We treated two Japanese patients withPneumocystis cariniipneumonia. 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 13.6×103/μl with 25morphologically normal lymphocytes and 4abnormal. Lymphocyte surface markers were 72.6, CD4+, 13.6CD8+and 46.4CD3+. In patient no. 2, leukocytes numbered 13.8×103/μl, including 18lymphocytes, although no morphologically abnormal lymphocyte was evident. Lymphocyte markers were 36.6CD4+, 16.8CD8+and 46.6CD3+. 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 cariniiinfectious, 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 ce
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