ABSTRACT
Oral mucositis is a painful inflammatory response that can lead to infection, cachexia, and therapy termination. This immune-related adverse event (IRAE) has been well documented within the newly developing field of immunotherapy. This case series presents three patients, aged 73 to 81 years, who were undergoing treatment with programmed death-1 (PD-1) immunotherapy for cancer; each patient developed grade III mucositis, one after the fourth cycle and two after the seventh. All three patients had no prior history of oral pathology, yet each patient reported ulcerated and inflamed oral mucosa that was swollen and painful. These lesions involved various locations within the oral cavity and caused irritation to the point of dysphagia and odynophagia. Conservative treatments such as oral anesthetic and mouthwashes with antimicrobial properties had minimal effects. Each patient thereafter was started on systemic glucocorticoids in addition to the local treatments. The initiation of a systemic treatment resulted in a resolution of the oral lesions allowing each patient the option to return to their prior immunotherapy. Mucositis is uncommon and has no standardized treatment. This case series emphasizes the debilitative result of immunotherapy-induced mucositis and illustrates the need for systemic glucocorticoids. While conservative treatments such as oral mouthwashes can be effective in treating the symptoms of mucositis, the initiation of high-dose steroids with a prolonged taper has been shown to treat the condition at its source. Early recognition of mucositis with prompt initiation of steroids has proven to be the effective mainstay treatment to relieve mucositis while limiting pauses in cancer treatment.
ABSTRACT
Statins are well tolerated in general but can be associated with myopathies. Statin-induced myopathies can range widely from mild myalgias to necrotizing autoimmune myopathies. We present a case of an 81-year-old man on statins for five years with no complications, who developed progressive muscle weakness, rhabdomyolysis, and dysphagia. His laboratory workup revealed elevated inflammatory markers with creatine kinase (CK) levels above 2000 U/L. The myositis panel was negative, and the anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase antibody was positive. His muscle biopsy showed randomly scattered necrotic fibers with minimal perivascular inflammation confirming statin-induced necrotizing autoimmune myopathy (SINAM). Statins were discontinued immediately after initial suspicion. The patient was started on intravenous immunoglobulin followed by hydrocortisone and mycophenolate mofetil. The patient continued to have muscle weakness and progressive dysphagia to the point that he could not handle his secretions. His disease course was complicated by recurrent aspiration pneumonia. Percutaneous endoscopic gastrostomy tube placement was considered, but his family decided on hospice care given his overall comorbidities. Physicians should note that SINAM can occur after a few months to several years of statin use. This disease can be rapidly debilitating and progress even after discontinuation of statins, and treatment requires immunosuppressants, including steroids and steroid-sparing agents.
ABSTRACT
Gout typically affects the peripheral joints but uncommonly can involve the axial skeleton and rarely the intervertebral discs. We present a rare case of gouty spondylodiscitis affecting the intervertebral disc in the lumbar spine. Our patient with a gout history not on any maintenance therapy presented intractable right-sided back pain radiating to the right lower extremity. Computed tomography scan findings were consistent with spondylosis, while magnetic resonance imaging showed concern of infectious discitis. Initially, he was treated for infectious discitis with IV antibiotics. Biopsy of the L5-S1 disc space revealed monosodium urate crystals, confirming the diagnosis of gouty spondylodiscitis. He was managed with IV dexamethasone and recovered well on a tapering dose of steroids and colchicine followed by allopurinol once acute flare resolved.
