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PubMed2001

Effect of chronic treatment with haloperidol on vasopressin release and behavioral changes by osmotic stimulation of the supraoptic nucleus.

Chronic treatment with dopamine D2 blockers in schizophrenic patients has been proposed as one of the causes of polydipsia and water intoxication, but this conclusion is still controversial. To investigate the relationship between dopamine D2 blockers and these syndromes, we designed a behavioral and neurochemical study using hyperosmotic stimulation in the supraoptic nucleus (SON) by microdialysis after chronic treatment with haloperidol in rats. Animals were injected with haloperidol decanoate (20 mg/kg, i.m.) or sesame oil at 2-week intervals for 8 successive weeks. During the 7th week, water-intake was increased 30-60 min after the hyperosmotic stimulation in both groups, but more so in haloperidol-treated animals compared to that in the control group. Moreover, arginine vasopressin (AVP) was released by the hyperosmotic stimulation in SON, but was not significantly different between groups. In addition, striatal dopamine levels 3-4 days after the microdialysis study showed a significant decrease in the haloperidol-treated animals. These results suggest that chronic treatment with haloperidol enhances water-intake produced by hyperosmotic stimulation in the SON but does not increase AVP levels in dialysates following hyperosmotic stimulation. Thus, these symptoms may be mediated by dopaminergic systems in brain.

Animals↗

PubMed2003

Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy.

BACKGROUND: Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin. CASE: While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. Urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. CONCLUSION: Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.

Adult↗

PubMed1997

Diabetes insipidus in pregnancy: a treatable cause of oligohydramnios.

BACKGROUND: Diabetes insipidus, which presents with polyuria, polydipsia, and profound electrolyte abnormalities, occurs rarely in pregnancy. We report a patient with severe oligohydramnios that resolved after treatment of diabetes insipidus. CASE: A 14-year-old girl was admitted at 33 weeks' gestation with cramping and vaginal spotting. A sonogram indicated oligohydramnios and an amniotic fluid index (AFI) of 2.6, with normal fetal kidneys and bladder. On hospital day 2, the AFI was 0.0. Recorded fluid was 8 L in and 13.6 L out. Serum sodium was 153 mEq/L. Diabetes insipidus was diagnosed and treated with intranasal desmopressin acetate. The oligohydramnios resolved rapidly, and the patient delivered a healthy 2700-g male infant at 38 weeks. CONCLUSION: Although rare, diabetes insipidus may present initially in pregnancy and should be considered in patients with oligohydramnios. Simple diagnosis with determination of 24-hour urine volume and serum electrolytes can identify this potentially reversible cause of oligohydramnios and poor obstetric outcome.

Adolescent↗

PubMed1997

Effects of lentinan on abnormal ingestive behaviors induced by tumor necrosis factor.

Lentinan (LNT), a beta-glucan derived from Lentinus edodes (Berk.) Sign., is known to work positively against cachexia in patients with malignant tumors. Because the cachectin/tumor necrosis factor (TNF) is supposed to be one of the factors that mediate cancer cachexia, we tested the effects of LNT on TNF-induced cachexia in rats. First, we analyzed in detail the cachectic actions of TNF (0.2 mg/kg/day, 5 days, IV) on food and water intake, body weight, and locomotor activity. The day after the first administration of TNF (acute phase), food and water intake, as well as body weight, of all rats decreased. However, over the next few days of treatment (chronic phase), the rats gradually developed a tolerance to the cachectic actions of TNF. Specifically, after the third administration, the rats treated with TNF had a higher amount of water intake than the control rats. This was mainly due to an increase in daytime water intake. We also analyzed the effects of LNT (0.1 or 1.0 mg/kg, twice/wk. IV) on TNF-induced cachexia, and compared the data with those from the rats treated with TNF alone. The higher dosage of LNT significantly suppressed TNF-induced daytime polydipsia and increased the amount of nighttime water intake, as well as the meal size of nighttime food intake. These results suggest that LNT partially normalizes TNF-induced cachexia in rats.

Animals↗

PubMed1997

Schedule induction conditions not only exaggerate intake but also enhance drug solution choice.

