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Clinical features were studied in 125 patients with sarcoidosis (72 females and 53 males) diagnosed at Okayama University Hospital during a recent 10-year period. The age distribution had two peaks in patients in their 20s and the 50s. Over half of the patients were detected at health screening check and were asymptomatic, while the remaining were symptomatic. Twelve patients were in stage 0, 41 were in stage I, 54 were in stage II, 16 were in stage III, and 2 were in stage IV according to the chest x-ray findings. Serum angiotensin converting enzyme levels and serum lysozyme levels were elevated in 60% and 76% of the patients, respectively. The bronchoalveolar lavage fluid showed lymphocytosis, especially of helper T-cells. The clinical features of sarcoidosis appear to depend on the duration of the disease.

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A 61-year-old woman, who had engaged in "tatami" mat production for 20 years, showed a gradually increasing large conglomerate mass shadow associated with small irregular opacities on chest X-ray film. Transbronchial lung biopsy revealed findings consistent with pneumoconiosis, with no suggestion of pulmonary tuberculosis or lung cancer. After 6 years' observation, right upper lobectomy was performed because the mass shadow was still increasing in size. Histological examination revealed a well-defined large mass composed of numerous macrophages containing abundant silicate minerals and fibroblasts proliferating in storiform fashion. No evidence of tuberculosis or malignancy has ever been detected. These findings are compatible with the previously reported pathological findings of "IGUSA-SENDO" pneumoconiosis; however, PR4 type "IGUSA-SENDO" pneumoconiosis has never been previously reported. This is the first reported case of PR4 type "IGUSA-SENDO" pneumoconiosis.

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To determine the genesis of the high incidence of stenotic lesions of the left anterior descending artery (LAD) in the young, we have investigated the anatomical characteristics of coronary arteries in the following 3 groups; young (less than or equal to 40 yr) myocardial infarction (MI) patients with LAD lesions, young (less than or equal to 40 yr) patients without coronary stenosis and aged (greater than or equal to 60 yr) MI patients. The angle between the left main coronary artery (LMT) and the LAD in the young MI patient group (146.7 +/- 7.4 degrees) was significantly wider than those of the young normal (126.0 +/- 13.4 degrees) or the aged MI patient groups (127.1 +/- 18.6 degrees) (p less than 0.01, p less than 0.02, respectively). The angle between the LMT and the left circumflex artery (LCX), and the angle between the LAD and the LCX were not significantly different among the 3 groups. The LMT length in the young MI patient group was 18.3 +/- 4.7 mm, which was not significantly longer than those of the young normal (12.7 +/- 6.9 mm) or the aged patient groups (14.8 +/- 6.0 mm). The internal diameter ratio of the LAD and LCX was also not significantly different among the 3 groups. These results suggest that the angle between the LMT and LAD was significantly wider in young MI patients, and should be regarded as an inherited characteristic influencing the development of coronary atherosclerosis of the LAD, particularly in young MI patients.

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Thirty seven patients with sarcoidosis were examined using ultrasound (US) to determine the size of the spleen. A Spleen Index (SI) was employed to evaluate splenomegaly and the SI was calculated using long (a) and short (b) dimensions on the sectional splenotomogram (SI = a x b). In 21 (57%) of these patients the spleen was judged ultrasonographically to be enlarged (SI 30), but in only 3 was it palpable. The clinical records of patients with and without splenomegaly detected by US were compared. There were no differences between patients with or without splenomegaly in hematologic findings (peripheral blood and bone marrow) or blood chemistry; furthermore no patients with hypersplenism were seen. In immunological parameters, the serum immunosuppressive acid protein level was significantly (p less than 0.05) higher in patients with splenomegaly than in those without splenomegaly; however, there were no differences in serum angiotenins converting enzyme activity, serum lysozyme level, PPD skin test or bronchoalveolar lavage fluid analysis. The patients with splenomegaly had significantly higher evidence of increased uptake of 67-Gallium in lung fields and positive lung infiltrates in chest X-ray than those without splenomegaly (p less than 0.01, p less than 0.05). These data suggest that ultrasound is a promising diagnostic tool for the assessment of the size of the spleen and is useful to detect disease activity and extent of disease in sarcoidosis. Patients with sarcoidosis who had splenomegaly had more disseminated disease, especially pulmonary parenchymal disease, than did those without splenomegaly.

