Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 59 year old man presenting fever, serum hyponatremia and hypoosmolality in association with hyperosmotic urine was hospitalized in our unit in February 1988. We demonstrated evidence of systemic sarcoidosis and inappropriate secretion of antidiuretic hormone (ADH). The patient was treated with corticosteroid therapy for a period of about 1 year, with regression of signs of the inappropriate vasopressin secretion as well as the symptomatology related to systemic sarcoidosis. This study identified systemic sarcoidosis as a definite cause of "syndrome of inappropriate ADH secretion".
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PMID:Inappropriate antidiuretic hormone secretion in a patient with systemic sarcoidosis. 143 16

Sarcoidosis is a generalized disorder which involves the central nervous system in 5 per cent of patients presenting with the disease. We describe the case of a 22-year-old man who developed central diabetes insipidus with a daily urine production of 14,81 seven weeks after diagnosis of pulmonary sarcoidosis and parotid gland enlargement. Computed tomography showed a contrast enhancement of pituitary gland and stalk, no other intracranial manifestations were demonstrated. Intranasal administration of synthetic antidiuretic hormone (ADH) reduced urine volume to normal levels immediately. After discontinuation of 15 months therapy with corticosteroids and administration of ADH for 29 months spontaneous urine volume didn't exceed 31. The patient has been free of symptoms since discontinuation of therapy.
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PMID:[Diabetes insipidus in sarcoidosis]. 203 Oct 45

Herein we will describe a case of chronic hypernatremic-hyperosmolar syndrome with cerebral localization of systemic sarcoidosis. Several determinations of plasma arginine vasopressin (p-AVP) at various plasma sodium levels were carried out in this patient. During the study p-AVP values varied between 2.6 and 9.5 pg/ml. A high percentage of them was related to plasma osmolality, pointing out that p-AVP secretion was osmotically mediated. This behavior is in contrast with the tendency of hypernatremic patients previously reported in the literature, in whom p-AVP values were inappropriately low for the corresponding degree of plasma osmolality, suggesting that vasopressin secretion was not influenced by osmotic stimulation. Furthermore, our case, unlike those previously described, showed high values of urinary osmolality. In conclusion, our patient represents, in essence, the 'middle' of the spectrum of the hypodipsic-hypernatremic syndrome, because she is to be inserted between the majority of patients who have little or no osmotically mediated AVP release and the case of a child, recently described, who had completely normal AVP secretion.
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PMID:Fluctuation of vasopressin secretion in chronic hypernatremia. 231 41

A syndrome of chronic hypernatremia (range 148 to 161 mmoles/l) and partial hypopituitarism (growth hormone and gonadotropin deficiencies) is reported in a 27 year-old man with sarcoid hypothalamic involvement. The patient did not complain of thirst and spontaneous fluid intake was not sufficient to restore the serum sodium to normal. However, when larger amounts of water were given (50 ml/kg for 180 min), the plasma osmolality returned to normal values in 3 hours. Blood volume values were found subnormal on two occasions on free diet (63 and 74% of the theorical normal values) and plasma renin activity was elevated (22 ng/ml/hour). Plasma vasopressin (AVP) concentrations (range < 1 to 1.9 pg/ml) were inappropriately low for the degree of plasma osmolality and remained markedly subnormal when hypertonic saline was infused (NaCl 5%, 10 ml/min for 60 min). However, the secretory stores and hemodynamic control of AVP release were intact since a rise in plasma AVP to 10.8 pg/ml was observed after induction of arterial hypotension with sodium nitroprusside infusion. These results provide further direct evidence fo the dysfunction of the thirst mechanism and the osmotic contol of AVP release. They support the concept that osmoreceptor areas are anatomically distinct from the neurohypophyseal AVP secretory system and that neural inputs from baroreceptor and osmoreceptor cells are completely separated.
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PMID:Chronic hypernatremia, hypovolemia and partial hypopituitarism in sarcoidosis: a case report. 699 62

We evaluated water metabolism in 11 patients with hypothalamic-pituitary sarcoidosis. Seven patients had abnormal water metabolism: one had partial antidiuretic hormone (ADH) deficiency, one had severe ADH deficiency, one had severe ADH deficiency and deficient thirst, one had only deficient thirst, and three had excessive thirst. In four of the five with thirst disturbances, there was loss of congruence of osmotic thresholds for thirst and ADH release. Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH. That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition.
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PMID:Disordered control of thirst in hypothalamic-pituitary sarcoidosis. 742 13