In previous research, rats exposed to daily, 3 h sessions of schedule-induced polydipsia (SIP) self-administered high doses of cocaine orally. However, a strong and durable preference for cocaine solution to water requires training in addition to mere oral self-administration exposure. If cocaine is dissolved in a preferred vehicle solution, and the vehicle is subsequently faded to water, then a strong preference for cocaine remains. A similar preference can be instituted for lidocaine solution. Such preferences may develop because the gustatory property of a drug becomes associated with the preferred vehicle and remains to function as a durable conditioned reinforcer after vehicle fading. To determine if drug preference is solely a function of this posited conditioning mechanism, or whether it also depends upon the SIP condition, rats were exposed to daily, 3 h sessions of single-ration feeding, rather than the SIP condition. A preferred vehicle (glucose/saccharin solution) was slowly faded from a 0.19 mg/ml lidocaine solution, which was presented concurrently with a choice for water. Although a preference for lidocaine solution to water could be generated, it occurred for only 5 out of 9 rats, and the preference was relatively unstable. By contrast, in two previous studies using SIP, 26 out of 27 rats maintained a preference for lidocaine solution. Thus, SIP not only exaggerates the amount of drug solution ingested but also contributes to the fixation of the associative drug solution choice.

Animals↗

PubMed1998

Schedule-induced polydipsic consumption of hypertonic NaCl solutions: effects of chlordiazepoxide.

Rats were exposed to daily, 3-h sessions of schedule-induced polydipsia (SIP) in which either water, hypertonic NaCl solution (1.5% or 2.2%), or concurrent water and 1.5% NaCl were available. Each condition was in effect for several, consecutive weeks. Presession subcutaneous injections of chlordiazepoxide (CDZP) produced dose-related increases in the polydipsic ingestion of both NaCl solutions but had smaller and less certain effects on water consumption. Under the concurrent-fluid presentation condition, CDZP primarily increased NaCl solution consumption. Conditions generating SIP may function to attenuate what might be viewed as the punishing effects of ingesting highly hypertonic NaCl solutions, thereby permitting the chronic self-administration of large, daily amounts. Like many benzodiazepines, CDZP can attenuate the effects of punishment and thereby also increase NaCl solution ingestion. The two sources of punishment attenuation may be additive, with both differentially effecting greater increases in hypertonic NaCl ingestion, compared to water, when both fluids are presented concurrently.

Animals↗

PubMed2001

Behavioral sensitization following exposure to low doses of trimethylolpropane phosphate.

Behavioral sensitization is commonly studied within the context of drugs known to directly increase activity in the brain's dopamine system, particularly drugs of abuse. However, the present research suggests such behavioral changes can also be observed following exposure to other compounds that indirectly affect the dopamine system. One such compound is trimethylolpropane phosphate (TMPP), a bridged organophosphate that can be produced by the partial pyrolysis of certain synthetic lubricants used on military ships and aircraft. Although TMPP is a potent convulsant, it has been demonstrated that treatment with doses below seizure threshold results in long-term behavioral sensitization. The effect has been demonstrated with a number of neurobehavioral endpoints, particularly those assessing appetitive responding. More specifically, sensitization has been observed in acquisition of schedule-induced polydipsia (SIP), appetitive reinforcer approach sensitization (ARAS) and social interaction as measured in neonatal ultrasonic vocalizations, juvenile play and adult conspecific approach. Overall, the rats demonstrated a heightened appetitive response pattern. More specifically, TMPP reliably reduced the number of SIP sessions necessary to induce asymptotic drinking level and increased the time spent investigating (sniffing) a food reinforcer as measured in the ARAS task. Specific effects of TMPP on social interaction were an increase in ultrasonic vocalizations when the neonate was isolated from the dam and littermates and an increase in both measures of juvenile play (pins and dorsal contacts). A complex set of interactions emerged for the measures of adult social investigation where the drug effect was modulated by such factors as sex and neutral vs. stress-inducing experiences coincident with the drug treatment. In contrast to the above results, no behavioral changes were recorded for measures in the elevated plus maze and open field exploration. These results suggest that TMPP produces neurophysiological changes that persist much longer than the pharmacological effect of the compound, particularly in the neural correlates for appetitive behavior.

Aging↗

PubMed1992

Neurologic manifestations of hypothalamic disease.

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.

Adult↗

PubMed2001

Neurohypophyseal germinoma traced from its earliest stage via magnetic resonance imaging: case report.

BACKGROUND: We report a case in which magnetic resonance imaging (MRI) documented the formation of a neurohypophyseal germinoma from its earliest stage. CASE DESCRIPTION: A 9-year-old girl presented with polyuria, polydipsia, and growth retardation. Urinary and endocrinological examination indicated diabetes insipidus (DI) and growth hormone deficiency. No clear evidence of a mass in the hypothalamo-pituitary area was apparent on the first MRI scan. Follow-up MRIs and endocrinological examinations revealed that a tumor, arising from the stalk and posterior lobe of the pituitary gland, formed a mass and caused anterior pituitary function to deteriorate. Histologic diagnosis was germinoma based on open biopsy. CONCLUSION: Radiologic findings in this case indicated the primary site of this intrasellar germinoma to be the hypothalamo-neurohypophyseal region, designating this a "neurohypophyseal germinoma."

