Diurnal variation of urinary excretion for patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome)

Ten patients [8 men and 2 women, mean age (SD) 37.6 +/- 6.5 years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent serial determinations at 6:00 AM, 12 noon, 6:00 PM, and 12 midnight of levels of urinary creatinine concentration (UCR), urinary specific gravity (SPGR), and urinary osmolality (UOSM) on 8 consecutive Thursdays. Diurnal variation (p less than 0.015) was present in the case of each parameter of urinary excretion (UCR, SPGR, and UOSM). These three parameters remained very low throughout the day (mean UCR 19.0 mg/dl, mean SPGR 1.0033, and mean UOSM 112.6 mosmol/kg), which is consistent with severe and persistent hyposthenuria, and each parameter correlated well with the other two parameters (r between 0.78 and 0.93, p less than 0.001). The 6:00 PM (UC6PM) value for UCR correlated best with the daily mean UCR (UCM), providing the simple linear regression UCM = 0.7615 X UC6PM + 6.1503 (r = 0.912, p = 0.0005) for the 10 PIP patients. Twenty-four-hour urinary volume (24UV) could then be estimated using UCM and values of 17.5 and 12.5 mg creatinine/kg body weight for male and female PIP patients, respectively, to calculate the daily urinary excretion of urinary creatinine. The group mean 24UV was 6963 ml, with a range of 4934-9884 ml. We hope that information about the diurnal variation of urinary excretion (21.6%, 20.5%, 27.4%, and 30.4% of 24UV excreted in consecutive quartiles commencing with the 12 midnight to 6:00 AM quartile), coupled with the utilization of the equation UCM = 0.7615 X UC6PM + 6.1503 (r = 0.912, p = 0.0005) to estimate UCM as an index of 24UV in the PIP syndrome, will provide tools to better elucidate the relationship between psychosis and water dysregulation.     

Serum ANP and ADH after subarachnoid hemorrhage and hyponatremia]

We determined serum atrial natriuretic peptide (ANP) and anti-diuretic hormone (ADH) on a time course basis in cases of subarachnoid hemorrhage and studied their influence on the development of hyponatremia. Twenty six cases of subarachnoid hemorrhage were admitted to our hospital in the past 1 year, and by the site of ruptured aneurysms, there were Acom 6 cases, ICA 6 cases, MCA 5 cases and VA BA 4 cases. Serum ANP and ADH levels were determined in the acute phase on Day 1-4, in the hyponatremia phase on Day 5-14 and in the chronic phase on Day 15 downward. Levels of not more than 130 mEq/l were regarded as hyponatremia. Cases showing other evident causes such as heart failure and renal insufficiency were excluded. In the normal control group (n = 20) which was admitted to this hospital for a close check-up, serum ANP was 26.5 +/- 11.6 pg/ml (10-50); levels of more than 50 pg/ml were regarded as being abnormally high. 1) Hyponatremia was observed in 7 cases (26-9%); the day of onset was 11.9 hospital day. The duration was 5.0 days and the minimum serum Na level was 126.4 mEq/l. 2) The serum ADH level was high regardless of whether or not there was the development of hyponatremia in the acute phase but tended to decrease gradually and became normal in the hyponatremia phase. 3) The serum ANP level in the cases of hyponatremia was 40.7 +/- 9.1 pg/ml in the acute phase, 69.0 +/- 25.7 pg/ml in the hyponatremia phase and 40.2 +/- 21.5 pg/ml in the chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diurnal weight gain as a predictor of serum sodium concentration in patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome)

Ten male patients (mean age 37.3 +/- 6.4 years) with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent measurement of weight, sitting and standing blood pressure, and serum sodium concentration at 7 a.m. and 4 p.m. weekly for 8 consecutive weeks. Blood pressure was higher in the afternoon than in the morning. The diurnal decrease in serum sodium (141.4 +/- 2.8 to 134.2 +/- 4.8 mEq/l) was associated with a diurnal increase in weight (78.4 +/- 9.7 to 80.0 +/- 10.3 kg). When the weight increase was normalized by dividing by 7 a.m. weight (NDWG), the following relationship evolved: diurnal serum sodium decrease = 3.060 + [201.728 x NDWG]. Therefore, NDWG accounted for 63.1% of the variability of serum sodium. Using the known relationship of plasma water, total body water, and total body weight, we calculated that antidiuresis (afternoon weight gain) accounted for 62.5% of afternoon hyponatremia. Thus, two separate methods of calculating the relationship between antidiuresis and hyponatremia provided remarkably similar findings. We derived a table to predict 4 p.m. serum sodium values based on 7 a.m. weight, 7 a.m. serum sodium, and 4 p.m. weight.     

