Abstract
Introduction
Alcoholic myopathy is a well-recognised but often underdiagnosed complication of chronic alcohol misuse. It typically presents in two distinct forms: a chronic painless muscle atrophy and an acute, necrotising presentation that can mimic other inflammatory myopathies. The acute form, though rare, may present with severe muscle weakness, elevated creatine kinase (CK), and rhabdomyolysis. Here, we describe a case of acute necrotising myopathy associated with a history of chronic alcohol misuse, highlighting diagnostic challenges and management considerations.
Case description
A 59-year-old man with a background of ethanol-induced liver disease (including oesophageal varices), hypertension, and hypercholesterolemia presented with a two-week history of progressive, bilateral lower limb weakness and pain. He could not mobilise and reported malaise, poor appetite, and significant weight loss. There was no history of fever, viral prodrome, or connective tissue disease features. He consumed excessive alcohol for over 30 years, though had reportedly abstained for 18 months. Initial investigations showed elevated creatine kinase (CK) of 7,950 U/L and creatinine of 142 µmol/L, and urine dip was positive for blood. He was treated for presumed rhabdomyolysis with intravenous fluids and statin discontinuation, resulting in renal improvement; however, weakness and CK elevation persisted. Neurological examination revealed significant proximal weakness (MMT 98/150), with preserved distal strength. He had bilateral lower limb oedema and hypoalbuminemia (25 g/L), but no rash or dermatomyositis signs. MRI thighs showed diffuse muscle oedema, especially in the quadriceps and gluteals, consistent with myositis. MRI spine ruled out cord compression. EMG showed myopathic features with spontaneous activity, without neuropathy. CT of neck, thorax, abdomen, and pelvis showed cirrhotic liver and ascites but no malignancy. Given the degree of weakness, he received empirical intravenous methylprednisolone for three days with improvement in strength. Autoimmune screen, including ANA, ANCA, myositis-specific antibodies, HMGCR, and viral serologies, were negative. Muscle biopsy showed necrotizing myopathy with prominent fibre necrosis, minimal inflammation, and type 2 fibre atrophy. He was commenced on high-dose oral prednisolone (50 mg/day) with maintained clinical improvement and CK normalisation. Lacking other identifiable causes, and based on clinical, radiological, and histopathological findings, a diagnosis of seronegative immune-mediated necrotising myopathy, potentially alcohol-induced, was made. Myositis remained suppressed on a weaning dose of steroids although his inpatient stay was complicated by liver disease complications. Disease modifying agents would include lower dose mycophenolate if a myositis relapse occurred.
Discussion
Alcoholic myopathy is a spectrum of muscle pathology resulting from chronic alcohol misuse, ranging from insidious, painless muscle wasting to rare, acute necrotising presentations. The acute form is under-recognised and often mimics autoimmune inflammatory myopathies, presenting with rapid-onset proximal muscle weakness, markedly elevated creatine kinase (CK), and systemic features such as malaise and weight loss. In such cases, differentiating toxic myopathy from autoimmune or paraneoplastic causes is clinically challenging, particularly in the presence of comorbidities such as alcoholic liver disease. Our patient presented with classic features of acute myopathy but lacked serological or imaging evidence of systemic autoimmune disease or malignancy. The EMG findings supported a myopathic process, and muscle biopsy confirmed necrotising myopathy with minimal inflammatory infiltrate, favouring a toxic rather than autoimmune aetiology. While the patient maintained abstinence from alcohol, there was concern over the reliability of this duration from family members; this, alongside decades of heavy alcohol consumption, implicated alcohol as the underlying cause. Although abstinence remains the cornerstone of management in alcoholic myopathy, the severity of presentation in this case warranted immunosuppressive therapy. Empirical corticosteroids led to clinical improvement and CK normalisation. While the role of steroids in toxic myopathies is not well established, selected severe cases may benefit from short-term immunomodulation to reduce muscle inflammation and support functional recovery. This case underscores the importance of maintaining a high index of suspicion for alcohol-induced myopathy in patients with unexplained weakness and elevated CK, especially in those with established liver disease. Muscle biopsy remains essential for diagnostic clarity in the absence of serological markers. A multidisciplinary approach, including hepatology and alcohol liaison services, is vital to ensure both acute management and long-term relapse prevention.
Key learning points
1. Acute necrotizing myopathy is a rare but important manifestation of alcohol-induced muscle injury and should be considered in the differential diagnosis of elevated CK and proximal weakness.
2. Muscle biopsy remains key to differentiating between immune-mediated and toxic myopathies, especially when inflammatory markers and antibody panels are negative.
3. Alcohol-induced myopathy may mimic inflammatory myositis; however, a thorough history and exclusion of other causes are essential to reach the correct diagnosis.
4. Chronic alcohol misuse may cause myopathy even months after cessation, highlighting the lasting impact of ethanol on skeletal muscle.
5. Empirical corticosteroids may be beneficial in selected severe or progressive cases of toxic myopathy, although their role remains controversial.
6. Multidisciplinary care, including alcohol liaison services, plays a vital role in long-term recovery and prevention of relapse.