Endocrine function in multiple sclerosis

Abstract

In 31 patients with multiple sclerosis (MS) the endocrine functions of the hypothalamus, the pituitary and several peripheral endocrine glands were assessed with a combined pituitary test; 3/31 patients had an endocrine disease: one primary hypothyroidism, one primary amenorrhea and one primary male hypogonadism. We found no patient with endocrine disease of the hypothalamus, the pituitary or the adrenals. However, the poststimulatory secretion of cortisol, growth hormone or thyroid-stimulating hormone was impaired in 7/31 patients, suggesting a possible preclinical 1 endocrine insufficiency in these patients.When clinical improvement of multiple sclerosis (MS) with ACTH therapy became apparent (1,2), the question arose, whether this indicated a defect of the adrenal and/or pituitary. Measurements of cortisol and corticosteroid metabolites in urine and later in plasma showed conflicting results with normal values in some reports, yet elevated basal or depressed stimulatory values in others (3-13). The abnormal values were hypothetically related to MSinduced stress, to MS lesions in the hypothalamus, to an insufficiency of the pituitary, or to an adrenal disturbance associated with MS. Other anterior pituitary hormones also showed unexplained abnormal values in some MS patients (12, 14-16). Manifest endocrine diseases of these organs were not identfied. In fact, there are only singular reports on the coincidence of MS and such diseases (17-21).Because of the unresolved abnormal endocrine findings, we evaluated MS patients with a combined pituitary test, by which the interactions between hypothalamus, pituitary and several endocrine endorgans including the adrenals can be determined. Patients and methodsOf 101 consecutively admitted patients with clinically definite or probable MS (65 f, 36 m) 3 1 patients (16 f, 15 m) participated after thorough information and written consent. 46 patients were excluded because of medical or ethical reasons, 24 patients refused. The 3 1 patients were 20-58 years old (median 42 yrs), the disease duration was 1-21 years (median 7 yrs), the total disability score (22) was 0-2 in 18 patients, 3-5 in 7 patients, and 6-7 in 6 patients. The MS course was relapsing-remitting in 16 patients, relapsing-remitting/progressive in 10 and pri-

Coagulation status and biochemical and inflammatory markers in multiple sclerosis

“…8 Although we have not evaluated the thyroid status of our patients, both hyper-and hypothyroidism is shown in MS patients. [26][27][28] These studies suggest that MS patients may have different metabolic rates which may affect biochemical parameters. These findings should be further investigated with prospective studies using a greater number of MS subjects.…”

Acute and chronic neuroendocrine effects of interferon‐β 1a in multiple sclerosis

“…Since clinically overt or subclinical endocrinological disturbances have been described in multiple sclerosis, 7,8,10–13 these patients might also display a different endocrine response to cytokines. More specifically, Reder et al .…”

“…Because cortisol, like exogenously administered glucocorticoids, attenuates the immune response, such an endocrine effect might contribute to the therapeutic actions of IFN‐β in multiple sclerosis. Several groups have found disturbances of the hypothalamo‐pituitary‐adrenal (HPA) axis in multiple sclerosis, 7–14 suggesting that the neuroendocrine responses to IFN‐β may be altered or heterogeneous. If such responses were associated with varying therapeutic effects, they could be useful to predict benefit of treatment.…”

Heterogeneity of hypothalamic-pituitary-adrenal system response to a combined dexamethasone-CRH test in multiple sclerosis

“…From other studies in patients with MS that measured corticosteroids in plasma and urine at baseline or following stimulation conflicting data emerged, showing increased, decreased or unaltered HPA activity (Cazzullo et al, 1968;Ketelaer & Delmotte, 1972;Klapps et al, 1992;Maida & Summer, 1979;Millac et al, 1969). Following insulin hypoglycemia the plasma cortisol increase was found to be blunted in MS, which was interpreted as indicative of an impaired ability to adapt to a humoral stressor (Teasdale et al, 1967).…”