Haemostatic Mechanisms are Normal Despite Increased Vascular Mortality in Hypopituitary Adults

Beshyah, Salem A.; Markussis, V.; Harbourne, T.; An, Nicolaides; Johnston, Desmond G.

doi:10.1055/s-2007-1002144

Cited by 10 publications

(8 citation statements)

References 8 publications

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“…(1990) showed normal levels of plasma fibrinogen, tissue plasminogen activator, fibronectin, factor VIII and Von Willbrand factor in 22 GH‐deficient adults, mainly of childhood onset disease. Plasma fibrinogen, euglobulin lysis time (ECLT), plasminogen activator inhibitor‐1 (PAI‐1) and prothrombin III were normal in 23 hypopituitary adults compared with 21 matched controls (Beshyah et al ., 1993). However, Johansson et al .…”

Section: Cardiovascular Risk Factors In Hypopituitarismcontrasting

confidence: 55%

“…Jorgensen et al (1990) showed normal levels of plasma fibrinogen, tissue plasminogen activator, fibronectin, factor VIII and Von Willbrand factor in 22 GH-deficient adults, mainly of childhood onset disease. Plasma fibrinogen, euglobulin lysis time (ECLT), plasminogen activator inhibitor-1 (PAI-1) and prothrombin III were normal in 23 hypopituitary adults compared with 21 matched controls (Beshyah et al, 1993). However, Johansson et al (1994) comparing 20 hypopituitary adults and 20 matched controls demonstrated higher plasma fibrinogen (3·2 Ϯ 0·7 vs 2·4 Ϯ 0·6 g/l, P < 0·0001) and PAI-1 activity 13·2 Ϯ 10·6 vs 6·8 Ϯ 4·3 U/ml, P ¼ 0·013) in the patients, suggestive of a defective fibrinolytic system.…”

Section: Haemostatic Mechanismsmentioning

confidence: 99%

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Cardiovascular disease and risk factors in adults with hypopituitarism

Beshyah¹,

Johnston²

1999

Clinical Endocrinology

119

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In 1992, Cuneo et al. (1992) reviewed, in this journal, the consequences of growth (GH) deficiency during adult life and coined the term 'Growth hormone deficiency (GHD) syndrome in adults'. Limited information was available then on cardiovascular disease and risk factors in adults with hypopituitarism. More data have been published since on cardiovascular morbidity in symptom-free hypopituitary adults. Several groups have also published results on the effects of GH therapy on cardiac structure and function and on the cardiovascular risk factors.We shall review here the epidemiological and experimental data on cardiovascular morbidity and mortality in adult hypopituitarism. We shall also examine the prevalence of cardiovascular risk factors in this group of patients and their potential causes focusing on the possible role of GH deficiency and the effects of GH replacement. Cardiovascular disease in hypopituitarism

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Section: Cardiovascular Risk Factors In Hypopituitarismcontrasting

confidence: 55%

Section: Haemostatic Mechanismsmentioning

confidence: 99%

Cardiovascular disease and risk factors in adults with hypopituitarism

Beshyah¹,

Johnston²

1999

Clinical Endocrinology

119

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“…A prothrombotic state has been described in patients with hypopituitarism in whom plasma fibrinogen and plasminogen activator inhibitor-1 activity was increased (17), although this has not been confirmed in other studies (61,62).…”

Section: Other Cardiovascular Factorsmentioning

confidence: 89%

Cardiovascular risk factors in hypopituitary GH-deficient adults

Verhelst¹,

Abs²

2009

European Journal of Endocrinology

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Design: Data on lipids, body composition, and blood pressure (BP) from all published KIMS papers are summarized and compared with a literature review. Results: KIMS data confirm and extend previous research showing that adults with GH deficiency (GHD) have an adverse cardiovascular risk profile. GHD patients have high levels of dyslipidemia, elevated body mass index, unfavorable waist-to-hip ratio and body composition, and a high risk of hypertension. These abnormalities are likely to explain the increased cardiovascular mortality observed in patients with hypopituitarism. When given GH replacement therapy, an improvement is seen in KIMS as well as earlier studies for lipid profile, body composition, and BP. The added value of the different KIMS papers over previous research is that KIMS involves a much larger number of patients, that lipid concentrations and IGF1 are measured in a single central laboratory, and that the effects of GH replacement therapy can be followed longer than the duration of earlier trials. By the large number of patients, KIMS gives insight into the effects of GH in different patients' subgroups such as elderly patients, patients with idiopathic GHD, patients with craniopharyngioma, patients after irradiation, and so on. In addition, KIMS has made it possible to calculate more exactly the influence of baseline parameters on these cardiovascular risk parameters and their response to GH. Conclusions: Taken together, data from KIMS confirm earlier knowledge about the important benefits of GH replacement therapy, but also on the use of GH in specific subgroups such as isolated GHD, patients above 65 years, and patients after irradiation. No subgroup yet has been identified as not responding well to GH.

