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)

We studied the systemic manifestations of myasthenia gravis and its putative pathogenesis. 644 clinically, pharmacologically and electrophysiologically diagnosed patients with myasthenia gravis (MG) were studied. 33 patients had Graves disease, 5 periodic paralysis, 4 Hashimoto disease, and 4 epilepsy, polymyositis, rheumatoid arthritis and Guillain-Barre syndrome each. 45 patients had positive anti-skeletal-muscle antibodies, 9 positive anti-thyroid antibody, and 3 positive SSA and SSB. 11 MG patients with positive pyramidal signs (MG+PS) had no evidence of multiple sclerosis (MS) or other neurologic diseases. Compared with 12 MG patients without pyramidal signs (MG-PS) and 23 normal controls (NCs), they had not only high levels of IgGcsf and IgG syn, but also increased ratio of AChRAbcsf/AChRAbs (P < 0.05). Four MG patients had epilepsy. Four MG patients had severe memory disorders. Three MG patients had diseases of the peripheral nerves without diabetes mellitus and toxin. SGPT was significantly increased in 22 MG patients than in 9 normal controls (P < 0.05). These systemic manifestations were improved while MG was improved by immunological therapy. MG is a systemic autoimmune disease predominantly involving AChR on the postsynaptic membrane of N-M conjunction.
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PMID:[Systemic manifestations of myasthenia gravis and its putative pathogenesis]. 1037 93

A 10 year old boy with a superior division palsy of the left oculomotor nerve is reported. He had a flu-like illness 1 week before the onset. The computed tomography and magnetic resonance imaging scans were normal. Laboratory data for evaluation of infection, diabetes mellitus and myasthenia gravis were normal. The symptoms spontaneously disappeared after 2 months. The course of the illness in conjunction with the negative laboratory findings made this case an example of partial paralysis of the third nerve related to viral infection. In the literature, only several cases with isolated divisional palsy of the oculomotor nerve were found after a viral infection. Inferior division palsy has been reported in five children. Superior division palsy has been published in only two cases. Divisional palsy is more common among children and resolves spontaneously. This rare but important clinical entity is one of the differential diagnoses in oculomotor nerve palsies, particularly in children, which are neuroradiologically undiagnosed. It occurs after a viral infection and may affect a superior or inferior division alone.
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PMID:Isolated superior division oculomotor palsy in a child with spontaneous recovery. 1084 55

In numerous animal models, DNA immunization has been shown to induce protective immunity against infectious diseases (viral, bacterial and protozoan) and cancers (1, 2). In these situations it is desirable to induce a strong immune response to the DNA-encoded antigen in order to generate an immune memory that enables the vaccine to respond more rapidly to subsequent challenge. The success of DNA vaccination in this regard has led to its rapid introduction into several human clinical trials (3, 4). However, in autoimmunity, undesirable immune responses to autoantigens are thought to lead to the destruction of target cells or organs, resulting in diseases such as myasthenia gravis, diabetes or multiple sclerosis. Thus, at first sight, it appears that immunization would more likely trigger autoimmunity than ameliorate it. Nevertheless, clinical experience has shown that certain immune-mediated diseases may be countered by low-dose antigen administration ('desensitization'), although the underlying mechanisms remain somewhat conjectural. Here, we will describe an intriguing approach to the prevention of autoimmune disease, in which we use a DNA vaccine encoding a self-antigen to abrogate autoimmune diabetes. The success of this strategy relies on the nature of the immune response induced by the DNA vaccine.
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PMID:DNA vaccination to treat autoimmune diabetes. 1094 59

