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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats treated chronically with dopamine receptor blockers were found to have an increase in striatal 3H-dopamine binding and adenylate cyclase activity as manifestations of receptor supersensitivity. Both the increase in binding and in adenylate cyclase activity were reversed by chronic 1-dopa treatment, presumably by increasing the supply of specific ligand (dopamine). The use of deliberate receptor sensitivity manipulation may be useful as a treatment for conditions involving disturbances in receptor sensitivity such as tardive dyskinesia and insulin resistant diabetes.
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PMID:Reversal of two manifestations of dopamine receptor supersensitivity by administration of L-dopa. 84 96

Two studies examine the prevalence of tardive dyskinesia (TD) in neuroleptic-treated diabetic patients. Study 1 compared 38 diabetic patients with 38 nondiabetic patients treated for psychotic disorders with low to moderate doses of neuroleptics (mean chlorpromazine equivalents = 300 mg/day) for an average of 18 years. Study 2 compared 24 diabetic and 27 nondiabetic patients treated for an average of 2.6 years with a mean 31 mg/day of metoclopramide for gastrointestinal disease. Patients were examined for TD using standardized scales by raters blind to all treatment and illness variables. In both studies, there were no differences between the diabetic and nondiabetic groups in age, sex, type of psychiatric illness, and dose and duration of neuroleptic treatment or severity of parkinsonism. In both studies, the diabetic patients had significantly greater prevalence and severity of TD. No measures of diabetes severity were associated with TD in either study. Possible pathophysiologic mechanisms for the increased prevalence of TD in neuroleptic-treated patients with diabetes will be discussed.
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PMID:Tardive dyskinesia and diabetes mellitus. 136 76

In a controlled study, we compared the prevalence of tardive dyskinesia in 38 neuroleptic-treated diabetics with the prevalence of tardive dyskinesia in a group of 38 nondiabetic neuroleptic-treated controls, matched for age, sex, psychiatric diagnosis, and dose and duration of neuroleptic treatment. Members of each group were evaluated for movement disorders by a rater who used standard rating scales and was "blind" to all diagnoses and treatments. Neuroleptic-treated diabetics had a significantly higher prevalence and severity of tardive dyskinesia. There were no differences between groups on other possible risk factors for tardive dyskinesia, including parkinsonism, anticholinergic drug treatment, or cognitive function. These data suggest that diabetes mellitus should be examined further as a risk factor for tardive dyskinesia.
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PMID:The prevalence of tardive dyskinesia in neuroleptic-treated diabetics. A controlled study. 167 43

Chronic neuroleptic therapy may be associated with the development of diverse movement disorders including Tardive dyskinesia (TD), Parkinsonism, dystonia, and akathisia in a subset of schizophrenic patients. It is presently unknown why only a proportion of neuroleptic-treated patients develop these movement disorders. In the following communication, we present a series of studies which demonstrate that the development of these movement disorders may be facilitated by certain risk factors including disturbances in pineal melatonin functions, diabetes mellitus, cognitive deficits, suicidal behavior, and disturbances in the functions of the choroid plexus. Recognition of these biological factors may prove useful in: (a) further understanding of the pathophysiology of these disorders, and (b) identifying patients at risk for these movement disorders.
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PMID:Risk factors for neuroleptic-induced movement disorders. 168 14

Diabetes mellitus has been identified as a possible risk factor for tardive dyskinesia. The authors examined 160 elderly individuals who were beginning neuroleptic treatment; 24 had diabetes and 136 did not. After 43 weeks of neuroleptic exposure, the cumulative incidence rates of tardive dyskinesia were 54.1% (SE = 5.6%) for the diabetics and 25.6% (SE = 16.1%) for the nondiabetics.
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PMID:Diabetes and development of tardive dyskinesia. 809 87

A retrospective analysis of 812 patients admitted to the Ross Tilley Burn Centre between 1984 and 1992 resulted in 37 cases of burn injuries which were directly related to premorbid disabilities. The majority of these burns (83.8 per cent) occurred in the patient's home, most commonly as scald injuries in the bath tub, the shower, or following hot water spills. Nineteen patients were male, 17 were female. The median age was 58 years. Six patients had spinal cord disorders: four had traumatic cord damage, two had spina bifida. Six patients had seizure disorders. Five of these patients had been taking anti-seizure medications, but all had subtherapeutic blood levels on admission to hospital. Two patients had diabetes mellitus with peripheral neuropathies. Thirteen patients had four miscellaneous neurological disorders, including: tardive dyskinesia (two), CVA (four), Parkinson's disease (two), Alzheimer's disease (two), cerebral palsy (one), multiple sclerosis (one) and blindness (one). Three patients had a diagnosis of syncope. Two patients had emphysema, and four were morbidly obese. The average length of stay (LOS) for the disabled patients was 27.6 days for a median burn size of 10 per cent body surface area (BSA), compared to an average LOS for the general population of 25.7 days for a larger median burn size of 21 per cent BSA. The mortality rate was also much higher in the disabled population (22.2 per cent vs. 6.0 per cent). Most of these burn injuries were preventable. A series of burn prevention guidelines is presented, in an attempt to reduce the incidence of these burn injuries in disabled patients.
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PMID:Burns in the disabled. 850 62

