Hwa Young Cho, Young Min Cho, Myoung Hee Park, Mi Yeon Kang, Ki Hwan Kim, Yun Hyi Ku, Eun Kyung Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee
Korean Diabetes J. 2007;31(4):372-376. Published online July 1, 2007
Autoantibody negative fulminant type 1 diabetes mellitus is a novel subtype of type 1 diabetes, which is characterized by a remarkably abrupt onset, metabolic derangement such as diabetic ketoacidosis at diagnosis, low HbA1c level at onset and a negative islet-related autoantibodies. The prevalence of fulminant type 1 diabetes has large difference between Japan and other countries. The precise reason for this regional variation remains to be clarified. One of the possible explanations is genetic background such as genotype of class II HLA molecule. In addition, environment factors including viral infection are suggested as possible pathogenesis of the disease. Only a few cases with fulminant type 1 diabetes have been reported outside Japan, and most of these cases with definite diagnosis have been reported in Korea. We report here on two Korean patients that met the criteria for diagnosis of fulminant type 1 diabetes in accordance with their HLA genotypes.
Transient hypoglycemic hemiparesis is a rare but important presentation of hypoglycemia that is frequently misdiagnosed as stroke. The development of hemiparesis as a result of hypoglycemia was first described in 1928. Thereafter over the years, several cases have been sporadically reported in Korea, but case reports of recurrent hypoglycemic hemiparesis are rare. We recently experienced a case of recurrent hypoglycemic hemiparesis in an adult with type 1 diabetes mellitus. A 30-year-old woman with type 1 diabetes receiving daily multiple subcutaneous insulin injections was admitted with right hemiparesis. She had had admitted with the same symptom and recovered with oral carbohydrates in twice 2 years ago. Her clinical course improved over 2 hours after infusion of dextrose solution. Further investigations such as CT, MRI and MRA revealed no abnormality
Rhino-orbital mucormycosis was a rare, but mostly fatal fungal infection, usually found in poorly controlled diabetics or other immunocompromised hosts. This fungal infection begins from the nose, and rapidly spreads to the paranasal sinus (PNS), orbits and central nervous system(CNS), and finally extends to the entire organ. Early diagnosis and treatment is the only way to increase the survival rate. Herein Is reported We experienced a case of rhino-orbital mucormycosis, with type 1 diabetes mellitus, which was confirmed by a maxillary sinus biopsy. A 38-year-old male had been frequently treated for tonsillitis, but with no history of diabetes mellitus. He was admitted with mental change, accompanied by a fever, facial tenderness and swelling, with progressive visual acuity loss. During admission, CT and MRI of the in orbital area were performed. A biopsy in of the nasal cavity was also performed, and the mucormycosis was diagnosed through the pathological finding. The patient was treated with intravenous amphotericn B and an endoscopic antrostomy.
BACKGROUND Type 1 diabetes develops due to the destruction of insulin-secreting beta-cells by an autoimmune process, in which both genetic and environmental factors are involved. In children with newly diagnosed type 1 DM, the prevalence of ICA (Islet cell cytoplasmic antibody) is 60~86% and is highest at the time of onset after which it decreases. But, GADA (glutamic acid decarboxylase anti- bodies) are characterized by substantial fluctuations in the humoral immune response over a long period after clinical manifestation. This study was performed to evaluate the persistence of type 1 DM associated autoantibodies, including ICA and GADA, and their relation to clinical characteristics of the disease after clinical manifestation. METHODS: Eighteen childhood onset type 1 diabetes patients (mean age 13.7 years; duration 3.9 years) were included in this study. ICA was measured by indirect immunofluorescence using conventional ICA-IgG and positive samples were titered by serial dilutions. Also the sera were screened for GADA by radioimmuno-assay. RESULTS: The positivities of ICA and GADA at the time of study were 55.6% and 61%, falling to 44.4% and 41.2% 5 years later, respectively. There was no case of an ICA negative patient becoming positive or whose ICA titer was increased later. One case of a GADA negative patient became positive later. Initial c-peptide levels didn't have any correlation with initial ICA titers or ICA prevalence, but did with initial GADA titer. There were significant correlations between initial GADA titer and ICA prevalence (p<0.001), and between initial GADA titer or ICA titer and later ICA persistence (p<0.05). CONCLUSION: ICA and GADA persisted long after the clinical diagnosis of type 1 diabetes. And the persistence of autoantibody positivity showed a weak relation with endogenous insulin secretion and clinical characteristics, both at and after diagnosis of overt type 1 diabetes.
