Abstract

Background: Diabetic amyotrophy is a rare complication of type 2 diabetes mellitus. There is little existing evidence contributing to projected outcomes for patients recovering from diabetic amyotrophy.Clinical Case: A 42 year-old man presented with lower extremity muscle pain and progressive proximal muscle weakness over 8 months. He developed asymmetrical muscle weakness in the lower extremities with diffuse pain and sensitivity to touch. He also had 80 pounds weight loss, diarrhea, and erectile dysfunction over the same time period. He had a past medical history of asthma, chronic migraines, and type II diabetes mellitus with A1c 7.1. His medications included high dose prednisone to treat his chronic migraines and asthma. Exam revealed generalized muscle atrophy, asymmetric proximal weakness, areflexia, with sensory loss in bilateral lower limbs.ESR, CRP, ANA, anti-HMG CoA reductase, CK, aldolase, SPEP, and myomarker panel were all within normal limits. Treponema pallidum and Bartonella serologies were negative. CSF evaluation was not suggestive of any demyelinating or neuromuscular disease. Full body STIR MRI demonstrated muscle edema in abductor, gluteus minimus, and paraspinal muscles bilaterally. EMG testing revealed acute to subacute active asymmetrical polyradiculoneuropathy and evidence of chronic proximal myopathy.Based on clinical presentation, EMG findings, and lack of evidence to support alternative diagnoses, he was diagnosed with diabetic amyotrophy and was started on IVIG and methylprednisolone with improvement in pain but very minimal improvement in weakness. Unfortunately, the expected clinical course following a diagnosis of diabetic amyotrophy is one of minimal improvement with treatment, as was the case in our patient.Conclusion: Diabetic amyotrophy is a rare complication of type 2 diabetes mellitus which typically presents with muscle weakness followed by severe pain in the thighs, hips, and buttocks. Compared with other neurologic complications of diabetes, amyotrophy is relatively uncommon, affecting approximately 1 percent of patients. This low prevalence and the broad differential for proximal muscle weakness makes it challenging to diagnose. It remains a diagnosis of exclusion, though EMG studies showing polyradiculoneuropathy in the proximal leg musculature is suggestive. Clinical improvement is slow and often incomplete. Physical and occupational therapy are a mainstay of treatment which may also include IVIG and steroids aimed at treating associated pain. Endocrinologists should have a high clinical suspicion for diabetic amyotrophy in the appropriate clinical context. When considering the diagnosis and discussing treatment options with patients, this case highlights the important role of endocrinologists discussing expectations associated with projected outcomes while attempting to manage diabetic amyotrophy.

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