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PubMed2001

Gitelman's syndrome revisited: an evaluation of symptoms and health-related quality of life.

BACKGROUND: Gitelman's syndrome (GS), also called Gitelman's variant of Bartter's syndrome, is an autosomal recessive renal disorder characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. GS is caused by inactivating mutations in the thiazide-sensitive sodium chloride cotransporter gene (NCCT). It is also known as the "milder" form of Bartter's syndrome, as patients with GS are usually diagnosed in adulthood during routine investigation. Symptoms reported in the literature range from asymptomatic, to mild symptoms of cramps and fatigue, to severe manifestations such as tetany, paralysis, and rhabdomyolysis. This is the first systematic evaluation of a large group of patients with genetically defined GS. METHODS: We evaluated the symptoms and quality of life (QOL) in 50 adult GS patients with confirmed mutations in NCCT, using a standardized questionnaire. This cohort was compared with 25 age- and sex-matched controls. RESULTS: GS patients were significantly more symptomatic than controls. The most common symptoms were salt craving, with musculoskeletal symptoms such as cramps, muscle weakness, and aches and constitutional symptoms such as fatigue, generalized weakness and dizziness, and nocturia and polydipsia. Forty-five percent of GS patients consider their symptoms a moderate to big problem. Measures of health-related QOL were significantly lower in GS patients compared with controls, particularly in terms of role limitations caused by physical health, emotion, level of energy, and general health perception. CONCLUSIONS: This descriptive study indicates that GS is not an asymptomatic disease and adversely affects QOL in these patients. Further studies are needed to assess the impact of therapy on symptoms and QOL.

Adolescent↗

PubMed2002

Infantile cystinosis presenting as chronic constipation.

An infant presented with persistent constipation as the first clinical symptom of cystinosis before evidence of renal Fanconi's syndrome. The history of muscle weakness, failure to thrive, polydipsia, and polyuria prompted subsequent clinical and laboratory evaluations, leading to the correct diagnosis of cystinosis. Primary and persistent constipation as an initial manifestation of cystinosis has not been reported previously. Although rare, cystinosis should be considered in the differential diagnosis of constipation if other suggestive signs or symptoms are present.

Chronic Disease↗

PubMed2006

Nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus (NDI), which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone arginine vasopressin (AVP). Polyuria, with hyposthenuria, and polydipsia are the cardinal clinical manifestations of the disease. About 90% of patients with congenital NDI are males with X-linked recessive NDI (OMIM 304800) who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. In about 10% of the families studied, congenital NDI has an autosomal recessive or autosomal dominant mode of inheritance (OMIM 222000 and 125800). In these families, mutations have been identified in the aquaporin-2 gene (AQP2) (OMIM 107777), which codes for the vasopressin-sensitive water channel. Most missense AVPR2 mutations lead to receptors that are trapped intracellularly; a few mutant receptors reach the cell surface but are unable to bind AVP or to properly trigger an intracellular cyclic adenosine monophosphate signal. Similarly, most AQP2 mutant proteins are also misrouted. Prior knowledge of AVPR2 or AQP2 mutations in NDI families and perinatal mutation testing is of direct clinical value because early diagnosis and treatment can avert the physical and mental retardation associated with repeated episodes of dehydration.

Aquaporin 2↗

PubMed2003

Treatment of malignancy-associated hypercalcemia and cachexia with humanized anti-parathyroid hormone-related protein antibody.

