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Biomedical subjects

I Aoki

Publications and source records attributed to I Aoki.

At least 181 records · Page 10Linked to original sources
PubMed1980

Adenosquamous carcinoma of the pancreas: a clinicopathologic study and report of three cases.

Among 27 surgically resected carcinomas of the pancreas, 3 cases were diagnosed histologically as adenosquamous carcinoma (11.1%). This is the highest rate among the medical literature we reviewed. Since a very small focus of squamous cell carcinoma was detected through close observation in 1 case, it would seem that this sort of pancreatic tumor could be more common than is ordinarily expected. From the histologic studies of these 3 cases, it seems likely that the preexisting adenocarcinoma partially underwent malignant transformation into a malignant squamous component. When the different modes of spread of these two histologic elements are compared, the adenocarcinomatous element seems to be more invasive and more likely to metastasize than does squamous cell carcinoma.

Adenocarcinoma↗
PubMed1978

Budd-Chiari syndrome associated with protein-losing enteropathy.

Budd-Chiari syndrome associated with protein-losing enteropathy is reported. A 26-year-old male suffered from ascites, edema in the lower extremities, and engorgement of ascending veins on the abdominal wall. The diagnosis of Budd-Chiari syndrome was made by inferior vena cavography. The 131I-polyvinylpyrrolidone test showed the association of protein-losing enteropathy. The surgical operation was performed successfully, resulting in a marked improvement of signs and symptoms. To date, no similar case has yet been reported. There are, however, a number of reported cases of hypoproteinemia in Budd-Chiari syndrome, which might have been associated with a protein-losing enteropathy.

Adult↗
PubMed1975

Pancreatic excretion of 5,5-dimethyl-2,4-oxazolidinedione in patients with chronic pancreatitis.

Abnormal pancreatic excretion of 5,5-dimethyl-2,4-oxazolidinedione (DMO) was demonstrated in 44 patients with chronic pancreatitis (14 with calcification and 30 without calcification). Pancreatic excretion of DMO in patients with chronic pancreatitis, as well as in normal subjects, depended on plasma DMO concentration and secretory volume. In the postsecretin 60-min period, almost all patients showed a decrease in total DMO output of duodenal aspirate over the observed range of plasma DMO concentration. More than half the patients without calcification gave a discordant pattern between the DMO output and volume, ie, decreased DMO output with normal volume secretion, while most of patients with calcification had low DMO output with decreased volume flow. The data of the pancreozymin-secretin test suggested that chornic pancreatic inflammation was moderate or minimal in patients without calcification and far advanced in those with calcification. From these results the hypothesis was advanced that DMO diffusion into the pancreatic ducts might be primarily impaired in the relatively early stage of chronic pancreatitis, and as the inflammation progressed to the final stage, DMO outflow from the ducts to the duodenum would be disturbed with evolving diffusion impairment of the compound. Total DMO output, when expressed as the output at a level of 10 mg/100 ml of plasma DMO (standard DMO output), was significantly reduced in chronic pancreatitis during a 60-min period after secretin stimulation. DMO in duodenal content, when expressed in terms of maximal concentration ratio of duodenal juice/plasma for the compound (maximal J/P ratio), was significantly low in chronic pancreatitis during the last 40-min period after secretin stimulation. These two parameters can therefore be used as indices of pancreatic excretion of DMO. The present technique may well become an effective diagnostic tool for early detection of chronic pancreatitis.

Adult↗