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PubMedDate not supplied

Diabetes insipidus and increased serum levels of leptin and lactate-dehydrogenase (LDH) in an adolescent boy with a primary intracranial germinoma. Case report and an endocrinological revaluation of literature.

A 16-year-old boy presented with a four-month history of polyuria-polydipsia and a diplopia which had reverted after treatment. The neuroimaging studies performed had been strongly suggestive of an optic nerve glioma, while endocrinological investigation (beta-hCG 420 IU/L) has lead to the correct diagnosis later confirmed at the immunohystochemical analysis performed at biopsy. The high serum level of hCG was unaffected by bromocriptine nor octreotide, while the PRL level (80.0 microg/L) was reduced only by bromocriptine. Among the several tumor markers which may be secreted by such lesions, ours is the first reported case of an elevation of serum LDH for a primary intracranial germinoma. Moreover, the elevated value of serum leptin reported by us might be due to the insensitivity of the hypothalamic structures to endogenous leptin.

Adolescent↗

PubMed2006

A case of reversed pituitary dysfunction with intrasellar mass.

Hypopituitarism can be caused by tumor, inflammation, granuloma and injuries. Once pituitary function is disturbed, hormone replacement therapy is necessary for the remaining life span in most cases. We have experienced a rare case of a unique intrasellar mass associated with pituitary dysfunction in which both spontaneously reversed. A 61-yr-old woman developed hypoadrenalism and central diabetes insipidus (cDI). Magnetic resonance (MR) imaging revealed a lobular, strong hypointense lesion with spotty signal in the middle of the hypophysis. This spotty lesion showed isointensity on T1- and high-intensity on T2-weighted MR images. The spotty signal as well as the normal pituitary lobe were enhanced by the administration of gadolinium. As replacement therapies for hypoadrenalism and cDI, 10 mg of hydrocortisone and 2.5 microg of desmopressin acetate were prescribed. Three months later, slight shrinkage of intrasellar mass and spontaneous improvement of pituitary functions were found. Hydrocortisone was then discontinued. Furthermore, because polyuria and polydipsia were improved nine months later, desmopressin acetate was stopped. Currently, the intrasellar mass continues to shrink, and the patient shows no symptoms without medication. Based upon the unique features of MR images, we suspect that the origin of the mass is an intrasellar hemangioma.

Diabetes Insipidus, Neurogenic↗

PubMed1986

Insulin autoimmune syndrome with insulin-resistant diabetes at the incipient stage prior to hypoglycemic attacks.

Insulin autoimmune syndrome is characterized by spontaneous hypoglycemia, glucose intolerance, hyperinsulinemia and insulin-binding antibodies in serum without previous immunization. A 31-year-old man with Graves' disease developed insulin autoantibodies after therapy with methimazole. The patient was unique in that persistent hyperglycemia with polyuria and polydipsia had continued for several days before frequent hypoglycemic attacks appeared. We were able to extract a huge amount of immunoreactive insulin (116,000 microU/ml) with acid-ethanol from his serum obtained in the diabetic stage, and serum C-peptide immunoreactivity was as high as 268 ng/ml. The insulin-binding activity of his serum was quite potent, and when 1:5,000 diluted serum was incubated with 125I-porcine insulin, 71.2% of the label could be precipitated by polyethylene glycol. The insulin-binding protein was identified as mainly IgG with kappa light chains. Insulin-binding activity was not detected in serum obtained before methimazole therapy, suggesting that the drug was responsible for the induction of antibodies in this patient. The antibodies recognized porcine, sheep, bovine and horse insulins as well as human insulin. The mechanisms by which the antibodies produced hyper- and hypoglycemia have also been discussed.

Adult↗

PubMed2004

A case of insulin edema with inappropriate hyperaldosteronism.

Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.

Adult↗

PubMed1992

Central diabetes insipidus due to acute monocytic leukemia: case report and review of the literature.