BACKGROUND Type 1 diabetes mellitus (Type 1 DM) results from autoimmune destruction of -cells of the pancreas. Many treatments aimed at inducing remission of newly diagnosed type 1 DM or preventing of type 1 DM in high risk group are being conducted. BCG is known to modulate the development of spontaneous diabetes in animal model of type 1 DM. In some studies, single injection of BCG induced clinical remission in recent onset type 1 DM patients. However, the effect of BCG on human is still controversial. Thus, we performed a prospective study to evaluate the effect of BCG on type 1 DM. METHODS: We enrolled a total of 23 type 1 DM patients within 6 months period. Randomly selected 14 patients were injected 0.1 ml BCG intradermally and 9 patients were injected normal saline. Fasting and postprandial 2 hour C-peptides, and insulin requirements were measured in all patients at enrollment and at 6, 12 and 24 months after BCG vaccination. RESULTS: At enrollment, there was no significant difference in age, sex, duration of diabetes, HbA1-C, body mass index, fasting and postprandial 2 hour C-peptides, and insulin requirement between BCG group and control group. During follow-up, there was no significant difference in fasting and postprandial 2 hour C-peptides. However postprandial 2 hour C-peptides in BCG group were higher than those in control group at 12 and 24 months (p-value>0.05). Insulin requirements also were lower in BCG group than in control group at 12 and 24 months (p-value>0.05). Clinical remission has been sustained in 2 BCG vaccinated patients at 6 and 12 months. In one of the two patients, remission was sustained for 36 months. CONCLUSION: BCG vaccine is safe and convenient to use, however, a large study is warranted for the use of BCG as a therapy of type 1 DM.
Severe hypertriglyceridemia exceeding 5.6 mmol/L in diabetic ketoacidosis occasionally occur in patients with type 1 diabetes mellitus. The pattern of dyslipidemia is usually Fredrickson classification type lV. But it also exists in type III and type V. However, extreme triglyceridemia, triglyceride level exceeds 22.6 mmol/L, occur rarely in the modern era of insulin therapy. And the pattern is usually Fredrickson type I. The severe hypertriglyceridemia in diabetic ketoacidosis is mainly due to lipoprotein lipase deficiency, and secondly to insulin deficiency. The severity usually improves with insulin replacement. In patients with extreme hypertriglyceri-demia, serum electrolyte values of the patients are fallaciously low, and it leads to the misinterpretation of biochemical results and to the inappropriate treatment. We reported a case of a 25 years old female patient with diabetic ketoacidosis and extreme hypertriglyceridemia. At admission, the color of her serum was milky, her plasma triglyceride concentration was 144.7 mmol/L (12864 mg/dL), cholesterol was 25.5 mmol/L (982 mg/dl), and HDL-cholesterol was 0.77 mmol/L (40 mg/dL). The biochemical values at admission could not be measured. Empirical therapy was administered with the use of insulin and fluid. After the initial treatment with insulin and fluid, plasma triglyceride declined rapidly and was nearly normal after 72 hours. We also measured fasting blood glucose concentration and lipid profiles from her father and two sisters. Their plasma glucose and lipid profiles were normal.
Hong kyu Lee, Kee Up Lee, Sung Kwan Hong, Byuong Doo Rhee, Dong Seop Choi, Hyoung Woo Lee, Sang Wook Kim, Hee Jin Kim, Nan Hee Kim, Kyong Soo Park, Woo Je Lee, Kyung Soo Ko
Korean Diabetes J. 1999;23(4):541-551. Published online January 1, 2001
BACKGROUND American Diabetes Association (ADA) proposed new criteria for the classification of diabetic patients, which were mainly based on the presence of autoimmune markers. But it is questionable if we can apply the new ADA criteria to Korean type 1 diabetic patients directly. In this study, we measured several autoantibodies to islet cell in Korean subjects with typical and atypical clinical manifestations of type 1 diabetes mellitus. And mutation of mitochondrial DNA was analyzed in the same patients. METHODS: We measured fasting serum C-peptide in 1870 diabetic patients attending the diabetes clinic of Asan Medical Center. Among the 117 patients with fasting serum C-peptide less than 0.6 ng/mL, glucagon-stimulated C-peptide was measured, and 57 Patients showed the level less than 1 ng/mL and they were diagnosed as type 1 diabetic patients. They were subgrouped into typical (n=26, needed insulin injection within 1 year after diagnosis) and atypical (n=30, did not need insulin for more than l year after diagnosis) type 1 diabetic patients. ICA was measured by indirect immunofluorescence method. Anti-GAD antibody was measured by radioimmunoassay. Anti-ICA512 antibody was measured by western blotting. Mitochondrial DNA 3243 mutation was detected using restriction enzyme Apa-I digestion of the amplified genomic DNA from the subjects. RESULTS: 1) Median age of onset was 40 years for atypical type 1 diabetes patients, while it was 27.5 years for typical type 1 diabetes patients. Average duration of insulin requirement was 0.18 years for typical group and 5.73 years for atypical group. In this series, only typical type 1 diabetic patients experienced diabetic ketoacidosis. 2) Only 50 % of typical type 1 diabetic patients and 47 % of atypical type 1 diabetic patients had at least one autoantibody among ICA, anti-GAD antibody and anti-ICA512 antibody. 3) Mitochondrial DNA 3243 point mutation was detected in 3 patients with atypical type 1 diabetes (10 %), but it was not found in patients with typical type 1 diabetes. CONCLUSION: These results suggest that the prevalence of autoantibodies in Korean type 1 diabetic patients was lower than that reported in Caucasians irrespective of clinical features. Therefore, it may not be easy to apply this new diabetes classification of ADA to Korean type 1 diabetic patients. In addition, mitochondrial DNA mutation may be responsible for some of the Korean atypical type 1 diabetic patients.