A 70-year-old previously independent man developed progressive proximal leg weakness resulting in a fall at home suffering traumatic brain injury. He was prescribed a statin medication two years prior, but this was discontinued on admission to the hospital due to concern for statin myopathy. His weakness continued to progress while in acute rehabilitation, along with the development of dysphagia requiring placement of gastrostomy tube and respiratory failure requiring tracheostomy. Corticosteroids and intravenous immunoglobulin were administered without response. Nerve conduction study demonstrated no evidence of neuropathy; electromyography revealed spontaneous activity suggestive of myopathy. A muscle biopsy was performed and demonstrated myonecrosis. Serology was positive for autoantibodies to 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), verifying our diagnosis of statin-associated autoimmune myopathy (SAM). The patient was subsequently treated with rituximab and methotrexate and demonstrated mild clinical improvement. He was eventually liberated from the ventilator. However, later in the course of treatment, he developed respiratory distress and required ventilator support. The patient was discharged to long-term acute care two months after his initial presentation and died due to ventilator-acquired pneumonia three months later. Since their introduction 30 years ago, statin medications have been widely prescribed to prevent cardiovascular diseases. Myalgias and/or myopathic symptoms are among the most recognized side effects of the medication. Statin-associated autoimmune myopathy is a very rare complication of statin use and estimated to affect two to three for every 100,000 patients treated. Clinically, the condition presents as progressive symmetric weakness, muscle enzyme elevations, necrotizing myopathy on muscle biopsy, and the presence of autoantibodies to HMGCR. These findings will often persist and even progress despite discontinuation of the statin. Very few cases of SAM have been described in the literature. Describing this rare condition and the ultimately fatal outcome of our patient, we aim to further understanding of SAM, its presentation and clinical course to promote earlier diagnosis and prompt management.
Lung cancer is the number one cause of cancer-related deaths in the United States. Involvement of pericardium occurs once cancer has progressed to stage IV which can cause massive effusion in the pericardial sac. This can lead to cardiac tamponade which can be fatal very quickly if untreated. The following is a two patient case series in which both patients presented with large pericardial effusion. The first patient sought medical attention due to new onset palpitations and was found to have hemorrhagic pericardial effusion and pulmonary embolism (PE). The second patient presented with shortness of breath. Investigations revealed that she had pericardial and pleural effusions along with multiple metastases throughout the body. Both patients ended up with a diagnosis of non-small cell lung cancer (NSCLC) with BRAF mutation. One patient had V600E mutation; other patient had a variant p.D594N mutation. Both patients also had expression of PD-L1.
Collision tumors, consisting of two different histological types of cancer, are rare but may have important implications, both for the patient and possibly in terms of cancer risks and predisposition. This patient has had prior invasive ductal breast cancer treated with surgery and chemotherapy 5 years earlier, but she developed a pathological hip fracture and anemia. The workup uncovered a plasma cell dyscrasia and the bone biopsy from the hip showed the collision tumor with an interface between breast cancer and plasma cell cancer. Such combination tumors may be diagnostic and therapeutic challenges, but they also raise significant questions regarding pathogenesis. Local factors such as neuro-immune crosstalk or cytokine perturbations may be at play. Alternatively, or in addition, oncogenic growth factors or the effects of prior chemotherapy may be significant.
10694 Background: Despite the improvements related to introduction of neoadjuvant chemotherapy, the prognosis of patients with inflammatory breast cancer remains poor. The purpose of this study was to evaluate the efficacy, feasibility and outcomes of high dose chemotherapy in this group of patients. Methods: Between June 1991 and January 1999, twenty eight patients with pathologically confirmed inflammatory breast cancer were consecutively enrolled in this study. All patients were rendered free of clinically evident disease by using chemotherapy (adjuvant, neoadjuvant or both) either alone or in combination with surgery. Following stem cell collection patients received HD-CT with thiotepa 250mg/m2 days 1, 2 & 3(total dose of 750mg/m2), mitoxantrone 40mg/m2 on day 1 and carboplatin 333mg/m2 on days 1, 2 & 3 ( total dose of 1gm/m2). Previously stored stem cells were infused on the seventh day of HD-CT chemotherapy. Eligible patients received radiation to the chest wall and tamoxifen for 5 years. Results: With median duration of follow-up of 46.9 months( range 15.1–177.2), the median overall survival (OS) and progression free survival (PFS) were 42.5 months (range 9.7–135.7) and 34.8 months (range 3.3–135.7), respectively. The multivariate analysis showed a significantly better EFS and OS in patients with estrogen receptor (ER) positive tumors ( P value ≥ 0.003). Mucositis and Infection were the most severe non-hematological toxicities. Grade four cardiac and pulmonary toxicities developed in one patient. There was no transplant related mortality. One patient developed myelodysplastic syndrome. Conclusions: The results of our study suggest that high dose chemotherapy with thiotepa, mitoxantrone and carboplatin is a safe and efficacious regimen in patients with stage IIIB inflammatory breast cancer. No significant financial relationships to disclose.
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