Diabetes Insipidus

Author: Gianpiero Pescarmona
Date: 13/02/2024


Endocrine manifestations of histiocytosis, 1981

  • Diabetes insipidus and growth retardation are the prominent endocrine manifestations of histiocytosis. Galactorrhea, hypogonadism, and panhypopituitarism are rarely associated with this disorder. To date, the vast majority of morphologic and functional studies of the pituitary and hypothalamus in affected patients indicate that histiocytic infiltration results in a hypothalamic dysfunction with a secondary partial or complete hypopituitarism. This hypopituitarism is due to deficient trophic stimulation or inhibition by hypothalamic releasing or inhibitory factors.



Diabetes Insipidus and Galactorrhea Caused by Histiocytosis X,1975

  • A 44-year-old woman with diabetes insipidus of 3 years duration was found to have histiocvtosis X. This was based on clinical, radiological and pathological findings consistent with the diagnosis. Furthermore, she developed spontaneous galactorrhea during the course. Endocrine studies of hypothalamic-pituitary function revealed completely impaired secretion of gonadotropin, growth hormone and antidiuretic hormone, and possible partial impairment of adrenocorticotropic hormone secretion, while thyroid stimulating hormone secretion remained intact. Persistently elevated plasma levels of human prolactin were also demonstrated, which were unaffected by administration of either thyrotropin releasing hormone, l-DOPA or water loading, but suppressed significantly by CB-154, an ergot alkaloid. These results suggest that abnormalities of the patient's endocrine function may be mainly accounted for by a single hypothalamic lesion.


Effect of prolactin on the in vitro phagocytic capacity of macrophages, 1996

  • Abstract
    Prolactin (PRL) plays a modulatory role in immune function. Previous studies have demonstrated that physical activity (swimming until exhaustion) provokes a stimulation in the phagocytic function of peritoneal macrophages. In this study, we have investigated the possible role of PRL as a mediator of physical activity-induced stimulation of macrophage phagocytosis. Peritoneal macrophages from
    mice were incubated for 30 min with 1.1 (basal concentration in these animals), 2.2 (the concentration observed in plasma after swimming until exhaustion) and 8, 16 and 22,000 ng/ml of PRL. The results indicated that incubation of peritoneal macrophages with a concentration of PRL similar to that observed in plasma immediately after physical activity stress stimulates phagocytic capacity. This stimulation was also observed after incubation of macrophages with the higher concentrations of PRL. We conclude that PRL may be considered as a mediator of physical activity-induced stimulation of macrophage phagocytosis, confirming the immunoregulatory role of this hormone.

Enhancement of murine bone marrow macrophage differentiation by beta- endorphin, 1995

  • The present study was performed to investigate the effect of beta- endorphin on macrophage colony-stimulating factor (M-CSF)-induced differentiation of macrophages from bone marrow cells in a semisolid culture system. beta-endorphin increased the number of macrophage colonies when bone marrow cells were cultured in the presence of M-CSF plus lipopolysaccharide (LPS).


AddThis Social Bookmark Button