HYBRID EVENT: You can participate in person at Paris, France or Virtually from your home or work.

9th Edition of International Conference on

Neurology and Neurological Disorders

June 20-22, 2024 | Paris, France

Neurology 2024

Nidhi Patel

Speaker at Neurology and Neurological Disorders 2024 - Nidhi Patel
Renaissance School of Medicine at Stony Brook University, United States
Title : Progressive muscle weakness in a patient with diabetes and gout

Abstract:

Objective: Raise awareness of medication induced toxic myopathy.
Background: Myopathy encompasses increase of creatine kinase, myalgia, muscle weakness, rhabdomyolysis.  Statins and colchicine carry a risk of myopathy. The mechanism of statin-induced myopathy is interruption of the HMG-CoA reductase biosynthetic pathway and consequent intracellular depletion of downstream intermediate metabolites. Risk factors for colchicine myopathy include kidney disease, cirrhosis, high dose, and concomitant CYP3A4 inhibitor use.
Design/Methods: A 75-year-old man presented with proximal muscle weakness, difficulty walking and falls. He has had anorexia, anosmia and ageusia since 2019. He endorsed one month of dysphagia for both liquids and solids, shortness of breath, and dark tarry diarrheic stools. His medical history was remarkable for diabetes mellitus, hyperlipidemia, gout, Parkinson’s disease, and diabetic neuropathy. Medications included aspirin, statin, colchicine, and Sinemet. The physical examination showed proximal muscle weakness in upper and lower extremities, and distal hand weakness. He had depressed ankle jerks and length dependent sensory abnormalities. Guillain-Barre syndrome on a background of uncontrolled diabetes mellitus was diagnosed. After two days of IVIGs, kidney function deteriorated.
Results: NCS/EMG revealed axonal sensory motor neuropathy and irritative myopathy. The left vastus lateralis muscle biopsy showed necrotizing myopathy suggestive of statin toxicity and vacuolar myopathy likely triggered by colchicine. Colchicine toxicity was most likely precipitated by acute renal dysfunction. ANA and Anti-Ro antibodies were positive. Anti-HMG-CoA reductase antibodies and the myositis panel were negative. Statin, colchicine and IVIG were discontinued. The patient slowly became stronger, and gait improved. The hypercholesterolemia is treated with a PCSK9 inhibitor and gout with febuxostat.
Conclusions: A multitude of genetic and acquired factors increase the risk for statin and colchicine induced myopathy. This case illustrates the importance of awareness of medication interactions leading to toxic myopathy in patients with muscle weakness.

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