Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

H2-antagonists such as cimetidine and ranitidine are metabolized by cytochrome P-450. In this way they may interfere with theophylline metabolism. Cimetidine is known to have this effect and frequently to induce a theophylline toxic effect, while data concerning ranitidine are more uncertain. In this paper, we report the case of a 67-year-old woman with non-insulin dependent diabetes. She was taking aminophylline for respiratory failure and after ranitidine infusion exhibited generalized convulsions. Theophylline values which were monitored within the therapeutic range, increased toxic levels after ranitidine therapy and epileptic episodes. The increase in theophylline levels was associated with a further reduction in the clearance rate of the bronchodilator. We think that ranitidine may combine with other clinical factors known to reduce theophylline metabolism mainly in the elderly and severely ill patients. Theophylline-induced seizures may occur when theophylline serum levels are slightly above the therapeutic range, as in our case report.
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PMID:Seizures during concomitant treatment with theophylline and ranitidine: a case report. 209 63

The association of juvenile diabetes mellitus (DM), diabetes insipidus (DI), optic atrophy (OA) and sensorineural deafness (D) is known as DIDMOAD or Wolfram syndrome. Aside from these four cardinal features, a wide variety of abnormalities of the nervous system, urinary tract and endocrine glands have been described in this syndrome. In this report, the clinical features of six patients with DIDMOAD syndrome are presented. All six patients had DM. Five of the six patients had DI, five OA and five displayed abnormal audiogram findings. In addition, two had goiter, two delayed puberty, one seizure and one mental retardation with depression attacks. Urinary tract dilatation was recorded in five patients. Four patients developed typical complications of DM. One of them had overt nephropathy and arthropathy despite the short duration of DM. In addition, this patient had diabetic retinopathy, which is considered to be rare in this syndrome.
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PMID:Various clinical aspects of DIDMOAD (Wolfram) syndrome. 750 61

Wolfram's syndrome, also known as DIDMOAD syndrome, includes juvenile diabetes mellitus and optic atrophy variously associated with diabetes insipidus and deafness. We describe the neurological findings in 5 patients with Wolfram's syndrome. All patients had a neurological examination and were subjected electrophysiological and brain imaging including CT scan and, in one patient, MRI. There were two pairs of brothers and a sporadic case with paternal consanguinity suggesting recessive inheritance. Neurological abnormalities were found in four patients including dysarthria, seizures, anosmia, nystagmus, ataxia and changes in the electroencephalograms, electroretinograms and evoked potentials. In contrast with previous reports, four patients had abnormal brain CT scan with prominent atrophy of the brainstem. In the patient studied with NMR, severe brainstem and cerebellar atrophy was found. These neuroradiological findings are reminiscent of those described in olivopontocerebellar atrophy and are in agreement with previous pathological studies. We conclude that Wolfram's syndrome includes phenotypical manifestations of olivopontocerebellar atrophy. This reinforces the opinion that olivopontocerebellar atrophy is a nonspecific syndrome of varied causes.
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PMID:[Neurologic manifestations in Wolfram's syndrome]. 833 58

SEZ-12 is one of the seizure-related cDNAs which was isolated by differential hybridization from primary cultured neurons from the mouse cerebral cortex with or without pentylenetetrazol (PTZ). SEZ-12 expression is transiently down-regulated in the mouse brain by injection of PTZ. To characterize SEZ-12, isolation of full-length cDNA and nucleotide sequence analysis were performed. The deduced amino acid sequence of SEZ-12 revealed that it encodes membrane-bound C-type lectin and has a significant homology to that of human cDNA, DGCR2 and IDD, which were cloned from a balanced translocation breakpoint associated with the DiGeorge syndrome. The isolated cDNA was about 4 kb in length and the message was expressed ubiquitously in various organs with low-abundance. Previously, we also cloned a transmembrane protein which is probably involved in cell-cell interaction by the differential hybridization technique. These findings suggest that transmembrane signaling in neuronal cells may have an important role in PTZ-induced seizure.
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PMID:Cloning of SEZ-12 encoding seizure-related and membrane-bound adhesion protein. 863 60

A total of 1,441 patients with IDDM were randomly assigned to receive either intensive (n = 711) or conventional (n = 730) diabetes therapy in the Diabetes Control and Complications Trial (DCCT). The patients were followed for an average of 6.5 years. Subjects were instructed to report all episodes of suspected severe hypoglycemia to their health care team. In addition, at quarterly follow-up visits, each subject was asked about the occurrence of severe hypoglycemia. There were 3,788 episodes of severe hypoglycemia (requiring assistance); 1,027 of these episodes were associated with coma and/or seizure. A total of 65% percent of patients in the intensive group vs. 35% of patients in the conventional group had at least one episode of severe hypoglycemia by the study end; the overall rates of severe hypoglycemia were 61.2 per 100 patient-years vs. 18.7 per 100 patient-years in the intensive and conventional treatment groups, respectively, with a relative risk (RR) of 3.28. The relative risk for coma and/or seizure was 3.02 for intensive therapy. The increased risk with intensive treatment persisted over each of the 9 years of follow-up in the DCCT and over the calendar years 1984-1993 during which the study was conducted. When baseline patient characteristics were examined for effects on the risk of severe hypoglycemia, the relative risk of hypoglycemia for intensive versus conventional treatment was > or = 2 for all subgroups. Several subgroups defined by baseline characteristics, including males, adolescents, and subjects with no residual C-peptide or with a prior history of hypoglycemia, had a particularly high risk of severe hypoglycemia in both treatment groups. Analyses of the cumulative incidence of successive episodes indicated that intensive treatment was also associated with an increased risk of multiple episodes within the same patient (e.g., 22% experienced five or more episodes of severe hypoglycemia within the first 5 years of follow-up vs. 4% in the conventional group). Within both treatment groups, patients who experienced severe hypoglycemia were at increased risk of subsequent episodes. Approximately 30% of patients in each group experienced a second episode within the 4 months following the first episode of severe hypoglycemia. Within each treatment group, the number of prior episodes of hypoglycemia was the strongest predictor of the risk of future episodes, followed closely by the current HbA1c value. After adjustment for the current quarterly HbA1c level, intensive treatment was still associated with a significantly increased risk of hypoglycemia, indicating that the increased risk with intensive treatment is not completely explained by differences in HbA1c values.
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PMID:Hypoglycemia in the Diabetes Control and Complications Trial. The Diabetes Control and Complications Trial Research Group. 900 Jul 5

