A 48-year-old male with type A atrophic gastritis developed multiple gastric carcinoids and a pituitary adenoma. Laboratory tests revealed high levels of serum gastrin and growth hormone (GH). He underwent subtotal gastrectomy, resulting in a return of the previously elevated gastrin level to normal. Serum GHconcentration remained high. Three months after the surgery, the pituitary tumor, composed greatly of GH-immunoreactive cells, was partially removed. Since hypergastrinemia plays a pivotal role in gastric carcinoid formation and induces GH-releasing factor (GHRH)release resulting in GH-producing pituitary tumor formation, GH-producing pituitary adenoma might be a clinical manifestation in type A gastritis. (Internal Medicine 36: 787-789, 1997)
The ultrastructural changes of human or rabbit platelets in response to release inducers I were studied by using isolated cells from the respective platelet rich plasma. The changes of platelets were more dynamic in ADP than those in epinephrine and endotoxin though common changes occurred in all cases. In the platelets on release reaction, there were well preserved alphagranules and the disappearance of very dense granules accompanied by simultaneous appearance of round vesicles. The contraction wave of the microtubules rarely occurred and the microfibrils increased in amount in the cytoplasm of platelets. The canalicular system in response to ADP alone is morphologically interpreted as the open canalicular system. On the other hand, epinephrine and endotoxin did not cause obvious morphological changes of the open canalicular system. When the contents of very dense granules alone were discharged leaving the round vesicles behind in the release I, it seems likely that the microfibrils play a more important role than the microtubules. Furthermore, the author suggests that the dense tubular system or third canalicular system may play an essential role for the release I as a secretory pathway in place of the open canalicular system. ACTA PATHOL. JPN. 32: 961 N 980, 1982.
A case of a 44-year-old man with hepatic form of glycogenosis was presented. The patient had abdominal distension and muscular weakness. The glucose tolerance test showed a diabetic pattern, though he had hypoglycemia in fasting state. The fructose tolerance test showed an ability of conversion from fructose to glucose. The double glucagon test showed no rise of blood glucose in fasting state but a rise 2 hours after meal. These symptoms and laboratory data supported the clinical diagnosis of type I11 glycogenosis. At autopsy, glycogen was markedly deposited in the liver, and slightly in the kidneys and heart. The glycogen pooled in the hepatic cells histochemically showed a normal reaction to several glycogen stainings. Electron microscopy by using Thibry's method revealed that the pooled glycogen particles were clearly arranged as rosettes measuring 1,OOOA in largest diameter composed of clustered monoparticulates. There were marked hyalinization of the islets of Langerhans containing amyloid. As to its pathogenesis, this change can be interpreted as a morphological expression of the hypofunction of 8-cells ascribed to long-standing hypoglycemia. ACTA PATHOL. JPN. 30 : 599-612, 1980.
A 4-moth-old male infant predisposed to allergic dermatitis acquired widespread eczema vaccinatum by contacts with a recently vaccinated sibling. He died of acute purulent peritonitis following a perforation of multiple duodenal ulcers. Fluorescence immunocytochemical and electron microscopic studies on the skin lesions revealed the presence of viral antigens and numerous virus particles compatible morphologically with those of the mature form from the same batch of smallpox vaccine given to the sibling. A large number of virus particles in the developmental form were also predominantly scattered in the cytoplasm of cells at the stratum malpighii of the epidermis as well as in neutrophils and macrophages in the skin lesions. The virus isolation from the skin lesions was done by using the HeLa cells and the human embryonic lung fibroblasts. No abnormal laboratory data were noted in immunoglobulins. On the basis of atrophy of the thymus and other lymphatic tissues and an appearance of large pyroninophilic cells in association with blastoid transformation, the authors discussed a possible participation of the disturbance of cellular immunity secondary to the virus infection in the development of the disease. ACTA PATH. JAP. 29: 435-455, 1979.
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