[Two surgical cases of pulmonary aspergilloma with different postoperative prognosis].
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Biomedical subjects
Publications and source records attributed to H Morinari.
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In Japan a number of reported cases of diffuse panbronchiolitis (DPB) have been associated with human T lymphotropic virus type I (HTLV-I) infection. In this study the hypothesis that HTLV-I proviral DNA may be prevalent in DPB was examined using polymerase chain reaction (PCR) for the region of env or the two-step PCR for the pX region of this virus. The presence of HTLV-I proviral DNA was studied in the peripheral blood mononuclear cells (PBMC) obtained from 10 patients with DPB. The presence of proviral DNA in PBMC in 12 patients with chronic obstructive pulmonary disease (COPD), eight patients with idiopathic interstitial pneumonia (IIP), four patients disease were also studied as relevant controls. The lung tissue obtained from 11 patients with DPB, 12 patients with diffuse aspiration bronchiolitis (DAB) at autopsy, and the surgical lung samples obtained from 12 patients with bronchogenic cancer were also studied. Peripheral blood mononuclear cells obtained from one DPB patient and one bronchogenic carcinoma patient were positive for the HTLV-I pX region. The presence of the pX region was also found in the lung tissue of three DPB patients (27.3%) and one DAB patient (8.3%). None of other subjects were positive for HTLV-I proviral DNA, In conclusion, HTLV-I is not the causative virus in the pathogenesis of COPD, IIP, bronchiectasis and bronchogenic carcinoma. There is a likelihood that HTLV-I infection is associated with some cases of DPB; however this association needs further verification.
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To assess the feasibility and efficacy of rhGM-CSF in ameliorating chemotherapy-induced leukopenia in patients with advanced non-small-cell lung cancer, we conducted a double-blind placebo controlled phase III study in a multicenter setting. Patients were eligible if they had cytologically or histologically proven cancer, no prior chemotherapy, stage IIIB or IV disease, an Eastern Cooperative Oncology Group (ECOG) performance status of 0-2, an age of less than 76 years, and no symptomatic brain metastasis, disseminated bone metastasis, or previous vertebral/pelvic irradiation. The chemotherapy regimen consisted of mitomycin given at 8 mg/m2 on day 1, cisplatin given at 100 mg/m2 on day 1, and vindesine given at 3 mg/m2 i.v. on days 1 and 8 (MVP). If the granulocyte nadir count recorded after the first cycle of MVP was less than 1,000/mm3, patients were randomly assigned to receive recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) or placebo during the second cycle of MVP. The dose of rhGM-CSF was 125 micrograms/m2 given daily s.c. for 14 consecutive days starting on day 2. Of the 52 patients enrolled, 45 were evaluable. The nadir of granulocytes was significantly lower in the placebo group (P = 0.007). The period during which the granulocyte count was less than 1,000/mm3 was significantly longer in the placebo group (median, 6 vs 10 days; P = 0.04). The incidence of adverse effects related to rhGM-CSF, such as fever (> or = 38 degrees C) and skin rash, was significantly higher in the rhGM-CSF group (P = 0.011). The rate of response to chemotherapy did not significantly differ between the two groups. In conclusion, rhGM-CSF reduced the duration of chemotherapy-induced granulocytopenia. The clinical usefulness of this agent may be deminished because of the adverse effects encountered when it is used in combination with a moderately myelotoxic chemotherapy regimen.
A dose escalation study of teniposide (VM-26) plus cisplatin (CDDP) was carried out using recombinant human granulocyte colony-stimulating factor (rhG-CSF) in 46 previously untreated patients with advanced small cell lung cancer (SCLC). The dose of CDDP was 80 mg/m2/day intravenously (i.v.) (day 1) and VM-26 was escalated from 60 mg/m2/day to 80, 100 and 120 mg/m2/day i.v. x 5 days for four cycles. The dose of rhG-CSF was 90 micrograms/m2/day subcutaneously for 13 days. The feasibility of the regimen at the starting dose level of VM-26 with or without rhG-CSF was initially examined in 10 patients chosen through random allocation. WHO grade 4 neutropenia was observed in 17% (three out of 18 courses) of patients in the rhG-CSF group and in 63% (12 out of 19 courses) of the control group (P < 0.01). The number of patients with febrile episodes (> 38 degrees C) over the four courses of chemotherapy was 1 in the rhG-CSF group and 4 in the control group. According to these results, all 36 patients received rhG-CSF in the dose escalation stage. The incidence of WHO grade 4 neutropenia at the dose levels of 60, 80, 100 and 120 mg/m2/day of VM-26 was 66, 57, 76 and 85%, respectively (P > 0.1). The incidence of grade 4 thrombocytopenia was 19, 31, 18 and 46%, respectively (P > 0.1). The overall response rate was 100% in patients with limited stage SCLC and 83% in patients with extensive stage SCLC. The actual administered VM-26 dose per week at the dose level of 100 mg/m2/day was 1.6-fold higher than the planned starting dose (60 mg/m2/day) per week. At the dose level of 120 mg/m2/day, 50% of patients developed WHO grade 4 leucopenia, which lasted longer than 1 week and 67% of the patients had WHO grade 3 or 4 diarrhoea. At this same dose, all patients had at least one febrile episode (> 38 degrees C), and 1 patient died of cerebral bleeding with severe thrombocytopenia. The median survival time of all patients was 451 days (411 days, extensive disease; 497 days, limited disease). VM-26 plus CDDP with rhG-CSF was active in previously untreated patients with SCLC. The recommended dose of VM-26 in combination with CDDP for a phase II study is 100 mg/m2/day for 5 days with rhG-CSF support.
