To investigate the role of the mucus-bicarbonate barrier in the prevention of duodenal ulcer recurrence, duodenal mucosal neutralizing capacity and mucosal prostaglandin (PG) synthesis were examined in 5 normal controls (NC) and 12 duodenal ulcer (DU) patients. DU patients were divided into non-recurrent (NR, 7) and recurrent (R, 5) groups based on endoscopic follow-up study. The recovery time (RT) was significantly longer and the mucosal PGE₂ synthesis was significantly lower in R than in NC and NR groups. There was a proportional correlation between mucosal PG synthesis and RT in DU patients. These results indicate that impaired neutralizing capacity caused by reduced endogenous PG synthesis in duodenal mucosa may contribute to recurrence of DU.

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Adenosine deaminase (ADA) activity and free interleukin (IL)-2 receptor levels were assayed in serum samples from patients with mycoplasma and bacterial pneumonia to evaluate the usefulness of these parameters in distinguishing between these diseases at an early stage. Serum ADA and free IL-2 receptor levels in patients with mycoplasma pneumonia (32.4±9.2 U/l, 960±204 U/ml) were significantly higher than those in patients with bacterial pneumonia (12.5±3.3 U/l, 425±86 U/ml) and in healthy controls (14.0±3.4 U/l, 286±49 U/ml) (p<0.001). Of the 20 mycoplasma pneumonia cases, 19 showed increased levels of ADA over 20.8 U/l; in 17 of the 19, the increase of ADA was seen before the elevation of the specific antibody to Mycoplasma pneumoniae. In contrast, serum ADA levels in all 20 cases of bacterial pneumonia were lower than 20.8 U/l. These results indicate that assays for serum ADA and free IL-2 receptor levels are useful in distinguishing between bacterial and mycoplasma pneumonia at an early stage.

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Pulmonary sarcoidosis is a granulomatous disorder of unknown cause, characterized by an accumulation of active T lymphocytes in the lung. We measured the levels of soluble interleukin-2 receptor (IL-2R) in bronchoalveolar lavage fluid (BALF) of patients with active pulmonary sarcoidosis and normal subjects by a sensitive enzyme-linked immunosorbent assay. Soluble IL-2R was detectable in BALF from 6 of 11 patients with sarcoidosis but in only 1 of 8 normal control subjects, the mean levels of IL-2R in BALF of the two groups being 2.8±0.9 U/ml and 0.1±0.1 U/ml, respectively (p<0.01). A slight correlation was found between the soluble IL-2R level and the number of CD4-positive cells. Sarcoidosis patients were classified by radiographical staging. Soluble IL-2R was not detectable in the BALF of any stage I patients, but was found in the BALF of 6 of the 7 stage II and stage III patients. These results suggest that in the clinical management of patients with sarcoidosis, measurement of soluble IL-2R in BALF is useful for evaluating the activity of the lung disease is sarcoidosis.

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The kappa/lambda (κ/λ) ratios of IgG, IgA and IgM in the cerebrospinal fluid (CSF) and in the sera of 10 patients with Guillain-Barré syndrome were analyzed. The κ/λ ratios of IgG, IgA and IgM in the CSF and in the serum were not significantly different between the acute and the late stages of Guillain-Barré syndrome nor between Guillain-Barré syndrome and the normal controls. In the CSF, however, the concentration of albumin, IgG, IgA and IgM in the acute phases of Guillain-Barré syndrome were significantly higher than in the normal controls. These results suggest that in Guillain-Barré syndrome, the increase of immunoglobulins may not be due to intrathecal synthesis and therefore there are no significant changes in the κ/λ ratios in the CSF.

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A 43-year-old male with non-Hodgkin's lymphoma accompanied by autoimmune hemolytic anemia (AIHA). His blood group was group B, CcDEe. Alloantibody was absent in his serum, but autoantibody, a combination of IgG and C3d type which showed anti-e specificity, was present. Although transient improvement of AIHA was achieved by treatment with 60 mg/day of prednisolone, subsequent worsening of the anemia resulted in the patient's death. Identification of blood group-specific autoantibodies may be beneficial in such a case for blood transfusion.

