Endothelial function and coagulant factors in growth hormone-treated hypopituitary adults receiving desmopressin.
Although GH deficiency may underlie the increased cardiovascular risk in adult hypopituitarism, other coexisting hormonal deficiencies and/or unphysiological hormone replacement may contribute. L-Deamino-8-D-arginine (DDAVP), when administered parenterally, potentiates hemostasis by increasing plasma procoagulant factors. We investigated whether chronic intranasal DDAVP therapy influences clotting factors (plasma fibrinogen, factor VIII, and von Willebrand factor antigen) and endothelial function (flow-mediated dilation of the brachial artery) in 30 GH-treated hypopituitary subjects, including both DDAVP-treated subjects (group A) (mean age, 46 +/- 11 yr) and vasopressin-sufficient subjects (group B) (mean age, 47 +/- 16 yr). Fifteen healthy controls (group C) (mean age, 48 +/- 12 yr) were also studied. All hypopituitary patients were receiving stable GH replacement (median duration, 19 months). Comparing the three groups, concentrations of fibrinogen (mean +/- SD) (A, 3.3 +/- 1.0 g/liter vs. B, 3.5 +/- 0.9 vs. C, 2.6 +/- 0.8, P < 0.05), factor VIII (A, 130% +/- 30% vs. B, 128% +/- 30% vs. C, 104% +/- 35%, P < 0.05) and von Willebrand factor antigen (A, 124% +/- 35% vs. B, 134% +/- 45% vs. C, 93% +/- 36%, P < 0.05) were higher in hypopituitary subjects, compared with controls. However, there were no differences in clotting factors between groups A and B. Flow-mediated dilation did not differ significantly between the two hypopituitary groups (A, 5.9% +/- 2.0% vs. B, 4.7% +/- 1.6%) and was similar to that in the control group (C, 5.7% +/- 2.1%). In conclusion, although endothelium-dependent vasodilation is intact in GH-treated hypopituitary adults, elevated concentrations of hemostatic markers suggest the persistence of a prothrombotic tendency and endothelial dysfunction. Intranasal DDAVP does not appear to influence this proatherogenic profile in hypopituitary adults with vasopressin deficiency.
Department of Medicine, University Hospital of Wales, Cardiff CF14 4XN, United Kingdom. jamie.smith@virgin.net
J C
JC
Smith
H A
HA
Lane
J
J
Lewis
S
S
Dann
J
J
Goodfellow
P
P
Collins
L M
LM
Evans
M F
MF
Scanlon
J S
JS
Davies
D000281:Administration, Intranasal; D000328:Adult; D001161:Arteriosclerosis / Q000209:etiology; D001779:Blood Coagulation Factors / Q000032:analysis*; D001916:Brachial Artery / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003430:Cross-Sectional Studies; D003894:Deamino Arginine Vasopressin / Q000627:therapeutic use*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005169:Factor VIII / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D007018:Hypopituitarism / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood; D014664:Vasodilation; D014841:von Willebrand Factor / Q000032:analysis
D001779:Blood Coagulation Factors; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D014841:von Willebrand Factor; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D005169:Factor VIII; D005340:Fibrinogen; D002784:Cholesterol; D003894:Deamino Arginine Vasopressin