Docetaxel-Induced Acute Myositis: A Case Report with Review of Literature
Docetaxel is a widely used chemotherapeutic agent belonging to the taxane family, primarily employed in the treatment of various solid tumors, including breast, prostate, lung, gastric, and head and neck cancers. Its mechanism of action involves stabilizing microtubules, thereby disrupting cell division and leading to apoptosis of rapidly proliferating cancer cells. While docetaxel is effective, its use is associated with a range of side effects, including myelosuppression, neuropathy, fluid retention, skin reactions, and nail changes. Musculoskeletal toxicities, though less common, have also been reported, ranging from arthralgia and myalgia to more severe conditions like myositis. Acute myositis, characterized by inflammation of the muscles, can present with muscle pain, tenderness, and elevated muscle enzymes, and can significantly impact a patient’s quality of life and adherence to treatment. This case report describes a rare instance of docetaxel-induced acute myositis and provides a comprehensive review of the relevant literature to better understand this adverse event.
Case Presentation
A [patient’s age, gender, and relevant medical history, e.g., 65-year-old female with breast cancer] was initiated on docetaxel chemotherapy. After [specific number] cycles of treatment, the patient began to experience [describe initial symptoms, e.g., severe muscle pain and weakness, particularly in the lower extremities]. These symptoms were progressive and significantly debilitating, interfering with daily activities. Physical examination revealed [findings on physical examination, e.g., diffuse muscle tenderness and decreased strength in the affected limbs]. Laboratory investigations showed a significant elevation in muscle enzymes, specifically creatine kinase (CK), lactate dehydrogenase (LDH), and aldolase, confirming muscle damage. Other potential causes of myositis, such as infectious, autoimmune, or other drug-induced etiologies, were thoroughly investigated and ruled out. Based on the temporal relationship with docetaxel administration and the exclusion of other causes, a diagnosis of docetaxel-induced acute myositis was made.
Clinical Course and Management
Upon diagnosis, docetaxel was promptly discontinued. Management of the myositis involved symptomatic treatment, including pain control with analgesics and corticosteroids to reduce inflammation. The patient’s muscle pain and weakness gradually improved following the discontinuation of docetaxel and initiation of corticosteroids. Muscle enzyme levels also trended downwards, returning to near normal ranges over several weeks. The patient’s overall clinical condition improved significantly, allowing for the continuation of alternative oncological treatment strategies. This case highlights the importance of early recognition and prompt management of docetaxel-induced myositis to prevent severe complications and ensure patient well-being.
Review of Literature
Docetaxel-induced myositis is a recognized, albeit uncommon, adverse effect. A review of the existing literature reveals that its incidence is relatively low, typically ranging from less than 1% to a few percent of treated patients. The onset of symptoms can vary, usually occurring after several cycles of treatment, but acute presentations after the first few doses have also been reported. The underlying pathogenesis of taxane-induced myositis is not fully understood but is believed to involve several mechanisms:
1. Direct Myotoxicity:
Docetaxel, like other taxanes, affects microtubule dynamics. While this is crucial for its anti-cancer activity, it may also directly interfere with microtubule function in muscle cells, leading to muscle damage and inflammation. Microtubules are important for various cellular processes, including intracellular transport and structural integrity in muscle fibers.
2. Immune-Mediated Response:
Some evidence suggests an immune-mediated component. Docetaxel can potentially act as an antigen, triggering an immune response that targets muscle tissue. This hypothesis is supported by the inflammatory infiltrate sometimes observed in muscle biopsies of affected patients. Cytokines and chemokines, which play a role in inflammation, may also be involved.
3. Oxidative Stress:
Chemotherapeutic agents can induce oxidative stress, leading to cellular damage. Increased production of reactive oxygen species (ROS) in muscle cells due to docetaxel exposure could contribute to muscle injury and inflammation.
4. Individual Susceptibility:
Genetic polymorphisms in drug-metabolizing enzymes or drug transporters, or variations in immune response genes, may predispose certain individuals to developing docetaxel-induced myositis. This could explain why only a subset of patients experiences this side effect.
5. Drug Accumulation:
In some cases, accumulation of the drug or its metabolites in muscle tissue due to impaired clearance or prolonged exposure might contribute to myotoxicity.
The diagnosis of docetaxel-induced myositis is primarily clinical, based on the temporal relationship between drug administration and symptom onset, characteristic muscle pain and weakness, and elevated muscle enzymes. Muscle biopsy, if performed, may show non-specific inflammatory changes or myonecrosis. Differential diagnosis is crucial to exclude other causes of myositis, such as viral infections, autoimmune diseases (e.g., polymyositis, dermatomyositis), hypothyroidism, or other drug-induced myopathies.
Management typically involves immediate discontinuation of docetaxel, supportive care, and, in some cases, corticosteroids. The prognosis is generally favorable with prompt intervention, with most patients experiencing resolution of symptoms. However, severe cases can lead to significant morbidity.
Conclusion
Docetaxel-induced acute myositis is a rare but potentially serious adverse event of docetaxel chemotherapy. Clinicians should maintain a high index of suspicion for this toxicity in patients presenting with muscle pain and weakness during or after docetaxel treatment. Early recognition, discontinuation of the offending drug, and appropriate supportive management, including corticosteroids when indicated, are essential for improving patient outcomes. Further research into the precise mechanisms underlying this toxicity and the identification of predictive biomarkers would be beneficial for personalized risk assessment and the development of targeted preventive or therapeutic strategies.