RESUMEN
Drug reaction with eosinophilia and systemic symptoms (DRESS) is a delayed adverse drug reaction that is characterized by fever, cutaneous manifestation, enlarged lymph nodes, hematologic abnormalities, and organ involvement. Multiple medications have been reported to cause DRESS with the presentation varying from drug to drug. Some cases are mild and can be managed by stopping the causative agent along with supportive measures; however, other cases can lead to multi-organ failure requiring systemic corticosteroids and organ transplant. Acute liver failure is a rare manifestation of DRESS. We report a patient who had recently completed a course of trimethoprim-sulfamethoxazole and presented with low-grade fever, diffuse skin rash, eosinophilia, elevated liver enzymes, acute kidney injury, and thrombocytopenia. DRESS was subsequently diagnosed based on history, physical examination, and relatively negative workup for an alternate diagnosis. The patient eventually showed improvement with steroid therapy without the need for a liver transplant. Due to its pharmacogenetic susceptibility, it is essential to recommend avoiding the causative medication for the patient's family members.
RESUMEN
Drug-induced lupus erythematosus (DILE) is a syndrome that manifests with symptoms similar, but with less severity, to that of systemic lupus erythematosus (SLE). Many medications are reported to be involved in DILE; however, terbinafine (Lamisil) is not a well-known causative agent of this syndrome. In this case report, we present a 22-year-old male patient with no prior medical history presented with worsening fever, rash, joint pain, and weight loss a couple of weeks after starting terbinafine. He underwent an extensive workup which revealed worsening kidney function, proteinuria, and microscopic hematuria, for which he underwent a renal biopsy which revealed class IV lupus nephritis. He was treated with prednisone taper and immunosuppressants with subsequent resolution of his symptoms. Close monitoring for the development of DILE symptoms is recommended after starting terbinafine, especially in patients with a known personal or family history of SLE.
RESUMEN
Osteomalacia is a widely prevalent bone disorder that is caused by an imbalance in body calcium and phosphate. Tumor-induced osteomalacia (TIO) is a rare form of osteomalacia that is associated with mesenchymal tumors. It is caused by overproduction of fibroblast growth factor 23 (FGF-23), a hormone involved in phosphate regulation. A 59-year-old male with a history of factor V Leiden mutation, pulmonary embolism, and deep vein thrombosis was diagnosed with oncogenic osteomalacia in 2008 following laboratory findings significant for low phosphorus and elevated FGF-23 levels. He underwent a resection of a right suprascapular notch mass with the biopsy confirming a phosphaturic mesenchymal tumor. He was maintained on oral phosphorus and calcitriol replacements with a regular follow-up with oncology and nephrology. Eight years later, the patient's phosphorus levels started declining despite replacement. A repeat test showed FGF-23 levels once again elevated. A whole-body magnetic resonance imaging (MRI) scan showed no significant findings. The patient was continued on oral replacement therapy with a close follow-up. Two years later, urine phosphorus excretion was elevated at 2494 mg per 24 hours with low plasma phosphorus (1.2 mg/dL) and an elevated FGF-23 level of 1005 relative units (RU)/mL. A repeat MRI of the right shoulder revealed a mass in the supraspinatus muscle and another in the spinal glenoid notch. The masses were resected and the biopsy was consistent with a recurrence of the phosphaturic mesenchymal tumor. Follow-up serum phosphate levels remained in the normal range. FGF-23 plays a critical role in bone mineralization through the regulation of phosphate levels. Overproduction, as seen in mesenchymal tumors, results in hyperphosphaturia, hypophosphatemia, and low calcitriol levels. While the definitive treatment of TIO involves the resection of the mesenchymal tumor, localization of the tumor is often challenging given its small size and slow growth. This leads to delayed diagnosis and treatment. For individuals whose tumor cannot be resected or detected, burosumab is the preferred form of therapy. Interestingly, FGF-23 is shown to have a potential cardiovascular (CV) morbidity and mortality through various mechanisms like activation of myocardial FGF-23 receptors, endothelial dysfunction, inflammation, and altered phosphorus and vitamin D metabolisms. While studies have shown possible FGF-23 effects on CV outcomes in patients with chronic kidney disease, this has not been proven in cases of TIO.
RESUMEN
Use of the hospitalist model has reduced the number of primary care physicians taking care of inpatients. Physician shortages in primary care has forced many healthcare systems to use locum physicians as part of their delivery system and physician practice plan. With value-based purchasing and new payment models, measuring quality and patient-satisfaction with the hospitalist model is important. Hospital administrators need to carefully monitor the use of locum hospitalists, especially around quality of care and clinical outcomes.