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Five children who developed diabetes insipidus as a manifestation of severe brain injury received continuous intravenous treatment with a solution containing both aqueous vasopressin and appropriate crystalloid replacement. Polyuria, hypernatraemia, and decreased urine osmolalities were safely corrected in all patients within eight to 28 hours.
Fifty five children with nocturnal enuresis referred to a hospital enuresis clinic entered a controlled trial to compare the efficacy of one month and three month courses of intranasal desmopressin (Desmospray). There was no significant difference in outcome between the two groups. Overall 36% improved by at least two dry nights/week during treatment, but only five children (18%) in the one month group and three (11%) in the three month group became completely dry and only one in each group remained dry after treatment. To determine whether nocturnal polyuria was associated with a therapeutic response to desmopressin, the nocturnal urine volume, osmolality, and vasopressin concentration were measured in desmopressin responsive enuretics, desmopressin non-responders, and non-enuretic control children. There were no significant differences between the three groups. A three month course of desmopressin is no more effective than a one month course. Although many children will improve during treatment, only a small number become dry and most will relapse when treatment is stopped.
Nephrogenic diabetes insipidus (NDI) is characterised by the inability of the kidney to concentrate urine in response to arginine vasopressin. The consequences are severe polyuria and polydipsia, often associated with hypertonic dehydration. Intracerebral calcification, seizures, psychosomatic retardation, hydronephrosis, and hydroureters are its sequelae. In this study, four children with NDI were treated with 3 mg/kg/day hydrochlorothiazide and 0.3 mg/kg/day amiloride orally three times a day for up to five years. While undergoing treatment, none of the patients had signs of dehydration or electrolyte imbalance, all showed normal body growth, and there was no evidence of cerebral calcification or seizures. All but one had normal psychomotor development and normal sonography of the urinary tract. However, normal fluid balance was not attainable (fluid intake, 3.8-7.7 l/m2/day; urine output, 2.2-7.4 l/m2/day). The treatment was well tolerated and no side effects could be detected. Prolonged treatment with hydrochlorothiazide/amiloride appears to be more effective and better tolerated than just hydrochlorothiazide. Its efficacy appears to be similar to that of hydrochlorothiazide/indomethacin but without their severe side effects.
OBJECTIVE: To determine the impact of posters advertising symptoms of diabetes on public knowledge of these symptoms. DESIGN: Structured street interviews of members of the general public before, at the end of, and 10 weeks after a campaign advertising the main symptoms of diabetes. SETTING: Basingstoke and Wolverhampton. SUBJECTS: Three samples of 1000 members of the general public were interviewed. Samples were selected randomly but stratified to match the local population's age (20-75), sex, social class, and racial characteristics. MAIN OUTCOME MEASURES: Knowledge of symptoms of diabetes; perceived seriousness of diabetes; and induction of anxiety about symptoms in the target population. RESULTS: Advertising significantly raised knowledge (without prompting) of symptoms: thirst, 245 before v 411 at end of campaign (P < 0.0001) v 341 after (P = 0.0012 v before); polyuria, 72 v 101 (P = 0.0211) v 92 (P = 0.5169); lethargy, 180 v 373 (P < 0.0001) v 298 (P < 0.0001); knowledge of weight loss and visual disturbance was unaffected. The number of subjects lacking knowledge of any symptoms was reduced from 550 to 388 (P < 0.0001). The perceived seriousness of diabetes was unaffected (mean 7.6 in each phase on a scale of 1 (not) to 10 (very). Before advertising, 449 (45%) claimed to have one or more symptoms of diabetes, but this number fell at the end of the campaign (403; P = 0.0419) and 10 weeks afterwards (278; P < 0.0001). CONCLUSIONS: An advertising campaign raised public knowledge of diabetes symptoms without inducing fear of diabetes or anxiety about symptoms. Its potential for achieving earlier detection of non-insulin dependent diabetes should be evaluated.