Diurnal variation in water homeostasis among schizophrenic patients subject to water intoxication

Among seven schizophrenic patients subject to water intoxication (six men and one woman, mean age 39.1 +/- 6.9 years), we measured serum sodium, plasma arginine vasopressin, and urine osmolality at 7 a.m. and 4 p.m. on eight consecutive Thursdays. On the days of greatest diurnal change in serum sodium, the 7 a.m. serum sodium was 141.1 +/- 1.8 mEq/l and the 4 p.m. value was 129.9 +/- 3.2 mEq/l. Plasma vasopressin also tended to be lower at 4 p.m. but, in many cases, was inadequately suppressed for the level of hyponatremia. The urine was dilute at both 7 a.m. and 4 p.m. and mean urine osmolality did not differ at the two times. In three patients, urine osmolality was consistently subnormal relative to plasma vasopressin at both 7 a.m. and 4 p.m. This abnormality was consistent with nephrogenic diabetes insipidus secondary to lithium and, possibly, phenytoin which the patients received to protect them against hyponatremia. We conclude that the combination of polydipsia and abnormal osmoregulation of vasopressin secretion contributes importantly to the afternoon hyponatremia found in schizophrenic patients subject to water intoxication.     

Roles of arginine vasopressin and atrial natriuretic peptide in polydipsia-hyponatremia of schizophrenic patients

Respective contributions of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) to the urinary sodium concentration were evaluated in 23 naturalistic incidents of polydipsia-hyponatremia observed in 11 hospitalized schizophrenics (10 males and 1 female). The sodium concentration of the spontaneously excreted urine was examined before and after the forced water restriction. Before the water restriction, mean (+/-S.D.) plasma ANP was 52.8 +/- 33.9 pg/ml (range = 6.9-137). Plasma AVP levels were below 0.3 pg/ml in 15 episodes; relatively high levels (> or = 0.3) were noted in eight episodes. Means of urinary sodium concentration (mEq/l) were significantly higher in episodes with high AVP (> or = 0.3) alone (25.0 +/- 8.2, n=4), with high ANP (> 43) alone (21.3+/-7.4, n = 9), and with high AVP and ANP (26.8 +/- 6.4, n = 4) as compared to that of the low AVP (< 0.3) and ANP (< or = 43) group (13.5 +/- 3.7, n = 6). The data indicate that the elevated urinary sodium in polydipsic patients is possibly due to the AVP-induced antidiuresis and/or the ANP-induced natriuresis. In addition, we observed a close relationship between elevated plasma AVP and vomiting, suggesting that vomiting is one of the causal factors responsible for AVP elevations in this syndrome.     

The use of demeclocycline in the treatment of patients with psychosis,intermittent hyponatremia,and polydipsia (PIP syndrome)

Eight patients (7 men and 1 woman, mean age 43.1 ± 8.9 years) with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent treatment with demeclocycline in an effort to normalize serum sodium levels and thereby protect the PIP patients against complications including hyponatremic seizures and coma. There tended to be an improvement (p=.080) in early morning serum sodium following treatment with demeclocycline (baseline 132.6±SD 3.3 and treatment serum sodium 134.8±SD 3.3 mEq/1). At the same time, there was an increase (p=.043) in urinary specific gravity following treatment with demeclocycline (baseline 1.0047±SD .0029 and treatment urinary specific gravity 1.0063±SD .0026). Clinical indications for and potential mechanisms of action of demeclocycline treatment in the PIP syndrome are discussed.     

