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Hydralazine/immunosuppressants Anti neutrophil cytoplasmic antibody associated vasculitis and Clostridium difficile induced systemic inflammatory response syndrome: case report

A 67-year-old woman developed antineutrophil cytoplasmic antibody vasculitis during treatment with hydralazine for hypertension. Additionally, she also developed Clostridium difficile–induced systemic inflammatory response syndrome during immunosuppression with methylprednisolone, prednisone and rituximab for hydralazine induced antineutrophil cytoplasmic antibody vasculitis (HIAV) [not all durations of treatment to reactions onset stated]. The woman, presented with progressive, tense necrotic and haemorrhagic bullae on both sides of the neck, face and extremities of two weeks duration. She had history of hypertension and a thyroid nodule following unilateral thyroid lobectomy. She further had worsening of dyspnoea and generalised weakness. Her anamnesis revealed medications including oral hydralazine 75mg thrice daily for 13 months along with concomitant medications including metoprolol, amlodipine and levothyroxine sodium. The bullae first appeared on the scalp and further progressed to cephalocaudal pattern with a propensity of nostrils, eyes and labial mucosa. Her tongue was covered by an eschar. She had diffuse periorbital oedema and an eschar on the tongue. Additionally, concentric purpuric patches on the lower legs and thighs were noted. Pertinent laboratory findings showed perinuclear antineutrophil cytoplasmic antibody (ANCA) titer of 1:160, positive antinuclear antibody titer of 1:320 and elevated serum creatinine level 2.31 mg/dL. Chest radiograph showed bilateral perihilar infiltrates along with bilateral pleural effusions. During hospitalisation, she developed progressive decline in respiratory status and pulmonary haemorrhages. She was transferred to the medical intensive care unit. She required aggressive support. Skin biopsy and endobronchial biopsy of the right middle lobe were obtained. Skin histopathology showed a necrotic vasculitis. Lung histopathology revealed bronchial tissue fragments with acute and chronic inflammation, oedema, granulation tissue formation, focal necrosis and squamous metaplasia. The clinical history and findings were suggestive of HIAV. Hydralazine was discontinued. The woman started receiving IV methylprednisolone 65mg daily. Afterwards, methylprednisolone was switched to oral prednisone 30mg daily. IV rituximab 375 mg/m2 weekly for 4 weeks was initiated as per lymphoma protocol due to multiple organ involvement including lung and kidney. Within two weeks of initiation of therapy, her respiratory status and renal function improved. The skin lesion had completely resolved by week 4. Initially she did well on immunosuppressive therapy with resolution of symptoms, however five weeks after rituximab initiation, she developed Clostridium difficile–induced systemic inflammatory response syndrome attributed to immunosuppressive therapy and died. Schrom KP, et al. Antineutrophil cytoplasmic antibody