OBJECTIVE: To quantify efficacy and harm of pharmacological prevention of acute mountain sickness. DATA SOURCES: Systematic search (Medline, Embase, Cochrane Library, internet, bibliographies, authors) in any language, up to October 1999. STUDY SELECTION: Randomised placebo controlled trials. DATA EXTRACTION: Dichotomous data on efficacy and harm from 33 trials (523 subjects received 13 different interventions, 519 a placebo). DATA SYNTHESIS: At above 4000 m the mean incidence of acute mountain sickness with placebo was 67% (range 25% to 100%); incidence depended on the rate of ascent, but not on the altitude or the mode of ascent. Across all ascent rates, dexamethasone 8-16 mg prevented acute mountain sickness (relative risk 2.50 (95% confidence interval 1.71 to 3.66); number needed to treat (NNT) 2.8 (2.0 to 4.6)), without evidence of dose responsiveness. Acetazolamide 750 mg was also efficacious (2.18 (1.52 to 3.15); NNT 2.9 (2.0 to 5.2)), but 500 mg was not. In two trials, adverse reaction (including depression) occurred after dexamethasone was stopped abruptly (4.45 (1.08 to 18); NNT 3.7 (2.5 to 6.9)). With acetazolamide, paraesthesia (4.02 (1.71 to 9.43); NNT 3.0 (2.0 to 6.0)) and polyuria (4.24 (1.92 to 9.37); NNT 3.6 (2.5 to 6.2)) were reported. Data were sparse on nifedipine, frusemide (furosemide), dihydroxyaluminium-sodium, spironolactone, phenytoin, codeine, phenformin, antidiuretic hormone, and ginkgo biloba. CONCLUSIONS: At above 4000 m, with a high ascent rate, fewer than three subjects need to be treated with prophylactic dexamethasone 8-16 mg or acetazolamide 750 mg for one subject not to experience acute mountain sickness who would have done so had they all received a placebo. Acetazolamide 500 mg does not work.
Plasma concentrations of immunoreactive atrial natriuretic polypeptide were raised in 22 of 23 patients with paroxysmal supraventricular tachycardia and in all seven patients with atrial flutter. Plasma concentrations of atrial natriuretic polypeptide rose soon after the onset of supraventricular tachycardia. A sample taken 30 minutes after reversion to sinus rhythm (pharmacological or non-pharmacological) showed a significant fall in 19 of the 23 patients with paroxysmal supraventricular tachycardia and all seven patients with atrial flutter. Because atrial natriuretic polypeptide has powerful natriuretic and diuretic properties, an increase may contribute considerably to the polyuria that is often associated with episodes of supraventricular tachycardia.
The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.
INTRODUCTION: Medullary cystic kidney disease 2 (MCKD2) and familial juvenile hyperuricaemic nephropathy (FJHN) are both autosomal dominant renal diseases characterised by juvenile onset of hyperuricaemia, gout, and progressive renal failure. Clinical features of both conditions vary in presence and severity. Often definitive diagnosis is possible only after significant pathology has occurred. Genetic linkage studies have localised genes for both conditions to overlapping regions of chromosome 16p11-p13. These clinical and genetic findings suggest that these conditions may be allelic. AIM: To identify the gene and associated mutation(s) responsible for FJHN and MCKD2. METHODS: Two large, multigenerational families segregating FJHN were studied by genetic linkage and haplotype analyses to sublocalise the chromosome 16p FJHN gene locus. To permit refinement of the candidate interval and localisation of candidate genes, an integrated physical and genetic map of the candidate region was developed. DNA sequencing of candidate genes was performed to detect mutations in subjects affected with FJHN (three unrelated families) and MCKD2 (one family). RESULTS: We identified four novel uromodulin (UMOD) gene mutations that segregate with the disease phenotype in three families with FJHN and in one family with MCKD2. CONCLUSION: These data provide the first direct evidence that MCKD2 and FJHN arise from mutation of the UMOD gene and are allelic disorders. UMOD is a GPI anchored glycoprotein and the most abundant protein in normal urine. We postulate that mutation of UMOD disrupts the tertiary structure of UMOD and is responsible for the clinical changes of interstitial renal disease, polyuria, and hyperuricaemia found in MCKD2 and FJHN.