The aim of the current study was the introduction and standardization of two experimental conditions for dynamic pupillometry. Pupillometry is a method that can provide valuable data concerning the functioning of the autonomous nervous system. The system for recording the pupil reaction was developed in the Laboratory of Clinical Neurophysiology of the 1st Department of Neurology of Aristotle University of Thessaloniki, in co-operation with the Laboratory of Fluid Mechanics of the Aristotle University of Thessaloniki. This system is fully automated. It includes an infra-red video camera, which has the capacity to record in complete darkness, and an SLE (clinical photic stimulator) lamp. A software application automatically performed all the procedures. During the first experiment, one flash was administered. During the second experiment, a series of 25 flashes (1 Hz frequency) was administered. Fifty physically and mentally healthy subjects aged 23-48 years took part in the study. Means, standard deviations and ranges for all variables characterizing normal subjects during both experimental conditions are reported. Test/re-test results and comparisons of the two eyes are also reported. The combined use of these two experimental conditions in dynamic pupillometry may be a very useful tool in medical research. There are already reports on the usefulness of pupillometry in the research of various diseases, including depression and Alzheimer's disease. It is expected that it will also be a valuable research tool in the study of diabetes, alcoholism, myasthenia gravis, cancer, multiple sclerosis, etc.
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PMID:Automated standardized pupillometry with optical method for purposes of clinical practice and research. 1097 44

A 32-year-old student reported fatigue and malaise since two months in the absence of specific symptoms. Clinical examination and extensive laboratory testing revealed no abnormalities at his first presentation. Some weeks thereafter, on re-admission, hyperpigmentation suggestive of Addison's disease was observed and pathognomonic autoantibodies directed against the thyroid gland and the adrenal cortex were detected. Further evaluation led to the diagnosis autoimmune polyglandular deficiency syndrome, also named "Schmidt syndrome", comprising adrenocortical insufficiency (Addison's disease) and lymphocytic thyroiditis (Hashimoto thyroiditis). The diagnosis of polyglandular insufficiency is often delayed due to non-specific symptoms at early disease stages and progression may be rapid, culminating in Addisonian crisis under physical stress or infection, requiring immediate high-dose hormone replacement therapy. Hence, careful re-examination is mandatory to ensure adequate treatment before life-threatening complications occur. Nowadays this type of disease is classified as autoimmune polyglandular syndrome type II (APS type II) with an increased risk of developing insulin-dependent diabetes mellitus (IDDM), vitiligo, alopecia, pernicious anaemia, coeliac disease, myasthenia gravis and primary hypogonadism. The cause of the disease remains obscure but in addition to an autosomal dominant trait with variable penetrance some hints at viral infection triggering the disease process exist.
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PMID:32-year old patient presenting with autoimmune polyglandular syndrome. 1131 87

A 57 year-old man with a history of diabetes mellitus was admitted to our hospital for the complaint of slowly progressive muscle weakness involving proximal limbs and head dropping. His serum CK level was within normal range, and muscle biopsy showed no inflammatory changes. To rule out myasthenia gravis, computerized tomography was done for the detection of thymoma, and detected an adrenal tumor in stead. He was not over-weighted, and his morning plasma levels of ACTH and cortisol were within normal ranges. Additional hormonal examinations revealed daily autonomous hypersecretion of cortisol. He received diagnosis of preclinical Cushing syndrome. After resection of the tumor, muscle weakness improved and his diabetes mellitus was controlled better. The muscle symptoms seem to be related with steroid myopathy. Preclinical Cushing syndrome should be included as a differential diagnosis for myopathy of unknown etiology.
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PMID:[A patient with myopathy due to preclinical Cushing syndrome]. 1196 44

A 61-year-old woman had repeated episodes of muscle weakness of face, neck and limbs for 18 years. She was diagnosed as having myasthenia gravis (MG) by the positive anti-acetylcholine receptor antibody and findings of electromyogram. Simultaneously, she was noticed to have diabetes mellitus with high titers of anti-glutamic acid decarboxylase (GAD) antibody. Magnetic resonance imaging showed a large thymoma. In spite of the improvement of MG after thymectomy, the insulin secretion slowly exacerbated during next two years. The clinical course of her disease was characteristic as slowly progressive insulin dependent diabetes mellitus (SPIDDM). She continued to have positive autoantibody against beta-cell of pancreas. Recently, anti-GAD antibody is detected in patients with SPIDDM and stiffman syndrome (SS) in high rate, and it is closely associated with the cause of these syndromes. The patient did not reveal the symptoms of SS. From the clinical course, MG and SPIDDM in this patient may be caused by a common underlying autoimmune abnormality resulting from the long presence of the thymoma. MG and SPIDDM may be derived from organ-specific autoimmunopathy from the defect of self-tolerance.
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PMID:[A case of myasthenia gravis accompanied by large thymoma and anti-GAD antibody]. 1208 Jun 17

