PMC:6636912 / 7984-9630
Annnotations
2_test
{"project":"2_test","denotations":[{"id":"31232947-10868861-68672924","span":{"begin":88,"end":89},"obj":"10868861"},{"id":"31232947-17130187-68672925","span":{"begin":227,"end":228},"obj":"17130187"},{"id":"31232947-26071380-68672925","span":{"begin":227,"end":228},"obj":"26071380"},{"id":"31232947-29600506-68672925","span":{"begin":227,"end":228},"obj":"29600506"},{"id":"31232947-28668376-68672926","span":{"begin":905,"end":907},"obj":"28668376"},{"id":"31232947-30280274-68672927","span":{"begin":908,"end":910},"obj":"30280274"},{"id":"31232947-3543673-68672928","span":{"begin":1064,"end":1065},"obj":"3543673"},{"id":"31232947-26530207-68672929","span":{"begin":1111,"end":1112},"obj":"26530207"},{"id":"31232947-26071380-68672930","span":{"begin":1113,"end":1114},"obj":"26071380"},{"id":"31232947-26171144-68672931","span":{"begin":1115,"end":1117},"obj":"26171144"},{"id":"31232947-27657549-68672931","span":{"begin":1115,"end":1117},"obj":"27657549"},{"id":"31232947-22704172-68672931","span":{"begin":1115,"end":1117},"obj":"22704172"},{"id":"31232947-22611441-68672932","span":{"begin":1374,"end":1376},"obj":"22611441"},{"id":"31232947-20170930-68672933","span":{"begin":1640,"end":1642},"obj":"20170930"},{"id":"31232947-26372299-68672934","span":{"begin":1643,"end":1645},"obj":"26372299"}],"text":"The distinction between type 1 and type 2 diabetes mellitus is usually straightforward.[7] However, as reported in this case, there may be an overlap in the presentations of the 2 disorders, which creates a diagnostic dilemma.[8–10] Questions raised as we review the clinic process of the young ketosis prone diabetes patients. How to classify type of diabetes for the young patient based on his initial presentation? What was the likely reason for his metabolic decompensation? The young patient presented with marked dehydration and uncontrolled hyperglycemia in the absence of any precipitating factor such as infection., along with diabetic acidosis and ketosis resulting from deficient insulin secretion, However, the phenotypic features of obesity, acanthosis nigricans, marked insulin resistance and strong family history of adult onset diabetes which are classically associated with classic T2DM.[11,12] All findings were consistent with atypical diabetes or ketosis-prone diabetes, which first systematically reported by Winters and his colleges in 1987.[5] KPDM is an emerging heterogeneous syndrome.[6,9,13–15]This syndrome of episodic diabetic ketoacidosis without immunologic markers of type 1 diabetes is characterized by insulin dependence at the time of presentation, but followed by absence of insulin requirements for years as observed in type 2 diabetes.[16] Because of the mixed features of type 1 and type 2 diabetes, this variant of diabetes has been referred to in the literature as diabetes type 1B, idiopathic type 1 diabetes, atypical diabetes, Flatbush diabetes, and more recently, ketosis-prone type 2 diabetes.[17,18]"}