Polymyositis: A Case Report.

Inflammatory myopathies are a group of diseases whose common pathway is immune-mediated muscle damage, one of which is polymyositis. The definition of polymyositis is controversial, with proponents advocating a definition based on immunohistochemical and histopathological findings in muscle biopsies, while other proponents advocate a definition based on clinical manifestations and histopathological findings. Polymyositis is a quite rare disease that is clinically characterized by progressive proximal muscle weakness with a symmetric distribution. Within the diagnostic approach, laboratory studies show elevation of sarcoplasmic enzymes; nerve conduction tests are performed, which may aid in distinguishing myopathic causes of weakness from neuropathic disorders; and muscle biopsy is considered the gold standard to diagnose inflammatory myopathy and to distinguish the subclasses. We report the case of a 61-year-old male patient who presented generalized symmetrical weakness, predominantly in the upper extremities, and dysphagia, whose laboratory studies, autoantibodies, and muscle biopsy were confirmatory of this entity.

Acute Bilateral Stroke in a Moyamoya Patient With High Risk of Thrombosis Due to Multiple Myeloma With Chemotherapy.

Multiple myeloma (MM) is a common hematologic malignancy. Multi-agent chemotherapy and anti-myeloma immunomodulatory drugs increase the incidence of arterial and venous thrombosis. We present a moyamoya patient with MM who had a stroke shortly after induction chemotherapy. We present the case of an adult female patient who arrived at the ER due to automatism seizures, dysarthria, and left hemiparesis. The patient had a medical history of MM and underwent six cycles of induction chemotherapy (cyclophosphamide, dexamethasone, thalidomide, and bortezomib). MRI of the brain showed bilateral watershed ischemic strokes. Angiogram showed occlusion at the supraclinoid segment of both internal carotid arteries consistent with moyamoya. The patient was discharged with full-dose anticoagulation, levetiracetam, and physical therapy. At three years of follow-up, the patient has no recurrent cerebrovascular disease. MM patients treated with thalidomide/lenalidomide in combination with high-dose dexamethasone, doxorubicin, or multiagent chemotherapy should be on anticoagulation for venous thromboembolism (VTE) prophylaxis. There are no clear recommendations for arterial thrombosis prevention. Moyamoya is a vasculopathy characterized by progressive intracranial artery stenosis with a high risk of ischemic stroke, ischemia recurrence, and intracerebral hemorrhage. Despite the risk of intracerebral hemorrhage, we decided on anticoagulation due to the high risk of thrombosis due to MM, multi-agent chemotherapy, and moyamoya.

Tumor-Induced Osteomalacia With Normal Fibroblast Growth Factor-23 (FGF23) and Idiopathic Hypercalciuria.

Tumor-induced osteomalacia (TIO) is a rare acquired paraneoplastic syndrome characterized by low serum phosphate, phosphaturia, inappropriately low/normal levels of serum calcitriol, and normal or elevated levels of fibroblast growth factor-23 (FGF23). Finding this mesenchymal tumor is challenging since it is usually benign, small, slow-growing, and is localized in the appendicular skeleton. We report a 58-year-old male patient who arrived at the endocrinology outpatient clinic due to slowly progressive low back pain and generalized weakness since the age of 48. On physical examination, only a reduced range of motion was noted. Laboratory tests revealed hypophosphatemia with normal parathyroid hormone (PTH) levels, normal serum calcium, high 24-hour urine calcium, normal 1,25-dihydroxyvitaminD levels, low renal threshold phosphate concentration (TmPO4/GFR), and high FGF23. The 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) reported a hypermetabolic extramedullary lesion in the C1-C2 vertebral bodies measuring 1.5 x 1.1 cm. Two months after the 18F-FDG PET/CT, complete excision of the cervical tumor was performed. The pathology ward reported a histiocytic mesenchymal neoplasm with accumulations of multinucleated giant cells compatible with phosphaturic mesenchymal tumor. After surgery, the patient's hypophosphatemia was completely resolved. With this, the diagnosis of TIO was confirmed. The patient remains asymptomatic, with normal phosphate levels at one year of follow-up. Hypophosphatemia due to renal losses in an adult patient is a challenging diagnosis and one must consider TIO, autosomal dominant hypophosphatemic rickets, fibrous dysplasia, and even Fanconi syndrome. FGF23 can be extremely useful during the diagnostic approach since acquired dependent hypophosphatemia (FGF23 ≥ 30 RU/mL) highly suggests TIO. In this case report, we want to highlight the paramount importance of adequate tumor screening in adult patients with acquired FGF23-dependent hypophosphatemia. TIO is a reversible cause of hypophosphatemia with potentially disabling consequences if left untreated. These manifestations are non-specific (bone pain and muscle weakness), while others are progressive and severely disabling (bone deformities and multiple fractures). In this case report, we want to highlight the paramount importance of adequate tumor screening in adult patients with acquired hypophosphatemia, and the crucial lead that phosphate and vitamin D regulating hormones (FGF23) have for suspecting TIO.