[Atypical condyloma latum of anus].
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Biomedical subjects
Publications and source records attributed to A Kinugasa.
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The present report concerns a patient who was first diagnosed as having adenoma in the duodenal bulb and subsequently was discovered to have adenomas in the stomach and colon. Surgical procedures including endoscopic resection could not be carried out because the patient had advanced liver cirrhosis. Follow-up colonoscopy no longer detected any polyp in the colon. Ultrasonography demonstrated a slowly growing hypoechoic mass in the liver, which was indicative of hepatocellular carcinoma. Then, single chemotherapy with oral administration of 5'-deoxy-5-fluorouridine was initiated. Surprisingly, repeated esophagogastroduodenoscopy revealed gradual regression of the gastric and duodenal tumors. Findings from the endoscopy and biopsy materials 10 months after the start of therapy showed disappearance of the gastric and duodenal adenomas. Despite enlargement of the hepatic mass, no recurrence of gastric and duodenal tumors has been noted during the past 1 1/2 yr.
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Administration of monosodium L-glutamate (MSG) to neonatal mice produces a hypothalamic syndrome consisting of stunted growth and later development of obesity. We assayed plasma insulin (IRI), thyroxine (T4) and insulin-like growth factor-I (IGF-I) to investigate their roles in the growth of the mice. Two mg/g body weight of MSG was injected into newborn male mice daily for five successive days after birth. Plasma IRI levels were increased on the after 8 weeks of age in MSG-treated mice. There was no significant difference between the plasma T4 levels in MSG-treated mice and those in controls at any age studied. In contrast to this, plasma IGF-I levels in MSG-treated mice were reduced at one week and after. These results suggest that a decreased plasma IGF-I level contributes to the retarded linear growth which develops soon after the administration of MSG, and hyperinsulinemia contributes to the later development of obesity in MSG-treated mice.
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A 3 year old girl was admitted to hospital in an emaciated condition and with polydipsia in October 1974. Following the diagnosis of diabetes mellitus, she received treatment with insulin. On the first admission, a systolic murmur was noted at the apex of the heart. In 1981, the murmur was found to be continuous with a systolic click, and echocardiography demonstrated a mitral valve prolapse. In 1982, electrocardiography revealed left ventricular hypertrophy, and the patient's X-ray showed vertebral kyphoscoliosis. Ophthalmological examination revealed slightly impaired visual acuity and a mild case of cataracts in 1986. The patient grew to be tall and thin with arachnodactylia of the hands, fingers, feet and toes. These symptoms and findings were compatible with Marfan syndrome, although the ophthalmological findings are not specific for this disease. This patient is the first case in Japan of Marfan syndrome associated with insulin-dependent diabetes mellitus, although the relation between Marfan syndrome and IDDM remains unclear.
An indirect immunofluorescence test using a flow cytometer (FACS420) was useful for detection of antineutrophil antibodies (anti-NA2 antibodies) in a case of monozygous twins with alloimmune neonatal neutropenia. When high-dose intravenous gammaglobulin (300 mg/kg for five consecutive days) was given to one twin, the increase in neutrophils was not obvious. Although neutropenia persisted for about three months, no infections were observed in either of the twins.
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In order to elucidate the relation between the hepatotoxicity of salicylate (SA) and the pathogenesis of Reye's syndrome (RS), urea production, gluconeogenesis and ketogenesis were investigated in isolated perfused rat livers in the presence of salicylate (SA) and oleate. Although urea formation from 0.5 mM NH4Cl, 2 mM ornithine and 0.3 mM oleate was not inhibited by infusion of SA, 3 mM SA caused a 26% decrease of ketogenesis, 85% decrease of 3-hydroxybutyrate/acetoacetate ratio (30HB/AcAc) and 45% increase of oxygen consumption. Glucose production from 2 mM pyruvate in the presence of 0.3 mM oleate decreased by 33% after administration of 3 mM SA, and 30HB/AcAc ratio also decreased by 33%. The decrement of gluconeogenesis and that of the 30HB/AcAc ratio were very close. These results suggested that ATP production was maintained but that the intra-mitochondrial redox state was changed to a more oxidized state after SA administration in perfused rat livers. This change in redox state could be responsible for the decrease of gluconeogenesis. Metabolic characteristics found in RS were not obtained by infusion of 3 mM SA and 0.3 mM oleate in rat livers. Therefore, some other factors in addition to SA seem necessary to establish an animal model of RS.
We report a boy with some clinical symptoms compatible with a diagnosis of incomplete DiGeorge syndrome. He had a dismorphic face, micrognathia, cleft palate, and heart anomalies similar to DiGeorge syndrome, but lacked aplasia of the thymus or hypoparathyroidism typical of the syndrome. High-resolution banding analysis revealed that his karyotype was 45,XY,-14,-22, +der(14)(14pter----14q32.32::22q11.21----22qter), the consequence of a maternal reciprocal translocation between chromosomes 14 and 22. Precise localization of the gene responsible for the present DiGeorge syndrome was assigned to subband 22q11.1.
Arteriovenous malformation of the intestine is an uncommon cause of gastrointestinal hemorrhage, and the diagnosis can be made only by selective mesenteric arteriography to demonstrate the characteristic appearance. This is a case report of a 16-year-old boy with arteriovenous malformation of the jejunum causing massive rectal bleeding. We advocate the use of selective visceral angiography for diagnosing arteriovenous malformations of the intestine, even in children.
We describe a very rare case of adrenocortical carcinoma (ACC) presenting with Cushing's virilising syndrome in a female child with congenital hemihypertrophy (CHh). CHh was of more value for early detection of ACC than Cushing's virilisation.
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The effect of glucagon on gluconeogenesis was measured in periportal and pericentral regions of the liver lobule by monitoring changes in rates of O2 uptake on the surface of the perfused liver with miniature O2 electrodes after infusion of lactate. When lactate (2 mM) was infused into livers from starved rats perfused in the anterograde direction, O2 uptake was increased 2.5-fold more in periportal than in pericentral regions, reflecting increased energy demands for glucose synthesis. Under these conditions, glucagon infusion in the presence of lactate increased O2 uptake exclusively in periportal regions of the liver lobule. Thus, when perfusion is in the physiological anterograde direction, the metabolic actions of glucagon predominate in periportal regions of the liver lobule under gluconeogenic conditions in the starved state. When livers were perfused in the retrograde direction, however, glucagon stimulated O2 uptake exclusively in pericentral regions. Thus glucagon only stimulates gluconeogenesis in 'upstream' regions of the liver lobule irrespective of the direction of flow.
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