PDF(Pubmed)
Abstract：
BACKGROUND: Necrotizing myopathies and muscle necrosis can be caused by immune-mediated mechanisms, drugs, ischemia, and infections, and differential diagnosis may be challenging.
METHODS: We describe a case of diabetic myonecrosis complicated by pyomyositis and abscess caused by Escherichia coli. A white woman in her late forties was admitted to the hospital with a 1.5 week history of bilateral swelling, weakness, and mild pain of the lower extremities and inability to walk. She had a history of type 1 diabetes complicated by diabetic retinopathy, neuropathy, nephropathy, and end-stage renal disease. C-reactive protein was 203 mg/l, while creatinine kinase was only mildly elevated to 700 IU/l. Magnetic resonance imaging of her lower limb muscles showed extensive edema, and muscle biopsy was suggestive of necrotizing myopathy with mild inflammation. No myositis-associated or myositis-specific antibodies were detected. Initially, she was suspected to have seronegative immune-mediated necrotizing myopathy, but later her condition was considered to be explained better by diabetic myonecrosis with multifocal involvement. Her symptoms alleviated without any immunosuppressive treatment. After a month, she developed new-onset and more severe symptoms in her right posterior thigh. She was diagnosed with emphysematous urinary tract infection and emphysematous myositis and abscess of the right hamstring muscle. Bacterial cultures of drained pus from abscess and urine were positive for Escherichia coli. In addition to abscess drainage, she received two 3-4-week courses of intravenous antibiotics. In the discussion, we compare the symptoms and findings typically found in pyomyositis, immune-mediated necrotizing myopathy, and diabetic myonecrosis (spontaneous ischemic necrosis of skeletal muscle among people with diabetes). All of these diseases may cause muscle weakness and pain, muscle edema in imaging, and muscle necrosis. However, many differences exist in their clinical presentation, imaging, histology, and extramuscular symptoms, which can be useful in determining diagnosis. As pyomyositis often occurs in muscles with pre-existing pathologies, the ischemic muscle has likely served as a favorable breeding ground for the E. coli in our case.
CONCLUSIONS: Identifying the etiology of necrotizing myopathy is a diagnostic challenge and often requires a multidisciplinary assessment of internists, pathologists, and radiologists. Moreover, the presence of two rare conditions concomitantly is possible in cases with atypical features.
METHODS: We describe a case of diabetic myonecrosis complicated by pyomyositis and abscess caused by Escherichia coli. A white woman in her late forties was admitted to the hospital with a 1.5 week history of bilateral swelling, weakness, and mild pain of the lower extremities and inability to walk. She had a history of type 1 diabetes complicated by diabetic retinopathy, neuropathy, nephropathy, and end-stage renal disease. C-reactive protein was 203 mg/l, while creatinine kinase was only mildly elevated to 700 IU/l. Magnetic resonance imaging of her lower limb muscles showed extensive edema, and muscle biopsy was suggestive of necrotizing myopathy with mild inflammation. No myositis-associated or myositis-specific antibodies were detected. Initially, she was suspected to have seronegative immune-mediated necrotizing myopathy, but later her condition was considered to be explained better by diabetic myonecrosis with multifocal involvement. Her symptoms alleviated without any immunosuppressive treatment. After a month, she developed new-onset and more severe symptoms in her right posterior thigh. She was diagnosed with emphysematous urinary tract infection and emphysematous myositis and abscess of the right hamstring muscle. Bacterial cultures of drained pus from abscess and urine were positive for Escherichia coli. In addition to abscess drainage, she received two 3-4-week courses of intravenous antibiotics. In the discussion, we compare the symptoms and findings typically found in pyomyositis, immune-mediated necrotizing myopathy, and diabetic myonecrosis (spontaneous ischemic necrosis of skeletal muscle among people with diabetes). All of these diseases may cause muscle weakness and pain, muscle edema in imaging, and muscle necrosis. However, many differences exist in their clinical presentation, imaging, histology, and extramuscular symptoms, which can be useful in determining diagnosis. As pyomyositis often occurs in muscles with pre-existing pathologies, the ischemic muscle has likely served as a favorable breeding ground for the E. coli in our case.
CONCLUSIONS: Identifying the etiology of necrotizing myopathy is a diagnostic challenge and often requires a multidisciplinary assessment of internists, pathologists, and radiologists. Moreover, the presence of two rare conditions concomitantly is possible in cases with atypical features.
