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Biomedical subjects

K Tanikawa

Publications and source records attributed to K Tanikawa.

At least 181 records · Page 10Linked to original sources
PubMed1995

Relapsing polychondritis associated with subclinical Sjögren's syndrome and phlegmon of the neck.

A 25-year-old woman, diagnosed with Sjögren's syndrome at age 20, presented with painful edema of her left neck. Three days later, she additionally complained of bilateral auricular pain, and her nasal cartilage was tender to palpation. She was diagnosed as having phlegmon on the basis of her neck findings. Anti-human cartilage antibodies were demonstrated by indirect immunofluorescence, and the diagnosis of relapsing polychondritis was established. The patient was administered antibiotics and a non-steroidal anti-inflammatory drug, and her symptoms gradually improved. Relapsing polychondritis is one of the possible complications of autoimmune diseases, and infection might be a precipitating factor for this disease.

Adult↗
PubMed1995

A case of acute exacerbation of chronic hepatitis B accompanied by antibody to HBeAg with remission of liver damage after long-term treatment with interferon.

The patient was a 47-year-old female with chronic hepatitis B having antibody to HBe antigen (HBeAg). She was admitted to our hospital in March, 1994, because of acute exacerbation of chronic hepatitis B. Laboratory data revealed the elevated serum transaminase and DNA-polymerase levels, and decreased prothrombin activity. The histological examination of the liver showed chronic active hepatitis with severe hepatic necrosis. Point mutation of the precore region of HBV-DNA (pre-C mutant) was observed in clones from this case by polymerase chain reaction method. The patient was treated with recombinant interferon alpha-2a 9 MU daily for 2 weeks and thereafter 3 times weekly for 6 months. After interferon therapy, the pre-C mutant disappeared with the improvement of transaminase levels and prothrombin activity. These findings suggest the possibility that long-term treatment with interferon therapy is effective for the acute exacerbation of chronic hepatitis B accompanied by antibody to HBeAg.

Chronic Disease↗
PubMed1995

Thyroid dysfunction induced by interferon therapy for the treatment of hepatitis type C. A report of 4 cases.

We describe 4 patients with onset or aggravation of thyroid dysfunction induced by interferon (IFN) treatment of hepatitis type C. All 4 patients were females; 2 had hyperthyroidism and 2 had hypothyroidism during or after IFN therapy. The onset or aggravation of thyroid dysfunction occurred during administration of IFN in 1 patient and 4 weeks after the end of IFN therapy in the remaining 3 patients. The 2 patients who demonstrated hyperthyroidism were euthyroid and negative for thyroid autoantibodies before receiving IFN therapy. The remaining 2 patients who demonstrated hypothyroidism were positive for thyroid autoantibodies before IFN therapy. One of these patients had a slight decrease in thyroid function before IFN therapy. Anti-thyroid stimulating hormone (TSH) receptor antibodies became positive in all 4 patients. Since there may have been a causal relationship between IFN therapy and the onset or aggravation of thyroid dysfunction, IFN therapy should be administered with caution.

Adult↗
PubMed1995

Clinical evaluation of intramuscular administration of natural interferon-gamma in the treatment of chronic hepatitis B.

Natural interferon-gamma at a dose of 0.5 x 10(6) or 1 x 10(6) IU daily was intramuscularly administered daily for 4 weeks to 15 patients with chronic hepatitis B. The efficacy and safety of the treatment were evaluated for 24 weeks following the completion of the 4-week treatment period. Persistent disappearance of HBeAg was observed in 5 of 15 patients. Serum hepatitis B virus (HBV)-related DNA polymerase disappeared in 5 of 13 patients at the end of interferon therapy. On the other hand, serum ALT and beta 2-microglobulin levels showed a significant increase during the interferon therapy period. The side effects were completely reversible. These findings suggest that interferon-gamma has an antiviral effect in patients with chronic hepatitis B and that the main mechanism of the therapeutic effect may be associated with the elimination of HBV-infected hepatocytes due to the immunopotentiating effect of the substance.

Adult↗
PubMed1995

Transforming growth factor beta 1, extracellular matrix, and inflammatory cells in wound repair using a closed duodenal loop pancreatitis model rat. Immunohistochemical study.

BACKGROUND: Serial changes in the localization of various components of extracellular matrix in acute pancreatitis have been reported, but there have been no reports on serial changes in the localization of transforming growth factor beta and the determination of cells producing extracellular matrix. METHODS: In this study serial relationships between the localization of transforming growth factor beta 1, fibronectin and type-III collagen, inflammatory cells, and serum amylase levels in the process of tissue repair in acute pancreatitis were studied using a closed duodenal loop model rat. Furthermore, the cells producing transforming growth factor beta 1, fibronectin, and type-III collagen were investigated by immunoelectron microscopy. RESULTS: Three to 6 h after duodenal ligation slight localization of transforming growth factor beta 1 and fibronectin and inflammatory cell infiltration were observed in the interlobular space. Twelve to 24 h after duodenal ligation the infiltration of polymorphonuclear leukocytes and the deposition of transforming growth factor beta 1 and fibronectin were observed extensively in the interlobular and intralobular spaces. After release of the loop, infiltration of fibroblasts and marked deposition of fibronectin and type-III collagen were observed around the tubular complexes, but the deposition of transforming growth factor beta 1 was slight. Also, fibronectin and type-III collagen were shown to be produced by fibroblasts and acinar cells. CONCLUSIONS: These findings suggest that transforming growth factor beta 1 appears at the injured sites from the early stage of acute pancreatitis. Moreover, it is extensively related to the production of extracellular matrix such as fibronectin and type-III collagen. Furthermore, these substances are closely involved in the healing process of acute pancreatitis.

