hg, P < 0.05). All SS patients were hypothyroid, and all except one were hypocortisolaemic. Triglyceride (TG) levels were significantly higher in SS patients (165.6 ± 83.3 vs. 117.2 ± 56.1, P < 0.01), but no difference in the prevalence of metabolic syndrome (MetS) was found. hs-CRP (9.1 (5.2–18.5) vs. 1.5 (0.6–2.8), P < 0.001) and IL-6 (4.9 (3.7–7.3) vs. 3.1 (2.0–4.2), P < 0.001) were significantly higher in SS patients. CIMT was significantly increased in SS patients, but no difference in FMD was found. Echocardiography revealed no significant difference in left ventricular (LV) dimensions, interventricular thickness, posterior wall thickness, ejection fraction, LV mass and diastolic function. Conclusion: SS patients show increased cardiovascular risk with hypertension, dyslipidaemia and increased atherosclerotic and inflammatory markers.

show abstract

Growth hormone replacement normalizes impaired fibrinolysis: New insights into endothelial dysfunction in patients with hypopituitarism and growth hormone deficiency

Miljić

Doknic

et al. 2013

Growth Hormone & IGF Research

View full text Add to dashboard Cite

Glucocorticoid replacement therapy and fibrinolysis in patients with hypopituitarism

Abstract: An increased dose of hydrocortisone for 2 weeks creates excessive glucocorticoid exposure, but does not significantly affect fibrinolytic-coagulation parameters.

Cited by 5 publications

References 38 publications

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

MECHANISMS IN ENDOCRINOLOGY: The spectrum of haemostatic abnormalities in glucocorticoid excess and defect

Cardiovascular Risk Factors in Sheehan’s Syndrome: A Case-Control Study

Growth hormone replacement normalizes impaired fibrinolysis: New insights into endothelial dysfunction in patients with hypopituitarism and growth hormone deficiency

Contact Info

Product

Resources

About