Chymoral Forte Should Not Be Given to Patients with Polymyositis or Dermatomyositis
Chymoral Forte (chymotrypsin) has no role in the treatment of polymyositis or dermatomyositis and should not be used. These conditions require immediate immunosuppressive therapy with high-dose corticosteroids combined with steroid-sparing agents, not proteolytic enzymes.
Why Chymoral Forte Is Inappropriate
The Disease Requires Immunosuppression, Not Enzymatic Therapy
Polymyositis and dermatomyositis are autoimmune inflammatory myopathies driven by CD8+ cytotoxic T-cell invasion and immune-mediated muscle destruction that demand prompt immunosuppressive intervention 1, 2.
Chymoral Forte contains the proteolytic enzyme chymotrypsin, which is marketed for reducing inflammation and edema in various conditions, but has no established mechanism of action against autoimmune muscle inflammation and is not mentioned in any evidence-based treatment guidelines for inflammatory myopathies 1, 2, 3.
Delaying appropriate immunosuppressive therapy in favor of ineffective treatments like proteolytic enzymes can allow progression to rhabdomyolysis, myocardial involvement, and potentially fatal outcomes 3.
The Correct Treatment Approach
First-Line Therapy: Immediate Dual Immunosuppression
For adult patients with idiopathic inflammatory myositis, initiate high-dose corticosteroids (prednisone approximately 1 mg/kg/day) concurrent with a steroid-sparing agent from the outset 1, 2, 3.
The recommended steroid-sparing agents are methotrexate, azathioprine, or mycophenolate mofetil, introduced early rather than later to facilitate corticosteroid tapering and minimize steroid toxicity 1, 2, 4, 5.
Combination therapy with azathioprine is most common for dermatomyositis/polymyositis 6, 4.
Severe or Refractory Disease
For patients with severe myositis, extensive extramuscular organ involvement, or refractory disease, use high-dose intravenous methylprednisolone plus intravenous immunoglobulin (2 g/kg divided over 2-5 days), cyclophosphamide, rituximab, or cyclosporine 1, 2, 3.
Intravenous immunoglobulin is particularly effective for dermatomyositis when the disease remains active despite initial therapy 2, 7, 5, 8.
Monitoring Disease Activity
Serial measurements of creatine kinase and inflammatory markers (ESR, CRP) guide treatment adjustments, with regular assessment of muscle strength using standardized manual muscle testing 2, 3.
Myositis-specific autoantibodies (anti-Jo-1, anti-Mi-2, anti-MDA5, anti-TIF1-γ, anti-NXP2) define clinical subsets, predict extramuscular organ involvement such as interstitial lung disease and cardiac complications, and offer prognostic information 1, 2.
Critical Pitfalls to Avoid
Do not use symptomatic treatments like NSAIDs or proteolytic enzymes as primary therapy for immune-mediated inflammatory myopathies; these conditions require immunosuppression to prevent irreversible muscle damage and life-threatening complications 3.
Do not delay corticosteroid treatment; postponing immunosuppression can allow progression to necrotizing myopathy with markedly elevated CK levels (>10 times upper limit of normal), rhabdomyolysis, and myocardial involvement 2, 3.
Prolonged administration of high-dose corticosteroids as monotherapy should be avoided; introduce a steroid-sparing agent early to minimize corticosteroid toxicity 5.