Parathyroid hormone-related protein (PTHrP) plays a central role in humoral hypercalcemia of malignancy (HHM), which is one of the most frequent paraneoplastic syndromes. PTHrP produced by the tumor acts through a common PTH/PTHrP receptor to promote bone resorption, inhibit calcium excretion from the kidney, and induce hypercalcemia. Patients with HHM often develop cachexia associated with typical symptoms such as anorexia, malaise, nausea, constipation, polyuria, polydipsia, and confusion. The etiology of the cachexia is not fully understood but is thought to be caused by hypercalcemia and various cytokines such as interleukin-6, tumor necrosis factor-alpha, leukemia inhibitory factor, and others. In this study, we investigated the role of PTHrP in hypercalcemia and cachexia in HHM by using humanized anti-PTHrP antibody. A mouse monoclonal antibody that binds to PTHrP amino acid sequence 1-34 and inhibits PTHrP function has been humanized to create a specific and potent agent for the treatment of patients with HHM. The mouse monoclonal antibody has been shown to have antihypercalcemic activity against nude mice bearing human tumors. Because a mouse antibody is highly immunogenic in human patients, the complementarity-determining regions from the mouse antibody were grafted into a human antibody. The resulting humanized antibody specifically recognizes PTHrP(1-34) and neutralizes PTHrP functions in vitro and in vivo. The humanized anti-PTHrP antibody was administered intravenously to HHM model animals bearing tumors such as LC-6 human lung carcinoma. These animals showed symptoms similar to those of patients with HHM (eg, hypercalcemia and cachexia). The humanized anti-PTHrP antibody-treated animals responded with normalization of blood ionized calcium level through an improvement of bone metabolism and calcium excretion. Moreover, the treated animals also showed an improvement in body weight, ultromotivity, metabolic alkalosis, food consumption, water intake, serum phosphorus, and renal function. Consequently, the humanized antibody-treated animals experienced complete resolution of hypercalcemia and cachexia. These results suggest that the humanized antibody would be an effective and beneficial agent for patients with HHM, and that PTHrP is a major pathogenetic factor of hypercalcemia and cachexia in patients with HHM.

Animals↗

PubMedDate not supplied

Multiple endocrine neoplasia in a dog.

Multiple endocrine neoplasms, including an insulinoma, bilateral adrenocortical adenocarcinomas and an aortic paraganglioma, were diagnosed after euthanasia in a 12-year-old spayed female dog of mixed breed with a history of progressive anorexia, vomiting, diarrhoea, weight loss, polyuria and polydipsia, regenerative anaemia and hypoglycaemia. The clinical, gross pathological, microscopical, immunohistochemical and ultrastructural findings were consistent with the human syndrome of multiple endocrine neoplasia.

Adrenal Gland Neoplasms↗

PubMed2001

Aspergillus species cystitis in a cat.

A Persian male cat with a history of lower urinary tract disease was presented because of polydipsia, polyuria, constipation and nasal discharge. Ten weeks before admission, the cat had been treated for lower urinary tract disease by catheterisation and flushing of the bladder. The animal was thin, dehydrated, anaemic and azotaemic. Urine culture revealed Aspergillus species cystitis. Antibodies against Aspergillus nidulans were identified in serum. Fluconazole was administered orally (7.5 mg/kg, q 12 h) for 10 consecutive weeks. The azotaemia was resolved, the kidney concentrating ability was recovered and the cat has remained healthy without similar problems.

Animals↗

PubMed2002

Diabetes mellitus and bilateral cataracts in a kitten.

An 18-week-old male domestic long-hair kitten was presented with a history of polyuria and polydipsia for several weeks. The general condition was unremarkable, but the kitten was considerably smaller than expected for the age and showed cataracts in both eyes. Serum glucose concentrations were persistently elevated and based on clinical findings and an elevated serum fructosamine concentration, a diagnosis of diabetes mellitus was established. Diabetes mellitus is not commonly diagnosed in young kittens, nor are cataracts recognised as a frequent feature of this disease in cats. The cataracts progressed in spite of the insulin therapy and the kitten was euthanised 10 weeks after referral. Histopathological examination of the pancreas revealed few and small islets of Langerhans compared to the examination of pancreas from a healthy kitten of the same age. Histopathological changes in the eyes included cataracts affecting both cortex and nucleus.

Animals↗

PubMed2001

Retrovesical echinococcal cyst causing renal failure and nocturnal enuresis in a child.

