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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polydipsia and polyuria have a long association with schizophrenia. To assess the prevalence of polydipsia and polyuria in schizophrenia, urine volume was examined in medication-free chronic schizophrenic patients, normal controls, and nonschizophrenic patients. Mean urine volume was significantly higher in the schizophrenic patients (2319 +/- SD 2052 ml/24 hours) than in the other two groups (1054 +/- SD 471 ml/24 hours for nonschizophrenic patients and 1265 +/- SD 613 ml/24 hours for normals). Seven of 35 patients with schizophrenia but 0/7 nonschizophrenics had urine volumes greater than any normal control. Polyuria was associated with a good premorbid history and a positive neuroleptic response. Among polyuric patients, those with hyponatremia may represent a different, distinct subgroup. Neuroleptic treatment was associated with a further, significant increase in urine volume. Hence, polydipsia and polyuria appear to be relatively common in schizophrenia.
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PMID:Increased urine volume in chronic schizophrenic patients. 386 Aug 85

Review of 60 consecutive records of patients who died before the age of 53 years in a state mental hospital revealed that 27 of those patients (45%) had a schizophrenic disorder. Of those 27 patients, five (18.5%) died of the complications of self-induced water intoxication and schizophrenic disorders (SIWIS). Clinical, laboratory, and autopsy features of those five SIWIS patients and of an additional five SIWIS cases obtained from the literature include psychosis, polydipsia, polyuria, severe hyposthenuria (specific gravity 1.003 or less), hyponatremia, seizures, coma, and cerebral and visceral edema. SIWIS characteristically develops during Arieti's third or "preterminal" stage (5 to 15 years after onset of psychosis) of schizophrenic disorders and it must be included in the differential diagnosis of unexplained death among psychiatric patients. As there are no pathognomonic SIWIS tissue changes, the pathologist must carefully integrate clinical, laboratory, and autopsy findings to arrive at the proper diagnosis. When premortem findings of polydipsia and hyponatremia are not available, evidence of antecedent severe hyposthenuria and postmortem vitreous humor hyponatremia of less than 120 mEq/1 are strongly supportive of the diagnosis of death due to SIWIS.
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PMID:Death from self-induced water intoxication among patients with schizophrenic disorders. 397 77

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.
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PMID:Psychogenic polydipsia and water intoxication--concepts that have failed. 406 21

The complications of water intoxication are well documented in the medical literature. Less well appreciated is the frequent appearance of self-induced water intoxication in patients with schizophrenic disorders. Six such patients are described and compared with the findings in the literature. Nonedematous, nonhypovolemic hyponatremia is the invariable biochemical abnormality in this syndrome and its multiple causes are discussed, including the syndrome of inappropriate antidiuresis. Severe hyposthenuria (urinary specific gravity 1.003 or less) is the silent biological marker that always antedates the complications of self-induced water intoxication and schizophrenic disorders (SIWIS). While recognizing that all patients with polydipsia do not go on to develop water intoxication, this biological marker provides the means to detect patients who may be destined to develop SIWIS; early recognition may prevent the major complications of this syndrome.
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PMID:Evaluation of patients with self-induced water intoxication and schizophrenic disorders (SIWIS). 647 Jun 99

Compulsive water drinking (psychogenic polydipsia) is a well-recognized clinical entity that is often seen in individuals with psychiatric disorders, especially schizophrenia. Although urinary tract abnormalities including enlarged bladders and hydronephrosis have been reported, the presence of chronic renal failure is rarely reported in this disorder. We report four patients with psychogenic polydipsia who presented with chronic renal failure due to obstructive uropathy in the absence of demonstrable anatomic causes of obstruction. The likely mechanism of functional obstructive uropathy is bladder failure due to a combination of excessive water ingestion, enlarged bladder volumes, and use of anticholinergic medications.
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PMID:Compulsive water drinking in the setting of anticholinergic drug use: an unrecognized cause of chronic renal failure. 757 11

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

In this paper a detailed argument will be advanced in support of the notion that schizophrenia is fundamentally a diabetic brain state, henceforth referred to as 'cerebral diabetes'. Many extraneous features of cerebral diabetes have been observed, including positron emission tomography (PET) scans which reflect abnormal distribution patterns and diminished supplies of glucose in the brain. Equally, empirical research has demonstrated that plasma levels of essential fatty acids and prostaglandins are abnormally low, and low levels of glycoproteins in the urine of cerebral diabetics have also been observed. In addition, cerebral diabetics manifest a wide range of disturbing physical symptoms, such as, impaired sexual function, temperature control, low blood pressure, disrupted sleep patterns, excessive thirst, poor memory, insensitivity to pain, and chronic unhappiness, all of which can be attributed to disrupted neuroendocrine function. Thus, in order to persuasively assert the redefinition of schizophrenia as 'cerebral diabetes', we shall first explicate glucose regulation and transport in the brain and then outline how this interacts with essential fatty acids and prostaglandins, neurotransmission, and the neuroendocrine system. In so doing, we shall provide a metabolic explanation for all the prominent symptoms currently known to be associated with cerebral diabetes and indicate some future therapeutic interventions.
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PMID:Schizophrenia is a diabetic brain state: an elucidation of impaired neurometabolism. 773 17