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A 67-year-old woman was admitted for nephrotic syndrome. In spite of the lack of lymphadenopathy, hepatosplenomegaly and serum hyperviscosity, remarkable monoclonal IgM-proteinemia was demonstrated. Amyloid kidney was shown by renal biopsy. However, in the bone marrow and other organs, neither proliferation nor invasion of monoclonal immunoglobulin-producing cells was revealed by immunohistological investigations of the specimens biopsied or examined at autopsy, excluding Waldenström's macroglobulinemia. Immunosuppressive chemotherapy with cyclophosphamide, vincristine and prednisolone was effective in reducing serum IgM, but could not slow the progression of renal failure. This case suggested the association of generalized amyloidosis with excessive IgM-proteinemia caused by a non-malignant mechanism.

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Fungal infections are often reported, but Trichosporon infection is very rare. A 78-year-old man with adult T-cell leukemia complicated with pulmonary infections is presented. Bronchial exudate culture revealed many yeast-like colonies, which were morphologically and biochemically identified as Trichosporon pullulans.

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A 71-year-old female visited our outpatient unit with chief complaints of anorexia and a sense of abdominal distension. The abnormalities found after admission were conspicious increases in CA125 levels in serum and ascites as well as anemia, accelerated erythrocyte sedimentation and increased serum LDH. The patient underwent an emergency operation for ileus. The histological diagnosis was serous papillomatous cancer. Immunohistologic staining of the cancer tissue demonstrated the production of CA125. In this very rare the remnant of the Müllerian duct in the peritoneum is thought to have been cancerous.

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A patient with subarachnoid hemorrhage who exhibited changes suggestive of myocardial infarction by electro- and echocardiography and underwent coronary angiography is reported. Echocardiography demonstrated marked hypokinesis in the left ventricular anterior wall to the septum. Since the possibility of concomitant myocardial infarction could not be excluded, coronary angiography was performed with cerebral angiography. No abnormalities were observed in the coronary arteries, and the myocardial damage was considered to be due to subarachnoid hemorrhage. Echocardiograms showed improvements in left ventricular wall motion within a short time after operation of the intracranial lesion.

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The proband, a 42-year-old woman without any symptoms or hypertension, was admitted for examination of accidentally discovered bilateral adrenal masses. Physical examination disclosed bilateral nodular goiter and mild sinus tachycardia. Pheochromocytomas and medullary thyroid carcinomas were revealed by biochemical and histopathological examinations. Hypercholesterolemia and abnormal glucose metabolism returned to normal after bilateral total adrenalectomy and thyroidectomy. Screening examination showed four affected family members. Three of them were also asymptomatic and normotensive. In pheochromocytoma patients, normotension, hypercholesterolemia, and impaired glucose metabolism might be signs of excess secretion of epinephrine rather than norepinephrine.

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A case of infective endocarditis of the tricuspid valve is described in a young female patient with no history of intravenous drug abuse. The patient suffered from symptoms of septic emboli of the lung and right heart failure. She was ultimately treated by tricuspid valve replacement. There was no recurrence of symptoms following surgery.

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Factor V deficiency associated with rheumatoid arthritis was found in a 54-year-old woman. Hereditary factor V deficiency is very rare; only about 150 cases have been reported since its discovery in 1943. This appears to be the first case report of factor V deficiency associated with rheumatoid arthritis in the literature.

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A 45-year-old woman presented with persistent headache which was of acute onset and occurred daily. Laboratory findings included thrombocytosis, elevated levels of antinuclear antibody, rheumatoid factor, and antibodies to Epstein-Barr virus (EBV). Magnetic resonance image of the head, left selective external carotid angiography, temporal arterial biopsy, and cerebrospinal fluid revealed no abnormal findings that could explain her headache. Her headache was compatible with NDPH, which has been reported by Vanast, and was thought to be related to EBV reactivation.

