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At least 253 records · Page 14Linked to original sources
PubMed2003

[Central diabetes insipidus with Behçet disease. A case report].

Vasculitis with central diabetes insipidus is a rare condition which must be recognized for an appropriate management. We report a case of Behçet disease with central diabetes insipidus. A forty seven year old men presented recurring oral and genital ulcers, skin lesions, polyarthralgia. Two years later, he showed right uveitis and central diabetes insipidus without dysfunction of the pituitary gland. Computed tomographic scan showed normal neurohypophysis and pituitary gland. Later on, he presented hemiplegia. The cerebral computed tomographic scan showed hypodense lesions. Central diabetes insipidus should not be systematically searched because it is a rare feature of the Behçet disease.

Behcet Syndrome↗
PubMed1987

Diabetes insipidus: a postpartum complication.

Sheehan's syndrome and diabetes insipidus were diagnosed in a 31-year-old woman seven months after postpartum bleeding with a short duration of hypotension. The diagnosis of diabetes insipidus was established by the inability to concentrate urine during water deprivation and the marked increase in urinary osmolality after administration of 1-Desamino-8-D-arginine-vasopressin (DDAVP). Obstetricians should be aware of diabetes insipidus as a postpartum complication.

Adult↗
PubMed1983

[Autoimmune form of central diabetes insipidus with antibodies against vasopressin-producing hypothalamic cells].

Autoantibodies against vasopressin (AVP)-producing cells of the human pituitary gland as well as conventional antibodies were determined in 67 patients with central diabetes insipidus and in 141 controls without diabetes insipidus using an immunofluorescence technique. Eleven out of 30 patients (37%) with nonfamilial idiopathic diabetes insipidus, two out of 28 patients (7%) with symptomatic diabetes insipidus and none of the control persons had AVP-cell antibodies. Antibody titres were between 1 : 2 and 1 : 32, in 8 of the 13 cases the antibodies were complement-binding. In 9 patients with idiopathic diabetes insipidus and in none of the symptomatic cases one or more autoimmune diseases were demonstrable. Demonstration of autoantibodies against AVP-cells of the pituitary in the serum of patients with so-called idiopathic diabetes insipidus indicates an autoimmune basis of the disease. This interpretation of the new antibody results is supported by a frequent association of idiopathic diabetes insipidus with recognized auto-immune diseases.

Adolescent↗
PubMedDate not supplied

Nephrogenic diabetes insipidus. Radiological and clinical features.

Two brothers with nephrogenic diabetes insipidus are presented. The importance of early recognition and treatment to reverse the consequential complications are underscored. The disorder has a sex-linked recessive transmission, where all male offspring of an affected mother show the extreme thirst characteristic of the disease; in whom hyposthenuria persisted despite arginine vasopressin infusion, and in whom the serum arginine vasopressin concentrations correlate with the serum osmolality which serves to discriminate nephrogenic diabetes insipidus from the pituitary diabetes insipidus. The radiological features of "non-obstructive" hydronephrosis and hydroureters, the combined use of hydrochlorothiazide and the potassium-sparing diuretic amiloride in comparison to the prostaglandin inhibitor are discussed.

Adolescent↗
PubMed2006

A novel heterozygous missense mutation in the vasopressin moiety is identified in a Japanese person with neurohypophyseal diabetes insipidus.

The autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is caused by diverse mutations in one allele of the gene that encodes the arginine vasopressin (AVP) precursor protein, AVP-neurophysin II (AVP-NP II). Most of the mutations identified so far are located in either the signal peptide or NP II moiety. Two recently published mutations in the AVP gene identified in kindreds with adFNDI predict a substitution of histidine for tyrosine at position 2 and a deletion of phenylalanine at position 3 in AVP. They are unique among adFNDI mutations in that they are the only adFNDI mutations that affect amino acid residues in the AVP moiety of the pro-hormone. Here, we report a novel heterozygous missense mutation in the AVP moiety of the AVP-NP II gene in a Japanese person with neurohypophyseal diabetes insipidus (DI). This mutation occurs at position 2 in AVP and predicts a substitution of serine for tyrosine (Y21S). It is expected to interfere with normal binding of AVP with NP II, and thus result in misfolding of the precursor proteins. The data of this study support the notion that mutations affecting the AVP moiety can result in the initiation of the pathological processes.

