An autopsy was performed on a 42-year-old Japanese female who had been suffering from both ulcerative colitis (UC) and Takayasu's disease. Her UC started at age 27 with bloody stool, and Takayasu's disease was diagnosed at age 30 on the basis of absence of pulse in her left arm. After more than ten years she died of multiple cerebral infarction. An autopsy study revealed the scarring stage of UC in the entire colon and aortitis in the aortic arch and its major branches and pulmonary arteries. Her HLA type was positive for HLA-A2, 24, Bw52 and 61. Clinical features of a total of 13 Japanese cases that had both UC and Takayasu's disease have been reviewed in the Japanese and Western literature.
The established assay method used to assess S- and MB-COMT activities in human erythrocytes could be useful to elucidate catecholamine metabolism in the normal physiological state as well as in the pathology of certain diseases.
Background Catechol-().methyltransferase (COMT) catalyses the inactivation of catecholamines. It is widely distributed in most tissues in soluble (S-COMT) and membrane-bound (MB-COMT) forms. Recently, we used a new assay for COMT activity and demonstrated that COMT plays an important role in blood pressure regulation in spontaneously hypertensive rats. In order to investigate whether this is true for human hypertension, we have evaluated the erythrocyte COMT assay in humans. Method The assay procedure included the use ofnorepinephrine (NE) as a natural substrate and the quantification ofthe reaction product. normetanephrine, followed by high-performance liquid chromatography separation and fluorescence or chemiluminescence detection.
Two patients with polymyositis (PM) or dermatomyositis (DM) complicated with massive pleural effusion are reported here. Both patients presented a high-grade fever, pleural effusion prominent on the right, and good response to steroid therapy. In a 50-year-old womanwith PM, combined process of pleural inflammation, cardiomyopathy and coexisting hypothyroidism were considered to be responsible for the accumulation of the massive pleural effusion. However, in a 34-year-old manwith DM,pleural inflammation associated with interstitial pneumonia or pleural microvasculopathy in DMwasconsidered to be responsible for the accumulation of the massive pleural effusion.
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