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A 70-year-old woman with Cogan's syndrome first presented with central diabetes insipidus and then developed secondary hypothyroidism. Magnetic resonance imaging revealed a diffuse pituitary swelling without evidence of tumor. High-dose glucocorticoid therapy administered to treat Cogan's syndrome was very effective in suppressing the inflammatory process, and resulted in the reversal of the pituitary swelling and partial recovery of thyroid stimulating hormone secretion. This is the first case of hypopituitarism associated with Cogan's syndrome, a form of autoimmune vasculitis. The glucocorticoid-responsive pituitary lesion is best explained by autoimmune hypophysitis which shows pituitary swelling and is known to often associate with other autoimmune phenomena.

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A pair of 37-year-old identical twins with diabetes mellitus are described. One of the brothers was admitted for heart failure without pain, and autonomic neuropathy was found. The clinical diagnosis was inferior myocardial infarction with anteroseptal healed myocardial infarction. Cardiac catheterization revealed triple coronary vessel involvement. The diagnosis was confirmed at autopsy after sudden death. The other brother was also examined by cardiac catheterization, which revealed total right coronary occlusion and hypokinesis of the wall. There had been no previous pain nor upper body discomfort until that time in either twin. Thus, genetic factors should possibly be considered in the genesis of asymptomatic or silent myocardial infarction.

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Literature reviews have indicated that thrombotic complications in leukemic patients are rare that prompt diagnosis is very difficult, and that morbidity and mortality are extremely high. We describe the successful treatment of a 36-year-old housewife suffering from chronic myelogenous leukemia with secondary myelofibrosis.

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A 30-year-old woman with thyroid crisis and impaired renal function presented with severe hypocalcemia. She had already had hypocalcemia one yr previously when her serum creatinine level was normal. A normal level of serum amino terminal fragment of parathyroid hormone in spite of severe hypocalcemia suggested impairment of parathyroid function. Since her serum magnesium was normal and she had no history of neck surgery or radioiodine therapy, her hypoparathyroidism was considered to be idiopathic. This is the seventh case with co-existing Graves' disease and idiopathic hypoparathyroidism reported in the literature.

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Twocases of necrotizing myelopathy, one with lung carcinoma and the other with adult T cell leukemia (ATL), displayed flaccid paraplegia and sphincter dysfunction. Both cases did not show any direct neoplastic cell invasion of the spinal cord. Pathologically, diffuse and random necrosis was found in the spinal cord in both cases. In the case of ATL, small numbers of inclusion bodies in the nerve cell nuclei were demonstrated. Using polyclonal and also monoclonal antibodies, herpes simplex virus type 2 (HSV-2) was clearly demonstrated in the spinal cord in both cases. By electron microscopy, numerous herpes virus particles were observed in the spinal cord in both cases. The usefulness of electrophysiological studies should be emphasized in the differentiation of these cases from others which might also display flaccid paraplegia. The possibility of necrotizing myelopathy caused by HSV-2 should always be considered in the differential diagnosis of spinal cord diseases displaying flaccid paraplegia.

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This report describes a case of cerebrotendinous xanthomatosis (CTX) accompanied by clinical manifestations of parkinsonism, including oily and masked face, marked akinesia, muscle rigidity and resting hand tremor. Magnetic resonance imaging (MRI) of the brain showed high intensity areas on T2 weighted imaging, and slightly low intensity areas on T1 weighted imaging in the right globus pallidus and the left putamen. Cerebral cortical atrophy with slight ventricular dilatation and cerebellar atrophy were present as well. This is a case report of CTX which manifested parkinsonism. Parkinsonism may not be a coincidental manifestation in CTX, but rather represent a symptom of the same underlying diathesis.

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