Cerebral salt wasting syndrome in children with acute central nervous system injury

The purpose of this investigation was to describe the causes, clinical pattern, and treatment of cerebral salt wasting syndrome in children with acute central nervous system injury. This retrospective study focused on patients120 mEq/L), and volume depletion. Fourteen patients were identified with cerebral salt wasting syndrome, 12 after a neurosurgical procedure (8 brain tumor, 4 hydrocephalus) and 2 after severe brain trauma. In 11 patients the cerebral salt wasting syndrome was diagnosed during the first 48 hours of admission. Prevalence of cerebral salt wasting syndrome in neurosurgical children was 11.3/1000 surgical procedures. The minimum sodium was 122+/-7 mEq/L, the maximum urine osmolarity 644+/-59 mOsm/kgH2O. The maximum sodium supply was 1 mEq/kg/h (range, 0.1-2.4). The mean duration of cerebral salt wasting syndrome was 6+/-5 days (range 1-9). In conclusion, cerebral salt wasting syndrome can complicate the postoperative course of children with brain injury; it is frequently present after surgery for brain tumors and hydrocephalus and in patients with severe head trauma. Close monitoring of salt and fluid balance is essential to prevent severe neurologic and hemodynamic complications.     

Possible malignant neuroleptic syndrome that associated with hypothyroidism

A 54-year-old woman with schizophrenia presented to hospital with unconsciousness, fever and marked muscle rigidity. She had been given fluphenazine decanoete 20 mg intramuscularly 15 days before the admission and she had continued taking haloperidol 20 mg daily and oral biperiden 2-4 mg. She was extremely rigid and unresponsive. On laboratory investigations revealed: serum sodium 120 mEq/l, creatinine phosphokinase 12,980 IU/l (normal up to 170), lactate dehydrogenase 1544 IU/l (150-500), free trioidothyronine < 1.00 pg/ml (1.5-4.5), free throxyine 0.76 ng/dl (0.8-1.9), thyroid stimulating hormone 1.14 microU/ml (0.4-4), cortisol (at 8.00 a.m.) 9 microg/dl (5-25). Antipsychotic drugs were withdrawn after admission. A diagnosis of secondary adrenal insufficiency and secondary hypothyroidism was made. Hormonal substitution with hydrocortisone and levothyroxine and correction of hyponatremia with intravenous hypertonic saline solution resulted in rapid improvement of symptoms and signs. It seems that the symptoms and signs of hypothyroidism and hyponatremia were attributed to acute psychosis in this patient. As a conclusion failure to recognize the endocrinopathy may not only produce recovery difficulties but also psychiatric and endocrine repercussions if psychotropic medications are given in such masked cases.     

Hyponatremia: cerebral symptoms and role in central pontine myelinolysis

Central nervous system symptoms due to hyponatremia is highly dependent on its acuteness and cause. Severe acute hyponatremia (serum sodium less than 125 mEq/l) often causes confusion, lethargy, seizures or frank coma due to brain oedema. If therapy is delayed, hyponatremia carries a high mortality rate, and risk of irreversible brain damage. Hyponatremia should probably be corrected to 125-130 mEq/l at a rate of 1.5-2.0 mEq/l/h. Malnourished alcoholic patients with hyponatremia may represent a special case with possible dangers of central pontine myelinolysis if a very low serum sodium is corrected acutely to normonatremic or hypernatremic levels. Mortality in this subgroup is high whatever the therapy.     

A case of amyotrophic lateral sclerosis with SIADH and throbbing headache induced by selective serotonin reuptake inhibitor]

A 57-year-old man with amyotrophic lateral sclerosis (ALS) was admitted because of depressive state. Selective serotonin reuptake inhibitor (SSRI), an antidepressant, was started on the admission day. The throbbing headache in the right temporal region appeared on day 3, and an analgesic drug was not completely effective. Serum sodium value on admission was 131 mEq/l. After SSRI was started the hyponatremia rapidly progressed, and it became 112 mEq/l on day 4. SSRI was discontinued, and headache disappeared; serum sodium was improved to 129 mEq/l. It has been reported that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may be associated with ALS. We consider that subclinical SIADH was manifested by SSRI in this case. SSRI seems to be a cause of headache, since headache disappeared completely by discontinuation of SSRI.     

Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances. METHODS: We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. RESULTS: Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. CONCLUSIONS: A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.     

