The involvement of antigen-specific T cells in the pathogenesis of collagen diseases is still controversial. The final stages of collagen diseases are usually characterized by the dominance of inflammation. Therefore, antigen non-specific factors, such as inflammatory cytokines, probably play an important role in this process. On the other hand, the methods available to analyze the antigen-specific aspects of the immune response are still limited. Here we review our novel system of T cell clonality analysis based on the idea that activated antigen-specific T cells should form accumulating clones among the lymphocyte population. Using this method, dynamic changes of clonal accumulation of T cells could be evaluated during antigenic stimulation in vivo and in vitro. The significance of antigen-specific T cell clones in collagen diseases is discussed using data obtained from patients with rheumatoid arthritis and systemic lupus erythematosus.
(Internal Medicine 36: 242-247, 1997)

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The serum autoantibodies, antinuclear antibody, anti-DNA antibody, anti-smooth muscle antibody, antithyroglobulin antibody, antimicrosomal antibody, antimitochondrial antibody, rheumatoid factor and antibody to deoxyribonucleoprotein were measured at the baseline and on completion of interferon-α2a (IFN-α2a) treatment in chronic hepatitis C (CHC) patients who did not present with any autoimmune disease prior to treatment. Of the 57 patients examined, 27 spontaneously manifested at least one autoantibody. Only the prevalence of rheumatoid factor (26%) was significantly higher in the CHC patients than in the control subjects. There were no differences in the prevalence of the 8 autoantibodies examined between hepatitis C virus (HCV) genotypes, Ib and 2a/2b. Twenty-six patients responded to IFN-α2a. Subclinical hypothyroidism developed in two patients with elevated antithyroid antibody titers during treatment. No relationship was observed between changes in the status of autoantibodies and either response to IFN-α2a or HCV genotype. Irrespective of the HCV genotype, autoantibodies might be present in CHC patients before and during the IFN-α2a treatment. The presence of such antibodies does not represent a contraindication to the use of IFN-α2a in CHC patients not complicated by autoimmune diseases. Careful observations are necessary for CHC patients positive for antithyroid antibodies during the IFN-α2a treatment. Preexisting or newly developed autoantibodies do not necessarily predict a poor response to IFN-α2a.
(Internal Medicine 36: 248-254, 1997)

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To assess the relationship between coronary artery calcification and the late success rate of percutaneous transluminal coronary angioplasty (PTCA), we performed electron beam computed tomography (EBCT) in 22 patients with ischemic heart disease who underwent PTCA. The calcification score in each coronary artery vessel was estimated and compared with the occurrence of restenosis at 3 months after PTCA. Angioplasty had been performed in 28 sites in 22 patients, and 12 sites exhibited restenosis. The mean calcium score in the unsuccessful PTCA vessels was significantly higher than in successful sites (228 vs 92). The overall late success rate of PTCA with moderate to severe calcification was extremely low at 29%. Coronary segments with diffuse and extensive calcification were not optimal target lesions for PTCA. Prediction of the late success rate after PTCA may be possible by prior evaluation of coronary artery calcification utilizing EBCT.
(Internal Medicine 36: 255-262, 1997)

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To investigate the left ventricular hypertrophic patterns and wall motion dynamics in hypertrophic cardiomyopathy, 51 patients were studied using electron beam computed tomography. The subject consisted of 26 asymmetrical hypertrophy, 9 diffuse hypertrophy, 14 apical hypertrophy and 2 papillary muscle hypertrophy. Concerning the wall motion dynamics in hypertrophic wall, 7 demonstrated homogeneous wall thickening involving the non-hypertrophic wall, 36 showed decreased wall thickening, 6 showed normal wall thickening, and 2 cases of papillary muscle hypertrophy had increased wall thickening in the apical wall. The percent wall thickening in hypertrophic wall was significantly reduced in relation to the increase of wall thickness; 14±8% in the wall over 20 mm, 23±12% in 16-19 mm and 56±36% in 13-15 mm. The reduced wall motion dynamics in hypertrophic wall were clearly observed by electron beam computed tomography.
(Internal Medicine 36: 263-269, 1997)