The effect of streptozotocin (STZ)-induced diabetes and a combination of chronic treatment with haloperidol (HPD) on dopamine (DA)D2, serotonin (5-HT) 5-HT1A and 5-HT2A receptors was investigated in rat brain. Rats were randomly assigned to one of four groups: vehicle-vehicle, STZ-vehicle, vehicle-HPD, and STZ-HPD groups. Four weeks after single administration of STZ (65 mg/kg IV) or vehicle (citrate buffer), rats received depot HPD (4 mg/kg IM) or vehicle (sesame oil) once a week for 4 weeks. Sixteen days after the last injection of HPD or vehicle, rats were sacrificed, and the density of binding sites was determined using [3H]spiperone as ligand in the striatum (D2),[3H]8-hydroxy-2-(di-n-propyl)-aminotetraline in the hippocampus (5-HT1A), and [3H]ketanserin in the frontal cortex (5-HT2A). The density of D2 receptors was significantly increased in the vehicle-HPD compared to vehicle-vehicle controls. However, striatal D2 receptor density of the STZ-HPD and the STZ-vehicle were not significantly different from the vehicle-vehicle group. A significant increase in cortical 5-HT2A receptor density was observed only in the group of STZ-vehicle. Treatment with STZ, HPD, or the combination thereof, did not affect the density of 5-HT1A receptors. The affinity constants for D2, 5-HT1A, and 5-HT2A receptors were not affected by any treatment. These results suggest that diabetic state may affect brain serotonergic activity via an increase in the density of 5-HT2A receptors. This may indicate an increased vulnerability to major depression in patients with diabetes. The lack of an effect of the combined chronic treatment with STZ and HPD on the D2 receptor density may correspond to the increased risk to develop tardive dyskinesia in patients with diabetes.
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PMID:The effect of streptozotocin-induced diabetes on dopamine2, serotonin1A and serotonin2A receptors in the rat brain. 913 34

The incidence of S(-)-apomorphine-induced vacuous chewing movements (VCMs) as a model for tardive dyskinesia was investigated in streptozotocin (STZ)-induced diabetic rats. A single dose of STZ (65 mg/kg, intravenously) caused a diabetic state (hyperglycemia, 480-490 vs. 116-118 mg/dl in naive rats). S(-)-apomorphine (250 micrograms/kg, subcutaneously)-induced VCMs were significantly intensified in diabetic rats which had received STZ 9 weeks previously. The enhancement of VCMs was also observed in nondiabetic rats which received subsequent treatment with depot haloperidol (4 mg/kg, intramuscularly, once a week, every week for 4 weeks) followed by a 2-week washout period. The ability of haloperidol to enhance VCMs was attenuated in diabetic rats. The implications of these results in relation to altered neurotransmissions in STZ-induced diabetes are discussed.
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PMID:Increased S(-)-apomorphine-induced vacuous chewing and attenuated effect of chronic haloperidol treatment in streptozotocin-induced diabetic rat. 916 49

Typical antipsychotic agents produce central nervous system effects, especially extrapyramidal symptoms (EPS) and tardive dyskinesia (TD). Nearly every patient who receives neuroleptic therapy has one or more identifiable risk factors for TD, among the most significant of which are older age, female gender, presence of EPS, diabetes mellitus, affective disorders, and certain parameters of neuroleptic exposure (i.e. dose and duration of therapy). The typical course of TD is a gradual onset after several years of drug therapy, followed by slow improvement or remission, but a large number of patients have persistent TD with irreversible symptoms. In the management of TD, the patient's mental status is of primary concern. Currently, no uniformly safe and effective therapies for TD exist, though a variety of therapeutic agents, including some of the atypical neuroleptics, have been reported to treat TD successfully in some patients. Because TD liability is so much lower with novel antipsychotic therapy, all patients who have TD or are at risk for TD, as well as EPS, should be considered candidates for switching to these new drugs.
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PMID:Tardive dyskinesia and atypical antipsychotic drugs. 1019 Feb 26

It has been reported in the earlier literature that many patients with psychoses had abnormalities in glucose metabolism as revealed by glucose tolerance testing. This observation is reinforced by the fact that the schizophrenic population appears to have about a 2-3-fold increased risk for Type II diabetes mellitus. However, some uncertainty remains about the relative risk value because there have been numerous case reports of patients who developed hyperglycemia and even Type II diabetes apparently as a consequence of treatment with antipsychotic drugs. Schizophrenic patients with abnormal glucose metabolism have a higher prevalence of drug-induced tardive dyskinesia than patients with a normal glucose profile. Treatment with the new atypical antipsychotics has a much lower risk of movement disorders; however, weight gain, hyperglycemia, and diabetes are emerging as significant side effects. Because glucose is essential for energy metabolism in neurons, any change in the effective glucose levels in brain that result from drug therapy may have significant clinical implications. It is not clear whether the glycemic state of schizophrenics contributes to their psychotic symptoms or modulates the incidence of drug side effects. Basic research shows that the drugs which cause hyperglycemia in patients appear to inhibit neuronal glucose transport which may partly explain their effects. This paper reviews the relevant literature in a preliminary attempt to understand the implications of such clinical findings in the light of basic research.
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PMID:Glucose metabolism in relation to schizophrenia and antipsychotic drug treatment. 1195 67


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