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“…In particular high fibrinogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) levels which normalized with treatment have been described both in GHD and acromegalic patients (Wildbrett et al, 1997;Johansson et al, 1994;Sartorio et al, 1995;Johansson et al, 1996). With the exception of hyperfibrinogenaemia in acromegaly, these results are in contrast with previous observations showing normal haemostatic and fibrinolytic parameters in these two clinical conditions (Jùrgensen et al 1990;Markussis et al, 1992;Scelles et al, 1992, Beshyah et al, 1993Landin-Wilhelmsen et al, 1997).…”

Section: Introductionmentioning

confidence: 87%

Alterations of haemostatic and fibrinolytic markers in adult patients with growth hormone deficiency and with acromegaly

Sartório

Cattaneo

Bucciarelli

et al. 2000

Exp Clin Endocrinol Diabetes

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Alterations of coagulation and fibrinolytic systems might contribute to the increased cardiovascular and cerebrovascular mortality observed in patients with both chronic growth hormone (GH) excess (acromegaly) and deficiency (GHD). However, contrasting results have been so far reported. To assess the importance of GH in modulating haemostatic system, several haemostatic variables in patients with GHD and acromegaly were measured. Twenty-four adult patients with GHD (8 childhood- and 16 adult-onset; age: 41+/-12 years, insulin like growth factor-I, IGF-I: 6.7+/-4 nmol/L), 10 non-diabetic acromegalic patients (age: 39+/-15 years; IGF-I: 109+/-37 nmol/L) and 64 healthy volunteers age- and sex-matched with cases were studied. The plasma levels of tissue-type plasminogen activator antigen (t-PA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) were measured by ELISA. Plasminogen activator inhibitor type I (PAI-1) was measured by an immunoactivity assay and fibrinogen by von Clauss method. GH levels were measured by IFMA and IGF-I by RIA. GHD patients had higher PAI-1 (12.7+/-16.7 vs 4.8+/-5.3 U/ml, p<0.01), fibrinogen (363+/-104 vs 291+/-71 mg/dL, p< 0.05) and TAT levels (6.8+/-9 vs 3.6+/-2.8 ng/ml, p<0.05) than controls. Taking the 95th pecentile of the normal distribution in the control group as the cut-off point for normal plasma levels of the haemostatic variables, high PAI levels were found in 25% of patients with GHD (P<0.01), while high fibrinogen and TAT levels were observed in 21% (P<0.05). The alterations were mostly present in patients with adult-onset GHD, with the exception of hyperfibrinogenaemia which was equally present in adult- and childhood-onset patients. Acromegalic patients had higher mean fibrinogen levels than controls (398+/-111 vs 291+/-71 mg/dL, p< 0.05), 40% having hyperfibrinogenaemia (P<0.01, vs controls). They also had t-PA levels lower than controls and GHD. No correlations between hormonal and haemostatic variables were found. Body mass index and waist to hip ratio correlated positively with PAI-1 levels in GHD patients only. In conclusion, this study shows that several abnormalities of coagulation variables (increased PAI-1. fibrinogen and TAT levels) are present in patients with GHD, while only hyperfibrinogenaemia is found in patients with acromegaly. These changes do not appear to be directly related to IGF-I levels or to the degree of GH deficiency/excess. However, these abnormalities may be an additional trigger for the development of coronary heart disease and thromboembolic complications mostly in patients with GHD.

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Haemostatic Mechanisms are Normal Despite Increased Vascular Mortality in Hypopituitary Adults

Cited by 10 publications

References 8 publications

Cardiovascular disease and risk factors in adults with hypopituitarism

Cardiovascular disease and risk factors in adults with hypopituitarism

Cardiovascular risk factors in hypopituitary GH-deficient adults

Alterations of haemostatic and fibrinolytic markers in adult patients with growth hormone deficiency and with acromegaly

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