摘要：
背景：坏死性肌病和肌肉坏死可由免疫介导的机制引起，毒品,缺血,和感染，和鉴别诊断可能具有挑战性。
方法：我们描述了一例由大肠杆菌引起的糖尿病性肌坏死并发化脓性肌炎和脓肿的病例。一名四十多岁的白人妇女因双侧肿胀1.5周病史入院,弱点,下肢轻度疼痛和无法行走。她有1型糖尿病合并糖尿病视网膜病变的病史，神经病,肾病，和终末期肾病.C反应蛋白为203mg/l,而肌酐激酶仅轻度升高至700IU/l。她下肢肌肉的磁共振成像显示广泛的水肿，肌肉活检提示坏死性肌病伴轻度炎症。未检测到肌炎相关或肌炎特异性抗体。最初，她被怀疑患有血清阴性免疫介导的坏死性肌病，但后来她的病情被认为可以通过多灶性累及的糖尿病性心肌坏死得到更好的解释.她的症状在没有任何免疫抑制治疗的情况下缓解。一个月后,她的右大腿后部出现了新发作和更严重的症状。她被诊断为气肿性尿路感染，气肿性肌炎和右腿筋脓肿。从脓肿和尿液中排出的脓液的细菌培养物对大肠杆菌呈阳性。除了脓肿引流，她接受了两个3-4周的静脉注射抗生素疗程.在讨论中,我们比较了在化脓性肌炎中常见的症状和发现，免疫介导的坏死性肌病，和糖尿病性心肌坏死（糖尿病患者的骨骼肌自发性缺血性坏死）。所有这些疾病都可能导致肌肉无力和疼痛，成像中的肌肉水肿，和肌肉坏死.然而,他们的临床表现存在许多差异，成像,组织学,和肌外症状，这对确定诊断很有用。由于化脓性肌炎通常发生在具有预先存在的病理的肌肉中，在我们的病例中，缺血性肌肉可能是大肠杆菌的有利滋生地。
结论：确定坏死性肌病的病因是一个诊断挑战，通常需要对内科医生进行多学科评估，病理学家,和放射科医生。此外，在具有非典型特征的情况下，可能同时存在两种罕见情况。
方法：我们描述了一例由大肠杆菌引起的糖尿病性肌坏死并发化脓性肌炎和脓肿的病例。一名四十多岁的白人妇女因双侧肿胀1.5周病史入院,弱点,下肢轻度疼痛和无法行走。她有1型糖尿病合并糖尿病视网膜病变的病史，神经病,肾病，和终末期肾病.C反应蛋白为203mg/l,而肌酐激酶仅轻度升高至700IU/l。她下肢肌肉的磁共振成像显示广泛的水肿，肌肉活检提示坏死性肌病伴轻度炎症。未检测到肌炎相关或肌炎特异性抗体。最初，她被怀疑患有血清阴性免疫介导的坏死性肌病，但后来她的病情被认为可以通过多灶性累及的糖尿病性心肌坏死得到更好的解释.她的症状在没有任何免疫抑制治疗的情况下缓解。一个月后,她的右大腿后部出现了新发作和更严重的症状。她被诊断为气肿性尿路感染，气肿性肌炎和右腿筋脓肿。从脓肿和尿液中排出的脓液的细菌培养物对大肠杆菌呈阳性。除了脓肿引流，她接受了两个3-4周的静脉注射抗生素疗程.在讨论中,我们比较了在化脓性肌炎中常见的症状和发现，免疫介导的坏死性肌病，和糖尿病性心肌坏死（糖尿病患者的骨骼肌自发性缺血性坏死）。所有这些疾病都可能导致肌肉无力和疼痛，成像中的肌肉水肿，和肌肉坏死.然而,他们的临床表现存在许多差异，成像,组织学,和肌外症状，这对确定诊断很有用。由于化脓性肌炎通常发生在具有预先存在的病理的肌肉中，在我们的病例中，缺血性肌肉可能是大肠杆菌的有利滋生地。
结论：确定坏死性肌病的病因是一个诊断挑战，通常需要对内科医生进行多学科评估，病理学家,和放射科医生。此外，在具有非典型特征的情况下，可能同时存在两种罕见情况。
