Chronic hypopituitarism is uncommon in survivors of aneurysmal subarachnoid haemorrhage

Hannon, Mark J; Behan, Lucy Ann; O'Brien, M. M.; Tormey, William; Javadpour, Mohsen; Sherlock, Mark; Thompson, Christopher J.

doi:10.1111/cen.12533

Cited by 26 publications

(19 citation statements)

References 31 publications

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“…Thus, the prevalence obtained from our analysis in the acute phase is higher compared to their results because we included endocrinal dysfunction in the very acute phase of aSAH (including \3 months). Many results from authors who studied both the acute and the chronic phase [10,18,20,44] confirm the improving trend of pituitary dysfunction with time. However, some authors [24,25] reported that new onset of hormone deficiency can occur in the follow up period as well.…”

Section: Prevalence Of Pituitary Dysfunctionmentioning

confidence: 73%

“…Some are focused on the acute phase of aSAH [13,15], others on the chronic phase of aSAH [16,17], while some adress both [10,18]. There is substantial heterogeniety in the conclusions of these studies: although some suggest that hypopituitarism after aSAH affects only exceptional cases [19,20], others describe a high incidence reaching up to 50 % of cases [9,11,14]. Further, the clinical impact of any endocrine abnormalities that are present after aSAH remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

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Clinical prevalence and outcome impact of pituitary dysfunction after aneurysmal subarachnoid hemorrhage: a systematic review with meta-analysis

et al. 2016

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Section: Prevalence Of Pituitary Dysfunctionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Clinical prevalence and outcome impact of pituitary dysfunction after aneurysmal subarachnoid hemorrhage: a systematic review with meta-analysis

et al. 2016

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“…Several patients with Sheehan's syndrome have demonstrated acquired FVIII and vWF deficiency, thrombocytopenia, shorter PT and aPTT and higher FBG levels (111). The incidence of hypopituitarism after aneurysmal subarachnoid haemorrhage is unclear because of conflicting reports in the literature (112,113).…”

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

101

107

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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.

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“…In a well-designed study by Gardner, using two different confirmatory tests for GHD adjusted for body mass index (BMI), 12% of patients had hypopituitarism at 12 months (88). GH deficiency is most common pituitary hormone deficiency reported after SAH (49,69,89). Pituitary hormone deficiencies after SAH recover in the majority of cases.…”

Section: Chronic Hypopituitarismmentioning

confidence: 99%

“…Pituitary hormone deficiencies after SAH recover in the majority of cases. For instance, in a prospective study of 100 SAH patients, 14% had acute glucocorticoid deficiency defined by inappropriately low plasma cortisol concentrations (89). However, only two of 41 (5%) had long-term ACTH deficiency and four of 41 (10%) had GHD when formally tested, with either insulin hypoglycaemia or, if contraindicated, glucagon or Synacthen testing, at a median of 15 months (89).…”

Section: Chronic Hypopituitarismmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

Garrahy

Sherlock

Thompson

2017

European Journal of Endocrinology

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Advances in the management of traumatic brain injury, subarachnoid haemorrhage and intracranial tumours have led to improved survival rates and an increased focus on quality of life of survivors. Endocrine sequelae of the acute brain insult and subsequent neurosurgery, peri-operative fluid administration and/or cranial irradiation are now well described. Unrecognised acute hypopituitarism, particularly ACTH/cortisol deficiency and diabetes insipidus, can be life threatening. Although hypopituitarism may be transient, up to 30% of survivors of TBI have chronic hypopituitarism, which can diminish quality of life and hamper rehabilitation. Patients who survive SAH may also develop hypopituitarism, though it is less common than after TBI. The growth hormone axis is most frequently affected. There is also accumulating evidence that survivors of intracranial malignancy, who have required cranial irradiation, may develop hypopituitarism. The time course of the development of hormone deficits is varied, and predictors of pituitary dysfunction are unreliable. Furthermore, diagnosis of GH and ACTH deficiency require dynamic testing that can be resource intensive. Thus the surveillance and management of neuroendocrine dysfunction in neurosurgical patients poses significant logistic challenges to endocrine services. However, diagnosis and management of pituitary dysfunction can be rewarding. Appropriate hormone replacement can improve quality of life, prevent complications such as muscle atrophy, infection and osteoporosis and improve engagement with physiotherapy and rehabilitation.

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Chronic hypopituitarism is uncommon in survivors of aneurysmal subarachnoid haemorrhage

Abstract: Both anterior and posterior hypopituitarism are very uncommon following SAH and are not predicted by acute clinical, haemodynamic or endocrinological parameters. Routine neuroendocrine screening is not justified in SAH patients.

Cited by 26 publications

References 31 publications

Clinical prevalence and outcome impact of pituitary dysfunction after aneurysmal subarachnoid hemorrhage: a systematic review with meta-analysis

Clinical prevalence and outcome impact of pituitary dysfunction after aneurysmal subarachnoid hemorrhage: a systematic review with meta-analysis

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

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

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