We report a case of phosphate diabetes in a patient with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with sarcoidosis. Our patient was affected by systemic sarcoidosis and he fits the criteria of Schwartz for the diagnosis of SIADH. He presented with phosphate diabetes which appeared during demeclocycline (DMC) therapy and persisted for about 1 month from the end of DMC. It constitutes the fourth case of phosphate diabetes induced by tetracycline described in the literature and it is the third case of SIADH associated with sarcoidosis.
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PMID:Demeclocycline-induced phosphate diabetes in a patient with inappropriate ADH secretion and systemic sarcoidosis. 845 Sep 17

Central diabetes insipidus (DI) can be the outcome of a number of diseases that affect the hypothalamic-neurohypophyseal axis. The causes of the condition can be classified as traumatic, inflammatory, or neoplastic. Traumatic causes include postoperative sella or transection of the pituitary stalk, while infectious or inflammatory causes include meningitis, lymphocytic hypophysitis, and granulomatous inflammations such as sarcoidosis and Wegener's granulomatosis. Various neoplastic conditions such as germinoma, Langerhans cell histiocytosis, metastasis, leukemic infiltration, lymphoma, teratoma, pituitary adenoma, craniopharyngioma, Rathke cleft cyst, hypothalamic glioma, and meningioma are also causes of central DI. In affected patients, careful analysis of these MR imaging features and correlation with the clinical manifestations can allow a more specific diagnosis, which is essential for treatment.
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PMID:MR imaging of central diabetes insipidus: a pictorial essay. 1175 30

Diabetes insipidus is a heterogeneous condition characterized by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. In many patients, it is caused by the destruction or degeneration of the neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus. Known causes of these lesions include: germinoma or craniopharyngioma; Langerhans cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma following surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Magnetic resonance imaging (MRI) allows identification of the posterior pituitary hyperintensity and of hypothalamic-pituitary abnormalities. Thickening of the pituitary stalk is the second most common finding on MRI scans in several local inflammatory pathologies and autoimmune diseases or germinoma, but it is not specific to any single subtype. A progressive increase in the size of the anterior pituitary gland should alert physicians to the possibility that a germinoma is present, whereas a decrease can suggest the presence of an inflammatory or autoimmune process. Most children with acquired central diabetes insipidus and a thickened pituitary stalk have anterior pituitary hormone deficiencies during follow-up. Biopsy of enlarged pituitary stalk should be reserved for patients with a hypothalamic-pituitary mass and progressive thickening of the pituitary stalk, since spontaneous recovery may occur.
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PMID:Diabetes insipidus. 1256 20

Literature data and original experience of the authors with 6890 cases of respiratory sarcoidosis (stage I-III) suggest that diabetes ipsipidus in respiratory sarcoidosis (RS) can present as hypothalamic-hypophysial form (observed at the stage I-II by physicians since 1935) and a new form--nephrogenic (vasopressin-resistant) at stage II of pulmonary sarcoidosis. The latter form is little known. It was found that in stage III sarcoidosis patients who have severe fibrosis of the lungs and a long history of corticosteroid hormone treatment the nephrogenic form of the pathogenesis is caused by defects in calcium metabolism leading to nephrocalcinosis with low sensitivity of renal tubular receptors to ADH. Adiurecrine treatment is unefficient. It is recommended to use chlorpropamide which raises sensitivity of the tubules to ADH.
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PMID:[Stage I-III pulmonary sarcoidosis complicated by nephrogenic (vasopressin-resistant) form of diabetes insipidus]. 1269 55

Diabetes insipidus is a heterogeneous condition characterised by polyuria and polydipsia caused by a lack of secretion of vasopressin, its physiological suppression following excessive water intake, or kidney resistance to its action. The clinical and laboratory diagnosis is confirmed by standard tests, but recent advances in molecular biology and imaging techniques have shed new light on the pathophysiology of this disease. In many patients, central diabetes insipidus is caused by a germinoma or craniopharyngioma; Langerhans' cell histiocytosis and sarcoidosis of the central nervous system; local inflammatory, autoimmune or vascular diseases; trauma from surgery or accident; and, rarely, genetic defects in vasopressin biosynthesis inherited as autosomal dominant or X-linked recessive traits. Thirty to fifty percent of cases are considered idiopathic. Tumour-associated central diabetes insipidus is uncommon in children younger than 5 years old. Biopsy of enlarged pituitary stalk should be reserved for patients with hypothalamic-pituitary mass and progressive thickening of the pituitary stalk since spontaneous recovery may occur. Molecular biology in selected patients may identify those with apparently idiopathic diabetes insipidus carrying the vasopressin-neurophysin II gene mutation.
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PMID:Current perspective on the pathogenesis of central diabetes insipidus. 1612 39


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