Hitoshi Funatomi

A case of autoimmune pancreatitis complicated with immune thrombocytopenia during maintenance therapy with prednisolone.

A unique form of chronic pancreatitis, primary inflammatory sclerosis of the pancreas, which may result from an autoimmune mechanism, was first reported by Sarles et al (1). Since then, several authors have reported similar cases, and Yoshida et al (2) first proposed the concept of autoimmune pancreatitis. One of the characteristics of so-called autoimmune pancreatitis is an occasional association with other autoimmune diseases such as Sj ̈ ogren’s syndrome (3), primary biliary cirrhosis (4), and primary sclerosing cholangitis (4, 5). However, autoimmune pancreatitis rarely associates with immune thrombocytopenia, and only one case has been previously reported in the Japanese literature (6). According to this report, autoimmune pancreatitis and immune thrombocytopenia occurred concomitantly. We report a case complicated with immune thrombocytopenia during maintenance therapy with prednisolone for autoimmune pancreatitis. In our case, elevation of serum level of total immunoglobulin (Ig) G was thought to be suggestive of the development of other autoimmune disease, and the determination of IgG subclass would provide a useful tool to differentiate exacerbation of autoimmune pancreatitis from the development of other autoimmune disease.

Hepatocyte growth factor stimulates cell growth and enhances the expression of transforming growth factor α mRNA in AsPC-1 human pancreatic cancer cells

Abstract: We investigated the effects of hepatocyte growth factor (HGF) and transforming growth factor α (TGF α) on cell growth in four human pancreatic cancer cell lines. Changes in the expression of mRNAs of HGF, c-met, TGF α, and epidermal growth factor receptor (EGFR) by treatment with HGF and TGF α were observed. Cell growth with growth factors was assessed with the MTT assay and compared with basal growth without growth factors. Although HGF stimulated cell growth in AsPC-1, COLO-357, and T3M4 cells, Panc-1 cells showed no response to HGF. TGF α stimulated the growth of all the above cells. The expression of c-met mRNA under nonstimulated conditions was detected with Northern blotting in all cells. Treatment with HGF slightly enhanced the expression of c-met mRNA only in COLO-357 cells. The intensity of EGFR expression was consistent, and HGF mRNA was not detected during induction experiments in any cell type. Concomitant treatment with HGF and TGF α exerted an effect that was additive or less on the growth of all cells. Expression of TGF α was enhanced by HGF treatment only in AsPC-1 cells. These results suggested that HGF and TGF α stimulated cell growth through a final common pathway of signal transduction.

Hyperamylasemia and S-type isozyme dominance in liver cirrhosis

SummaryTo investigate the mechanisms of serum amylase abnormalities in liver disease, we determined serum amylase levels, S-type isozyme proportion, clinical symptoms, and laboratory data in 38 cases of histologically confirmed liver cirrhosis and 19 controls. Of the 12 patients who were hyperamylasemic (12/38, 32%), 5 showed S-type isozyme dominance (5/12, 42%), whereas in the 26 normoamylasemic cirrhosis patients, only 5 were S-type isozyme dominant (5/26, 19%). Isozyme percentages were significantly higher (P<0.01) in the dominant-S-type cases than in the controls, and S-type dominance was found more frequently in the hyperamylasemic than in the normoamylasemic cirrhosis cases. Only ascites and esophageal varices were observed more frequently as clinical symptoms in the dominant-S-type cases. Our results suggest that amylase is not produced in the human liver, but that the decreased clearance rate of amylase, especially the S-type isozyme, may be a cause of hyperamylasemia and S-type isozyme dominance in cirrhosis.

Changes in immunoreactive insulin, C-peptide immunoreactivity, and immunoreactive glucagon in acute viral hepatitis

Insulin and glucagon are thought to play important roles as hepatotrophic factors in acute viral hepatitis (AVH); however, few reports have investigated the responses and relationships of each of these hormones to liver damage in detail. We studied insulin and glucagon responses during the acute and recovery phases of AVH. We performed a glucose tolerance test (GTT) and an insulin sensitivity test (IST) in each phase in 11 patients with AVH. In 8 additional patients in the acute phase (totaln=19), were compared immunoreactive insulin (IRI) and C-peptide immunoreactivity (CPR) levels with transaminase levels. In the acute phase, IRI concentrations were normal from fasting to 60 min, despite an increased CPR level. In the recovery phase, IRI and CPR levels increased significantly. Immunoreactive glucagon levels in both phases did not differ significantly from those in controls. During the IST, the insulin sensitivity index in both phases was significantly lower than that in the controls. Fasting IRI and ΣIRI showed significant negative correlations with transaminase levels. We found enhanced insulin secretion and a decrease in plasma insulin in the acute phase of AVH. The discrepancy between IRI and CPR responses in the acute phase suggests an increase in the degradation or consumption of insulin in the liver.