Child↗

PubMed1976

Acute diabetic abdomen in childhood.

Three children presented as acute surgical emergencies due to undiagnosed diabetes mellitus. Where diabetic ketoacidosis mimicks the acute abdomen three clinical features are important in reaching the right diagnosis-namely, a history of polydipsia, polyuria, and anorexia preceding the abdominal pain, the deep sighing and rapid respirations, and severe dehydration.

Abdomen, Acute↗

PubMed1996

A new stress-related syndrome of growth failure and hyperphagia in children, associated with reversibility of growth-hormone insufficiency.

BACKGROUND: Growth failure without organic aetiology but associated with behavioural disturbance and psychosocial stress has been termed psychosocial short stature. This condition is not a valid diagnostic entity, but encompasses failure to thrive, stunting secondary to chronic malnutrition, and idiopathic hypopituitarism. Some children show spontaneous catch-up growth when removed from the source of stress, without further treatment, but until now precise definition of this subgroup for the purpose of clinical identification has not been possible. METHODS: Hospital-referred children with growth failure unrelated to organic pathology, who came from stressful homes, were compared with children of short-normal stature identified from an epidemiological survey (n = 31). Growth-hormone dynamics were studied in the hospital group by a combination of diurnal profiles and provocation tests. The tests were repeated after a hospital stay of 3 weeks away from familial stress. Standard behavioural measures were obtained from home and school. FINDINGS: In a distinctive subgroup (n = 29), growth-hormone insufficiency was associated with characteristic behavioural features, especially hyperphagia and polydipsia, and a normal body-mass index. When the children were removed from their stressful home circumstances, growth-hormone insufficiency spontaneously resolved only in formerly hyperphagic subjects. 74% of the non-hyperphagic cases (n = 23) were anorexic, with a low body-mass index and normal growth-hormone responses to provocation tests. INTERPRETATION: We present explicit behavioural and developmental criteria by which the novel syndrome of hyperphagic short stature may be recognised clinically. Such children have a capacity for spontaneous recovery of growth-hormone production on removal from or reduction of stress. Discriminant and predictive validity of the core symptoms are demonstrated. Preliminary familial studies indicate a possible genetic predisposition.

Adolescent↗

PubMed1998

Acute fatty liver of pregnancy.

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that occurs during the third trimester. The obstetric team must be familiar with this disease because early diagnosis and prompt delivery have dramatically improved prognosis, which was often fatal for both mother and child. Clinicians must have a high index of suspicion for this condition when a woman has nausea or vomiting, abdominal pain (particularly epigastric), jaundice, polyuria-polydipsia (without diabetes), increased serum transaminase activity or thrombocytopenia in late pregnancy. The disease rarely recurs during a subsequent pregnancy. The cause is unknown, but some cases of acute fatty liver of pregnancy have been associated with a genetic deficiency of fatty acid beta-oxidation. Because of the possibility of this congenital deficiency, infants of affected mothers should undergo close follow-up from birth.

Acute Disease↗

PubMed1992

The aggression theory of schizophrenia: revisited.

The aggression theory of schizophrenia is a psychoanalytic theory which proposes that schizophrenia results from uncontrolled, deprivation-induced aggressive impulses. An animal model of the aggression theory is presented using predatory aggression as the source of arousal. Although neurochemical control of predatory aggression is nonspecific, anatomic control is located in the lateral hypothalamus across species. The lateral hypothalamus also controls schedule-induced polydipsia which has been implicated in schizophrenia. The aggression theory could be empirically evaluated by determining if schizophrenics respond differently than normals to scheduled feedings. Implications of the aggression theory are discussed.

Aggression↗

PubMed1986

Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome.

This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.

Acidosis↗

PubMed1985

Suppression of schedule-induced drinking and food-reinforced bar pressing by tail-pinch is not reversed by naloxone.

In Experiment 1 eleven food-deprived rats were tested in a schedule-induced drinking paradigm under both tail-pinch and non-tail-pinch conditions. Tail-pinch produced a strong suppression of schedule-induced drinking, licking, licks per milliliter, bar presses, and number of reinforcers received during 30-min test sessions. Experiment 2 showed that the narcotic antagonist naloxone (2 and 4 mg/kg) did not reverse the tail-pinch suppression of schedule-induced drinking and food-reinforced bar pressing. Experiment 3 demonstrated that the suppression of schedule-induced drinking by tail-pinch could not be attributed to a suppression of drinking behavior in general, as tail-pinch had no effect on deprivation-induced drinking. The failure of naloxone to reverse this blockade suggests that endogenous opiate systems do not play a very important role in the suppression of schedule-induced polydipsia by tail-pinch. It was suggested that the combination of both the schedule-induction paradigm and the tail-pinch procedure increased arousal levels to such a high level that all behaviors were suppressed.