A 55 year old woman with multifocal eosinophilic granuloma (MEG) is described. She developed facial numbness and twitching followed by slowly progressive cerebellar symptoms. Two years later polyuria and polydipsia were noted. A CT of the brain showed multifocal enhancing lesions, and MRI showed areas of hyperintensity on T2 weighted studies in the cerebellar peduncles, pons, and midbrain. Radiographs of the skull, pelvis, and long bones were normal, but a 99mTc diphosphonate bone scan and MRI showed bone lesions compatible with granuloma. The diagnosis of MEG was made by bone biopsy. This is believed to be the first case of MEG with such unusual clinical profiles and radiographical findings. Skeletal surveys are indicated for patients with unexplained focal or multifocal inflammatory changes in the cerebellum.
Infundibulohypophysitis is an unusual inflammatory condition that affects the infundibulum, the pituitary stalk, and the neurohypophysis and may be part of a range that includes lymphocytic hypophysitis. Lymphocytic hypophysitis occurs mainly in women and most often presents in the later stages of pregnancy. Infundibulohypophysitis usually presents with diabetes insipidus and the cause remains unclear. The case of a 46 year old man with a 12 week history of polyuria and polydipsia is reported. Cranial diabetes insipidus was diagnosed on the basis of a water deprivation test. Initial cranial and pituitary imaging studies were normal. He subsequently developed symptoms of panhypopituitism over a period of 6-9 months and then, more acutely, developed diplopia secondary to a fourth nerve palsy. Further brain imaging studies disclosed an enhancing pituitary stalk and a left cavernous sinus lesion. An initial trial of immunosuppressive treatment did not help symptoms significantly. The diagnosis of infundibulohypophysitis was made on histological evidence. The patient was treated with prednisolone and methotrexate. At 9 months he is well, without symptoms, and the radiological abnormalities have resolved.
Office workers who became sensitised to antigens derived from humidifier sludge developed episodes of fever, malaise, and other symptoms, including polyuria and mild chest tightness. The episodes usually occurred on a Monday evening and were to some extent dose-related. Lung function was assessed over a day shift on two occasions, including one after which almost all the susceptible subjects developed symptoms. The symptoms were preceded by a 6% reduction in forced expiratory volume and vital capacity, a corresponding increase in residual volume, and a reduction in flow rate after 75% vital capacity had been expired. There were no changes in peak expiratory flow, forced expiratory flow at 50% of vital capacity, or transfer factor. In some subjects the transfer factor was apparently reduced 36 hours later, but for this there may have been another explanation. The physiological features were considered to reflect narrowing of small airways in the lung. The changes, however, were minimal and not the main cause of the symptoms. A feature of the episode was the severity of the constitutional symptoms despite the low airborne dust levels.
A female patient, aged 44, with diabetes insipidus as a complication of acute myelomonocytic leukaemia (AMML) is described. She presented with bleeding, anaemia, polyuria and polydypsia. She was treated with intranasal vasopressin for diabetes insipidus and responded well to treatment. Chemotherapy was administered for the leukaemia and a full remission was achieved. The patient relapsed a few days before final admission to hospital and died of septicaemia 7 months after initial diagnosis. A short review of the literature related to this subject is also presented.
A 36 year old man presented with headache, polyuria, thirst and weakness of the lower limbs. Hypertension and a high haematocrit were striking features on initial assessment. Subsequently the full picture of Guillain-Barré syndrome developed. Hormone measurement revealed marked sympathetic nervous system and renin-angiotensin system activation with a return to normal of both blood pressure and hormones with neurological recovery.
