ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2007) 14 P3

Study of the hypothalamic-pituitary-adrenal axis in patients with the antiphospholipid syndrome

Renato Carignola1, Valeria Data1, Rosetta Vitetta1, Adriana Severino1, Tiziana Bertero2, Mario Bazzan3, Giuseppe Reimondo1, Fulvia Daffara1, Alberto Angeli1 & Massimo Terzolo1

1Dipartimento di Scienze Cliniche e Biologiche – Medicina Interna I, ASO San Luigi, Orbassano, Italy; 2UONA Immunologia e Allergologia Clinica, Ospedale Mauriziano, Torino, Italy; 3UOA Ematologia e Malattie Trombotiche, Humanitas Cellini, Torino, Italy.

Objective: The Antiphospholipid Syndrome (APS) is a thrombophilic disorder characterised by recurrent venous and/or arterial thromboses and increased pregnancy morbidity. There is growing evidence supporting a functional interplay between the neuroendocrine and immune system; the hypothalamic-pituitary-adreal (HPA) axis plays a pivotal role in this network. Previous studies have described normal cortisol levels in APS patients while occurrence of acute adrenal failure was reported as a manifestation of this syndrome. However, it is still unknown whether subtle alterations of the HPA axis do exist in APS patients without overt hypoadrenalism.

Method: In the present study, we performed either a low-dose (1 μg) short Synacthen test (LDSST) or a 250 μg Synacthen test (SST) in 15 subjects of both sexes with primitive APS (diagnosed according to the Sapporo Criteria) and in 11 age and sex-matched healthy subjects. In addition, the patients underwent 1 mg dexamethasone suppression test (DST). None of the evaluated subjects were receiving any drug known to affect the HPA axis. The local Ethical Committee approval has been obtained.

Results: The patients with APS showed significantly higher cortisol levels than controls either at baseline (31.2±15.6 vs. 18.3±9.0 μg/dl, P<0.01) or at +30 min following 250 μg ACTH (57.3±14.2 vs. 39.6±12.8 μg/dl, P<0.01). Cortisol levels after 1 μg ACTH were also significantly increased in the subjects with APS compared to controls (P<0.01). Moreover, in only 2 patients we observed cortisol levels lower than 1.8 μg/dl after 1 mg DST (mean, 3.4 μg/dl; range 1.4–9.2) and two patients had cortisol values above 5.0 μg/dl after suppression.

Conclusions: In conclusion, although APS may cause adrenal insufficiency in selected cases, the present data seem to suggest that the HPA axis is not suppressed in APS patients. A possible explanation might be the state of chronic stress that usually accompanies long-standing autoimmune diseases.

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