Although retrovesical hydatid cysts are observed in adulthood albeit very rarely, to our knowledge there is no case reported in childhood. In the current case, a huge retrovesical hydatid cyst caused obstructive uropathy, polydipsia, and secondary nocturnal enuresis in a child. Because the retrovesical hydatid cyst was firmly adherent to the neighboring structures, partial cystectomy could be performed. Perioperative and postoperative complications did not occur, and the symptoms relieved in the early postoperative period.

Child↗

PubMed1999

Pituitary abscess.

A 28-year-old Caucasian woman presented with a 12 month history of secondary amenorrhoea, polyuria and polydipsia with fatigue and weight loss. Investigations revealed panhypopituitarism, diabetes insipidus, an intrasellar mass and papilloedema, thought to be due to benign intracranial hypertension. She was treated conservatively. However, a repeat magnetic resonance image showed enlargement of the pituitary mass with compression of the optic nerves. The pituitary abscess was drained by a transsphenoidal approach. Postoperatively the patient received antibiotics with no recurrence of the pituitary abscess. Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗

PubMed1979

[Hypothalamic hyperosmolarity in childhood (author's transl)].

Hypothalamic lesions occasionally lead to excessive hypernatraemia and hyperosmolarity which cannot be explained by defective ADH secretion alone. As osmoregulation is a complex system the clinical features differ widely from one patient to another. In general central dysregulation of osmolarity is due to diffuse hypothalamic lesions, e.g. inflammatory inflammatory infiltration by histiocytosis X or by large suprasellar tumours. We report on a ten-year-old girl suffering from a suprasellar spongioblastoma and a twelve-year-old-girl, who had been operated for a large craniopharyngioma. Polyuria and polydipsia were not present. Whereas one patient presented hypernatraemic crises and showed normal osmolarity at the intervals, the other patient suffered from sustained hypernatraemia and hyperosmolarity. In the first patient water loading led promptly to clinical and laboratory normalisation. In the other case water loading failed to decrease hyperosmolarity but led to oedema. In the first patient hypernatraemic crises were combined with decreased serum potassium levels and elevated urinary aldosterone excretion. Therefore acute and long-term trials of spironolactone treatment were successful. Exogenous ADH-derivatives failed to normalize hyperosmolarity. In the other patient, however, DDAVP decreased the serum sodium level seen with small doses.

Astrocytoma↗

PubMed1977

Improved method and its clinical application of a radioimmunoassay of arginine vasopressin in human serum.

A sensitive and specific double-antibody radioimmunoassay for measuring circulating levels of arginine vasopressin in human serum is described. It is possible to detect arginine vasopressin levels of 1 microU/ml serum without extraction procedure. Normal subjects were found to have 5.7 +/- 4.4 microU/ml after a dehydration period of 12 hours. Water loading diminished arginine vasopressin concentrations while dehydration increased it. Application of furosemide over a period of 14 days brought forth constant but not significant decreases. Subjects suffering from psychogenic polydipsia showed normal levels in spite of drinking 8-12 liters of water per day. Patients suffering from liver cirrhosis with ascites showed significantly higher arginine vasopressin levels, approaching normal values, when ascites was under control.

Arginine Vasopressin↗

PubMed1978

Effect of carbamazepine in polyuria associated with lithium therapy.

Ten patients, suffering from affective disorders, were treated with carbamazepine for polyuria and polydipsia associated with long-term lithium therapy. Oral carbamazepine (300--600 mg daily for six weeks) was observed to have no beneficial effect in alleviating these symptoms when compared with placebo tablets in a double blind crossover study. Plasma and urinary osmolality were observed to be within normal range in these patients and there was no antidiuretic response following subcutaneous Pitressin injection. There was 50% drop-out due to severe side-effects like ataxia, dizziness, restlessness and confusional states. It appears that lithium exacerbates carbamazepine induced CNS side-effects or vice versa, the mechanism of which is not very clear. It may be due to their mutual effect on sodium metabolism or on nervous conduction velocity. Hence, simultaneous administration of these two drugs should preferably be avoided.