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We report one operated case (a 71-year-old female) of intralobar pulmonary sequestration (Pryce's type 1) associated with an accessory diaphragm. The patient had hemoptysis for 5 years. Lateral chest X-ray showed an oblique line attaching to the central portion of the right diaphragm. Selective angiography and ultrasonography showed an aberrant vessel originating from the abdominal aorta. At the time of operation, the pleural cavity was divided into two compartments by a fibrous membrane. The bronchus of the lower compartment and the pulmonary veins ran through a hole in the accessory diaphragm. The aberrant artery flowed into the parts of lung in the upper and lower compartments.
Bone mineral density (BMD) of the lumbar spine (L2-L4) was measured using dual-energy X-ray absorptiometry (DEXA), and its relationship to total dose of prednisolone and duration of prednisolone therapy was studied in 57 patients with bronchial asthma. There was a significant negative correlation between BMD and total dose of prednisolone (r = -0.463, p < 0.001) and between BMD and duration of prednisolone treatment (r = -0.30, p < 0.05). The half-yearly percent decrease of BMD measured in 17 asthmatic patients was 0.83% (p < 0.01) after correction for age-associated decline. These findings suggest that the reduction of BMD was related to the total dose of prednisolone and the duration of therapy in asthmatics.
In seven normal adult males the authors studied diaphragmatic fatigue by analysis of the power spectrum of the diaphragmatic electromyogram obtained with an esophageal electrode, and of the change of transdiaphragmatic pressure. Diaphragmatic fatigue was produced by inspiring through a resistive load, and mean value of the index of the tension time of the diaphragm (TTdi) maintained until fatigue was 0.33 +/- 0.09, which has been known to produce fatigue. The mean value of ratios of power at high frequencies to power at low frequencies (H/L) decreased to 61.2 +/- 16.8% of the initial value at just before breaking time. Breaking time was 4.88 +/- 1.37 minutes in average. The selection of low and high band widths for analysis of H/L ratio has differed slightly in the literature, but such differences do not have any substantial influence on the estimation of the changes of H/L ratio.
A 24 year-old male with pulmonary tuberculosis in right upper lobe developed two lesions of extrapulmonary pleural tuberculoma during the course of antituberculous therapy. He had no history of lung tuberculosis nor pleurisy. However, the chest X-ray film on first admission showed scattered nodular shadows in right upper lung field. He had no subjective symptoms and no abnormalities of laboratory findings except mild iron deficiency anemia, from which he recovered completely without specific therapy. Three months after starting the antituberculous therapy including SM, INH, and RFP, a new round homogeneous opacity appeared in the right lower lung field (S4). Chest CT scan revealed the lesions in S10 as well as in S4. Microscopic examination of the specimen obtained by ultrasound-guided needle aspiration biopsy disclosed positive acid-fast bacilli. Because of the lack of effect of drug therapy on pleural lesions, surgical treatment was performed. The visceral pleura was found adherent fibrously to parietal pleura, which was easily separated by hand. However, at the site of lesions, the adhesion was so tight that extrapleural resection was needed. Because lung tissue and tumor were connected tightly, the lung had to be partially resected. Most content of tumors were caseous necrosis. Although main lesion was located outside of the lung, intrapulmonary invasion was also noticed. Double lesions of this kind of disease seem to be very rare. There is no evidence of relapse until eight months after surgery.
Hypersensitivity pneumonitis (HP) is believed to be induced by immunological mechanisms, the details of which remain to be clarified. While a role for cellular immunity is accepted in the pathogenesis of HP, several clinical observations also suggest a role for immune-complex-mediated lung injury. We have previously demonstrated the presence of chemotactic factors for polymorphonuclear cells (PMNs) in bronchoalveolar lavage (BAL) fluids of acutely ill patients with the summer type of HP found in Japan. The present study correlated chemotactic factors for PMNs with the level of C5a des Arg in BAL fluids obtained from patients with summer type HP. Furthermore, this study demonstrated that PMNs were increased in BAL fluids obtained after 2 days of avoidance of exposure to the presumptive causative agent. The percentage of PMNs in the BAL increased in proportion to the activity of the chemotactic factors. Finally, leukotriene B4 was not detected in concentrated BAL or supernatant fluids of cultured macrophages. These results suggest that complement activation in the respiratory tract may occur as the early event in the pathogenesis of HP.
We studied the antiemetic effects of a combination therapy consisting of metoclopramide (MCP) and high-dose lorazepam (HiLor; 3-4.5 mg/day) in patients with lung cancer who were being treated with cis-diamminedichloroplatinum (CDDP). This study was designed in order to compare the antiemetic efficacy of two different-term treatments. In the short-term treatment, MCP and HiLor were given for three days after the beginning of the CDDP regimen (group 1). In the long-term treatment (group 2), the same dose of MCP and a decreased dose of HiLor (1.5-3 mg/day) were administered for another three days (eventually for 6 days). Thirty-one trials were evaluated in eighteen patients for 8 days after the CDDP treatments initiated. The frequency of episodes of vomiting was less than two times in 70% and 82% of trails, in group 1 and group 2, respectively. This finding indicates that the combination therapy of MCP and HiLor for a long period would be the same or more effective than that of MCP and steroid agents. Furthermore, in group 2, the frequency and severity of late emesis were significantly less than in group 1, and appetite recovery was observed significantly earlier than in group 1. There was no side effect related to the administration of MCP and HiLor during this study. These findings suggested that the combination treatment of MCP and HiLor with a decreased dose of HiLor for a long period was markedly effective for antiemesis in patients treated with CDDP, especially for the prophylaxis of CDDP-induced late emesis.
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