[Sarcoidosis localized in endocrine glands].

INTRODUCTION: There is a relationship between sarcoidosis and endocrine diseases: hypothalamus, hypophysis, thyroid gland, parathyroid gland, adrenal gland and calcium metabolism disorder. DISCUSSION: Neurological disorders, obesity, secondary hypogonadism, and thirst as a result of diabetes insipidus, dominate the clinical picture of hypothalanmic sarcoidosis. Diseases of adenohypophysis present with gonadotropic insufficiency and prolactin increase. They may cause disorders in menstruation and ovulation. Disorders of neurohypophysis manifest with moderate polyuria and polydipsia. Disorders of thyroid gland function in systemic sarcoidosis present with hyperthyroidism, hypothyroidism or thyroiditis. Sarcoidosis of the parathyroid gland is rare. Sarcoidosis of adrenal cortex may cause primary insufficiency of the suprarenal gland The secondary insufficiency of the suprarenal gland is caused by hypothalamic and pituitary sarcoidosis. In sarcoidosis, calcium metabolism disorder and hypercalcemia are frequent. Vitamin 1.25(OH)2D has an important role since it is increasingly produced in renal and extra renal regions. Hypercalcemia leads to hypercalciuria and nephrolithiasis, while the level of parathyroid hormone usually decreases. Increased levels of serum angiotensin converting enzyme (ACE) are also important markers in the diagnosis of sarcoidosis. CONCLUSION: Clinical manifestations of endocrine disorders depend on the localization of sarcoid lesions. The treatment of disorders is directed to the treatment of structure and functional disorders of glands involved, as well as to sarcoidosis. Successful treatment of sarcoidosis may cause regression of granulomatous lesions in the involved glands.

[Sarcoidosis and obesity].

INTRODUCTION: Polypliagia and morbid obesity appears in patients with sarcodosis may be signs of neurosarcoidosis in the medial hypothalmus where satiety center is located. It is estimated that about 1% of all patients with sarcoidosis may have sarcoidosis of the hxpothalamus. It is of utmost importance to diagnose and treat hxpothalamie sarcoidosis as early as possible, because lethality from neurosarcoidosis is active as high (10%) as the lethality from other localizations of sarcoidasis (5%). CASE REVIEWS: In a unique case report published so far, sarcoid granulomas were found by computerized tomography in the ventromedial hypothalamic nuclei of a 21-year-old man with a 7-year history of polyphagia and body mass index of 65.8. Another case report is of a 7-year-old boy with hyperphagia and obesity following an episode of meningoencephalitis, who presented with high Polypliagia insulin levels (1183 pmol/L) and strikingly high insulin release in response to glucose (7892 pmol/L) which were not accompanied by hypoglycemia. DISCUSSION AND CLUSION: These results have been supported withi experimental studies in animals. Cell groups of the medial hypothalamus are key to the regulation of energy balance. Functional disruption by colchicine injected in the hypothalamic arcuate, paraventricullar, and ventromedial cell groups produced increased food intake and obesity. After scanning, thiogliucose labeled with gold-198 (Au-198) at doses of 2 OmicroCi per patient, can be used to diagnose hypothalamic obesity in people with neurosarcoidosis, due to the ability of cell groups in hypothalamic satiety centers to take up thioglucose in their gluxcostat receptors.