Animals↗

PubMed2002

Sudden onset of diabetes with ketoacidosis in a patient treated with FK506/tacrolimus.

We report a 43-year-old man who presented diabetic ketoacidosis 1 year after receiving kidney transplantation. He was a recipient of renal transplantation treated with metyl-prednisolone and tacrolimus regimen. The serum level of tacrolimus was 12.4 ng/ml, and he showed hyperphagia before a month of admission. A week before admission, he was aware of polydipsia, polyuria, and general fatigue. He visited our hospital and was found to have severe hyperglycemia (925 mg/dl), significant ketosis and mild metabolic acidosis (pH 7.341), although he had not been diagnosed as diabetes mellitus. He administrated in our hospital, and was treated with insulin for 5 weeks. He was not obese (BMI = 18.2 kg/m(2)) and had no family history of type 2 diabetes. He was finally treated with diet therapy alone. The 24 h urine C-peptide secretion on the third hospital day was low (8.4 microg per day). However, no autoantibodies against pancreatic islets were positive, and his insulin secretion was recovered at discharge suggesting that he was not type 1 diabetes. Although, tacrolimus has been reported to cause or worsen diabetes mellitus, the present case suggests that it could cause severe decrease in insulin secretion which leading to diabetic ketoacidosis in lean subject without previous history of diabetes mellitus.

Adult↗

PubMed2002

Clinical features of a young Japanese woman having marked obesity and abrupt onset of diabetes mellitus with ketoacidosis.

The subject was a 26-year-old Japanese woman of 148 cm height, 96.2 kg of body weight (BW) (body mass index (BMI) of 43.8 kg/m(2)). She was referred to our hospital on May 1, 2000 for the evaluation of marked hyperglycemia with clinical symptom of general malaise, polydipsia, and ketonuria (3+). She did not smoke, or drink alcohol. But, she tended to eat lots of sweet food every day before the onset of this symptom. Her father was diagnosed type 2 diabetes mellitus. Her fasting plasma glucose and HbA(1c), and serum C-peptide were 398 mg/dl, 7.8% and less than 0.05 ng/ml [normal range: 0.94-2.8], respectively. She tested negative for anti-glutamic acid decarboxylase (GAD) antibodies and islet-cell antibodies. C-peptide level in her urine was as low as 3.4 microg/day. We immediately started insulin treatment under the diagnosis of abrupt onset of diabetes mellitus with diabetic ketoacidosis on the day of her admission, and the insulin treatment was continued after her being discharged. She showed continuous BW reduction until her BW reached approximately 60 kg, followed by her BW being plateau. During the period, intra-abdominal visceral fat (VF) and subcutaneous fat (SF) volume assessed by helical computerized tomography (CT) showed a substantial reduction [3.9-0.5 l for VF, 19-3.2 l for SF volume]. Pre-heparin plasma lipoprotein lipase (LPL) mass showed a considerably lower value when she had continuous BW reduction than did it when her BW reduction discontinued. These findings suggest that in this subject, continuous BW reduction after the abrupt onset of diabetes is closely associated with intra-abdominal fat mass reduction, which may be related to decreased production of LPL.

Adipose Tissue↗

PubMedDate not supplied

Reversal of diabetes by syngeneic transplantation of a radiation-induced rat insulinoma.

The growth and metabolic effects of a radiation-induced rat insulinoma were examined after subcutaneous subscapular transplantation into normal and streptozotocin diabetic NEDH rats. Streptozotocin diabetic rats exhibited hyperglycaemia, hypoinsulinaemia, impaired glucose tolerance without an insulin response, polyuria, polydipsia, hyperphagia and weight loss. Transplantation of tumour fragments gradually improved the physical and metabolic state over the following 3 weeks. Coincident with a progressive rise in plasma insulin between 10 and 17 days, the diabetic rats gained weight and reduced their food intake. The rats remained hyperglycaemic during this time, but developed hypoglycaemia with marked hyperinsulinaemia by 24 days. Furthermore, plasma glucose and insulin concentrations were not increased by an intraperitoneal glucose challenge, indicating greatly accelerated glucose clearance. Both the streptozotocin-treated and normal insulinoma-bearing rats incurred a fatal hypoglycaemic coma by 28-33 days after transplantation. Final body weights, tumour weights and concentrations of glucose and insulin were similar in the two groups. This study demonstrates reversal of streptozotocin diabetes by insulinoma transplantation. The hyperglycaemia and the accompanying diabetic environment did not modify tumour growth and development.

Adenoma, Islet Cell↗