Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urine samples from members of 29 families of patients with Indian childhood cirrhosis (ICC) and nine families with related disorders gave positive reactions when tested with ferric chloride. Column chromatography showed that this was due to the presence of abnormally large amounts of tryptophan metabolites, notably 3-hydroxyanthranilic acid. Affected pedigrees had a significantly greater prevalence of peptic ulcer, adult cirrhosis, diabetes mellitus, migraine, and Parkinsonism than a control population. ICC may result from an inborn error of tryptophan metabolism in susceptible ethnic groups.
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PMID:Indian childhood cirrhosis: an inherited disorder of tryptophan metabolism? 69 56

The muscle, nerve terminal and end plates of 3 patients suffering from idiopathic Parkinson's disease have been studied electrophysiologically, histologically, histochemically and electron microscopically. No characteristic neuromuscular features of parkinsonism were discernible. Four additional patients suffering from idiopathic parkinsonism complicated by diabetes, myasthenia gravis and spinal atrophy were also studied.
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PMID:Peripheral neuromuscular changes in Parkinson's disease. 87 15

Amyotrophic lateral sclerosis and Parkinsonism-dementia are unusually prevalent on Guam. Carbohydrate metabolism was studied in 110 patients with evidence diagnostic of or suspecious for these diseases. The combined incidence of known diabetes in 29 per cent of them plus a high percentage of glucose tolerance tests interpreted as abnormal, even when most age-related criteria were considered, was considerably higher than the incidence of abnormal carbohydrate metabolism reported elsewhere in the general population of the United States, the tropical Pacific area, or in recent surveys on Guam itself. The diabetes was generally mild in nature and noteworthy for a lack of retinopathy and other complications. Hypertension, hypercholesterolemia, and hyperuricemia, although highly prevalent, were not consistently associated with abnormal glucose metabolism. Similarly, no consistent association was demonstrated with such factors as age, muscle atrophy, or physical activity.
Diabetes 1976 Nov
PMID:Abnormal carbohydrate metabolism in amyotrophic lateral sclerosis and Parkinsonism-dementia on Guam. 99 26

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

Thyroid disfunction in the aged is often misdiagnosed either due to scanty symptoms, masking by other ailments or because function tests can be altered by extrathyroid causes such as chronic diseases, drugs or undernutrition. We surveyed 93 patients from 60 to 104 years old (73 females) living in geriatric homes. Most received at least 2 drugs for control of hypertension, coronary artery disease, diabetes, parkinsonism or psycho-organic deterioration. No clinical evidence of thyroid disfunction was found in 75 patients. T3 was 73.6 +/- 25.5 ng/dl, T4 7.3 +/- 1.8 micrograms/dl, TSH 2.8 +/- 0.9 uU/ml and rT3 32.2 +/- 16.3 ng/dl. Antimicrosomal antibodies were negative in all. Significant differences were found comparing these values with those obtained in 26 normal adults with mean age 39.9 years: T3 was lower and TSH and rT3 were higher in the elderly (p less than 0.0001). T3 decreased and rT3 increased in relation to age and males had significantly lower values of T3, T4 and TSH than females. Some evidence of thyroid disfunction was present in the remaining 18 patients: 9 had multinodular and/or positive antimicrosomal antibodies with euthyroid hormone levels; 6 had elevated T3, T4 and fT4 so hyperthyroidism was suspected; the remaining 3 patients had TSH levels above 20 uU/ml indicating the presence of hypothyroidism of which only one had some clinical manifestation. Thus, thyroid disfunction in the elderly + is not uncommon (3.2% of hyperthyroidism and 2.6% hypothyroidism in this series) in the absence of clinical manifestation. Treatment may improve the quality of life in these patients.
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PMID:[Problems in the diagnosis of thyroid dysfunction of the elderly adult]. 213 50

A case of a 29-year-old woman with idiopathic hypoparathyroidism was reported. There were neither endocrine nor neurological disorders among her family, except for her mother's hearing loss. She had been suffering from insulin-dependent diabetes mellitus since 21 years of age, and was noticed to be hard of hearing for several years, but never been examined. At the age of 27, choreic movement on her left upper limb and gait disturbance appeared. A year before admission, gait disturbance gradually developed and she could not walk any more. On admission, her height was 137.2 cm and her weight 36.5 kg. She had a round face, uneven teeth and borderline metacarpal sign on her right hand. On neurological examination, Parkinsonism, bucco-lingo-masticatory dyskinesia and bilateral extensor planter reflex were present, but tetany was not observed anywhere. Serum calcium was 3.9 mEq/l, and serum phosphorus 5.3 mEq/l. A CT scan of brain revealed calcifications in the bilateral basal ganglia and thalami, low density area in the left putamen, and atrophy of both caudate nuclei. Serum PTH was less than 100 pg/ml. Ellsworth-Howard's test showed hyperresponsiveness in the secretion of urinary phosphorus and cyclic-AMP. Other endocrinological studies showed no abnormality except for hyporesponsiveness in the secretion of insulin on glucose tolerance test. On the basis of these results, a diagnosis of idiopathic hypoparathyroidism with insulin-dependent diabetes mellitus was made. Administration of alfacalcidol returned serum calcium and phosphorus to normal with considerable clinical benefit. Parkinsonism was gradually improved and she became to be able to walk with a cane after one year of treatment. But buco-lingo-masticatory dyskinesia were not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of idiopathic hypoparathyroidism with extrapyramidal signs and insulin-dependent diabetes mellitus]. 222 58

Aging is associated with a considerable number of alterations in function of the autonomic nervous system and with systems involved in the control of cardiovascular response to postural changes. However, these alterations themselves do not generally lead to symptomatic orthostatic hypotension. In combination with other factors, older patients can develop marked problems with orthostatic hypotension--notably, certain drug regimens, some degree of underlying heart failure, or such common geriatric illnesses as parkinsonism and diabetes. Treatment regimens must be designed to minimize side effects. While aggressive pharmacologic treatment may be helpful for young patients, among the elderly physical therapy or behavioral maneuvers may promote the most benefit with least risk. The simplest first step, however, is to focus on possible iatrogenic causes and eliminate them.
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PMID:Postural hypotension: its meaning and management in the elderly. 319 80

We describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease beginning between age 21-40 years should be called "young onset Parkinson's disease." Twenty percent of such patients in our series had at least one first- or second-degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called "juvenile parkinsonism." All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.
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PMID:Young onset Parkinson's disease. 350 66


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