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P300, somatosensory evoked potential (SEP) and brainstem auditory evoked potential (BAEP) are widely used neurophysiological methods for objectively evaluating cognitive, somatosensory and brainstem auditory functions. We studied the P300, SEP and B AEP in 17 patients with chronic respiratory insufficiency (PaO₂:58.2±7.0 mmHg; mean ± SD) and 15 age-matched healthy subjects (PaO₂: 84.4 ± 11.3 mmHg). The latency and amplitude of P300, the N9 latency, N9-N13 and N13-N20 interpeak latencies (IPL) in SEP, wave I latency and I-VIPL in B AEP were compared between the patients and controls. The P300 latency, N9-N13 and N13-N20 IPLs in SEP in the patients were significantly prolonged compared to the controls. In contrast, the amplitude of P300, N9 latency in SEP, wave I latency and I-V IPL in B AEP were not significantly different between the patients and controls. These results suggest that chronic respiratory insufficiency influences the cognitive and somatosensory functions, and indicate that there is a selective vulnerability of evoked potentials to this condition.
(Internal Medicine 36: 270-275, 1997)

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Eosinophils play a crucial role in bronchial asthma. As theophylline and procaterol (β₂-agonist) are used for the treatment of bronchial asthma, the specific functions of eosinophils in the presence of granulocyte/macrophage colony-stimulating factor (GM-CSF) or platelet activating factor (PAF) were examined using theophylline and procaterol alone and in combination. Eosinophil degranulation induced by PAF or GM-CSF was inhibited by theophylline (10^-6 M-10^-3 M and 10^-6 M to 10^-3 M, respectively) and procaterol (10^-7 M-10^-5 M and 10^-7 M-10^-5 M, respectively). The combination of 10^-4 M theophylline and various concentrations of procaterol provided higher inhibition than 10^-4 M theophylline or procaterol (10^-7 M-10^-5 M). CD11b, which is a triggering molecule for human eosinophil degranulation, showed a significantly inhibited expression of PAF stimulation with 10^-4 M theophylline. CD11b and another triggering molecule for eosinophil degranulation, CD18, showed a significantly inhibited expression of PAF stimulation using a combination of 10^-4 M theophylline and various concentrations of procaterol (10^-5 M-10^-7 M) compared with the inhibition of 10^-4 M theophylline or procaterol (10^-5 M-10^-7 M), but GM-CSF-stimulated eosinophils were not inhibited. Taken collectively, theophylline and/or procaterol have anti-inflammatory effects.
(Internal Medicine 36: 276-282, 1997)

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A 68-year-old man with moderate liver dysfunction diagnosed with atypical pneumonia showed serum alanine aminotransferase and γ-glutamyltranspeptidase levels which revealed a sustained abnormality over six months. Hepatitis GB virus type C/hepatitis G virus was demonstrated in his serum by reverse transcription-polymerase chain reaction. Liver histology showed Steatohepatitis typically observed in alcoholic hepatitis without a remarkable drinking history. This case suggests that hepatitis GB virus type C/hepatitis G virus may induce chronic hepatitis and that there may be cases with chronic hepatitis induced by this virus in patients who have been diagnosed with alcoholic liver disease, even in cases with typical histology of alcoholic hepatitis.
(Internal Medicine 36: 283-288, 1997)

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A 29-year-old man with von Recklinghausen's disease suddenly developed severe epigastric pain and was admitted to hospital. Physical examination revealed elevated blood pressure (200/130 mmHg) and tachycardia (162 bpm). Initially, he was suspected to have appendicitis, and appendectomy was performed immediately; however, appendicitis was not demonstrable pathologically. Retroperitoneal hematoma was found incidentally during the operation. Further clinical and laboratory examination demonstrated a marked increase in the urinary excretion of catecholamines. There was no evidence of pheochromocytoma on computed tomography or magnetic resonance imaging; however, these imaging studies simply showed a hematoma at the right adrenal gland. Transient hypertension and tachycardia, resembling pheochromocytoma, was caused by adrenal hemorrhage.
(Internal Medicine 36: 289-292, 1997)