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Current concepts of the pathogenesis of sarcoidosis suggest that the alveolitis in this disorder is related to increased numbers of helper T-cells within the lungs. However, the mechanism of this accumulation of lymphocytes is not known. We have reported that proliferation of alveolar lymphocytes induced by P. acnes is increased in patients with active sarcoidosis. To determine whether the response of alveolar lymphocytes would be useful in staging the activity of pulmonary sarcoidosis, we studied 34 untreated patients with this disorder, and correlated the response of alveolar lymphocytes with clinical, roentgenographic, physiologic, and bronchoalveolar lavage findings in these non-smoking patients. There was a significant correlation of the response in the numbers of lymphocytes (p less than 0.05) and CD4 (+) T-cells (p less than 0.01) recovered from the lungs of these patients by bronchoalveolar lavage. Furthermore, the response correlated significantly with the activity of Interleukin-2 released by alveolar lymphocytes stimulated by P. acnes (p less than 0.05). In contrast, no correlation was found between the response and the clinical, roentgenographic, or physiologic data. However, in patients who showed abnormality in all three clinical examinations, i.e. serum angiotensin converting enzyme activity, number of alveolar lymphocytes, and 67Ga scintigraphy of the lung, the response was significantly higher than in controls (p less than 0.001) or in patients with none of these abnormalities (p less than 0.01). Also, the response in patients with an abnormality in two of these three examinations was significantly elevated compared to that in normals (p less than 0.025) or in patients without an abnormal examination (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

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We previously reported that alveolar lymphocytes in patients with active sarcoidosis are sensitized to Propionibacterium acnes (P. acnes) which may play a significant role in the induction of alveolitis in these patients. However, the mechanism of lymphocyte activation is not fully understood. In this study, we further investigated the production of Interleukin-2 (IL-2), and the responsiveness to IL-2 of alveolar lymphocytes obtained from sarcoidosis patients and stimulated by P. acnes in vitro. In 21 untreated sarcoidosis patients, 7 treated patients and 13 control subjects, the mean IL-2 activity of fluid released from cultured alveolar lymphocytes was 9.8 +/- 15.7 u/ml (M +/- SD), 1.9 +/- 4.7 u/ml and 0.2 +/- 0.8 u/ml respectively. The IL-2 activity of lymphocytes from untreated patients was significantly higher than that of control subjects (p less than 0.02). The responsiveness of alveolar lymphocytes to recombinant IL-2 was evaluated by 3H-thymidine uptake in the presence and absence of P. acnes. Lymphocytes stimulated by P. acnes showed a significantly increased uptake (3766 +/- 3929 dpm) compared to unstimulated lymphocytes (1123 +/- 968 dpm) obtained from 11 untreated sarcoidosis patients (p less than 0.02). On the other hand, the responsiveness of lymphocytes obtained from 6 control subjects was low, regardless of stimulation by P. acnes. There was a significant correlation (p less than 0.05) between the P. acnes-induced production of IL-2 by alveolar lymphocytes and the blastogenesis of alveolar lymphocytes in untreated sarcoidosis patients. Our data indicate that P. acnes stimulates IL-2 production and IL-2 receptor induction in alveolar lymphocytes from patients with active sarcoidosis.