Acute Disease↗
PubMed1995

Leukocyte adhesion molecules in the liver and plasma cytokine levels in endotoxin-induced rat liver injury.

BACKGROUND: The interactions between polymorphonuclear neutrophils (PMNs) and sinusoidal endothelial cells (SECs) have been known to be involved in the pathogenesis of acute liver injury. It has been also reported that tumor necrosis factor-alpha (TNF-alpha) up-regulates ICAM-1 expression on SECs and that interleukin-8 (IL-8) provokes rapid activation of CD11/CD18 on PMNs. These findings expand into the relationship between the expression of leukocyte adhesion molecules (ICAM-1, CD11a/CD18 and CD11b/CD18) in liver tissues and plasma TNF and IL-8 levels after lipopolysaccharide (LPS)-induced liver injury in rats. METHODS: Male Wistar rats weighing 200-250 g were treated with 2 mg LPS/kg intravenously in a 0.2- to 0.25-ml volume. Liver and blood samples were obtained at 1, 3, 8, and 12 h after LPS exposure. Plasma TNF and IL-8 levels were measured using bioassay and specific enzyme-linked immunosorbent assay, respectively. Liver samples were fixed and studied by immunohistochemistry using specific monoclonal antibodies against ICAM-1, CD11a, and CD11b. RESULTS: The TNF level showed a peak at 1 h (23.3 +/- 11.4 IU/ml), and the IL-8 level showed a peak at 3 h (343.1 +/- 110.5 ng/ml) after LPS exposure. An increase in the number of PMNs in the liver was observed as early as 1 h and continued until 12 h after LPS exposure. PMNs adhered to degenerated SECs and hepatocytes. ICAM-1 on SECs was diffusely and strongly expressed at 8 h, and PMNs adhered to SECs expressed both CD11a and CD11b. ICAM-1 was also observed on hepatocytes. CONCLUSION: These data suggest that PMN-SEC and PMN-hepatocyte interactions via leukocyte adhesion molecules, related to inflammatory cytokines such as TNF and IL-8, exist and play an important role in the pathogenesis of acute liver injury.

Animals↗
PubMed1995

Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism.

We performed a partial splenic arterial embolization in 22 patients with cirrhosis associated with thrombocytopenia and then evaluated the changes in platelet kinetics after undergoing the procedure using 111In-tropolone-labeled platelets. The controls consisted of eight chronic hepatitis patients who showed a normal platelet count and normal spleen size. The mean splenic infarction ratio after the procedure was 54.9%. A platelet kinetics study was performed before and 2 months after the procedure. Before the procedure, the cirrhotic patients showed increases in the splenic volume and the spleen/liver uptake ratio of the 111In-labeled platelets on both the third and seventh days, and a decrease in the platelet recovery compared with the controls, which suggested an increased platelet pool in the spleen. In addition, the platelet survival time in cirrhotic patients was shortened, whereas the platelet-associated immunoglobulin G (PA-IgG) was higher than that of the controls, which suggested the involvement of immunologic mechanisms in the thrombocytopenia. With an increase of the platelet count after a partial splenic arterial embolization, the spleen/liver uptake ratio of the 111In-labeled platelets decreased, whereas the platelet recovery increased. Furthermore, the platelet survival time was prolonged, whereas the PA-IgG decreased. The platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG before and after the procedure. These results suggest that a transcatheter splenic arterial embolization not only may reduce the increased platelet pool in the spleen but also may improve the thrombocytopenia induced by immunologic mechanisms in patients with cirrhosis.

Adult↗
PubMed1995

Effects of extracellular matrices on tube formation of cultured rat hepatic sinusoidal endothelial cells.

To determine the effects of extracellular matrices on the function and morphology of hepatic sinusoidal endothelial cells, isolated rat hepatic sinusoidal endothelial cells were cultured in three-dimensional fashion on collagen gel containing various extracellular matrix components. Cells cultured on type I collagen gel with or without type IV collagen formed a cobblestone appearance on the surface of the gel. Cells cultured on laminin-containing type I collagen gel invaded the gel and exhibited three-dimensional tube formation with a decreased number of characteristic endothelial pores. Morphometrically, there was a significant relationship between the length of the tube formed and the concentration of laminin in the type I collagen gel. Cells cultured on Matrigel, which contains high concentrations of laminin, type IV collagen, fibroblast growth factor, tissue plasminogen activator, and other growth factors, formed a great number of tubes into a network on the surface of the gel, as is observed in the situ hepatic sinusoidal endothelial cells. Ultrastructurally, tube-forming endothelial cells cultured on Matrigel had many endothelial pores on the cell surface, with tubes (approximately 10 microns in diameter) formed by two or three hepatic sinusoidal endothelial cells. These results indicated that extracellular matrix components, especially laminin, induced the formation of tubes in cultured rat hepatic sinusoidal endothelial cells. Tube-forming sinusoidal endothelial cells cultured on Matrigel could provide more advantages than the two-dimensional culture model for investigating the function and morphology of these cells in vitro.

Animals↗