Aged, 80 and over↗
PubMed1950

Diabetes insipidus.

Explore the source record for details and available documents.

Diabetes Insipidus↗
PubMed1997

Systemic sclerosis associated with diabetes insipidus.

A rare case of systemic sclerosis that preceded the development of diabetes insipidus is reported. This 25-year-old man presented with Raynaud's phenomenon and ulceration of the tip of the right thumb. The diagnosis of systemic sclerosis was based on findings of proximal scleroderma, sclerodactyly, serological abnormalities, and skin abnormalities verified histologically. Partial central diabetes insipidus was later diagnosed after the sudden appearance of polyuria and polydipsia. Coexistence of systemic sclerosis with diabetes insipidus suggests that diabetes insipidus in this patient might have occurred via an autoimmune mechanism.

Adult↗
PubMed1988

Antibodies to vasopressin in patients with diabetes insipidus. Implications for diagnosis and therapy.

STUDY OBJECTIVE: To determine whether antibodies to vasopressin play a role in the development of diabetes insipidus or interfere with diagnosis and treatment. DESIGN: Random plasma or serum samples for determining of antibodies to vasopressin were collected from patients and controls. SETTING: Referral university hospital with most patients studied in the clinical research center. PATIENTS: Twenty-nine healthy controls and 113 patients with polyuria (15 with primary polydipsia; 86 with neurogenic diabetes insipidus [60 studied before, 28 during, and 10 after antidiuretic hormone treatment]; and 12 with nephrogenic diabetes insipidus). INTERVENTIONS: Antibodies were detected by incubating samples with radiolabeled 125I-arginine vasopressin. The effect of antibodies on diagnosis was studied by examining the relation of plasma vasopressin to osmolality measured during dehydration or infusion of hypertonic saline and the relation of urine osmolality to plasma vasopressin measured during dehydration. MEASUREMENTS AND MAIN RESULTS: Antibodies to vasopressin were not detected in patients with primary polydipsia, nephrogenic diabetes insipidus, or neurogenic diabetes insipidus studied before therapy with antidiuretic hormone. Antibodies were detected in 6 of 28 patients studied during such treatments. All 6 patients reported decreased antidiuretic response to previously effective therapy with arginine or lysine vasopressin but had normal response to desmopressin or chlorpropamide. CONCLUSION: Diabetes insipidus does not result from spontaneously occurring antibodies to vasopressin. The antibodies occasionally develop during treatment with antidiuretic hormone and, when they do, almost always result in secondary resistance to its antidiuretic effect. Antibodies usually do not impair the response to other forms of therapy; they only rarely interfere with the diagnosis of diabetes insipidus, by falsely suggesting the presence of the partial nephrogenic form.

Adolescent↗
PubMed1985

Plasmatic arginine vasopressin levels in total and partial diabetes insipidus.

Plasma arginine vasopressin (AVP) was measured in 24 patients with polyuria exceeding 3.5 l/day diagnosed as severe or partial diabetes insipidus according to the dehydration test. All patients with severe diabetes insipidus diagnosed by the dehydration test had very low or undetectable basal AVP values and always subnormal plasma osmolality. Patients with partial diabetes insipidus diagnosed by the dehydration test had a wide range of AVP and osmolality values. The stimulation test performed on these patients was able to differentiate patients with primary polydipsia from patients with partial diabetes insipidus. The measurement of basal plasma AVP is capable of diagnosing all patients with severe diabetes insipidus; when we combine the stimulation test with the measurement of AVP, we can differentiate partial diabetes insipidus from other forms of polyuria.

Adolescent↗