Case Presentation: An 83-year-old male with past medical history of hypertension managed chronically with hydralazine presented to the hospital complaining of acute onset of dyspnea, fever, and cough. He was treated for community acquired pneumonia with incomplete resolution of his symptoms. One month later he returned with fatigue and hemoptysis. Work up was significant for new anemia and acute hypoxemic respiratory failure. Physical examination revealed an aphthous ulcer on his tongue and diffuse bilateral pulmonary crackles. Imaging of his chest showed bilateral multifocal ground glass opacities and consolidations concerning for pneumonia and antibiosis was resumed. Subsequent urinalysis showed hematuria, raising suspicion for possible pulmonary renal syndrome. He underwent bronchoscopy, which was consistent with diffuse alveolar hemorrhage. Extensive infectious work up was unremarkable. Serological workup showed positive ANA, positive dsDNA, positive anti-histone antibody consistent with a picture of drug induced lupus. A positive p-ANCA did bring up the question of whether this could be ANCA vasculitis however follow up MPO was negative and PR-3 antibodies were equivocal on two separate occasions making this less likely. Patient underwent lung biopsy with histology demonstrating intra-alveolar hemosiderin laden macrophages, capillaritis, and vasculitis in medium-sized arteries. He later underwent kidney biopsy which demonstrated diffuse mesangial proliferative glomerulonephritis consistent with lupus vasculitis further supporting the diagnosis drug-induced lupus. He was treated with steroids with resolution of his hemoptysis and improvement in his respiratory status and safely discharged home with instructions to never resume hydralazine.

Discussion: Although recently falling out of favor, hydralazine is still frequently used to treat hypertension. Generally thought a benign medication, 5-10% of patients develop a syndrome called drug induced lupus or in some cases a more severe syndrome called ANCA associated vasculitis. Both are drug triggered autoimmune phenomena of unknown etiology. Onset of symptoms can be months to years after initiation of medication making diagnosis difficult. This case demonstrated features of both drug induced ANCA vasculitis and drug induced lupus. Because neither MPO and PR3 antibodies were elevated and renal biopsy showed mesangial proliferation, a pattern more consistent with a lupus like picture, he was diagnosed with drug induced lupus. Hydralazine induced lupus commonly presents as arthralgias, myalgia, and fevers with skin involvement seen in up to one third of patients. It is rare to see glomerulonephritis in these patients and even rarer yet to see an associated pulmonary vasculitis presenting as diffuse alveolar hemorrhage. Diffuse alveolar hemorrhage is characterized by drop in hemoglobin, respiratory compromise and pulmonary opacities seen on imaging. Diagnosis requires bronchoscopy which will show increasing hemorrhagic return in the bronchial washings. Prompt diagnosis is vital in light of the high morbidity and mortality diffuse alveolar hemorrhage portends.

Conclusions: We present a rare case of hydralazine induced lupus presenting as diffuse alveolar hemorrhage in a hypertensive patient treated with hydralazine. Without frank hemoptysis milder forms of diffuse alveolar hemorrhage can easily be missed and diagnosis requires high suspicion. It is vital to keep it on the differential as outcomes can be fatal.

IMAGE 1: CT Chest demonstrating multifocal ground glass opacities with peribronchiolar opacities and wall thickening and bilateral pleural effusions more prominent on right than left.