Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient was 32-year-old man, who received olanzapine for schizophrenia and developed polyuria and thirst without drinking soft-drinks after 4 months. Five months after the initiation of treatment, he developed diabetic ketoacidosis (blood glucose: 490 mg/dL, HbA1c: 15.5%). He was diagnosed with type 1 diabetes (glutamic acid decarboxylase (GAD)-Ab: 5.6 U/mL, IA-2 Ab: 5.9 U/mL, fasting C-peptide: 0.12 ng/mL) and was put on intensive insulin therapy. At four months after the onset of 1A diabetes, he experienced a honeymoon phase that was sustained until the 40th month of treatment. We hypothesize that the administration of olanzapine to a patient with pre-type 1A diabetes induced marked hyperglycemia and accelerated the onset of type 1A diabetes.
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PMID:Acute-Onset Type 1 Diabetes that Developed During the Administration of Olanzapine. 2815 79

Primary polydipsia (PP) has been defined as excessive intake of fluids. However, the pathogenesis of PP remains unexplored. Different theories include a dysfunction in the thirst mechanism, involvement of the hippocampus, stress-reducing behaviour and lesion occurrences in specific areas of the brain. Most studies have been performed in the psychiatric setting, indicating that PP coincides with schizophrenia, anxiety disorder and depression. However, an increasing number of case reports emphasise the incidence of PP in non-psychiatric patients. As often recommended by healthcare professions and in life-style programmes, the phenomenon of excessive fluid intake appears to be growing, especially in health-conscious and active people. PP is part of the polyuria-polydipsia syndrome, so the differential diagnosis diabetes insipidus (central or nephrogenic) must be excluded. The gold standard when differentiating between these disorders has been the water deprivation test. However, new options for distinguishing between these entities have been proposed e.g., measurement of copeptin, a reliable surrogate marker of the hormone arginine vasopressin (AVP). The major risk of excessive drinking is the development of hyponatraemia and the ensuing complications. In patients with PP, factors reducing the renal excretory capacity of the kidney such as acute illness, medications or low solute intake may accumulate in hyponatraemia. Treatment options for PP remain scarce. Different medication and behavioural therapy have been investigated, but never on a large scale and rarely in non-psychiatric patients. This review provides an overview of the pathophysiology, characteristics, complications, and outcomes of patients with PP in the medical and psychiatric patient.
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PMID:Primary polydipsia in the medical and psychiatric patient: characteristics, complications and therapy. 2961 1

Psychogenic polydipsia is a well-described phenomenon in those with a diagnosed psychiatric disorder such as schizophrenia and anxiety disorders. Primary polydipsia is differentiated from psychogenic polydipsia by the lack of a clear psychotic disturbance. We present a case of a 27-month-old boy who presented with polyuria and polydipsia. Laboratory studies, imaging, and an observed water deprivation test were consistent with primary polydipsia. Polydipsia resolved after family limited his fluid intake and began replacing water drinking with other transition objects and behaviors for self-soothing. This case highlights the importance of water deprivation testing to differentiate between causes of polyuria, thereby avoiding misdiagnosis and iatrogenic hyponatremia. Secondly, primary polydipsia can result during the normal stages of child development without overt psychiatric disturbances.
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PMID:A 27-Month-Old Boy with Polyuria and Polydipsia. 3021 Aug 89

We present a patient with schizophrenia who developed dexmedetomidine-induced polyuria after superficial parotidectomy. Two hours after starting the dexmedetomidine infusion, urine output increased from a baseline rate of 80 mL/h to a 7-hour average rate of 400 mL/h (range, 280-560 mL/h), the serum sodium concentration increased from 132 to 139 mEq/L, and urine-specific gravity was 1.006. Following dexmedetomidine discontinuation, the urine output decreased to an average of 66 mL/h (range, 40-100 mL/h). Close monitoring of urine output and serum sodium concentration may be indicated during dexmedetomidine infusion.
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PMID:Postoperative Dexmedetomidine-Induced Polyuria in a Patient With Schizophrenia: A Case Report. 3187 58


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