Background: Diabetes mellitus (DM) is a disease characterized by hyperglycemia due to (a) insulin-insufficiency (type I DM), or (b) impaired glucose cell-entry (insulin resistance) due to the downregulation of insulin...Background: Diabetes mellitus (DM) is a disease characterized by hyperglycemia due to (a) insulin-insufficiency (type I DM), or (b) impaired glucose cell-entry (insulin resistance) due to the downregulation of insulin cell receptors (type II DM). Type I DM usually presents with florid manifestations contrary to a slowly-progressive type II. Patients and methods: Over the past 10 years, we encountered 9 obese patients with controlled insulin-requiring type II DM for years, at a dose of 62 ± 5 units/day, who developed sudden and severe insulin resistance (IR) that required 210 ± 25 units daily. All patients had very high levels of anti-Glutamic Acid Decarboxylase (GAD) antibodies. Despite a lack of previous testing for anti-GAD antibodies, they were treated, with Cyclosporin A (Cy), as an autoimmune disorder superimposed on their type II MD. Initially all patients were treated with 100 mg, of Cy, twice daily aiming at an initial trough level of 100 - 150 ng/ml. Three months later, the dose was reduced to 50 mg twice daily for a total of 2 years. Results: Amelioration of IR was achieved by 1 month with a reduction of daily insulin requirement to 123 ± 16 units that further decreased to 76 ± 11 by the end of the 3rd month. Such improvement persisted for 2 years and >1 year after Cy discontinuation. Moreover, a decline in insulin requirements was associated with a parallel decrease in anti-GAD antibody levels and an increase in C-peptide insulin without kidney disease. Conclusion: Anti-GAD antibodies can induce acute IR in type II DM, and this phenomenon can be treated safely and effectively with Cy.展开更多
BACKGROUND Anti-glutamic acid decarboxylase(GAD)antibody is known to cause several autoimmune-related situations.The most known relationship is that it may cause type I diabetes.In addition,it was also reported to res...BACKGROUND Anti-glutamic acid decarboxylase(GAD)antibody is known to cause several autoimmune-related situations.The most known relationship is that it may cause type I diabetes.In addition,it was also reported to result in several neurologic syndromes including stiff person syndrome,cerebellar ataxia,and autoimmune encephalitis.Decades ago,isolated epilepsy associated with anti-GAD antibody was first reported.Recently,the association between temporal lobe epilepsy and anti-GAD antibody has been discussed.Currently,with improvements in examination technique,many more autoimmune-related disorders can be diagnosed and treated easier than in the past.CASE SUMMARY A 44-year-old female Asian with a history of end-stage renal disease(without diabetes mellitus)under hemodialysis presented with diffuse abdominal pain.The initial diagnosis was peritonitis complicated with sepsis and paralytic ileus.Her peritonitis was treated and she recovered well,but seizure attack was noticed during hospitalization.The clinical impression was gelastic seizure with the presentation of frequent smiling,head turned to the right side,and eyes staring without focus;the duration was about 5–10 s.Temporal lobe epilepsy was recorded through electroencephalogram,and she was later diagnosed with anti-GAD65 antibody positive autoimmune encephalitis.Her seizure was treated initially with several anticonvulsants but with poor response.However,she showed excellent response to intravenous methylprednisolone pulse therapy.Her consciousness returned to normal,and no more seizures were recorded after 5 d of intravenous methylprednisolone treatment.CONCLUSION In any case presenting with new-onset epilepsy,in addition to performing routine brain imaging to exclude structural lesion and cerebrospinal fluid studies to exclude common etiologies of infection and inflammation,checking the autoimmune profile has to be considered.In the practice of modern medicine,autoimmune-related disorders are relatively treatable and should not be missed.展开更多
文摘Background: Diabetes mellitus (DM) is a disease characterized by hyperglycemia due to (a) insulin-insufficiency (type I DM), or (b) impaired glucose cell-entry (insulin resistance) due to the downregulation of insulin cell receptors (type II DM). Type I DM usually presents with florid manifestations contrary to a slowly-progressive type II. Patients and methods: Over the past 10 years, we encountered 9 obese patients with controlled insulin-requiring type II DM for years, at a dose of 62 ± 5 units/day, who developed sudden and severe insulin resistance (IR) that required 210 ± 25 units daily. All patients had very high levels of anti-Glutamic Acid Decarboxylase (GAD) antibodies. Despite a lack of previous testing for anti-GAD antibodies, they were treated, with Cyclosporin A (Cy), as an autoimmune disorder superimposed on their type II MD. Initially all patients were treated with 100 mg, of Cy, twice daily aiming at an initial trough level of 100 - 150 ng/ml. Three months later, the dose was reduced to 50 mg twice daily for a total of 2 years. Results: Amelioration of IR was achieved by 1 month with a reduction of daily insulin requirement to 123 ± 16 units that further decreased to 76 ± 11 by the end of the 3rd month. Such improvement persisted for 2 years and >1 year after Cy discontinuation. Moreover, a decline in insulin requirements was associated with a parallel decrease in anti-GAD antibody levels and an increase in C-peptide insulin without kidney disease. Conclusion: Anti-GAD antibodies can induce acute IR in type II DM, and this phenomenon can be treated safely and effectively with Cy.
文摘BACKGROUND Anti-glutamic acid decarboxylase(GAD)antibody is known to cause several autoimmune-related situations.The most known relationship is that it may cause type I diabetes.In addition,it was also reported to result in several neurologic syndromes including stiff person syndrome,cerebellar ataxia,and autoimmune encephalitis.Decades ago,isolated epilepsy associated with anti-GAD antibody was first reported.Recently,the association between temporal lobe epilepsy and anti-GAD antibody has been discussed.Currently,with improvements in examination technique,many more autoimmune-related disorders can be diagnosed and treated easier than in the past.CASE SUMMARY A 44-year-old female Asian with a history of end-stage renal disease(without diabetes mellitus)under hemodialysis presented with diffuse abdominal pain.The initial diagnosis was peritonitis complicated with sepsis and paralytic ileus.Her peritonitis was treated and she recovered well,but seizure attack was noticed during hospitalization.The clinical impression was gelastic seizure with the presentation of frequent smiling,head turned to the right side,and eyes staring without focus;the duration was about 5–10 s.Temporal lobe epilepsy was recorded through electroencephalogram,and she was later diagnosed with anti-GAD65 antibody positive autoimmune encephalitis.Her seizure was treated initially with several anticonvulsants but with poor response.However,she showed excellent response to intravenous methylprednisolone pulse therapy.Her consciousness returned to normal,and no more seizures were recorded after 5 d of intravenous methylprednisolone treatment.CONCLUSION In any case presenting with new-onset epilepsy,in addition to performing routine brain imaging to exclude structural lesion and cerebrospinal fluid studies to exclude common etiologies of infection and inflammation,checking the autoimmune profile has to be considered.In the practice of modern medicine,autoimmune-related disorders are relatively treatable and should not be missed.