Adult↗

PubMed1997

Atherosclerosis, aortic stenosis and sudden onset central diabetes insipidus.

The majority of cases of central diabetes insipidus are still pathogenetically unclear (idiopathic). Atherosclerotic cholesterol emboli might be partly responsible for some of these idiopathic cases. A 54-year-old woman with known aortic valve stenosis and a history of a transitory ischemic attack presented with sudden-onset polyuria and polydipsia of up to eight l/d, which had started acutely with headaches. She had been treated with lithium for 3 years because of cyclothymic depression. Plasma sodium was in the upper normal range (142-148 mmol/l). Hypertonic saline infusion during lithium therapy revealed a normal threshold of thirst and resetting of vasopressin secretion (osmotic threshold > 300 mosmol/l), whereas vasopressin reserve was normal. Lithium withdrawal led to an even greater delay of vasopressin release upon hypertonic saline infusion (> 310 mosmol/l). Pituitary function tests revealed a normal anterior pituitary function. MR imaging of the hypothalamo-hypophyseal region showed a normal hypothalamic region and a highly intensive neurohypophyseal signal in the T1-weighted image. The patient responded well to desmopressin. We suggest that in this rare case clinical symptoms as well as biochemical findings like impairment of AVP release might be related to a minor structural hypothalamic damage by a vascular lesion, caused, for example, by an atheromatous (cholesterol) embolism in the hypothalamic region responsible for integration of osmoreceptor function and AVP-secretion. The patient's atherosclerosis and aortic stenosis might be responsible for this event.

Aortic Valve Stenosis↗

PubMed2000

Diabetes insipidus in a patient with a highly malignant B-cell lymphoma and stomatitis.

A 37-year-old male patient with a diffuse pleomorphic B-cell-lymphoma, which has been diagnosed two month earlier with the primary site at the pterygopalatine fossa on both sides with infiltration of the clivus and cavernous sinus was referred to our hospital for continuation of the third course of CHOP chemotherapy. At admission he reported about a recent history of painful swallowing and intermittent substernal chest pain. Alleviation of the pain on swallowing and the chest pain was apparently only possible by drinking 10 to 15 l of cold coca cola throughout the day and night, a regimen that resulted in polyuria. Physical examination revealed extensive thrush stomatitis and soor esophagitis. Despite successful treatment with fluconazole, polydipsia continued unabated. The classic osmotic test of dehydration and exogenous vasopressin revealed hypothalamic diabetes insipidus (DI). Basal hormones and stimulated endocrine function tests of the adenohypophysis were found to be normal. MRI-scan revealed lymphoma infiltration of the neurohypophysis. After the third course of CHOP chemotherapy the patient surprisingly recovered completely from his excessive thirst. The present report shows that clinical disorders such as thrush stomatitis can mask diabetes insipidus caused by an early relapsing lymphoma.

Adult↗

PubMed2001

A new mutation of the arginine vasopressin-neurophysin II gene in a family with autosomal dominant neurohypophyseal diabetes insipidus.

Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomally dominant inherited disorder with a typical onset at one to six years of age. The genetic locus of FNDI is the arginine vasopressin-neurophysin II (AVP-NPII) gene. The gene encoding the precursor hormone (prepro-AVP-neurophysin II) is located in the chromosomal region 20p13 and contains three exons. Mutations that cause FNDI have been found to occur within the signal peptide of the prepro-AVP-neurophysin II precursor, within the coding sequence for neurophysin II and the vasopressin-coding sequence. A family (four members with FNDI, two without FNDI) in three consecutive generations was investigated. Index case was a now 22-year old man with a history of severe polyuria (18 L/day) and polydipsia first recognized at about 4-5 months of age. The arginine vasopressin-neurophysin II gene was investigated by direct sequencing of PCR products amplified from each exon. Subsequently, a restriction analysis was performed to verify the sequencing results. The affected individuals were found to have a missense mutation in exon 2 at nucleotide position 1887 (G to C) of the AVP-NPII gene. Using both restriction enzyme digestion and sequence analysis, the mutation was found in all affected family members, but not in the unaffected members studied. This mutation (1887 G to C) represents a novel mutation of the AVP-NPII gene.

