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At least 613 records · Page 34Linked to original sources
PubMed2006

Central diabetes insipidus: Is it Langerhans cell histiocytosis of the pituitary stalk? A diagnostic pitfall.

Central diabetes insipidus (CDI) is a rare disorder that may be caused by a variety of diseases. In pediatric and adolescent patients the most common causes for CDI are Langerhans cell histiocytosis (LCH) and germinoma. To avoid a potentially hazardous biopsy of the hypothalamic pituitary region it is recommended to evaluate patients with CDI carefully to identify potential extracranial lesions. Since LCH is the most common systemic disease that may cause CDI, special focus is paid to the identification of LCH lesions. We report on a 9(1/2) year old girl who presented with central diabetes insipidus and a thickening of the pituitary stalk on magnetic resonance imaging. Diagnostic workup revealed a history of recurrent ear infections and a compressed 6th thoracic vertebral body on radiographs. Based on these findings LCH was anticipated. Upon growth of the pituitary stalk lesion the patient was treated with LCH standard chemotherapy. After an initial shrinkage of the lesion, a further growth of the pituitary stalk lesion was observed and the tumor was resected. Histopathology revealed germinoma. This case underscores the importance of a istopathologically proven diagnosis in patients with HPR tumors before the initiation of a specific therapy, even if the clinical findings are highly suggestive.

Biopsy↗
PubMed1979

Diabetes insipidus in children. I. Arginine-vasopressin determination in plasma during short dehydration test.

Plasma vasopressin as well as plasma and urinary osmolality are measured during an overnight dehydration test in vasopressin is undetectable. It is present in plasma from patients with partial diabetes insipidus but the level is not appropriate for plasma osmolality. In patients with polyuria of renal origin plasma vasopressin was significantly higher than in patients with neurogenic diabetes insipidus. Plasma vasopressin measurement is of diagnostic values in partial neurogenic diabetes insipidus and may be of considerable help to distinguish this group of patients from children with polyuria of renal origin.

Adolescent↗
PubMed2003

A case of anterior hypopituitarism showing recurrent pituitary mass associated with central diabetes insipidus.

We report a case of anterior hypopituitarism showing recurrent pituitary mass associated with central diabetes insipidus. A 76-year old woman was hospitalized with general fatigue and 5 kg body weight loss. Endocrinological examinations and pituitary provocative tests demonstrated hypopituitarism and central diabetes insipidus. T1-weighted image of magnetic resonance imaging (MRI) revealed an intrasellar cystic mass with ring enhancement suggesting pituitary abscess. MRI films subsequently obtained from another hospital and studied retrospectively showed intrasellar cystic mass with ring enhancement 4 years earlier, and a mass shape that was decreased after 2 years. Over the subsequent years, the patient has remained asymptomatic with hormone replacement therapy only. Cystic pituitary adenoma or Rathke's cleft cyst with repeated infection may be involved in the repeated change of pituitary mass shape although neither pituitary surgery nor a pituitary biopsy was performed because of the patient's age and condition. It is reported that apparent recurrence of Rathke's cleft cysts after initially successful surgery was higher than suggested by previous reports, and that long-term follow-up with pituitary imaging and neuroophthalmological assessment is essential. Careful evaluation by follow-up brain MRI is needed in the present case to prevent future recurrence of pituitary abscess.

Aged↗
PubMed2005

Diabetes insipidus presentation before renal and pulmonary features in a patient with Wegener's granulomatosis.

We report a case of a 47-year-old woman with Wegener's granulomatosis complicated by central diabetes insipidus. The patient had initially seronegative polyarthritis which mostly responded well to methotrexate and steroid therapy. Eight months later the patient suffered from polyuria and polydipsia. There were no abnormalities of the anterior pituitary hormones. MR images showed only loss of brightness of the posterior pituitary. Extensive evaluation of the patient revealed the presence of ANCA, in c-ANCA pattern and also PR3 positivity. Three months later findings of glomerulonephritis, as suggested by an active urine sediment and gradual proteinuria, and, finally, asymptomatic pulmonary nodules completed the clinical picture of Wegener's disease within 1 year. Renal biopsy showed crescent formation in two glomeruli, consistent with ANCA-related glomerulonephritis which showed pauci-immün depositions by direct immunofluorescence. Diabetes insipidus symptoms mostly regressed; renal and pulmonary findings completely disappeared with glucocorticoid and pulse cyclophosphamide treatment. These findings show that diabetes insipidus may rarely develop early in the disease process and ANCA positivity was directly indicative of Wegener's granulomatosis before the classic clinical signs of the disease.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1977

[Essential hypernatremia with hypovolemia caused by hypodipsia and partial diabetes insipidus].