Polydipsia among chronic psychiatric patients is poorly understood and underdiagnosed. It may have three stages: simple polydipsia, polydipsia with water intoxication, and physical complications. Epidemiological surveys have used staff reports and polyuria measures to identify polydipsic patients. Water intoxication has been screened by chart review, weight, or serum sodium data. According to these surveys, polydipsia, not explained by medically induced polyuria, may be present in more than 20% of chronic inpatients. Up to 5% of chronic inpatients had episodes of water intoxication although mild cases may have been missed. Single time point surveys show that 29% of polydipsic patients had presented water intoxication. Methodologically limited clinical studies suggest that polydipsia with water intoxication rather than simple polydipsia may be associated with poor prognosis in schizophrenia. Epidemiological surveys found polydipsia with water intoxication to be associated with chronicity, schizophrenia, smoking, some medications, male gender, and white race. New pathophysiological models need to elucidate these findings.
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PMID:Polydipsia and water intoxication in psychiatric patients: a review of the epidemiological literature. 801 88

Disturbances of water homeostasis have frequently been reported in schizophrenia. Water homeostasis is regulated by arginine vasopressin (AVP), the renin-angiotensin system and natriuretic hormones. The aim of this study was to determine the activity of the central renin-angiotensin system in schizophrenia by measuring levels of angiotensin-converting enzyme (ACE) in the cerebrospinal fluid (CSF) and blood in 14 in-patients with schizophrenia on neuroleptic medication and in 9 healthy volunteers. The levels of CSF ACE were significantly higher in the schizophrenia group. There were no correlations between CSF ACE and gender, age, age at first episode, duration of illness, term of hospitalization or neuroleptic dosage. No correlations between CSF ACE and serum ACE were found in either group. The authors suggest an activated central renin-angiotensin system in schizophrenia at least during antipsychotic drug treatment, which may cause 'psychogenic' polydipsia in some patients. ACE and the brain renin-angiotensin system may also play a role in the regulation of neuron growth and differentiation in schizophrenia.
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PMID:Elevated angiotensin-converting enzyme (kininase II) in the cerebrospinal fluid of neuroleptic-treated schizophrenic patients. 809 92

506 patients with schizophrenia, diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-III) criteria, were included in a long term treatment programme with remoxipride, a selective dopamine (D2)-receptor antagonist. This overview includes pooled data from all patients who have been treated long term with remoxipride in clinical trials, focusing on patients treated for more than 6 months (n = 283). Remoxipride was administered in daily doses of 75 to 600mg. The assessment tools were Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression (CGI), Simpson and Angus scale, Abnormal Involuntary Movements Scale (AIMS) for abnormal involuntary movements, adverse events/symptoms using a 26-item checklist, clinical chemistry, and haematology and cardiovascular investigations. The majority of patients had a long duration of illness (median 11 years). 67% of patients (340/506) withdrew from treatment before 12 months and 44% (223/506) stopped treatment before 6 months. The median BPRS total score decreased during the first 3 months from 23 to 12, and this level of improvement was maintained throughout the 12-month period. Treatment-emergent adverse events reported by more than 5% of the patients were insomnia, tiredness, drowsiness and tremor in the group treated for 6 to 12 months. No symptoms, including checklist extrapyramidal symptoms (EPS), were reported by more than 5% of patients treated for 12 months. Low frequencies of EPS according to the Simpson and Angus scale were seen in patients treated for more than 6 months (n = 147). A small but statistically significant reduction of the mean total AIMS score from baseline to last rating was observed. There were infrequent changes in heart rate, resting diastolic blood pressure and electrocardiogram (ECG). Clinical chemistry and haematology data showed no evidence of clinically significant changes over time during the 12 months of treatment. Among 506 patients, 7 suicides and 7 suicide attempts occurred during the study period. Other serious adverse events were abnormal liver function test (2 cases), gastrointestinal, urinary retention, status epilepticus (psychotic polydipsia), granulocytopenia (1 each) and myocardial infarction (5 cases). Remoxipride is of potential value as a drug which is both effective and well tolerated in the long term management of patients with schizophrenia.
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PMID:Tolerability of remoxipride in the long term treatment of schizophrenia. An overview. 832 49


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