Treatment of psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) using lithium and phenytoin

Six patients [5 men and 1 woman, mean age 37.3 +/- 8.2 (SD) years] with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent a sequence of treatments in an effort to normalize basal serum sodium levels and thereby protect the patients against complications, including hyponatremic seizures and coma. The morning baseline group mean basal serum sodium value was 132.5 +/- 3.8 meq/liter. Over a 20-month period, the sequence of treatments was salt-added diet, lithium and phenytoin, and lithium alone. Each treatment program yielded morning group mean basal serum sodium determinations superior to baseline values, except for the program of lithium alone, which could not be tolerated. The combination of lithium and phenytoin provided a morning group mean basal serum sodium level of 140.6 +/- 3.2 meq/liter, which was superior (p less than 0.01) to all other treatment modalities. Early morning hyposthenuria persisted throughout the 20-month period of observation.     

Psychogenic polydipsia and water intoxication—Concepts that have failed

Ten patients (8 men, 2 women; mean age 38.7 ± 8.1 years), 7 of whom had schizophrenic disorders and 3 of whom had bipolar disorder (manic-depressive illness), manifested psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome). The relationship between serum sodium and urinary water excretion among the 10 PIP patients is described in detail. The success of lithium in improving serum sodium levels and in decreasing urinary water excretion among the three PIP patients with bipolar disorder and the failure of changes in urinary water excretion to explain changes in serum sodium levels among the 10 PIP patients argue against “psychogenesis” as the explanation for the polydipsia and excessive water intake as the sole explanation for hyponatremia or complications ascribed to water intoxication.     

Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Following subarachnoid hemorrhage, the plasma concentration of atrial natriuretic factor is elevated and appears to be independent of atrial stretch. While the hypothalamus and circumventricular organs contribute to sodium and intravascular volume regulation, their influence on atrial natriuretic factor is not known. We tested the hypothesis that, following subarachnoid hemorrhage, suprasellar cisternal blood, intraventricular blood, or ventricular enlargement would be associated with elevated plasma levels of atrial natriuretic factor. Computed tomograms of 26 patients performed less than or equal to 3 days after hemorrhage were analyzed to determine the presence of suprasellar or intraventricular blood and enlargement of the third or lateral ventricle. These results were correlated with the plasma atrial natriuretic factor and serum sodium concentrations. The initial atrial natriuretic factor concentration was elevated and was higher in patients with suprasellar or intraventricular blood than in those without (suprasellar: 131 +/- 20 and 54 +/- 10 pg/ml, respectively; intraventricular: 137 +/- 25 and 84 +/- 31 pg/ml, respectively). The atrial natriuretic factor concentration remained higher over the week following hemorrhage in patients with suprasellar blood than in those without (127 +/- 16 and 68 +/- 12 pg/ml, respectively). The atrial natriuretic factor concentration was not correlated with hyponatremia (125-134 meq/l) or age-corrected ventricular size. Hyponatremia did not correlate with the presence of intraventricular or suprasellar blood. Our data suggest that suprasellar and intraventricular blood disturb hypothalamic function, resulting in an elevated plasma atrial natriuretic factor concentration. The presence of a direct relation between atrial natriuretic factor and hyponatremia remains unclear.     

Abnormal diurnal weight gain among institutionalized patients with manic-depressive spectrum disorders

We found diurnal weight gain to be abnormal among 41 institutionalized patients with manic-depressive spectrum disorders. They were weighed at 7 AM and 4 PM weekly for three weeks. We normalized the diurnal weight gain (NDWG) as a percentage by subtracting the 7 AM weight from the 4 PM weight, multiplying the difference by 100, and then dividing the result by the 7 AM weight. NDWG was 2.216 +/- 1.513 percent for the study population, .631 +/- .405 percent for 16 young, newly admitted controls, and .511 +/- .351 percent for 29 normals. Abnormal NDWG may be an additional feature of manic-depressive spectrum disorders.     

Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage]

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.     

Hyponatremia and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage]

We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. It was mild (126 to 130 mEq/l) in 15 patients, moderate (121 to 125 mEq/l) in 3 patients, and severe (116 to 120 mEq/l) in 1 patient. Cerebral vasospasm was evaluated by angiography, symptoms and CT finding. Angiographical vasospasm was found in 57 patients, symptomatic vasospasm in 38 patients and low density area on CT in 20 patients. Angiographical vasospasm developed in 15 of the 19 patients (78.9%) with hyponatremia, symptomatic vasospasm in 16 patients (84.2%), low density area on CT in 8 patients (42.1%), the difference being significantly high. (respectively, p < 0.01, p < 0.001 and p < 0.01 by chi-square test) Polyuria of 2500 ml or more immediately before the onset of hyponatremia developed in 14 patients (87.5%). When symptomatic vasospasm and hyponatremia coincided, there were only 4 patients in which symptomatic vasospasm was preceded by hyponatremia. So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.     