The authors report the case of 13 year old girl presenting with chronic hypernatremia. This case should be considered as either neurogenic or essential hypernatremia. Partial diabetes insipidus and hypodipsia hypernatremia. Partial diabetes insipidus and hypodipsia are the cause of chronic hypovolemia and a new homeostasis with an exceptionally high level of sodium (isoosmotic point 154 mEq/l). No cause was found and in particular, the search for a cerebral disease was until now proved negative.

Adolescent↗
PubMed1995

[Rhino-orbito-cerebral zygomycosis (mucormycosis) in diabetes insipidus].

A case of rhino-orbito-cerebral zygomycosis in a diabetic patient treated with insulin is reported. Diagnosis was suspected because of extensive necrotic lesions of the face and was confirmed by mycologic tests. During hospital stay the patient developed a diabetes insipidus and the outcome was lethal because of the extension of lesions in spite of convenient antimycotic therapy.

Adult↗
PubMed1985

Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats.

A polyuric syndrome with nephrogenic diabetes insipidus (NDI) is a frequent consequence of prolonged administration of lithium (Li) salts. Studies in the past, mainly the acute and in vitro experiments, indicated that Li ions can inhibit hydroosmotic effect of [8-arginine]vasopressin (AVP) at the step of cAMP generation in vitro. However, the pathogenesis of the NDI due to chronic oral administration of low therapeutic doses of Li salts is not yet clarified. We conducted a comprehensive study to clarify the mechanism by which Li administered orally for several weeks induces polyuria and NDI in rats. Albino rats consuming a diet which contained Li (60 mmol/kg) for 4 wk developed marked polyuria and polydipsia; at the end of 4 wk the plasma Li was 0.7 +/- 0.09 mM (mean +/- SEM; n = 36). Li-treated rats had a significantly decreased (-33%) tissue osmolality in papilla and greatly reduced cortico-papillary gradient of urea (cortex--43%; medulla--64%; papilla--74%). Plasma urea was significantly (P less than 0.001) lower in Li-treated rats (5.4 +/- 0.2 mM) compared with controls (6.8 +/- 0.3 mM). Medullary collecting tubules (MCT) and papillary collecting ducts (PCD) microdissected from Li-treated animals had higher content of protein than MCT and PCD from the control rats. The cAMP accumulation in response to AVP added in vitro was significantly (delta = -60%) reduced. Also, the cAMP accumulation in MCT and PCD after incubation with forskolin was markedly lower in Li-treated rats. Addition of 0.5 mM 1-methyl,3-isobutyl-xanthine did not restore the cAMP accumulation in response to AVP and forskolin in MCT from Li-treated animals. In collecting tubule segments from polyuric rats with hypothalamic diabetes insipidus (Brattleboro homozygotes) the AVP-dependent cAMP accumulation was not diminished. The activity of adenylate cyclase (AdC) in MCT of Li-treated rats, both the basal and the activity stimulated by AVP, forskolin, or fluoride, was significantly (delta approximately equal to -30%) reduced, while the activity of cAMP phosphodiesterase (cAMP-PDIE) in the same segment showed no significant difference from the controls. Also, the content of ATP in MCT microdissected from Li-treated rats and incubated in vitro did not differ from controls. The rate of [14C]succinate oxidation to 14CO2 in MAL was inhibited (-77%) by 1 mM furosemide, which indicates that this metabolic process is coupled with NaCl cotransport in MAL. The rate of (14)CO(2) production from [14C]succinate in MAL was not significantly different between control and Li-treated rats. In MCT of control rats, the rate of [14C]succinate oxidation was approximately 3 times lower than in MAL. The rate of (14)CO(2) production from [(14)C]succinate in MCT of Li-treated rats was significantly (delta +33%) higher than in MCT dissected from control rats. Based on these results, we conclude that at least two factors play an important role in the pathogenesis of NDI consequent to chronic oral administration of Li: (a) decreased ability of MCT and PCD to generate and accumulate cAMP in response to stimulation by AVP; this defect is primarily due to diminished activity of AdC in these tubular segments caused by prolonged exposure to Li; and (b) lower osmolality of renal papillary tissue, due to primarily to depletion of urea, which decreases osmotic driving force for water reabsorption in collecting tubules. On the other hand, NaCI reabsorption in MAL is apparently not affected by chronic Li treatment.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

