(2008) (5) reported that this sensitivity and specificity for the combination of GAD and IA-2 antibody was 67 and 100% respectively, and the sensitivity and specificity for the GAD or IA-2 antibody was 98 and 99% respectively. insulin treatment, he was significantly sensitive to insulin therapy. Even the appropriate amount of insulin may result in dramatically decreasing blood sugar levels in patients with T1DM. We should therefore suspect WIN 55,212-2 mesylate T1DM in patients with HHS but not those with obesity. Moreover, age, clinical history and body type are helpful for identifying T1DM and HHS. Specifically, drinking an excess of beverages rich in sugars represents a risk of HHS in juvenile/adolescent T1DM patients. Learning points: Hyperglycemic hyperosmolar state (HHS) is characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis. The discrimination between HHS of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in initial presentation is hard. Pediatrician should suspect T1DM in patients with HHS but not obesity. Age, clinical history and WIN 55,212-2 mesylate body type are helpful for identifying T1DM and HHS. Children with T1DM are very sensitive to insulin treatment, and even appropriate amount of insulin may result in dramatically decreasing blood sugar levels. Background Hyperglycemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are the most severe acute complications of diabetes mellitus (DM). HHS is usually characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis. HHS has been frequently reported in adult Mouse monoclonal to IHOG patients with type 2 DM (T2DM), but other than at academic meetings, no pediatric cases with HHS have been reported in Japanese patients with type 1 DM (T1DM). Although HHS and DKA share some clinical appearances, they are unique clinical entities causing different complications and requiring different treatments. Here, we statement on a 14-year-old Japanese young man with HHS and T1DM and discuss the causes of this condition. Case presentation A 14-year-old Japanese young man presented at the emergency room with lethargy, polyuria and polydipsia. He had been healthy without a personal or family history of medical problems. He belonged to a baseball club team and experienced habitually drank sugar-rich beverages daily. Three weeks earlier he suffered from lassitude and developed polyuria and polydipsia 1 week later. He had been drinking more sugar-rich isotonic sports drinks (approximately 1000C1500?mL/day) than usual (approximately 500?mL/day). His excess weight decreased from 57 to 51.8?kg in the past month. At admission, his height, excess weight and BMI were 172?cm, 51.8?kg and 17.5?kg/m2 (Z score: ?0.74, https://zscore.research.chop.edu/index.php), respectively. His body temperature was 37.2C; heart rate, 81?beats/min; respiratory rate, 12?breaths/min; blood pressure, 129/73?mmHg; and pulse oximetry, 98% in room air. He appeared obtunded and developed significant WIN 55,212-2 mesylate dehydration with decreased skin turgor, he had dried mucous membranes, a capillary refill time 2?s and a cardiothoracic ratio of 32% on a chest radiograph. Investigation He presented with HHS (hyperglycemia (56.1?mmol/L, HbA1c 12.3%) and mild hyperosmolality (313?mOsm/kg)) without acidosis (pH 7.360), severe ketosis (589?mol/L) and ketonuria (Furniture 1 and ?and2).2). He did not present acanthosis nigricans or skin tags. His abdominal ultrasonography exhibited nonfatty liver disease. He was suspected of presenting HHS with T2DM. Table 1 Arterial blood and urine data before and after treatment in a patient with T1DM who developed HHS. thead th align=”left” valign=”bottom” rowspan=”1″ colspan=”1″ /th th align=”center” valign=”bottom” rowspan=”1″ colspan=”1″ Initial presentation /th th align=”center” valign=”bottom” rowspan=”1″ colspan=”1″ 14?h /th /thead pH7.367.39pCO2 (mmHg)42.044.0Bicarbonate (mM)23.726.6Base extra (mM)?1.81.2Lactate (mM)1.00.7Serum sodium (mEq/L)136.5137Serum potassium (mEq/L)4.94.1Serum chloride (mEq/L)87105Serum glucose (mg/dL)1010201Serum BUN (mg/dL)2315Serum creatinine (mg/dL)0.630.62Plasma osmolality (mOsm/L)313284Urine glucose3+CUrine ketone bodyCC Open in a separate window Table 2 Specific laboratory data for T1DM. thead th align=”left” valign=”bottom” rowspan=”1″ colspan=”1″ Parameters /th th align=”center” valign=”bottom” rowspan=”1″ colspan=”1″ Values /th th align=”center” valign=”bottom” rowspan=”1″ colspan=”1″ Reference range /th /thead HbA1c (%)12.34.6C6.2IRI (U/mL)3.991.84C12.2C-peptide (ng/mL)0.580.61C2.09Total ketone bodies (mol/L)5890C130Acetoacetic acid (mol/L)1980C55Beta-hydoroxybutyric acid (mol/L)3410C85GAD antibodies (U/mL)32.10C4.9IA-2 antibodies (U/mL)19.00C0.39TPO antibodies (U/mL)14.00C15.9TSH-R antibodies (U/mL) 1.00C0.9Tg antibodies (U/mL)Q100C27HLA-DNA DQB103:01:01 br / 03:03:02 Open in a separate windows GAD, glutamate decarboxylase; HHS, hyperglycemic hyperosmolar state; HLA, human leukocyte antigen; IA-2, islet antigen 2; IRI, immunoreactive insulin; T1DM, type 1 diabetes mellitus; Tg, thyroglobulin; TPO, thyroid peroxidase; TSH-R, thyroid-stimulating hormone receptor. Treatment Intensive transfusion with 0.9% saline was administered, and his blood glucose levels decreased to 47.3?mmol/L. Moreover, 5?U (0.1?U/kg) intravenous insulin was administered; infusions commenced at a rate of 0.06?U/(kgh). Two hours after hospitalization, insulin infusions were decreased to 0.01?U/(kgh) (Fig. 1). Twenty-four hours after hospitalization, the patient started oral intake and subcutaneous regular insulin treatment (6?U at every meal) while undergoing continuous insulin treatment of 0.01?U/(kgh). The continuous.