Nodular cystic fat necrosis in a patient with diabetes mellitus
Nodular cystic fat necrosis in a patient with diabetes mellitus
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糖尿病患者结节性囊性脂肪坏死
DOI：
10.1111/j.1346-8138.2009.00651.x
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
K. Yoneda
中科院分区：
文献类型：
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作者：
Y. Kubota;K. Nakai;T. Moriue;I. Yokoi;N. Fujita;I. Miyamoto;K. Yoneda
尊敬的编辑，结节性囊性脂肪坏死（NCFN），首先由Przyjemski等人于1977年描述，是一种独特的良性皮下病变，其组织学特征为包裹性脂肪坏死，显示膜囊改变。我们报告一个糖尿病患者发生结节性囊性脂肪坏死的病例。一位81岁的日本男性在他的背部和四肢出现多发性无症状的皮下结节，有2年的病史。体格检查时，在下背部、上臂和大腿的伸肌面散在约30个移动的、坚硬的皮下结节，直径为10-15 mm。(Fig. 1a，B）他的总体状况良好。他没有外伤史。临床鉴别诊断包括脂肪瘤、血管脂肪瘤、创伤后脂肪肉芽肿、皮下型结节病和Rothmann-Makai综合征。他还被诊断出患有糖尿病，并患有糖尿病视网膜病变超过10年。实验室数据显示，他的空腹血糖（FBS）水平为121 mg/dL，血红蛋白A1 c为6.1%。组织学上，切除的皮肤肿块显示界限清楚的包裹性脂肪坏死和明显的脂膜性改变。高碘酸-希夫染色脂膜呈阳性（图2a，B）。首次访视后2个月，结节大小略有下降，FBS和HbA 1c水平控制良好，但未使用皮肤病变药物。结节性囊性脂肪坏死具有独特的临床和组织学特征。诸如结节性囊性脂肪坏死、移动的包裹性脂肪瘤和包裹性脂肪坏死结节等名称已被用于指定病变。大多数病变是移动的皮下结节，位于易受创伤的区域，如肘部、膝盖和胫骨。组织学特征为包裹性脂肪坏死和脂膜变化，其中多个非活性脂肪细胞被浓缩的纤维组织包围。NCFN的病因尚不清楚。其发病机制似乎与创伤、快速血管功能不全和随后的纤维囊形成有关。然而，许多之前报道的患者都没有创伤史，我们的患者也是如此。在组织学上必须与脂肪瘤、血管脂肪瘤、α-1-抗胰蛋白酶缺乏相关性脂膜炎和胰腺脂肪坏死相鉴别。
Dear Editor, Nodular cystic fat necrosis (NCFN), first described by Przyjemski et al. in 1977, is a distinct, benign subcutaneous lesion characterized histologically by encapsulated fat necrosis showing membranocystic change. We report a case of nodular cystic fat necrosis in a patient with diabetes mellitus. An 81-year-old Japanese man presented multiple asymptomatic subcutaneous nodules on his back and extremities with a 2-year history. On physical examination, approximately 30 mobile, firm subcutaneous nodules measured 10–15 mm in diameter were scattered at the extensor aspect of the lower back, upper arm and thigh. (Fig. 1a,b) His general condition was good. He had no history of trauma. Clinical differential diagnosis included lipoma, angiolipoma, post-traumatic lipogranuloma, subcutaneous type sarcoidosis and Rothmann–Makai syndrome. He was also diagnosed with diabetes mellitus and had suffered from diabetic retinopathy for more than 10 years. Laboratory data revealed that his fasting blood sugar (FBS) level was 121 mg/dL and hemoglobin A1c was 6.1%. Histologically, the excised cutaneous mass showed well-demarcated encapsulated fat necrosis and marked lipomembranous changes. The lipomembrane was positive for periodic acid-Schiff staining (Fig. 2a,b). Two months after the first visit, the nodules decreased in size slightly with good control of FBS and HbA1c levels although no medication for skin lesions was used. Nodular cystic fat necrosis shows a distinctive spectrum of clinical and histological features. Names such as nodular cystic fat necrosis, mobile encapsulated lipoma and encapsulated fat necrotic nodules have been offered to designate the lesion. Most of the lesions are mobile subcutaneous nodules in regions vulnerable to trauma, such as the elbows, knees and shins. The histology is characterized by encapsulated fat necrosis and lipomembranous change in which multiple, non-viable adipocytes are surrounded by condensed fibrous tissue. The etiology of NCFN is still unclear. Its pathogenesis seems to be related to trauma, rapid vascular insufficiency and subsequent fibrous capsule formation. Many previously reported patients, however, had no history of trauma, as was the same with our patient. The lesion must be distinguished histologically from lipoma, angiolipoma, α-1-antitrypsin deficiency-associated panniculitis and pancreatic fat necrosis.