Abdulkadir J, Mengesha B, Welde Gebriel Z, Keen H, Worku Y, Gebre P, Bekele A, Urga K, Taddesse A S
Department of Internal Medicine, Faculty of Medicine, Addis Ababa University, Ethiopia.
Diabetologia. 1990 Apr;33(4):222-7. doi: 10.1007/BF00404800.
Cases of malnutrition-related diabetes mellitus conforming to the description of the protein deficient pancreatic diabetes type in Ethiopian patients were compared with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic. Fourteen of 39 malnutrition-related diabetes mellitus patients had fat malabsorption compared with only two of ten Type 1 diabetic patients and one of nine control subjects. Xylose absorption was normal favouring a pancreatic cause for the malabsorption. Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucagon secretion patterns were similar in malnutrition-related and Type 1 diabetic patients. Of 23 new malnutrition-related diabetic patients treated with glibenclamide after nutritional rehabilitation and insulin treatment, only three responded, 14 were unresponsive but remained ketosis free for over eight days while another six developed ketoacidosis or significant ketonuria within two to six days during the trial. Sixteen unselected Type 1 diabetic patients who discontinued their insulin therapy all developed frank ketoacidosis after a mean of 5.5 days. The similarity of the malnutrition-related and Type 1 diabetes mellitus in age of onset, insulin requirement for diabetic control and appearance of ketosis-proneness in some cases, together with the similarity of C-peptide and glucagon secretion patterns suggest that the protein deficient pancreatic diabetes variant of malnutrition-related diabetes mellitus may be Type 1 diabetes mellitus modified by the background of malnutrition rather than an aetiologically separate entity.(ABSTRACT TRUNCATED AT 250 WORDS)
将符合埃塞俄比亚患者蛋白质缺乏型胰腺糖尿病描述的营养不良相关性糖尿病病例与1型(胰岛素依赖型)和2型(非胰岛素依赖型)糖尿病患者进行比较。39例营养不良相关性糖尿病患者中有14例存在脂肪吸收不良,而10例1型糖尿病患者中只有2例,9例对照受试者中只有1例存在脂肪吸收不良。木糖吸收正常,提示吸收不良是由胰腺原因引起的。口服葡萄糖耐量试验期间的血浆C肽显著低于2型糖尿病患者和正常对照受试者(p小于0.01至0.001),并且始终但不显著高于1型糖尿病患者。营养不良相关性糖尿病患者和1型糖尿病患者的胰高血糖素分泌模式相似。23例新的营养不良相关性糖尿病患者在营养康复和胰岛素治疗后接受格列本脲治疗,只有3例有反应,14例无反应,但在超过8天的时间里没有酮症,而另外6例在试验期间的2至6天内发生了酮症酸中毒或显著酮尿。16例未选择的1型糖尿病患者停止胰岛素治疗后,平均5.5天后均出现明显的酮症酸中毒。营养不良相关性糖尿病和1型糖尿病在发病年龄、控制糖尿病所需胰岛素量以及某些情况下易发生酮症的表现方面相似,再加上C肽和胰高血糖素分泌模式的相似性,表明营养不良相关性糖尿病的蛋白质缺乏型胰腺糖尿病变体可能是在营养不良背景下发生改变的1型糖尿病,而不是病因上独立的实体。(摘要截短至250字)