A 30 year old woman with an 8-year history of thirst and polyuria was found to have cranial diabetes insipidus. There were no neurological abnormalities at presentation but she subsequently developed diverse signs and died 26 months later. Autopsy revealed a diagnosis of diffuse primary cerebral lymphoma. Cranial diabetes insipidus with otherwise minimal abnormality of hypothalamic/pituitary function has not previously been reported as a presentation of this neoplasm.
A 25 year old non-pregnant woman presented with a one-year history of amenorrhoea and polyuria. Three months before her admission, she had suffered lymphocytic meningitis. Hormonal studies revealed hypopituitarism and central diabetes insipidus, with associated primary autoimmune hypothyroidism. Computed tomographic scan and magnetic resonance imaging showed a pituitary mass with suprasellar extension and thickened stalk. Transsphenoidal surgery was performed and the histological study revealed fibrosis and diffuse lymphocytic infiltration with predominance of CD4 lymphocytes. This further case of lymphocytic hypophysitis was not related to pregnancy and produced diabetes insipidus, two uncommon associations. We discuss the features that can lead to a preoperative suspicion of this rare disorder.
Between 1989 and 1992, 22 Bernese mountain dogs (18 females and four males) aged between two and seven years, which had been suffering for some weeks from weight loss, anorexia, apathy, vomiting, polydipsia and polyuria, were examined. All of them had high blood urea nitrogen and serum creatinine concentrations, and many had hyperphosphataemia, hypercholesterolaemia, hypoproteinaemia and nonregenerative anaemia. All the dogs had very high protein: creatinine ratios in the urine, and macroproteinuria was identified by sodium dodecyl sulphate gel electrophoresis. The immunofluorescent titres against Borrelia burgdorferi, measured in 19 of the dogs, ranged between 256 and 32,768. In all cases, membrano-proliferative glomerulonephritis with concomitant interstitial nephritis was diagnosed. From an analysis of the dogs' pedigree it was concluded that the glomerulonephritis of these Bernese mountain dogs was inherited as an autosomal recessive trait and that its expression was influenced by a second gene locus with a sex-linked dominance exchange.
An 11-year-old female crossbred dog showed signs of polyuria, polydipsia, vomiting, posterior weakness and ataxia. Clinical and laboratory findings suggested the diagnosis of polycythaemia vera. The haematological values shown over a six-month period are presented. In four samples some aspects of erythrocyte function (glucose-6-phosphate dehydrogenase [G6PD] and pyruvate kinase [PK] activities, 2,3 diphosphoglycerate [2,3 DPG] concentration, osmotic fragility and intracellular sodium and potassium concentrations) were studied. Variable activities of G6PD and PK, probably related to different reticulocyte number, were detected together with normal osmotic fragility and intracellular sodium and potassium concentrations. 2,3 DPG concentration was higher than normal in all four samples. This could be interpreted as a response to a low tissue perfusion rather than a higher content of 2,3 DPG in red blood cells from the polycythaemic dog.
The efficacy of trilostane in the treatment of canine pituitary-dependent hyperadrenocorticism (PDH) was evaluated in 78 dogs with the condition which were treated for up to three years. The drug appeared to be well tolerated by almost all the dogs, and only two developed clinical signs and biochemical evidence of hypoadrenocorticism. Polyuria and polydipsia completely resolved in 70 per cent of the dogs that had these problems, and skin changes resolved in 62 per cent of the dogs that had skin abnormalities. There was a significant reduction (P<0.001 in each case) in both the mean basal and post-adrenocorticotrophic hormone (ACTH) cortisol concentrations after a mean of 12.3 days of treatment. The post-ACTH cortisol concentration decreased to less than 250 nmol/litre in 81 per cent of the dogs within one month of the start of treatment and in another 15 per cent at some later time. The median survival time of the 26 dogs which died was 549 days, and 51 of the dogs were alive at the completion of the study. One was lost to follow up after 241 days treatment.