We describe a 69-year-old man who presented with a four-month history of polyuria and polydipsia. Plasma vasopressin levels were undetectable, and a dehydration test was abnormal. Based on these findings, a diagnosis of central diabetes insipidus has been established. Hematologic studies showed acute monocytic leukemia. A relationship between the hematologic and endocrine disturbance has been hypothesized, and histological examination at autopsy showed leukemic infiltration of the pituitary stalk. This patient represents the third case in the world literature of central diabetes insipidus associated with acute monocytic leukemia.

Diabetes Insipidus↗

PubMed1994

Acquired nephrogenic diabetes insipidus secondary to distal renal tubular acidosis and nephrocalcinosis associated with Sjögren's syndrome.

A 52-year-old woman was referred to our hospital because of 16-year history of polyuria and polydipsia. Hyposthenuria, hyperchloremic metabolic acidosis and the inabilities to acidify the urine after acid-loading test and to concentrate the urine in responses to water-deprivation and antidiuretic hormone administration allowed us to diagnose renal tubular acidosis and nephrogenic diabetes insipidus. Radiographic examinations revealed bilateral nephrocalcinosis. The patient was also found to have clinical and laboratory findings characteristic for Sjögren's syndrome. Thus the longstanding, poorly monitored distal renal tubular acidosis associated with Sjögren's syndrome was considered to result in very rare renal complications-nephrocalcinosis and nephrogenic diabetes insipidus. In patients with renal tubular acidosis and/or nephrogenic diabetes insipidus of unknown etiology, therefore, Sjögren's syndrome should be considered as one of primary disorders.

Acidosis, Renal Tubular↗

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↗

PubMed2004

Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism.

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.

Adenoma↗

PubMed2005

[Generalized compartment syndrome after excessive drinking. A rare complication of psychological disorders?].

Psychogenic polydipsia can lead to compartment syndromes, which is too infrequently considered in psychiatric patients who binge-drink on hypotonic fluids. If masked by the leading clinical presentation of cerebral edema, compartment syndromes of the extremities may be diagnosed too late or remain undetected. Based on a literature review and case report, we discuss additional factors and the specific features of diagnosis and treatment.

Adult↗

PubMed2001

[Hypernatremia as a rare complication in change from lithium to valproate].

This paper is about a female patient who suffered from bipolar disorders for several decades. Due to a change in medication from lithium to valproic acid by infusion, the patient fell into a coma. Hypernatremia, which had developed unnoticed, was later discovered as the reason. This hypernatremia was due to renal diabetes insipidus stemming from the decades of lithium therapy, with accompanying polydipsia and polyuria, and also to the failure to give enough fluid to the somnolent patient.

Antimanic Agents↗

PubMed2005

Canine diabetes mellitus: can old dogs teach us new tricks?

BACKGROUND: Diabetes is common in dogs, with an estimated prevalence of 0.32% in the UK. Clinical signs, as in man, include polydipsia, polyuria and weight loss, associated with hyperglycaemia and glucosuria. Diabetes typically occurs in dogs between 5 and 12 years of age, and is uncommon under 3 years of age. Breeds predisposed to diabetes include the Samoyed, Tibetan Terrier and Cairn Terrier, while others such as the Boxer and German Shepherd Dog seem less susceptible. These breed differences suggest a genetic component, and at least one dog leucocyte antigen haplotype (DLA DRB1*009, DQA1*001, DQB1*008) appears to be associated with susceptibility to diabetes. METHODS: Canine diabetes can be classified into insulin deficiency diabetes (IDD), resulting from a congenital deficiency or acquired loss of pancreatic beta cells, or insulin resistance diabetes resulting mainly from hormonal antagonism of insulin function. RESULTS: There is no evidence for a canine equivalent of human type 2 diabetes. Adult-onset IDD, requiring insulin therapy, is the most common form, with pancreatitis and/or immune-mediated beta cell destruction considered to be the major underlying causes of the disease. DISCUSSION: Autoantibodies to insulin, recombinant canine GAD65 and/or canine islet antigen-2 have been identified in a proportion of newly diagnosed diabetic dogs, suggesting that autoimmunity is involved in the pathogenesis of disease in some patients. CONCLUSION: The late onset and slow progression of beta cell dysfunction in canine diabetes resembles latent autoimmune diabetes of the adult in man.