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While increased levels of circulating antibody to various microorganisms have been reported in sarcoidosis patients, the pathogenesis of the disease is still unknown. In this report, the levels of antibody activities against Propionibacterium acnes (P. acnes) were measured in bronchoalveolar lavage fluid (BALF) in patients with sarcoidosis, using an enzyme-linked immunosorbent assay method. Each immunoglobulin class of antibody activity to P. acnes was corrected by albumin concentrations in BALF. The levels of whole immunoglobulin antibody activities to P. acnes in BALF were as follows: 412.3 +/- 443.9 O.D./albumin 1 mg (M +/- SD) in 31 untreated sarcoidosis patients, 556.6 +/- 341.8 in 10 sarcoidosis patients treated with prednisolone, and 231.5 +/- 156.8 in 16 control individuals. The levels of antibody activities were significantly elevated in untreated patients (p less than 0.05) and in treated patients (p less than 0.02) compared to those of controls. However, considering the treated vs. untreated patients, there was no significant difference in levels. The serum levels of whole immunoglobulin antibody activities were 0.484 +2- 0.191 O.D. in 38 untreated patients, 0.410 +/- 0.166 in 13 treated patients and 0.571 +/- 0.254 in 52 controls. The levels of antibody activity were significantly lower in treated patients than in the controls (p less than 0.05). However, there was no significant difference between the untreated patients and controls. To assess the site of antibody production, the secretion ratio was calculated by dividing the levels in BALF to those in serum. For this purpose, each serum level of antibody activity was also corrected by serum albumin concentration as with BALF.(ABSTRACT TRUNCATED AT 250 WORDS)

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Regional cerebral blood flow (rCBF) during hypertension and hypercapnia was studied in 33 patients with putaminal hemorrhage, using a single photon emission CT by means of Xenon 133 inhalation method. The results obtained were as follows: 1) A significant relationship was obtained between the impairment of autoregulation, CO2 reactivity and the degree of cerebral ischemia, i. e., in most cases, these vascular responses were impaired in cases of ischemia showing the rCBF decrease over 30 to 40% of normal values. However, there were particular cases with cerebral ischemia of over 30 to 40% in which autoregulation seemed to be preserved in the acute stage, which was considered to be the similar phenomenon as so called "false autoregulation". 2) The cerebrovascular responses such as autoregulation and CO2 reactivity were preserved in cases of less than 50 ml of hematoma volume. In cases with 50 to 74 ml of hematoma volume however, autoregulation and CO2 reactivity were mostly impaired, especially in the affected hemisphere rather than the non-affected, in the period of 1 to 2 months from the onset. Furthermore, the impairment was also involved in both hemispheres if the hematoma was over 75 ml in volume. 3) The cerebrovascular responses were markedly impaired in the region of basal ganglia of the affected hemisphere which corresponded well to the hematoma site. 4) There was a close correlation between the cerebrovascular responses and the activity of daily life (ADL), i. e, the prognosis might be poor in cases with global impairment, but which seemed to be rather good in cases with local impairment. It might be concluded, from the results mentioned above, that the study of autoregulation and CO2 reactivity is probably significant in estimating the pathogenesis and the treatment of cerebral ischemia following hypertensive putaminal hemorrhage.

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The proliferation of lymphocytes induced by Propionibacterium acnes (P. acnes) was measured by the in vitro incorporation of 3H-thymidine. The mean response rate of alveolar lymphocytes obtained by bronchoalveolar lavage was 2.23 +/- 0.89 in nine untreated sarcoidosis patients, 0.85 +/- 0.17 in five sarcoidosis patients given corticosteroids and 0.78 +/- 0.29 in 11 controls. The proliferation was significantly enhanced in the untreated patients compared to both the treated patients (p less than 0.01) and controls (p less than 0.001), but there was no significant difference in response rates between the treated patients and controls. The response rate of alveolar lymphocytes was significantly higher in four active patients (3.05 +/- 0.61) than in four inactive patients (1.77 +/- 0.44) (p less than 0.05) and in the controls (p less than 0.001). In sarcoidosis patients, the response rates showed a good correlation with activities of serum lysozyme (r = 0.695, p less than 0.01), and with percentages of lymphocytes in bronchoalveolar lavage fluid (r = 0.591, p less than 0.05). There was a low correlation between angiotensin-converting enzyme activities and the response rates (r = 0.508, p less than 0.1). Neither peripheral blood lymphocytes in sarcoidosis patients nor in controls showed any response to P. acnes, but alveolar lymphocytes of the untreated active sarcoidosis patients were sensitive to P. acnes. The lymphocytes activated by P. acnes may play a central role in the induction of alveolitis in sarcoidosis patients.

