Studies on Duodenal Cyclic AMP Content in Pancreatic Disease after Administration of Pancreozymin and Secretin

Cyclic AMP (cAMP) output in the duodenal contents of 11 normal subjects, 18 patients with chronic pancreatitis, six convalescing from acute pancreatitis and five with pancreatic carcinoma was measured after a single dose of pancreozymin and secretin. The technic was indirect, utilizing recovery of duodenal contents by the Dreiling tube rather than direct measurements of fluid that was not contaminated by bile. In all patients groups, cAMP output reached a peak after this stimulation with a concomitant increase of bicarbonate and amylase outputs. A significantly decreased cAMP output was observed in all pancreatic disease groups compared to the normal group. Patients with chronic pancreatitis showed a slightly decreased cAMP output, considerably decreased bicarbonate output and normal amylase output. In acute pancreatitis cAMP output was reduced with normal bicarbonate and amylase outputs. In pancreatic carcinoma cAMP decreased significantly, bicarbonate output was moderately reduced and amylase output was normal. cAMP output in all groups studied did not correlate with either bicarbonate output or amylase output.     

Malignant Mesenchymoma of the Liver with Hypercalcemia Report of a Case

A case of malignant mesenchymoma of the liver is reported. Thediagnosis was confirmed on the surgical specimen. The patientshowed marked hypercalcemia. Parathyroid hormone assay was negative.     

A Case of Pachydermoperiostosis with Watery Diarrhea,Giant Gastri Rugae,and Endocrine Disorder

Abstract: A 31-year-old man, cook, who had had persistent watery diarrhea for about a month visited our hospital. He had already been diagnosed as having pachydermoperiostosis. An examination of the upper gastrointestinal tract revealed that he had giant gastric rugae. The histology was compatible with hypertrophic gastritis accompanied with marked hyperplasia of the fundic gland and foveolar epithelia. The output of gastric juice was high in volume, although its acidity normal. The barium transit time of the small intestine was reduced to 15 minutes. His diarrhea was, thus, considered to be induced by gastrointestinal hyperfunction. The patient's glucose tolerance was abnormal and basal Cortisol secretion level was high. Pachydermoperiostosis has been the focus of attention for skin and bone changes, and the frequency of this disease with endocrine disorders seems rather high, but accompanying gastrointestinal disorders have so far not often been reported in Japan. The results of our investigation strongly suggest that pachydermoperiostosis is a systemic disease.     

Monoclonal antibody HML-1 reactivity with adult T-cell leukaemia/lymphoma and other lymphomas

Human T-cell leukaemia/lymphoma virus type 1 (HTLV-1), a causative virus of adult T-cell leukaemia/lymphoma (ATLL), is known to be transmitted by breast-feeding. Using a monoclonal antibody HML-1 which labels human intestinal intra-epithelial T lymphocytes, we have immunohistochemically examined ATLL tissues in order to evaluate the possibility that HTLV-1 infected intestinal T cells are the origin of ATLL cells. Previously this antibody was reported to react with intestinal T-cell malignant lymphomas but not with peripheral tumours, or any B-cell lymphomas. We investigated 181 patients with malignant lymphomas and found that 19 out of 113 ATLLs were positive for HML-1. T-cell malignant lymphomas excluding ATLL also reacted with HML-1 (7/24), but all the B-cell lymphomas 0/33) and non-neoplastic lymph node and skin lesions (0/10) were negative for HML-1. In patients with ATLL and other T-cell malignant lymphomas, the positivity level of HML-1 was relatively higher in stomach (3/7) and tonsil (2/6) than that in lymph nodes (15/100) and skin (8/47). We observed one HML-1 positive ATLL patient with tumour formation in the skin and lymphadenopathy and marked infiltration of the large intestine but minimal involvement of other organs. Although HML-1 was frequently expressed in gastric infiltration of ATLL, the level of positivity was too low in lymph nodes to support the hypothesis that HTLV-1 infected intestinal T cells are the origin of ATLL cells. Some of the HML-1 positive ATLL cases co-expressed CD30. Furthermore, three of six cases of Ki-1 lymphoma (large anaplastic cell lymphoma) were positive for HML-1. We conclude that expression of HML-1 in ATLL reflects an activated state of the lymphoma cells, but not the intestinal origin of ATLL cells.