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At least 757 records · Page 42Linked to original sources
PubMed1984

Drinking-water-induced copper intoxication in a Vermont family.

Three of four family members reported recurrent episodes of gastrointestinal illness while residing in a house in a small northwestern Vermont village. The father and two daughters repeatedly experienced episodes of emesis and abdominal pain after drinking water drawn from their kitchen faucet. One early-morning water sample taken from the family household contained a copper level of 7.8 mg/L, which is above the standard for drinking water (1.0 mg/L). Values for the second daughter's copper in hair analysis (1,200 micrograms/g) and copper in nail analysis (100 micrograms/g) were elevated (normal range 11 to 53 micrograms/g). The household was at the end of a 3/4-in (19.05-mm) copper main, and it is suspected that copper levels increased in water when the water remained stagnant in the main. All symptoms of the family resolved when they stopped drinking water in their home. This is the first report of copper-induced gastrointestinal illness attributable to a public supply of drinking water.

Adult↗
PubMed1997

[Hyponatremia due to prolonged excessive ingestion of water].

We report a 1.5-year-old boy admitted for restlessness and constipation. He was found to have hyponatremia caused by voluntary drinking of excessive amounts of water. Although unusual in children, intoxication by oral water is a recognized clinical syndrome in infants, 3-6 months old, fed with dilute formula. Water intoxication in older children is rare. The diagnosis was established by the water deprivation test.

Adolescent↗
PubMedDate not supplied

Hemolysis associated with water administration using a nipple bottle for human infants in juvenile pygmy goats.

A 4-month-old, 6.8-kg, castrated male pygmy goat was examined for recurrent episodic fever and red urine of 7 days' duration. A second, 3-month-old, 7-kg, intact female pygmy goat was presented for similar clinical signs. The red discoloration of the urine in each case was determined to be due to hemolysis with subsequent hemoglobinuria. In both cases, hemolysis and hemoglobinuria were closely associated with the goats consuming large volumes of water from a human infant's nipple bottle. A diagnosis of water intoxication-induced hemolysis and hemoglobinuria was made. Episodes of hemoglobinuria in the first case were consistently associated with dilute (specific gravity < 1.010) urine. Water intoxication has been associated with bottle-feeding in human infants and is also widely reported in human psychiatric patients. The small erythrocytes in goats appear to be the most sensitive of the domestic species to hypotonicity-induced hemolysis.

Animals↗
PubMedDate not supplied

Peritoneal toxicity of water: a model of chronic peritonitis caused by osmotic dysequilibrium in rats.

The purpose of this work was to determine whether the osmotic dysequilibrium created by intraperitoneal (i.p.) injection of pure water has any permanent, damaging toxic sequelae. Rats were injected i.p. with pure water on five successive days. Necropsies were performed 1 week after the last injection. Necropsies revealed fibrosis of peritoneal surfaces of liver and spleen, similar to the effects of chemical irritants but milder. The severity of the lesions depended on the dose of water and the number of injections. A few minutes of contact with pure water was sufficient to ensure subsequent development of fibrosis. Soon after the initial injury, the inoculum became less hypotonic and then isotonic. Isotonic or moderately hypotonic electrolyte solutions did not produce peritoneal fibrosis but very hypotonic solutions were toxic. Injection of the synthetic compound 48/80, which is known to cause discharge of mast cell granules, did not produce peritonitis, nor was contamination by endotoxin or by blood responsible for the lesions. Injection of water may be a useful method for investigating the role, if any, of mast cells and/or mesothelial cells in the toxic effects of osmotic dysequilibrium.

Animals↗
PubMed1989

Development of water dysregulation during Arieti's third stage of schizophrenia?

We found abnormal diurnal weight gain among 25% of acutely psychotic patients with schizophrenia and 68% of chronically psychotic patients with schizophrenia. They were weighed at 7:00 AM and 4:00 PM weekly for 3 weeks. We normalized the diurnal weight gain (NDWG) as a percentage by subtracting the 7:00 AM weight from the 4:00 PM weight, multiplying the difference by 100, and dividing the result by the 7:00 AM weight, NDWG was 0.93% +/- 0.89% for the 36 acutely psychotic patients and 2.2% +/- 1.5% for the 68 chronically psychotic patients (F = 25.297, p less than 0.0001). Drugs did not explain this difference. Our data, though preliminary, suggest that water dysregulation, as manifested by abnormal diurnal weight gain, develops in schizophrenia as patients progress into Arieti's third stage of this disorder. A longitudinal study design, rather than our cross-sectional one, would be necessary to assess developmental changes in schizophrenia.

Adult↗
PubMed1989

Osteopenia, pathological fractures, and increased urinary calcium excretion in schizophrenic patients with polydipsia.

Ten male chronic schizophrenic patients with polydipsia and 10 nonpolydipsic controls, matched for gender, diagnosis, duration of illness, age, and race, were studied by dual- and single-photon absorptiometry to estimate bone density of the lumbar spine and radius and by 24-hr urine collections to estimate urinary electrolyte excretion. Bone density was normal in the control group, but was abnormally low in the polydipsic group, which had a markedly increased incidence of fractures. Electrolyte excretion was normal in the control group and in the polydipsic group when water intake was restricted to normal amounts; increased urinary sodium and calcium excretion occurred in proportion to polydipsia. As polydipsia is associated with a number of physiological changes, the cause of the osteopenia is unclear; we suggest that a negative calcium balance caused by increased urinary calcium excretion induced by extracellular space expansion may play an important role in the causation of the skeletal changes.

Adult↗
PubMed1993

Disordered water homeostasis and cognitive impairment in schizophrenia.

To investigate a possible association between disordered water homeostasis and cognitive impairment in schizophrenia, neuropsychological tests were applied to 16 schizophrenic patients with severely deranged water homeostasis and to 16 matched schizophrenic controls. The patients with disordered water homeostasis tended to obtain poorer scores than the controls throughout, the differences being statistically significant for two of the tests (Wechsler Memory Scale Visual Reproduction and Trial Marking Test part A). These results were not ascribable to differences in the duration of the illness, premorbid IQ, medication, or electroconvulsive therapy received, or prominence of any particular symptoms. The results suggest the co-existence of disordered water homeostasis and cognitive impairment in a subset of schizophrenic patients.

Adult↗