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A 78-year-old man was admitted to the hospital with exertional dyspnea and fever. Chronic idiopathic interstitial pneumonia (IIP) had been diagnosed a year before. Follow-up chest X-ray examination showed diffuse reticular shadows and progressive shrinkage of both lower lobes. Chest CT scan revealed honeycomb appearance of both lower lung fields. Moderate hypoxemia was found by arterial blood gas analysis. The patient responded to an orally administered corticosteroid. Because tapering of the medicine caused exacerbation of the hypoxemia, methylprednisolone pulse therapy was given with poor response. Then high-dose (750 mg) of cyclophosphamide (CPM) were given intravenously 6 times, every 3 or 4 weeks. After the second administration of CPM, decreases in hypoxemia and in blood LDH levels were observed. This treatment allowed as to taper the dose of oral corticosteroid from 60 mg/day to 15 mg/day. This case suggests that intravenous administration of high-dose CPM may be effective against IIP.

To elucidate whether or not human T-lymphotropic virus type I (HTLV-I) infected cells exist in the lungs of HTLV-I carriers, we examined bronchoalveolar lavage (BAL) cells for the presence of HTLV-I proviral DNA by the polymerase chain reaction (PCR) method. The cells were harvested from HTLV-I seropositive individuals with or without various respiratory diseases. The HTLV-I pX region was detected from separated BAL cells by dot blot hybridization after PCR in all 14 HTLV-I seropositive individuals tested. Four out of these 14 individuals were asymptomatic HTLV-I carriers, while the other ten had symptoms, including those of bacterial pneumonia, chronic respiratory tract infection, interstitial pneumonia, atypical mycobacterial infection, bronchitis, mediastinal lymphadenitis and bronchial asthma. HTLV-I proviral DAN was detected in BAL cells from patients with a normal proportion of lavage lymphocytes and a normal CD4/CD8 ratio. These findings suggest that HTLV-I infected cells may commonly exist in the lower respiratory tract and alveolar space without producing characteristic symptoms/signs, and that any causal relation to the pulmonary lesion must therefore be carefully elucidated, in HTLV-I carriers.

Serial lung images with N-isopropyl-p-[I-123]-iodoamphetamine (I-123 IMP) were obtained to assess the imaging findings and to clarify the lesion to uptake relationships in 74 lesions in 73 patients with various histological types of bronchogenic carcinoma. A decreased uptake area was observed in all 74 lesions in the initial one or two-min I-123 IMP image. The initial image was analogous to a Tc-99m MAA lung perfusion image in 70 patients in whom both lung imaging procedures were performed. The imaging findings changed following this initial phase. At 4 hr, the lesion was depicted as either areas of decreased uptake or increased uptake or a combination of the two. Comparison between the lesion findings in the 4-hr I-123 IMP images, radiograms and removed specimens revealed that areas of decreased uptake corresponded to the cancerous portions of the lung mass or pleural effusion and areas of increased uptake corresponded to inflammatory portions including obstructive pneumonitis and/or collapse. Thus, the 4-hr I-123 IMP lung images can be used to discriminate the cancerous portion from associated secondary changes, obstructive pneumonitis and/or collapse.

In complement-depleted condition induced by cobra venom factor (CoF), tissue macrophage reaction and macrophage chemotactic activity (MCA) in skin extract from skin lesions induced by DNP-Ascaris extract (DNP-As) were decreased, respectively. MCA in the fraction containing macrophage chemotactic factor b (B fraction) was decreased completely. While MCA in the fraction containing macrophage chemotactic factor a and c (A fraction) was affected only slightly. These results suggested that the decrease of MCA of B-fraction might be associated with depletion of complement system by CoF. Using anti-C5 antibody, it was confirmed that macrophage chemotactic factor-b (MCF-b) (MW 14,000: thermostable) might be derived from C5 fragment in vivo.