Hypoglycaemia is a frequent acute complication of IDDM and is usually defined as a blood glucose level below 3.0 mmol/l. Hypoglycaemia stimulates several neuroendocrine responses, such as secretion of glucagon, adrenaline, growth hormone and cortisol, which are generally increased during this phenomenon. The true prevalence of hypoglycaemia is not known. Studies of the epidemiology of severe hypoglycaemia give prevalences ranging from 2.7 to 85.7 episodes per 100 patients per year. The major risk factor for severe hypoglycaemia is hypoglycaemia unawareness, which occurs particularly in patients with type 1 diabetes of long duration and in those with a history of frequent episodes of hypoglycaemia. The first step in the management of hypoglycaemia is to check blood glucose and to treat hypoglycaemia on the basis of symptoms. Hypoglycaemia requires urgent treatment with a fast-acting carbohydrate or, if severe, with parenteral glucagon or intravenous glucose. Prevention measures should be instituted to prevent subsequent episodes, particularly in younger children with hypoglycaemic seizures or when seizures are recurrent.
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PMID:Hypoglycaemia in children with type 1 diabetes mellitus. 1019 51

Autism is an age-dependent neurologic disorder that is often associated with autoimmune disorders in the patients' relatives. To evaluate the frequency of autoimmune disorders, as well as various prenatal and postnatal events in autism, we surveyed the families of 61 autistic patients and 46 healthy controls using questionnaires. The mean number of autoimmune disorders was greater in families with autism; 46% had two or more members with autoimmune disorders. As the number of family members with autoimmune disorders increased from one to three, the risk of autism was greater, with an odds ratio that increased from 1.9 to 5.5, respectively. In mothers and first-degree relatives of autistic children, there were more autoimmune disorders (16% and 21%) as compared to controls (2% and 4%), with odds ratios of 8.8 and 6.0, respectively. The most common autoimmune disorders in both groups were type 1 diabetes, adult rheumatoid arthritis, hypothyroidism, and systemic lupus erythematosus. Forty-six percent of the autism group reported having relatives with rheumatoid diseases, as compared to 26% of the controls. Prenatal maternal urinary tract, upper respiratory, and vaginal infections; asphyxia; prematurity, and seizures were more common in the autistic group, although the differences were not significant. Thirty-nine percent of the controls, but only 11% of the autistic, group, reported allergies. An increased number of autoimmune disorders suggests that in some families with autism, immune dysfunction could interact with various environmental factors to play a role in autism pathogenesis.
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PMID:Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism. 1038 47

To ascertain if significant hypoglycaemic episodes can be avoided or managed more appropriately in children with insulin dependent diabetes mellitus (IDDM). A retrospective chart audit was performed on all children with IDDM admitted with hypoglycaemia between 1.1.90 and 31.8.97. Of the 21 children studied, 9 presented with seizures and 1 with coma. In 9 the hypoglycaemia was unexplained. Only 6 parents used glucagon. Five children were readmitted during the review with a further hypoglycaemic episode. Four of these had their first admission significantly sooner after diagnosis than those without recurrent episodes. Hypoglycaemic episodes are often unexplained and are unlikely to be completely avoidable. Improved support services during intercurrent illness may reduce the frequency of some hypoglycaemic episodes and increased use of glucagon at home may reduce the severity of some. Children who have their first hypoglycaemic episode within one year of diagnosis are at risk of having recurrent episodes.
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PMID:Hypoglycaemic episodes in children with insulin dependent diabetes mellitus--can the frequency or severity be reduced? 1132 Nov 69

A 6-year-old boy presented with epilepsia partialis continua 6 months after diagnosis of type 1 diabetes. Anti-glutamic acid decarboxylase 65 antibodies were found in his serum and cerebrospinal fluid. Anti-epileptic agents did not improve his seizures. High-dose steroids, plasmapheresis, and intravenous immunoglobulin resulted in decreased anti-glutamic acid decarboxylase 65 antibody levels and resolution of his seizures.
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PMID:Type 1 diabetes mellitus and epilepsia partialis continua in a 6-year-old boy with elevated anti-GAD65 antibodies. 1187 78

Degenerative diseases of the CNS, such as stiff-person syndrome (SPS), progressive cerebellar ataxia, and Rasmussen encephalitis, have been characterized by the presence of autoantibodies. Recent findings in individuals with Batten disease and in animal models for the disorder indicate that this condition may be associated with autoantibodies against glutamic acid decarboxylase (GAD), an enzyme that converts the excitatory neurotransmitter glutamate to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Anti-GAD autoantibodies could result in excess excitatory neurotransmitters, leading to the seizures and other symptoms observed in patients with Batten disease. The pathogenic potential of GAD autoantibodies is examined in light of what is known for other autoimmune disorders, such as multiple sclerosis, SPS, Rasmussen encephalitis, and type 1 diabetes, and may have radical implications for diagnosis and management of Batten disease.
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PMID:Glutamic acid decarboxylase autoimmunity in Batten disease and other disorders. 1559 40


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