Background : Prediabetes is an intermediate stage prior to development of diabetes mellitus. Preimpaired glucose tolerance state represents an early stage in the pathogenesis of diabetes wherein the normal glucose is attained by compensated hyperinsulinemia. Glycosylated hemoglobin is used in diagnosis and monitoring of diabetes but has not been explored in pre-IGT state. The objective of this study is to compare the 2-hour blood glucose, 2-hour insulin level, and HbA1c between normoinsulinemic-normal OGTT and pre-IGT groups. Methods: Conducted at University of Santo Tomas Hospital, this was a retrospective analytical study of high-risk individuals for evaluation of type 2 diabetes from 2000-2011 and underwent 75-gm OGTT with 2-hour blood sugar and insulin determinations. The 2-hour glucose, insulin level and HbA1c in normoinsulinemic-normal OGTT were compared with the preIGT group using t-test. Correlation between the 2-hour blood glucose and insulin level with the HbA1c was done using Pearson correlation analysis. Statistical signifi cance was considered for p-value of <0.05 Results: Second-hour blood glucose and insulin levels were signifi cantly higher in the pre-IGT group as compared to the normoinsulinemic-normal OGTT group (128.60±18 and 89.29±68.82 vs. 90.68±26 and 17.40±8.15). The HbA1c of the pre-IGT group was signifi cantly higher than the normoinsulinemic-normal OGTT group (6.09±0.55 vs. 5.15±0.25, p-value <0.001). There was weak positive correlation between the HbA1c and 2-hour blood glucose levels between the two groups but not with the insulin levels. Conclusion The pre-IGT groups have signifi cantly higher 2nd hour blood sugar, insulin and HbA1c levels. This suggests that indeed the metabolic abnormality must be addressed as early as the pre-IGT stage.
Prediabetic State ; Hyperinsulinism

Humans ; Consensus ; Congenital Hyperinsulinism

Hypoglycemic disorders are rare in persons without diabetes, and clinical evaluation to identify its etiology can be challenging. We present a case of insulin autoimmune syndrome induced by carbimazole in a middle-aged Chinese man with underlying Graves’ disease, which was managed conservatively with a combination of dietary modification and alpha-glucosidase inhibitor.
Hypoglycemia ; Hyperinsulinism ; Insulin Antibodies

Congenital Hyperinsulinism ; diagnosis ; therapy ; Humans

Autoimmune hypoglycemia is characterized by insulin autoantibody, hyperinsulinemia and fasting hypoglycemia without previous insulin immunization. Negative results on the anatomic studies of the pancreas and an inability to reproduce hypoglycemia during a prolonged fast may be helpful in excluding insulinoma. Autoimmune hypoglycemia is self-limited disorder. We recently experienced a case of autoimmune hypoglycemia in a patient with insulin antibody, and the patient was without previous insulin injection therapy or any evidence of insulinoma, during treatment with anti-tuberculosis drugs. We present this case along with a review of the literature.
Humans ; Hyperinsulinism ; Hypoglycemia ; Immunization ; Insulin ; Insulinoma ; Pancreas

Insulin autoimmune syndrome, a rare cause of endogenous hyperinsulinemic hypoglycemia, is characterized by insulin autoantibody, hyperinsulinemia and fasting hypoglycemia. It is well known that drugs containing a sulfhydryl group such as methimazole or α-mercaptopropionyl glycine can induce insulin autoimmune syndrome. However, insulin autoimmune syndrome caused by anti-tuberculosis treatment is very rare. We report a case of insulin autoimmune syndrome after anti-tuberculosis treatment with a review of the relevant literature.
Glycine ; Hyperinsulinism ; Hypoglycemia ; Insulin* ; Methimazole ; Tuberculosis

Congenital Hyperinsulinism ; diagnosis ; Humans ; Infant, Newborn ; Male

A 37-year old primigravid with HAIR-AN syndrome on Metformin therapy achieved spontaneous pregnancy after fifteen years of infertility.
Human ; Female ; Adult ; HAIR-AN SYNDROME ; HYPERINSULINISM ; HYPERANDROGENISM

Congenital hyperinsulinism is the most frequent cause of severe, persistent hypoglycemia in infancy and childhood. It is caused by an inappropriate insulin secretion from the pancreatic beta-cells secondary to various genetic disorders. Recognition of this entity becomes important due to the fact that hypoglycemia is very severe and frequent and that it may lead to severe neurological damage in the infant manifesting as mental or psychomotor retardation or even a life-threatening events if not recognized and treated effectively in time. Hypoglycemias can be detected by seizures, fainting, or any other neurological symptoms in the neonatal period or later, usually within the first two years of life. Hypoglycemias must be rapidly and intensively treated to prevent severe and irreversible brain damages. Next, a treatment to prevent the recurrence of hypoglycemia must be set, which may include frequent and glucose-enriched feeding, diazoxide and octreotide. We report a case of congenital hyperinsulinemia in a 2 months old infant presenting as atonic seizure which has been treated with diazoxide.
Brain ; Congenital Hyperinsulinism* ; Diazoxide ; Humans ; Hyperinsulinism ; Hypoglycemia ; Infant* ; Insulin ; Octreotide ; Recurrence ; Seizures* ; Syncope

Congenital hyperinsulinism (CHI), the most important cause of hyperglycemia in early infancy, is a heterogenous disease characterized by dysregulation of insulin secretion. Mutations in five proteins have been associated with CHI: sulfonyl urea receptor 1; Kir 6.2; glucokinase; glutamate dehydrogenase and mitochondrial enzyme short-chain 3-hydroxyacyl-coenzyme A dehydrogenase. Early recognition of hypoglycemia, diagnosis of CHI and appropriate management of the hypoglycemia are of the utmost importance to prevent neurologic damage. We report a case of persistent hyperinsulinemic hypoglycemia in 8-month-old male infant. This patient has no mutation in previously mentioned genes. Treatment with diazoxide was successful without any severe side effects in this patient.
Congenital Hyperinsulinism* ; Diagnosis ; Diazoxide* ; Glucokinase ; Glutamate Dehydrogenase ; Humans ; Hyperglycemia ; Hyperinsulinism ; Hypoglycemia ; Infant ; Insulin ; Male ; Oxidoreductases ; Urea