IMPACT OF b-D GLUCAN ON INVASIVE FUNGAL AND PNEUMOCYSTIS CARINII INFECTION AS A DIAGNOSTIC AND THERAPEUTIC MARKER FOR THE LIVING DONOR LIVER TRANSPLANT RECIPIENTS

Abstract

A176 Aims: Invasive fungal infection is potentially fatal complication in patients with liver transplantation, but the treatment is hampered by the non-specific nature of clinical and radiological signs and the insensitivity of current laboratory diagnostic methods. The aim of this study was to review the single-center experience with invasive fungal infections in LDLT and to report the impact of b-D glucan on invasive fungal and pneumocystis carinii infection as a diagnostic and therapeutic marker. Methods: From 1991 to 2003, 75 cases of LDLT were performed in our institution and since case no. 22 we measured the serum level of b-D glucan. Fungal colonization was defined as the presence of a fungus in one or more surveillance superficial cultures in the absence of any clinical symptoms or signs of infection. Invasive fungal infections were divided into definite and probable infections according to the following criteria : definite invasive fungal infection was diagnosed by one of these criteria as follows: 1) presence of fungus in the blood, cerebrospinal fluid, ascites and biopsy specimens; 2) ophthalmologic evidence; 3) more than 11pg/ml serum level of b-D glucan and isolation of fungus from at least two superficial sites with febrile condition; 4) isolation of fungus from bronchoalveolar lavage with radiological evidence of pneumonitis. Probable invasive fungal infection was defined as more than 11pg/ml serum level of b-D glucan together with febrile symptom above 38? which was not responded by antibiotics for more than one week or radiological evidence of pneumonitis or esophagitis. For the prophylaxis of the fungal infection (includes more than 11pg/ml serum level of b-D glucan), fluconazole and micafungin were administered. Active fungal infection was treated by fluconazole, amphotericin B, flucytosine and micafungin. Results: We experienced one definite and 5 probable invasive fungal infections (group A). The level of b-D glucan between group A and 20 recipients more than 11pg/ml of b-D glucan without clinical symptoms were significantly different (85.2 vs. 26.4 pg/ml, p<0.001). Six recipients were diagnosed as pneumonia by chest X-ray or CT. One definite invasive fungal infection had quite high serum level of b-D glucan (122 pg/ml) and isolation of fungus from three superficial sites with febrile condition. Two out of 5 probable fungal infections had high serum level of b-D glucan (39, 37 pg/ml) without isolation of fungal organisms from sputa with febrile symptom above 38? and radiological evidence of pneumonia. Only two out of 5 recipients with invasive fungal infections were alive. One recipient who was diagnosed as pneumocystis carinii pneumonia had quite high serum level of b-D glucan (169 pg/ml) and his clinical symptoms were correlated with the level of b-D glucan. Conclusion: In some cases b-D glucan was temporarily elevated within 2 weeks after LDLT. But it was very useful for the diagnostic and therapeutic marker for the invasive fungal and pneumocystis carinii infection.