We read with interest the report by Casavilla and colleagues [1] on the clinical course of patients with sarcoidosis who had no disease progression after liver transplantation. Their survival was similar to that of controls.

We describe a patient with a different clinical course. Our patient is a 59-year-old man who had end-stage liver disease secondary to well-documented sarcoidosis. Sarcoidosis was first detected in 1973 when he developed lymphadenopathy in the neck. Pulmonary involvement was minimal and subclinical. Despite long-term treatment with steroids, he developed a progressive elevation of the alkaline phosphatase level and, eventually, liver failure manifested by bleeding esophageal varices and hepatic encephalopathy. The patient showed marked fatigue and wasting and had liver transplantation in December 1991. His postoperative course was complicated by a bile leak with septic shock caused by peritonitis and subsequent development of the acute respiratory distress syndrome. His hospital course was prolonged when Pseudomonas pneumonia and cytomegalovirus colitis developed.

He recovered but noted dyspnea on exertion in September 1992. Investigations showed a restrictive defect with a diffusing capacity that was 67% of predicted. While the patient breathed room air, his PO₂ was 59 mm Hg, PCO₂ was 32 mm Hg, and pH was 7.33. Chest roentgenogram showed a diffuse interstitial infiltrate. A transbronchial biopsy specimen showed multiple noncaseating granulomas typical of sarcoidosis. After opportunistic infection was excluded, high-dose prednisone therapy was started; a prompt symptomatic and physiologic response was then shown by his pulmonary function test results. Symptoms and adverse physiologic responses recurred when prednisone doses were decreased to 30 mg or less. After 4 months of steroid treatment, superinfection with Pneumocystis carinii developed, which was treated satisfactorily with trimethoprim-sulfamethoxazole. Most recently, he has begun therapy with low-dose methotrexate in an attempt to reduce his steroid dose [2].

Liver function improved after liver transplantation, but the patient developed progressive pulmonary sarcoidosis 9 months later. This reactivated sarcoid has been unrelenting and responsive only to high-dose prednisone. The timing of the recurrence suggests that immunosuppression may have participated in the reactivation of disease. At the least, post-transplant immunosuppression with cyclosporine and low-dose steroids was insufficient to prevent reactivation.