Two different eosinophil chemotactic factors (delayed ECF-a and ECF-b) were isolated from the delayed phase (24 hr old) of eosinophil-rich inflammatory reaction sites induced by DNP-ascaris extract, which could be separated by DEAE-Sephadex. Both the factors were thermolabile (56 degrees, 30 min) and had a mol. wt of about 70,000, whereas they were clearly different in antigenicity. Delayed tissue eosinophilia was shown to be mediated by peritoneal exudate cells (PEC) and serum from immunized donors to recipients. A chemotactic factor, closely resembling a delayed ECF-a, was isolated from the skin lesions of recipients transferred by sensitized PEC and challenged. Another factor, closely resembling a delayed ECF-b, was isolated from those of recipients transferred by immune serum and challenged. Furthermore, we have shown that delayed ECF-b, but not delayed ECF-a, shared a common antigenicity with some guinea-pig serum component. Thus we concluded that delayed tissue eosinophilia was mediated by the combined actions of two different factors, delayed ECF-a and ECF-b.

Tissue eosinophilia in active cutaneous anaphylaxis reactions is biphasic: the early phase (6 hr) is induced by a low molecular (mol. wt. 300) factor (early ECF), and the delayed phase (24 hr) is mediated by synergy of two different factors (delayed ECF-a and -b). In this study, we report the mediation of tissue eosinophilia in passive cutaneous anaphylactic (PCA) reaction sites. Tissue eosinophilia in systemic PCA showed two phases with peaks at 6 hr and 24 hr, while that in local PCA was monophasic and peaked at 12 hr. A dialysable eosinophil chemotactic factor was isolated from the early stage (0-6 hr) of local PCA skin sites, and another chemotactic factor (mol. wt. 15,000), sharing a common antigenicity with guinea-pig serum C5, from 12-hr-old local PCA skin sites. On the other hand, a different chemotactic factor with a mol. wt. of about 70,000, sharing a common antigenicity with delayed ECF-b isolated from active cutaneous anaphylactic skin lesions, was isolated from 24-hr-old systemic PCA skin lesions. Although the dialysable factor was also isolated from systemic PCA skin sites, the factor from systemic PCA delayed skin sites may not contribute to delayed tissue eosinophilia, since the activity paralleled the intensity of basophil accumulation but not to that of eosinophils. It is thus suggested that tissue eosinophilia in systemic and local PCA reactions is mediated by different chemotactic factors.

In a patient with primary lung cancer, increased accumulation of I-123-IMP was observed in a pulmonary inflammatory lesion surrounding a lung cancer which was delineated as a photon deficient area. Ga-67-citrate uptake was observed in both the inflammatory and cancerous areas. These findings suggest that I-123-IMP may have the potential to accumulate differently in a variety of pathological conditions of the lung and thus may be a clinically useful lung imaging agent.

An eosinophil chemotactic factor (ECF) was produced in the cell-free culture supernatants (CFS) of peritoneal exudate cells (PEC) from guinea-pigs immunized with dinitrophenyl derivatives of ascaris extract (DNP-As), when stimulated by the antigen in vitro without activation by immune complexes. A 2 or 6 hr pulse of the antigen was sufficient for ECF production, whereas long time incubation (48 hr) was required for the production of a sufficient amount of the factor. Treatment of PEC by cycloheximide resulted in the reduction of ECF production, suggesting that protein synthesis is essential. Its generation appeared carrier-specific and the source of the factor is presumed to be lymphocytes, probably T lymphocyte. The factor with a molecular weight of 70,000 shared a common antigenicity with delayed eosinophil chemotactic factor-a (delayed ECF-a), which was isolated from the skin lesions showing delayed tissue eosinophilia in vivo.

The luteinizing hormone-releasing hormone (LH-RH) analog, less thanGlu-Pyr(1)Ala-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2, and the thyrotropin-releasing hormone (TRH) analog, less thanGlu-Pyr(1)Ala-Pro-NH2, were synthesized by azide couplings of the dipeptide hydrazide, less thanGlu-Pyr(1)Ala-NHNH2, to the C-terminal octapeptide of LH-RH and to proline amide, respectively. In an ovariectomized, steroid-blocked rat assay, the LH-RH analog was found to have only 1% of the LH-releasing activity of the natural hormone. The TRH analog was 1.5 times more effective than TRH itself in releasing TSH in vivo from the anterior pituitary of mice. This peptide is one of two synthetic peptides so far discovered which are more potent than TRH.