Patient: Male, 36Final Diagnosis: Rhabdomyolysis induced acute renal failureSymptoms: Diarrhea • generalized weaknessMedication: —Clinical Procedure: Hemodialysis • intubationSpecialty: Critical Care MedicineObjective:Unusual setting of medical careBackground:Rhabdomyolysis is a syndrome caused by muscle breakdown. It can be caused by traumatic as well as non-traumatic factors such as drugs, toxins, and infections. Although it has been initially associated with only traumatic causes, non-traumatic causes now appear to be at least 5 times more frequent. In rhabdomyolysis, the CK levels can range anywhere from 10 000 to 200 000 or even higher. The higher the CK levels, the greater will be the renal damage and associated complications.We present the case of a patient with exceptionally massive rhabdomyolysis with unusually high CK levels (nearly 1 million) caused by combined etiologic factors and complicated with acute renal failure.Case Report:A 36-year-old African American male patient with no significant past medical history and a social history of cocaine and alcohol abuse presented with diarrhea and generalized weakness of 2 days’ duration. He was found to be febrile, tachycardic, tachypneic, and hypoxic. The patient was subsequently intubated and admitted to the medical ICU. Laboratory work-up showed acute renal failure with deranged liver functions test results, and elevated creatine kinase of 701,400 U/L. CK levels were subsequently too high for the lab to quantify. Urine legionella testing was positive for L. pneumophilia serogroup 1 antigen and urine toxicology was positive for cocaine. The patient had a protracted course in the ICU. He was initially started on CVVH, and later received intermittent hemodialysis for about 1 month.Conclusions:In the presence of multiple etiologic factors, rhabdomyolysis can be massive with resultant significant morbidity. Clinicians should have a high index of suspicion for rhabdomyolysis in the presence of multiple factors, as early recognition of this diseases is very important in the prevention and active management of life-threatening conditions.

Patient: Male, 58Final Diagnosis: Levamisole induced leukocytoclastic vasculitisSymptoms: Arthralgia • skin rashMedication: —Clinical Procedure: Skin biopsySpecialty: RheumatologyObjective:Diagnostic/therapeutic accidentBackground:Levamisole is a common adulterant of cocaine. It can cause agranulocytosis and cutaneous vasculitis that can possibly lead to cutaneous necrosis.In all reported cases of levamisole-induced vasculitis, it has been described as a clinical syndrome characterized by a constellation of typical clinical features and a positive serum serology for ANCA levels, especially very high-titer p-ANCA levels, in the background of cocaine abuse. However, patients may have a negative serology and here, we present the first such case.Case Report:A 58-year-old African American man with a history of polysubstance abuse, 4 days after last cocaine use, presented with sudden onset of painful pruritic rash and polyarthralgias. He was found to have normal vital signs, with bilateral tender knees and erythematous-purplish maculopapular lesions involving the abdomen and the left thigh. Laboratory work-up was significant for elevated CRP, negative c-ANCA, p-ANCA ANA, and RA levels, and a positive urine toxicology for cocaine.Urine analysis by high-performance liquid chromatography was positive for levamisole. Ultimately, a final diagnosis was made by skin biopsy, which revealed findings suggestive of leukocytoclastic vasculitis.Conclusions:Cutaneous leukocytoclastic vasculitis can be caused by levamisole, which is used as an adulterant in cocaine. Most cases are associated with positive ANCA levels; however, a negative serology is also a possibility.

BackgroundMethotrexate has been implicated in a variety of lung complications, one of which is hypersensitivity pneumonitis. Hypersensitivity pneumonitis most often occurs within the first year of starting low-dose orally administered methotrexate. We present a case of methotrexate-induced hypersensitivity pneumonitis after 30 years of methotrexate use, which is the first case to be reported so far.Case presentationA 77-year-old African American woman with a history of rheumatoid arthritis presented with progressively worsening shortness of breath and nonproductive cough. She was on a daily dose of 2.5 mg of methotrexate that had been orally administered for the last 30 years. A physical examination was significant for fever of 38.2 °C (100.8 °F), tachycardia, bilateral basal crackles, and oxygen saturation of 88% on room air. A laboratory work up was significant for normal white blood cell count, increased eosinophil count of 18.3%, and erythrocyte sedimentation rate of 111 mm/hour. Sputum cultures were negative for any bacterial pathogens including acid-fast bacilli. Influenza and respiratory syncytial viral infection were ruled out. A (1-3)-B-D-glucan assay (Fungitell®) was within normal limits. Pulmonary embolism was ruled out and echocardiography was normal. A chest X-ray showed hazy opacity with prominent reticulation within the upper lung fields bilaterally, right greater than the left with no pleural effusion. Lung computed tomography revealed nonspecific bilateral upper lung opacification. A pulmonary function test was significant for no obstruction, normal maximum voluntary ventilation, and no restriction, with mildly decreased diffusion. Methotrexate was stopped, and our patient was started on prednisone 60 mg orally administered daily with dramatic clinical and radiologic improvement.ConclusionsMethotrexate-induced hypersensitivity pneumonitis usually occurs in the initial few weeks to months of starting treatment with methotrexate; however, it can occur late during therapy too, and prompt diagnosis is crucial as it is a reversible condition when diagnosed early.