糖尿病酮症酸中毒引起极度血小板增多症1例并文献复习

doi:10.3969/j.issn.1004-583X.2023.08.007

摘要/Abstract

摘要：

目的探讨糖尿病酮症酸中毒引起极度血小板增多症的临床特点及治疗。方法回顾性分析胜利油田中心医院收治的1例糖尿病酮症酸中毒引起的极度血小板增多症患者的临床特点及治疗转归。结果本例患者为青年女性,否认血小板增多病史及血液系统其他疾病病史,急性起病,血小板极度增多(多次报危急值),后完善骨髓穿刺活检及相关基因检测排除血液系统疾病,考虑糖尿病性酮症酸中毒导致继发性血小板增多。在充分补液,纠正酮症酸中毒的过程中血小板水平也随之降低,4天内血小板降至正常范围,且在日后随访过程中血小板维持正常水平。结论查阅相关文献,目前国内外尚无糖尿病酮症酸中毒合并血小板极度增多的病例报道,现就此例病例进行报道,以期在临床上发现糖尿病酮症酸中毒合并血小板极度增多时避免误诊及过度治疗。

关键词: 糖尿病酮症酸中毒, 极度血小板增多症

Abstract:

Objective To investigate the clinical characteristics and treatment of extreme thrombocytosis caused by diabetic ketoacidosis. Methods The clinical characteristics and treatment outcomes of a patient with extreme thrombocytosis caused by diabetic ketoacidosis who was treated in Shengli Oilfield Central Hospital were retrospectively analyzed. Results The present young female patient had a sudden onset of an extreme thrombocytosis, with multiple times of reporting critical values. She denied the history of thrombocytosis and other diseases of the blood system. After bone marrow biopsy and gene testing, hematological diseases were excluded, and secondary thrombocytosis caused by diabetic ketoacidosis was considered. Platelet count decreased during the treatment course. After adequate fluid rehydration and correction of ketoacidosis, platelet count returned to the normal range within 4 days, which remained normal during follow-up.Conclusion Through literature review, there is no case report of diabetic ketoacidosis with extreme thrombocytosis at home and abroad. This case report aims to provide reference to avoid misdiagnosis and excessive treatment of diabetic ketoacidosis patients with extreme thrombocytosis.

Key words: diabetic ketoacidosis, extreme thrombocytosis

中图分类号:

R587.22

张欣欣, 刘国庆, 王蓓蓓. 糖尿病酮症酸中毒引起极度血小板增多症1例并文献复习[J]. 临床荟萃, 2023, 38(8): 719-721.

Zhang Xinxin, Liu Guoqing, Wang Beibei. Extreme thrombocytosis caused by diabetic ketoacidosis: A case report and literature review[J]. Clinical Focus, 2023, 38(8): 719-721.

导出引用管理器 EndNote|Ris|BibTeX

链接本文: https://huicui.hebmu.edu.cn/CN/10.3969/j.issn.1004-583X.2023.08.007

https://huicui.hebmu.edu.cn/CN/Y2023/V38/I8/719

图/表 1

参考文献 17

[1]	Hsieh RW, Ravindran A, Hook CC, et al. Etiologies of extreme thrombocytosis: a contemporary series[J]. Mayo Clin Proc, 2019, 94(8):1542-1550. doi: S0025-6196(19)30211-3 pmid: 31378229
[2]	肖志坚. 原发性血小板增多症诊断与治疗中国专家共识(2016年版)[J]. 中华血液学杂志, 2016, 37(10):833-836.
[3]	Deutsch VR, Tomer A. Advances in megakaryocytopoiesis and thrombopoiesis: from bench to bedside[J]. Br J Haematol, 2013, 161(6):778-793. doi: 10.1111/bjh.2013.161.issue-6 URL
[4]	Heinrich PC, Castell JV, Andus T. Interleukin-6 and the acute phase response[J]. Biochem J, 1990, 265(3):621-636. doi: 10.1042/bj2650621 URL
[5]	Unsal E, Aksaray S, Koksal D, et al. Potential role of interleukin 6 in reactive thrombocytosis and acute phase response in pulmonary tuberculosis[J]. Postgrad Med J, 2005, 81(959):604-607. doi: 10.1136/pgmj.2004.030544 URL
[6]	Gordon MS, Nemunaitis J, Hoffman R, et al. A phase I trial of recombinant human interleukin-6 in patients with myelodysplastic syndromes and thrombocytopenia[J]. Blood, 1995, 85(11):3066-3076. doi: 10.1182/blood.V85.11.3066.bloodjournal85113066 URL
[7]	Ceresa IF, Noris P, Ambaglio C, et al. Thrombopoietin is not uniquely responsible for thrombocytosis in inflammatory disorders[J]. Platelets, 2007, 18(8):579-582. pmid: 18041648
[8]	Eulenfeld R, Dittrich A, Khouri C, et al. Interleukin-6 signalling: more than Jaks and STATs[J]. Eur J Cell Biol, 2012, 91(6-7):486-495. doi: 10.1016/j.ejcb.2011.09.010 pmid: 22138086
[9]	Dalton RR, Hoffman WH, Passmore GG, et al. Plasma C-reactive protein levels in severe diabetic ketoacidosis[J]. Ann Clin Lab Sci, 2003, 33(4):435-442. pmid: 14584758
[10]	Li J, Huang M, Shen X. The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis[J]. J Diabetes Complications, 2014, 28(5):662-666. doi: 10.1016/j.jdiacomp.2014.06.008 URL
[11]	Ivaska L, Elenius V, Mononen I, et al. Discrepancies between plasma procalcitonin and C-reactive protein levels are common in acute illness[J]. Acta Paediatr, 2016, 105(5):508-513. doi: 10.1111/apa.2016.105.issue-5 URL
[12]	Mousa SO, Sayed SZ, Moussa MM, et al. Assessment of platelets morphological changes and serum butyrylcholinesterase activity in children with diabetic ketoacidosis: A case control study[J]. BMC Endocr Disord, 2017, 17(1):23. doi: 10.1186/s12902-017-0174-6 pmid: 28376867
[13]	Sun Q, Li J, Gao F. New insights into insulin: The anti-inflammatory effect and its clinical relevance[J]. World J Diabetes, 2014, 5(2):89-96. doi: 10.4239/wjd.v5.i2.89 pmid: 24765237
[14]	Wolfsdorf JI, Nicole G, Mich Ae LA, et al. Diabetic ketoacidosis and hyperglycemic hyperosmolar state: A consensus statement from the International Society for Pediatric And Adolescent Diabetes[J]. Pediatric Diabetes, 2018, 19(Suppl 27):3. doi: 10.1111/pedi.2018.19.issue-S26 URL
[15]	Schafer AI. Thrombocytosis[J]. N Engl J Med, 2004, 350(12):1211-1219. doi: 10.1056/NEJMra035363 URL
[16]	Alberio L. Do we need antiplatelet therapy in thrombocytosis? Pro. Diagnostic and pathophysiologic considerations for a treatment choice[J]. Hamostaseologie, 2016, 36(4):227-240. pmid: 25707870
[17]	Harrison CN, Bareford D, Butt N, et al. Guideline for investigation and management of adults and children presenting with a thrombocytosis[J]. Br J Haematol, 2010, 149(3):352-375. doi: 10.1111/bjh.2010.149.issue-3 URL