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A 56-year-old Japanese man presented with a 2-month duration of polyuria and polydipsia. The diagnosis of diabetes insipidus was confirmed by water deprivation and vasopressin injection. The secretory function of the adenohypophysis was estimated as normal by a variety of provocative tests. Magnetic resonance imaging (MRI) displayed the loss of the hyperintense signal of the neurohypophysis and a tumor-like lesion confined to the neurohypophysis. The tissue specimen resected at transsphenoidal surgery showed diffuse lymphocytic infiltration. These findings suggest that this is a candidate case for lymphocytic infundibuloneurohypophysitis (LIN) that is not identical to classical lymphocytic hypophysitis. This patient will be followed up to determine whether this case simply represents an early stage of classical hypophysitis or a different clinical entity.
(Internal Medicine 36: 293-297, 1997)

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A 32-year-old immunocompetent man developed fever and malaise that persisted for three years. As he had no health insurance, he never received any medical treatment. On admission, chest X-ray revealed multiple cavitary lesions and his sputum yielded acid-fast bacilli, that were identified as Mycobacterium kansasii with multidrug resistance. Although his general status improved transiently by antituberculous agents, he died of respiratory insufficiency after four months. The prognosis of Mycobacterium kansasii pulmonary disease is reported to be relatively good among non-tuberculous mycobacteriosis, however, physicians must pay careful attention to cases of delayed start of therapy or multidrug resistance, or both.
(Internal Medicine 36: 298-300, 1997)

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A 39-year-old man with a known diagnosis of lung adenocarcinoma developed intermittent double vision with right pupil dilatation. His symptoms eventually progressed to complete oculomotor nerve palsy on the right. Postmortem examinations revealed a metastasis of the adenocarcinoma involving the root of right oculomotor nerve.
(Internal Medicine 36: 301-303, 1997)

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On hospitalization, the clinical examination of a 64-year-old female with polyarthralgia and an elevated fever revealed leukocytosis, an increased lactic acid dehydrogenase level, and a positivity for the C-reactive protein. Subsequently, the patient developed muscular pain in the lower limbs. Thus, a muscle biopsy was performed and B-cells with atypia were detected in the arteriolar lumen within the muscle. This led to the diagnosis of angiotropic lymphoma (AL). A combination chemotherapeutic regimen was initiated, and the patient's symptoms disappeared. AL is difficult to diagnose before death, but in this case, muscle biopsy facilitated an early diagnosis and subsequent chemotherapy resulted in the disappearance of the AL. We thus feel this report may be of value.
(Internal Medicine 36: 304-307, 1997)

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We describe a case of stiff-man syndrome accompanied by diabetes mellitus, Hashimoto's thyroiditis and the antecedent myasthenia gravis. The diagnosis of stiff-man syndrome was made based on not only clinical findings and the characteristic electromyographic pattern but also the presence of antibodies to glutamic acid decarboxylase in the serum and cerebrospinal fluid. Stiff-man syndrome is known to be associated with organ-specific autoimmunopathy including insulin-dependent diabetes mellitus. The present case is the first one that stiff-man syndrome was preceded by myasthenia gravis of organ-specific autoimmunopathy. Stiff-man syndrome in the present case probably represents the one of fully expressed manifestations from the broad spectrum of organ-specific autoimmunopathy caused by the loss of self-tolerance.
(Internal Medicine 36: 308-311, 1997)

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We report a case of amyotrophic lateral sclerosis (ALS) with anti-acetylcholine receptor (AChR) antibody in a 73-year-old female patient. She showed the typical course of ALS. She had no clinical findings of myasthenia gravis and had never undergone neurotoxin therapy using snake venom. Anti-AChR antibody was positive with a titer of 0.50 nmol/l on admission. We traced the titers during the progression of ALS; the titer was positive when muscle weakness worsened, and it became negative when the general condition became stable. We suppose that the occurrence of anti-AChR antibody may be partially relevant with abnormalities at the neuromuscular junction during the progression of ALS.
(Internal Medicine 36: 312-315, 1997)

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