Adult↗

PubMed2006

Successful switch to olanzapine after rhabdomyolysis caused by water intoxication and clozapine use.

We report on a case of rhabdomyolysis induced by the correction of hyponatremia after psychogenic polydipsia and clozapine use, where the switch to a high dose of olanzapine resulted in the non-recurrence of rhabdomyolysis. The 46-year-old patient with the diagnosis of schizophrenia paranoid type, who had been on clozapine treatment for the previous 4 years, was admitted with the symptoms of generalized seizure and vomiting, and as severe hyponatremia was proved, its correction with the parallel use of clozapine treatment was done. CK concentrations increased to 48 120 U/L without any symptom of neuroleptic malignant syndrome. To prevent acute renal insufficiency, high-volume alkaline diuresis was initiated and clozapine was tapered and stopped. On the day 12 of treatment, olanzapine was started and was elevated to 30 mg/day. CK concentration began to fall returning to the normal concentration on day 20. Six months after the switch to olanzapine no recurrence of rhabdomyolysis was detected; clinical and laboratory findings were normal. We suggest that after a benzodiazepine-type antipychotic-induced rhabdomyolysis, a switch to another atypical antipsychotic can be a cautious clinical strategy.

Antipsychotic Agents↗

PubMed1987

[Self-induced water intoxication in schizophrenic patients].

This case report concerns two schizophrenic patients with "psychogenic" polydipsia, without any underlying somatic disease. Although case A showed a correlation between excessive water intake and severity of psychomotor disturbance, this could not be safely diagnosed as a water intoxication because the sodium serum level was normal. The lowered sodium serum level in case B, however, allowed us to conclude that the manifestation of grand mal was a sign of a genuine water intoxication. 27 casuistic studies on 67 patients with the syndrome of self-induced water intoxication in schizophrenics are then reviewed. Finally, a variety of diagnostic and pathogenetic problems of this syndrome is discussed, with special reference to the role of inadequate ADH secretion.

Adult↗

PubMed1997

[The Wolfram syndrome: diabetes mellitus, hypacusis, optic atrophy and short stature in STH deficiency].

HISTORY AND CLINICAL FINDINGS: A 43-year-old man was known for 3 years to have diabetes mellitus. For 2 months before admission he had symptoms of hyperglycaemia with polyuria, polydipsia, weight loss, as well as impairment of vision and declining fitness. In addition to bilateral deafness he was clearly of normally proportioned short stature (150 cm). INVESTIGATIONS: The levels of blood sugar (221 mg/dl), HbA1c(10.2%), triglycerides (496 mg/dl) and cholesterol (323 mg/dl) were raised, while the concentration of somatotropic hormone was diminished, both before and after arginine administration. Fundoscopy revealed concentric diminution of the visual fields with left amblyopia. Visual evoked potentials and colour sense testing revealed bilateral optical atrophy, and the audiogram demonstrated deafness. These findings provided the diagnosis of Wolfram syndrome, namely insulin-dependent diabetes mellitus, deafness, optical atrophy and small stature with somatotropic hormone deficiency. TREATMENT AND COURSE: On insulin treatment the metabolic state became normal (HbA1c 7.5%, normal lipid profile). It was decided that the deficiency in somatotropic hormone regulation did not require treatment. CONCLUSION: Cardinal symptoms of the autosomally recessive Wolfram syndrome are insulin-dependent diabetes and optic nerve atrophy. Several types of hormonal abnormalities are associated with it, including a deficiency in the somatotropic axis. To obtain early and adequate hormonal substitution requires extensive endocrinological diagnosis of a disease which frequently becomes manifest in childhood or adolescence.

Adult↗