Th1 and Th2 serum cytokine profiles characterize patients with Hashimoto's thyroiditis (Th1) and Graves' disease (Th2)

OBJECTIVES: The aim of this study was to document the pattern of immune response, assessed by the measurement of both Th1 and Th2 serum cytokines, in patients suffering from autoimmune thyroid disease and toxic nodular goiter. METHODS: Both Th1 and Th2 serum cytokine levels were assayed in patients suffering from Graves' disease (GD, n = 25), Hashimoto's thyroiditis (HT, n = 21), and toxic nodular goiter (TNG, n = 7) and compared with corresponding levels of 25 healthy controls. Serum concentrations of IL-2, IL-1 beta, INF-gamma, TNF-alpha, IL-12, IL-15, IL-10, IL-18, IL-4 and IL-5 were assayed in fasting serum samples. RESULTS: It was found that patients with HT had higher IL-2 serum levels (12.16 +/- 0.66 pg/ml) compared to patients with TNG (9.25 +/- 0.84 pg/ml), GD (7.86 +/- 0.30 pg/ml) and controls (7.36 +/- 0.45 pg/ml; p = 0.0001), higher INF-gamma levels (7.60 +/- 0.33 pg/ml) compared to patients with TNG (5.77 +/- 0.55 pg/ml), GD (5.74 +/- 0.24 pg/ml) and controls (5.09 +/- 0.27 pg/ml; p = 0.0009), higher IL-12 levels (3.57 +/- 0.19 pg/ml) compared to patients with TNG (2.57 +/- 0.21 pg/ml), GD (2.48 +/- 0.13 pg/ml) and controls (2.59 +/- 0.23 pg/ml; p = 0.004), and higher IL-18 levels (27.52 +/- 1.75 pg/ml) compared to patients with TNG (18.71 +/- 2.24 pg/ml), GD (15.44 +/- 1.39 pg/ml) and controls (15.16 +/- 1.62 pg/ml; p = 0.0002). In contrast, patients with GD had higher serum levels of IL-4 (4.11 +/- 0.33 pg/ml) compared to patients with HT (3.0 +/- 0.16; p = 0.02) and higher IL-5 levels (4.22 +/- 0.30 pg/ml) compared to patients with TNG (3.21 +/- 0.58 pg/ml), HT (2.75 +/- 0.16 pg/ml) and controls (2.0 +/- 0.19 pg/ml; p = 0.0001). Patients had lower IL-1 beta serum levels (TNG 2.45 +/- 0.20, HT 2.52 +/- 0.14, GD 2.68 +/- 0.12 pg/ml) compared to controls (3.6 +/- 0.20 pg/ml; p = 0.008). CONCLUSIONS: The above findings suggest that a Th1 pattern of immune response characteristic of cellular immunity is dominant in HT, whereas the predominance of Th2 cytokines in GD indicates a humoral pattern of immune reaction.     

Correlation of parameters of urinary excretion with serum osmolality among patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome)

Nine patients (seven men and two women, mean age 36.3 +/- SD 6.7 years), six of whom had schizophrenic disorders, two of whom had bipolar disorder (manic-depressive illness), and one of whom had schizoaffective disorder, manifested psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome). Their stable pattern of hyposthenuria allowed us to predict 24-hr urinary volume on the basis of estimated daily urinary creatinine and early morning urinary creatinine concentration. Lithium and carbamazepine (Tegretol) had little, if any, effect on polyuria. Correlations of parameters of urinary excretion with serum osmolality among our nine PIP patients failed to implicate water consumption as the exclusive cause of serum hypoosmolality and attendant complications usually ascribed to "water toxicity" in the PIP syndrome. Discussed, also, is the overlap of the clinical and laboratory features of the PIP syndrome with the clinical and laboratory features of both diabetes insipidus and the syndrome of inappropriate antidiuresis.     

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.