Hypouricemia in Chronic Schizophrenic Patients With Polydipsia and Hyponatremia

Hanihara, Tokiji; Amagai, Isamu; Hagimoto, Hiroshi; Makimoto, Yasufumi

doi:10.4088/jcp.v58n0604

Cited by 12 publications

(3 citation statements)

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“…In a report of 3 chronic schizophrenic patients, hypouricemia was found in association with long-term polydipsia-hyponatremia syndrome [59]. However, patients in the present study were healthy, with no evidence for liver or kidney disease or significant calorie restriction.…”

Section: Discussioncontrasting

confidence: 62%

Homeostatic Imbalance of Purine Catabolism in First-Episode Neuroleptic-Naïve Patients with Schizophrenia

et al. 2010

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BackgroundPurine catabolism may be an unappreciated, but important component of the homeostatic response of mitochondria to oxidant stress. Accumulating evidence suggests a pivotal role of oxidative stress in schizophrenia pathology.Methodology/Principal FindingsUsing high-pressure liquid chromatography coupled with a coulometric multi-electrode array system, we compared 6 purine metabolites simultaneously in plasma between first-episode neuroleptic-naïve patients with schizophrenia (FENNS, n = 25) and healthy controls (HC, n = 30), as well as between FENNS at baseline (BL) and 4 weeks (4w) after antipsychotic treatment. Significantly higher levels of xanthosine (Xant) and lower levels of guanine (G) were seen in both patient groups compared to HC subjects. Moreover, the ratios of G/guanosine (Gr), uric acid (UA)/Gr, and UA/Xant were significantly lower, whereas the ratio of Xant/G was significantly higher in FENNS-BL than in HC. Such changes remained in FENNS-4w with exception that the ratio of UA/Gr was normalized. All 3 groups had significant correlations between G and UA, and Xan and hypoxanthine (Hx). By contrast, correlations of UA with each of Xan and Hx, and the correlation of Xan with Gr were all quite significant for the HC but not for the FENNS. Finally, correlations of Gr with each of UA and G were significant for both HC and FENNS-BL but not for the FENNS-4w.Conclusions/SignificanceDuring purine catabolism, both conversions of Gr to G and of Xant to Xan are reversible. Decreased ratios of product to precursor suggested a shift favorable to Xant production from Xan, resulting in decreased UA levels in the FENNS. Specifically, the reduced UA/Gr ratio was nearly normalized after 4 weeks of antipsychotic treatment. In addition, there are tightly correlated precursor and product relationships within purine pathways; although some of these correlations persist across disease or medication status, others appear to be lost among FENNS. Taken together, these results suggest that the potential for steady formation of antioxidant UA from purine catabolism is altered early in the course of illness.

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Section: Discussioncontrasting

confidence: 62%

Homeostatic Imbalance of Purine Catabolism in First-Episode Neuroleptic-Naïve Patients with Schizophrenia

et al. 2010

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“…In contrast, water intoxication causes hyponatremia by overwhelming the ability of the kidney to excrete a dilute urine; these patients have no natriuresis, and some may also present with depressed plasma uric acid. 11 Correction of asymptomatic hyponatremia due to water intoxication involves resumption of normal sodium and water intake, ensuring that correction occurs slowly as noted above. This child developed extreme hypona tremia associated with water intoxication and diminished sodium intake (<0.5 mmol/kg/ day) over 3 months, and correction occurred gradually over 7 days (<8 mmol/L/day) following resumption of a normal intake of both water and sodium.…”

Section: Discussionmentioning

confidence: 99%

Extreme Hyponatremia in a Child With Vegetative State and Water Intoxication

Baird

2009

Clin Pediatr (Phila)

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H yponatremia secondary to water intoxication is well known in infants. 1-8 However, extreme hyponatremia (serum [sodium] <100 mmol/L) from any cause, and at any age, is quite rare. This report of a 3-year-old male with vegetative state who developed extreme hyponatremia associated with gastrostomy tube feedings of a dilute formula includes a discussion of the differential diagnosis and therapy of this condition. Case ReportThe Integrated Scientific and Ethical Review Board of St Vincent Catholic Medical Center exempted this case report from review. A 3-year-old Hispanic male with vegetative state related to hypoxic ischemic encephalopathy (perinatally acquired) was transferred from a chronic care facility for the evaluation of coffee-ground secretions in both the gastrostomy and tracheostomy tubes. At his chronic care facility he did not require ventilatory support. Admission weight was 18.8 kg (increased slightly from 2 months prior [18.2 kg]), heart rate was 116 per minute, skin turgor was normal, and oral mucosa were pink and moist consistent with euvolemia. Other significant findings included microcephaly, contracted extremities, and nonpurposeful movements. There were no coffee-ground secretions in either the gastrostomy or tracheostomy tubes noted throughout this admission. Initial serum electrolytes were as follows: [sodium], 98 mmol/L; [potassium], 3.8 mmol/L; [chloride], <50 mmol/L; and [bicarbonate], 34 mmol/L. Initial urine studies provided the following values: [sodium], <5 mmol/L; osmolality, 295 mOsm/kg. The patient was admitted to the pediatric ward on restricted fluid intake (half of maintenance fluid requirements as dextrose 5% with 0.45% saline via a peripheral intravenous catheter) with a presumptive diagnosis of the syndrome of inappropriate antidiuresis (SIAD). Urinalysis revealed a specific gravity of 1.025; pH 5; protein, 30 mg/dL; glucose, 100 mg/dL; and urate crystals. Serum thyroid stimulating hormone was within the normal range (2.26 microunits/mL). After 8 hours, repeat serum electrolytes were as follows: [sodium], 103 mmol/L; [potassium], 5.4 mmol/L; [chloride], <50 mmol/L; and [bicarbonate], 36 mmol/L. Repeat urine [sodium] was still <5 mmol/L. After 18 hours, plasma [vasopressin] was elevated (13.8 pg/mL).He was then transferred to the pediatric intensive care unit where further history was obtained: he had been receiving gastrostomy tube feeding of a dilute formula (30 mL of Neocate with 40 mL of water every hour for 18 hours/day with an extra 60 mL water 4 times/day) for 3 months to limit excessive weight gain. Total water intake was 51 mL/kg/day. Fluid administration was then liberalized to maintenance with a routine formula (PediaSure) via the gastrostomy tube, and intravenous fluids were discontinued. Repeat laboratory evaluations over the next few days revealed a gradual increase in serum [sodium] without natriuresis, and a urine osmolality that remained >100 mOsm/kg until the fourth hospital day (Table 1), when the patient was transferred back to the pediatric ward. Urine ...

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“…La intoxicación acuosa aguda es frecuente en pacientes con patología psiquiátrica grave (como la esquizofrenia) con polidipsia crónica y osmolalidades en el límite bajo, con supresión permanente de ADH, que hacen hiponatremia aguda por otro factor de riesgo imprescindible: la ingestión masiva de agua en un momento determinado. Existen numerosas observaciones clínicas de este tipo de casos (5)(6)(7)(8). La intoxicación acuosa aguda en adultos sin patología psiquiátrica ni administración parenteral excesiva de líquidos hipotónicos es excepcional.…”

Section: Discussionunclassified