Diabetes mellitus, diabetes insipidus, and optic atrophy. An autosomal recessive syndrome?

Twenty-one families were selected from the published reports in which the propositus had the triad of juvenile diabetes mellitus, diabetes insipidus, and optic atrophy. The data were consistent with the hypothesis of an autosomal gene which, in the homozygote, causes juvenile diabetes mellitus and one or more of diabetes insipidus, optic atrophy, and nerve deafness. Heterozygotes appear to have an increased probability of developing juvenile diabetes mellitus.

Child↗
PubMed1975

Laurence-Moon-Biedl syndrome associated with diabetes insipidus neurohormonalis.

The case of a girl with Laurence-Moon-Biedl syndrome without polydactyly is described. Additional features were small stature, diabetes insipidus neurohormonalis and a renal disorder. The diabetes insipidus neurohormonalis was successfully treated with a new vasopressin analogue, DDAVP. The importance of renal studies in patients with Laurence-Moon-Biedl syndrome is emphasized.

Child↗
PubMed2000

Familial neurohypophyseal diabetes insipidus associated with a novel mutation in the vasopressin-neurophysin II gene.

Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder of renal water conservation due to deficiency of arginine vasopressin as the result of mutations in the arginine vasopressin-neurophysin II (AVP-NPII) gene that encodes the hormone or its carrier protein. Thirty-one different mutations have been reported. In this study, we evaluated the AVP-NPII gene in a family with FNDI and identified a new mutation (1911Gright curved arrow A) in the coding sequence for NPII in affected family members. This mutation substitutes Tyr for 74 Cys in the NPII moiety. NPII is an intracellular carrier protein for AVP during the axonal transport from the hypothalamus to the posterior pituitary and contains 14 conserved cysteine residues forming 7 disulfide bonds. Because the mutation cosegregates with the phenotype, it is possible that this mutation causes neurohypophyseal diabetes insipidus in this family.

Adolescent↗
PubMed1976

Does the rat with hereditary hypothalamic diabetes insipidus have impaired avoidance learning and/or performance?

Avoidance learning and extinction of rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) were studied in 2 experiments that differed only in shock intensity. In both experiments rats homozygous for diabetes insipidus were more deficient in both escape and avoidance responding than were their heterozygous or normal controls. Although the hterozygous animals showed improved escape performance at the higher shock intensity, their avoidance behavior was not improved. The superiority of normal and heterozygous animals in extinction performance, relative to the homozygous animals, was eliminated or reversed when the differences in terminal acquisition performance were taken into account by analyses of covariance. Deficiency of ADH, therefore, may not result in faster extinction of avoidance behavior.

Animals↗
PubMed1997

Autosomal dominant neurohypophyseal diabetes insipidus associated with a missense mutation encoding Gly23-->Val in neurophysin II.

Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) is an inherited disease caused by progressive degeneration of the magnocellular neurons of the hypothalamus leading to decreased ability to produce the hormone arginine vasopressin (AVP). Affected individuals are not symptomatic at birth, but usually develop diabetes insipidus at 1-6 yr of age. The genetic locus of the disease is the AVP-neurophysin II (NPII) gene, and mutations that cause ADNDI have been found in both the signal peptide of the prepro-AVP-NPII precursor and within NPII itself. An affected girl who presented at 9 months of age and her similarly affected younger brother and father were all found to have a novel missense mutation (G1758-->T) encoding the amino acid substitution Gly23-->Val within NPII. The mutation was confirmed by restriction endonuclease analysis. A T1-weighted magnetic resonance imaging of the father's pituitary gland demonstrates an attenuated posterior pituitary bright spot. This mutation may be valuable for developing models of dominantly inherited neurodegeneration, as the early age of onset of symptoms suggests that this mutation may be particularly deleterious to the magnocellular neuron.

