Histiocytosis of Langerhans cells and lymphocytic hypophysitis are the most common infiltrative diseases causing diabetes insipidus. About 10% of patients with histocytosis have diabetes insipidus diabetes, and polyuria may precede the detection of intracranial damage in a few months or even years. Lymphocytic infundibulo-neurohypophysitis can explain central diabetes insipidus in more than half of patients with an idiopathic form of pathology, and its association with other autoimmune diseases is possible. Magnetic resonance imaging reveals an enlarged pituitary gland and a thickening of the pituitary stalk. A biopsy of the neurohypophysis determines the lymphocytic infiltration of the pituitary gland, the pituitary stalk and the large cell hypothalamic nuclei.
Diabetes insipidus can also develop in the outcome of granulomatous lung diseases, including sarcoidosis.
The question of the possible antibody-induced destruction of vasopressin cells remains unresolved. Indeed, more than half of patients with central non-sugar diabetes of a non-traumatic nature have antibodies directed against vasopressin-containing cells. It is possible that these antibodies are not pathogenetic, but are markers of previous neuronal cell destruction.
Infections involving the base of the brain, such as meningococcal, cryptococcal, toxoplasmosis, congenital cytomegalovirus, etc., lead to the development of diabetes mellitus, often transient.