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In vivo animal studies support the concept that monocytes and macrophages are important in the immune surveillance of oncogenesis and that in vitro activated murine macrophages are cytocidal for tumour cells. In this study, the tumour cell cytotoxic activity of human peripheral blood monocytes was examined by measuring the inhibition of 3H-thymidine uptake in the human cancer cell line, established in our laboratory from human squamous cell lung cancer. The monocytes from 8 of the 31 lung cancer patients (26%) showed a percentage growth inhibition of less than 69.8%, which exceeded the 95% confidence limits of the percentage growth inhibition observed with healthy control monocytes. On the other hand, among the 16 sarcoidosis and the 8 tuberculosis cases no value was below 69.8%. However, there was no significant difference between the growth inhibition and the clinical stages or histological type. When OK-432, a Streptococcal agent, was administered in vivo to patients with lung cancer, an elevation of the growth inhibition was observed in 7 out of 8 patients. It was confirmed that the tumour cell cytostatic activity of the monocyte is suppressed in patients with lung cancer, and these monocyte deficits hinder the inhibition of tumour growth and metastasis.

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In order to determine the effect of immunosuppressive acidic protein (IAP) on the formation of pancreatic carcinoma, rats of the Sprague-Dawley strain were embedded with 7,12-dimethyl-benzanthracene (DMBA) in the pancreas with and without administration of IAP. In these animals, the growth of pancreatic cancer was studied both immunologically and histologically. Tumor was induced in 51 animals (85%) of 60 treated with embedding of 1 mg DMBA alone. Tumors began to appear from the 16th week after the embedding. Among animals in which tumor was induced, tubular adenocarcinoma and pleomorphic carcinoma accounted for 55% of the cases. When administration of IAP was combined, the period required for development of tumor was shortened. It became shorter with increases in the dosage and frequency of administration of IAP. In animals which received IAP in a mean dose of 75 mg/kg the area showing cancerous changes appeared as early as at the 8th week after the embedding of DMBA. A significant increase in the volume of tumors was seen in the group treated with IAP as compared to the group not treated with IAP. Animals which received IAP in increasing doses and frequencies showed an accelerated increase in the volume of the tumors which underwent cancerous changes. IAP was eliminated from the serum of rats within 72 hr after the administration, and acid protein was clearly recovered from the serum when tumors proliferated. These findings indicate that the acceleration of carcinogenesis in DMBA-induced pancreatic carcinoma may be attributable to the immunosuppressive effect of IAP administered and tend to be dependent on the dosage and frequency of its administration in the early phase of tumor induction.

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We report here an elderly woman who started vague complaints around the age of 50, was proved to be a sarcoidosis by negative skin reaction with purified protein derivative, bilateral hilar lymphadenopathy, and sarcoid lesions in biopsied liver and lymph nodes, and died of cardiac insufficiency after 15 years of the illness. Necropsy revealed a huge tumor-like left atrial thrombus with nonspecific fibrous lesions throughout the myocardium, a pulmonary hamartoma, pneumonia, liver cell necrosis, and cholecystopathy. To our knowledge, this may be the first case of myocardial sarcoidosis associated with this kind of atrial thrombus, although the sarcoidosis and thrombus may have occurred independently.

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In order to determine the effect of immunosuppressive acidic protein (IAP) on the formation of pancreatic carcinoma, rats of Sprague-Dawley strain were embedded with 7, 12-dimethylbenzanthracene (DMBA) in the pancreas with and without administration of IAP as a promotor, which was purified from the ascites obtained from cancer bearing patients, to induce pancreatic carcinoma experimentally. In these animals, growth of pancreatic cancer was studied both immunologically and histologically. Out of 60 rats treated with embedding of 1 mg DMBA alone, tumor was induced in 51 animals (85%). Tumors began to appear from the 16th week after the embedding. Among animals in which tumor was induced, tubular adenocarcinoma and pleomorphic carcinoma accounted for 55% of the cases. When administration of IAP was combined, the period required for development of tumor was shortened. It became shorter with an increase in the dosage and frequency of administration of IAP. In animals received IAP at a mean dosage of 75 mg/kg the area showing cancerous changes appeared as early as at 8th week after the embedding of DMBA. The acceleration of carcinogenesis in DMBA induced pancreatic carcinoma may be attributable to the immunosuppressive effect of IAP administered and tend to be dependent on the dosage and frequency of its administration in the early phase of tumor induction.

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