Age Factors↗

PubMed1997

Fatal hyponatraemic brain oedema due to common gastroenteritis with accidental water intoxication.

Acute symptomatic hyponatraemia is a life-threatening emergency which must be diagnosed and treated promptly. The initial symptoms are often dramatic, with seizures and coma, and there is therefore a risk that the diagnosis and the urgent sodium correction therapy may be delayed by procedures such as computed tomography (CT) of the brain. As the most common aetiological factors are psychotic polydipsia and different iatrogenic causes, this condition usually develops in hospitalised patients. Water intoxication alone is very unlikely to cause severe hyponatraemia in a person with normal renal function, unless for some reason the antidiuretic hormone secretion is increased. We describe a case in which dehydration due to common gastroenteritis in combination with excessive intake of water caused the death of a young, previously healthy woman. Increased awareness of this potentially fatal condition is recommended.

Acute Disease↗

PubMed2003

Amphetamine increases schedule-induced drinking reduced by negative punishment procedures.

RATIONALE: d-Amphetamine has been reported to increase schedule-induced drinking punished by lick-dependent signalled delays in food delivery. This might reflect a drug-behaviour interaction dependent on the type of punisher, because no such effect has been found when drinking was reduced by lick-contingent electric shocks. However, the anti-punishment effect of amphetamine could be mediated by other behavioural processes, such as a loss of discriminative control or an increase in the value of delayed reinforcers. OBJECTIVES: To test the effects of d-amphetamine on the acquisition and maintenance of schedule-induced drinking reduced by unsignalled delays in food delivery. METHODS: Rats received 10-s unsignalled delays initiated by each lick after polydipsia was induced by a fixed-time 30-s food reinforcement schedule or from the outset of the experiment. Yoked-control rats received these same delays but independently of their own behaviour. d-Amphetamine (0.1-3.0 mg/kg) was then tested IP. RESULTS: d-Amphetamine dose-dependently increased and then decreased punished schedule-induced drinking. The drug led to dose-dependent reductions when the delays were not contingent or when they were applied from the outset of training. CONCLUSIONS: These results support the contention that d-amphetamine has an increasing effect on schedule-induced drinking that has been previously reduced by a negative punishment procedure. This effect cannot be attributed to other potentially involved processes, and therefore support the idea that drug effects on punished behaviour depend on punishment being delays in food or shock deliveries.

Animals↗

PubMed2006

Behavioral effects of aminoadamantane class NMDA receptor antagonists on schedule-induced alcohol and self-administration of water in mice.

RATIONALE: Aminoadamantanes represent a class of NMDA glutamate receptor antagonists that reduce alcohol consumption and may prevent alcohol-induced neuronal adaptations and side effects. OBJECTIVE: Behavioral specificity of memantine and amantadine on alcohol drinking in a schedule-induced polydipsia (SIP) task was investigated in mice. METHODS: Male C57BL/6J mice were food-deprived and divided into four groups: 5% alcohol SIP, water SIP, 1 h limited access regulatory water drinking, and a control group to determine if either drug altered ethanol drinking. Behavioral specificity of memantine (5, 10, and 25 mg/kg, ip) and amantadine (20, 40, and 60 mg/kg, ip) was determined by comparing alterations in alcohol or water consumption in SIP and regulatory water drinking. Drug effects on SIP drinking-specific measures (grams per kilogram consumption) were also compared to nondrinking measures (locomotion, head-entries for food, and lick efficiency). RESULTS: Compared to saline, memantine reduced alcohol SIP drinking (10 and 25 mg/kg). Memantine increased locomotion during alcohol SIP (25 mg/kg) and during water SIP (5 and 25 mg/kg). In contrast, amantadine reduced both alcohol SIP (40 mg/kg) and water SIP (40 and 60 mg/kg). Both drugs reduced regulatory water consumption over the entire dose range tested. Blood alcohol concentrations indicated consumption of physiologically meaningful amounts of alcohol during SIP, and that changes in alcohol metabolism did not account for drug-induced reductions in alcohol drinking. CONCLUSIONS: In addition to reducing alcohol drinking, both drugs had other behavioral effects that included reductions in regulatory drinking. These results suggest that the therapeutic utility of these drugs for ameliorating human alcohol addiction remains questionable.