Arginine Vasopressin↗
PubMed1989

[Partial diabetes insipidus and ascitic liver cirrhosis in a patient].

The occurrence of hepatic cirrhosis with ascites and diabetes insipidus in the same patient is described. The stimulability of residual vasopressin was confirmed by water deprival and the partial vasopressin deficit by the administration of dDAVP. Water loading test referred to the possibility of suppression of residual vasopressin. Studying the specific renal functions in diets of different sodium content following the administration of dDAVP and diuretics, the diuretic without adding ADH was found to be the best therapy for these patients. Reviewing the literature the authors are taking into consideration the difficulties of differential diagnostics and the mechanisms which may explain the inhibiting effect of the liver disease on the polyuria associated with diabetes insipidus.

Aged↗
PubMed2002

Central diabetes insipidus and inv(3)(q21q26) and monosomy 7 in acute myeloid leukemia.

Chromosomal anomalies involving region 3q21q26 have been reported associated with thrombocytosis in various hematological malignancies, such as chronic myeloid leukemia, myelodysplastic syndrome, and acute myeloid leukemia (AML). Recent reports described the association of central diabetes insipidus with AML and chromosomal anomalies involving region 3q21q26. We review the database in our institution and report five cases of inv(3)(q21q26) in consecutive cytogenetic studies of AML and myelodysplastic syndromes from 1992 to 2000, two cases presented as sole abnormalities and three cases were associated with monosomy 7. Only one case was associated with central diabetes insipidus. The literature of 3q21q26 syndrome and central diabetes insipidus in myeloid leukemia is reviewed.

Adult↗
PubMed1996

Constitutive nitric oxide synthase in hypothalami of normal and hereditary diabetes insipidus rats and mice: role of nitric oxide in osmotic regulation and its mechanism.

Constitutive nitric oxide synthase (cNOS) was immunolocalized to study its role in osmotic regulation. Immunoreactivity was observed in all major hypothalamic osmoregulatory structures, the organum vasculosum laminae terminalis, subfornical organ, median preoptic nucleus, and supraoptic and paraventricular nuclei. These nuclei were compared in normal Long-Evans rats and homozygous Brattleboro rats with hereditary hypothalamic diabetes insipidus and in normal mice and mice with hereditary nephrogenic diabetes insipidus. About 50% of supraoptic neurons in Long-Evans rats and 90% in Brattleboro rats were cNOS immunopositive; a qualitatively similar difference occurred in the paraventricular nucleus. Mice with hereditary nephrogenic diabetes insipidus also showed a greater proportion of cNOS-positive supraoptic neurons (50%) than normal mice (20%). However, the number of cNOS-positive cells in the organum vasculosum laminae terminalis, subfornical organ, and median preoptic nucleus dis not differ significantly between diabetic and normal animals. The similar changes in cNOS in two mutant strains in which the only common feature is chronic osmotic stimulation shows that differences in vasopressin and oxytocin are not involved in the regulation of cNOS. The results suggest strongly that cNOS is involved in long term modulation of the hypothalamo-neurohypophysial system and, hence, body water and electrolyte homeostasis, and that cNOS is itself regulated by body osmotic status.

Animals↗
PubMed1979

Sheehan's syndrome with diabetes insipidus. A case study.

A case of a woman in whom Sheehan's syndrome and diabetes insipidus were found is presented. This association is very uncommon, but well-documented cases have been reported. Controversial opinions about the primary lesion still exist. To find out whether the pituitary gland responds to hypothalamic releasing factors, three kinds of test were performed. The failure of the pituitary to respond suggested pituitary damage. Because diabetes insipidus was present, presumably the hypothalamus was also damaged. A review of the literature and different opinions about the primary anatomic lesions in this syndrome are discussed.

Adult↗