Vaccines are by definition prophylactic, but in recent years an interest has developed in therapeutic vaccines for infectious diseases such as AIDS and tuberculosis, as well as gastric ulcers, cancer (with different approaches to combat various types of malignancy) and autoimmune diseases (a definite success was the development of a vaccine against multiple sclerosis) and there are potential vaccines in development for myasthenia gravis, lupus and diabetes. Therapeutic vaccines are also being developed against cognitive diseases such as Alzheimer's disease, prion diseases and Huntington's disease. All of these efforts are based on the therapeutic vaccine being closely related chemically to the etiological agent that causes the disease.
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PMID:Therapeutic vaccines: realities of today and hopes for the future. 1211 Feb 43

Interleukin-2 is an effective agent against renal cell carcinoma and melanoma, but it has been associated with autoimmune sequelae such as hypothyroidism and vitiligo. A 64-year-old man with non-insulin-dependent diabetes and metastatic renal cell carcinoma developed insulin-dependent diabetes after his first cycle of therapy with high-dose (HD) interleukin-2. After additional therapy with interleukin-2, the patient developed generalized myasthenia gravis (MG) and polymyositis, both of which responded to treatment with corticosteroids and plasmapheresis. To investigate the role of IL-2 in the development of these autoimmune complications, autoantibody titers were assayed from serum obtained before and after IL-2 treatment and after treatment with corticosteroids plus plasmapheresis. Before IL-2 treatment, the patient had antibodies directed against insulin, islet cell antigens, and striated muscle. Acetylcholine receptor antibody levels were normal before starting IL-2. After treatment with IL-2, the patient developed acetylcholine receptor binding antibodies and exhibited an increase in the striated muscle antibody titer from 1:40 to 1:160. Recovery from the MG and polymyositis was associated with substantial decreases in the acetylcholine receptor and striated muscle antibody titers. These findings suggest that HD IL-2 accelerated the progression of latent autoimmune diabetes and myositis in this patient whose tolerance to islet cell antigens and striated muscle had already been broken and precipitated a break in tolerance to the acetylcholine receptor resulting in the development of MG. This case demonstrates the importance of prompt recognition of IL-2-induced MG and shows how this complication can be successfully managed with aggressive therapy.
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PMID:Induction of myasthenia gravis, myositis, and insulin-dependent diabetes mellitus by high-dose interleukin-2 in a patient with renal cell cancer. 1214 60

Naive non-obese diabetic (NOD/LtJ) mice spontaneously produce natural IgG autoantibodies against self-antigens associated with the experimental autoimmune diseases to which they are susceptible: insulin-dependant diabetes mellitus, systemic lupus erythematosus and experimental autoimmune encephalomyelitis. We discovered recently that NOD/LtJ mice also spontaneously produce IgG antibodies to the acetylcholine receptor (AchR), an antigen that can induce experimental autoimmune myasthenia gravis (EAMG) in susceptible rodents. However, there are no reports indicating that NOD/LtJ mice are susceptible to EAMG. To test whether the presence of spontaneous IgG autoantibodies can predict susceptibility to an autoimmune disease, we challenged NOD/LtJ mice using a standard protocol to induce EAMG. We now report that NOD/LtJ mice developed EAMG, although to a somewhat lesser degree than did C57BL/6 mice, a strain regarded as highly susceptible to the disease. Both strains produced comparable levels of immune antibodies to AchR of the complement-fixing isotypes IgG2a and IgG2b; however, NOD/LtJ mice produced significantly more IgG1. An antigen-specific T cell proliferative response to AchR of the same magnitude was detected in both strains, together with the secretion of similar amounts of IFN-gamma. Thus, NOD/LtJ mice are susceptible to EAMG and disease induction is accompanied by immune responses comparable to those seen in the susceptible strain C57BL/6. These results support the association between specific, natural IgG autoantibodies and susceptibility to the induction of a particular autoimmune disease.
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PMID:Experimental autoimmune myasthenia gravis in naive non-obese diabetic (NOD/LtJ) mice: susceptibility associated with natural IgG antibodies to the acetylcholine receptor. 1250 21


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