Immunodeficiency in preclinical smoldering adult T-cell leukemia

We treated two Japanese patients with Pneumocystis carinii pneumonia. Inclusion bodies in both adrenal glands of patient no. 1 indicated a herpesvirus infection. The patient no. 2 recovered from the pneumonia upon sulfametoxazole-trimethoprim medication and high-dose methylprednisolone therapy. In both patients, anti-human T-cell leukemia virus type I (HTLV-I) antibodies were positive and anti-human immunodeficiency virus antibodies were negative. Peripheral leukocytes in patient no. 1 numbered 13.6 X 10(3)/microliter with 25% morphologically normal lymphocytes and 4% abnormal. Lymphocyte surface markers were 72.6%, CD4+, 13.6% CD8+ and 46.4% CD3+. In patient no. 2, leukocytes numbered 13.8 X 10(3)/microliter, including 18% lymphocytes, although no morphologically abnormal lymphocyte was evident. Lymphocyte markers were 36.6% CD4+, 16.8% CD8+ and 46.6% CD3+. Monoclonal integration HTLV-I proviral DNA in lymphocytes of patient no. 2 was demonstrated by Southern blotting. Thus, both patients must have had smoldering adult T-cell leukemia (ATL) without any cutaneous involvement, whereas the morphological diagnosis from peripheral blood smears was one of HTLV-I carrier status with a few atypical lymphocytes, i.e., the preclinical state of smoldering ATL. Pneumocystis carinii infections, a viral infection of the adrenals (no. 1), negative purified protein derivatives of the tuberculin reaction and suppressed blastogenesis of the peripheral lymphocytes indicated HTLV-I-induced impairment of the immune mechanism to have already occurred in both patients without there being a vast proliferation of ATL cells.