Immunohistochemical study of fibronectin, lysozyme, and alpha-fetoprotein (AFP) in human hepatocellular carcinoma

We have immunohistochemically localized fibronectin, lysozyme and alpha-fetoprotein (AFP) in 21 human hepatocellular carcinoma (HCC) tissues obtained by surgical resection at both light and electron microscopic levels. Three distinct distribution patterns of fibronectin (sinusoidal, periacinar, and pericellular patterns) were observed. The sinusoidal and periacinar patterns were mainly observed in HCC of pseudoglandular or trabecular patterns and of Edmondson's grade I or II, whereas the pericellular pattern was observed in HCC of compact or trabecular patterns and of Edmondson's III grade, suggesting that the pericellular fibronectin was rather associated with undifferentiated HCC. Electron microscopic observation of the pericellular fibronectin showed fibronectin to be present in the dilated intercellular spaces where microvilli were moderately developed. We observed intracytoplasmic staining of fibronectin in 2 of the 21 HCC cases. By immunoelectron microscopy, fibronectin was observed in the endoplasmic reticulum (ER) of some HCC cells. In the 21 HCC cases, lysozyme-positive cancer cells were observed in 10 cases, and AFP in 6 cases. At the ultrastructural level, lysozyme was identified in the ER and the perinuclear spaces of HCC cells, suggesting that lysozyme was synthesized by these cells. Lysozyme-positive cases tended to be more frequently observed in cases with the pericellular pattern of fibronectin rather than those with sinusoidal or periacinar patterns.     

Pyogenic liver abscess after choledochoduodenostomy for biliary obstruction caused by autoimmune pancreatitis

INTRODUCTION The differentiation of autoimmune pancreatitis (AIP) from pancreatic cancer is sometimes difficult because these diseases share many clinical features[1]. When pancreatic cancer cannot be ruled out, laparotomy or pancreatic resection may be p…     

Mesenteric panniculitis presenting as liver dysfunction

Mesenteric panniculitis is a non-specific inflammatory disorder affecting adipose tissues of the mesentery. Mesenteric adipose tissues contain macrophages and other inflammatory cells, which may secrete tumor necrosis factor ??, interleukin (IL)-1, and IL-6. These cytokines collect into the portal vein and thereby flow into the liver, possibly influencing hepatic function. Mesenteric panniculitis often occurs with inflammatory reactions such as fever and elevated erythrocyte sedimentation rates. Systemic inflammatory disorders can evoke acute cholestatic liver involvement, which is mediated by proinflammatory cytokines. However, no reports have focused on the association between mesenteric panniculitis and liver involvement. We report a rare case of mesenteric panniculitis presenting as liver dysfunction. Immunohistochemical staining of the liver demonstrated a marked decrease in expression of canalicular transport systems. These findings indicated cholestatic liver dysfunction associated with mesenteric panniculitis.     

HLA typing of a family with nephronophthisis-medullary cystic disease complex

A 25-year-old man developed renal dysfunction and his family showed autosomal dominant inheritance of endstage renal disease. The proband had trace albuminuria and a slightly raised serum creatinine level. Renal biopsy showed tubulointerstitial nephritis, which was compatible with the nephronophthisis-medullary cystic disease complex (N-MCD). His older brother (aged 31 years) had progressed to endstage renal failure by the age of 23 years after renal biopsy revealed N-MCD when he was 20 years old. Human leukocyte-associated (HLA) antigen typing was performed for the proband, the older brother, the mother (who showed endstage renal failure at the age of 50 years), and the sister (who showed no signs of renal disease at the age of 28 years). The HLA loci A24(9), B62(15), and DR2 were common to all 4 family members, while Cw1 was only found in the 3 with renal disease. These findings suggested the possible participation of the Cw1 locus in autosomal dominant N-MCD.     

Clinical and histological features of sporadic non-A, non-B hepatitis

The incidence of hepatitis A (HA), hepatitis B (HB), and non-A, non-B hepatitis (NANBH) was 27%, 30% and 43% among 73 patients with sporadic hepatitis. Epidemiological data (geographical distribution, seasonal variation, age, sex, and occupation) were not distinguishing of the type of hepatitis. Neither intrafamilial infection nor previous contact with viral hepatitis patients could be demonstrated in the NANBH cases. Fever and jaundice were less frequent in NANBH than in HA. Maximum levels of SGPT, serum bilirubin, ZTT, and gamma-globulin were significantly lower in NANBH than in HA and HB. Ten of 29 NANBH patients (35%) presented abnormal SGPT activities for more than 6 months, and four (14%) more than 12 months. In the ten patients with prolonged courses, jaundice was more frequent and maximum levels of SGPT were higher than in patients with transient courses. Histopathologic findings were not markedly different from those of HA and HB. Bile duct damage, fatty deposition, and giant multi-nucleated cells were recognized in 6, 12, and 2 NANBH patients, respectively. There were no characteristic ultrastructural changes in NANBH.     

Low-density lipoprotein apheresis for focal glomerular sclerosis.

We report on a 22-year-old female with focal glomerular sclerosis and hyperlipidemia who did not respond to long-term steroid or immunosuppressant therapy. When low-density lipoprotein (LDL) apheresis was performed, her total daily protein excretion decreased, serum albumin increased, total cholesterol decreased from 1,052 mg/dl to 148 mg/dl after 3 months, and the serum lipoprotein(a) level also decreased from 117.8 mg/dl to 9.1 mg/dl. After this therapy, her clinical course was well maintained. By controlling hyperlipidemia, including oxidized low-density lipoprotein and lipoprotein(a), low-density lipoprotein apheresis may produce clinical improvement in focal glomerular sclerosis.