Alcohol Drinking↗

PubMed1997

Normal MR appearances of the posterior pituitary in central diabetes insipidus associated with septo-optic dysplasia.

Magnetic resonance (MR) imaging of the pituitary in children with central diabetes insipidus usually shows absence of the normal high signal within the posterior gland. The high signal of the normal posterior pituitary is thought to be due to the presence of intra- cellular storage granules of vasopressin. MR imaging has been advocated as a useful investigation to aid in the distinction between central diabetes insipidus and other causes of thirst and polydipsia. We report the case of an infant with central diabetes insipidus in association with septo-optic dysplasia in whom MR imaging showed normal appearances of the posterior pituitary. The mechanism of central diabetes insipidus in this case may be related to a failure of hypothalamic function affecting osmoreception, rather than to a deficiency of vasopressin. Normal MR appearances of the pituitary do not exclude central diabetes insipidus in infants with midline cerebral malformations.

Abnormalities, Multiple↗

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↗

PubMed2006

Acute fatty liver of pregnancy.

OBJECTIVE: Acute fatty liver of pregnancy (AFLP) is a rare and serious entity associated with significant maternal and neonatal mortality and morbidity. We describe our experience with the clinical diagnosis, management and course patients with AFLP. STUDY DESIGN: Medical records of patients with AFLP were reviewed over a 10-year period. Records were reviewed for symptoms, laboratory findings, clinical course, and maternal and perinatal outcomes. RESULTS: The incidence of AFLP was 1 in 7,270 births. The mean gestational age at onset was 34.6 +/- 4.9 weeks. Eight percent of the patients were multiparous with more than three pregnancies. The prodromic phase was variable; patients complained of nausea, abdominal pain, malaise, polyuria-polydipsia syndrome and headaches followed by jaundice. The laboratory results indicated coagulopathy, liver function abnormalities and hypoglycemia. Emergency cesarean section was performed in two cases. The diagnosis has been assessed by transcutaneous hepatic biopsies processed in all patients between the 4th and 15th day (8.4 +/- 4.3 days). Maternal morbidity included hypoglycaemia (40%), coagulopathy (50%) encephalopathy (30%) and renal failure (40%). There were no maternal deaths but fetal mortality is high 66%. CONCLUSION: The early recognition of AFLP cases and prompt progressive management, including early termination of pregnancy and large dose infusion of fresh frozen plasma, the prognosis of AFLP is obviously improved.

Acute Disease↗

PubMed2003

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubular disorder that is frequently associated with progressive renal failure. The primary defect is related to impaired tubular reabsorption of magnesium (Mg) and calcium (Ca) in the thick ascending limb of Henle's loop. We have studied seven Arab patients with this syndrome who belong to four different families. The mean age at first presentation was 1.5+/-1.3 years (range 0.1-3 years) and at diagnosis 5.9+/-4.3 years (range 0.5-12 years). The presenting features were convulsions and carpopedal spasms (5 patients), polydipsia and polyuria (2 patients), rickets (2 patients), and recurrent urinary tract infections (1 patient). Bilateral nephrocalcinosis was observed in all patients. All patients had hypomagnesemia with a mean serum Mg of 0.45+/-0.09 mmol/l, an inappropriately high urine Mg of 2.07+/-0.73 mmol/24 h or fractional excretion of 15.3+/-7.1%, high urine Ca excretion of 4.1+/-1.2 mmol/24 h or urine Ca to creatinine ratio of 2.6+/-1.6, and normal serum potassium level of 4.4+/-0.34 mmol/l. All patients received Mg supplements and thiazide but exhibited slow worsening of their kidney function. After a mean follow-up of 4.4+/-3.9 years, one patient progressed to end-stage renal failure (ESRF). In conclusion, we report seven Arab patients with FHHNC syndrome. The clinical and biochemical data were similar to previous reports. However, they tend to show a slower rate of progression to ESRF.

Arabs↗