Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old female was admitted for treatment of refractory myeloma (IgG-lambda). Because of severe liver cirrhosis, the patient was treated with interferon (IFN) alone (natural IFN 6 x 10(6) IR/day i.m. for 28 days). Pneumonia developed during IFN therapy. The IFN therapy was completed, restoring suppressed IgM and IgA to their normal ranges, while pneumonia was cured by antibiotics. Because the M-component remained, an additional IFN therapy was resumed and M-protein disappeared. As the period within which the M-component disappeared in this case was shorter than that reported previously, we supposed that the pneumonia might have enhance the effects of IFN. To verify this, we administered OK-432 for 4 weeks as a model of immunoactivation by pneumonia between two successive courses of IFN therapy when M-protein reappeared. To monitor the immune state, natural killer (NK) and lymphokine activated killer (LAK) activities were measured: NK activity suppressed by IFN was restored by OK-432 and was suppressed less by subsequent IFN administration. LAK activity was increased by IFN and OK-432. These observations suggested synergic effects of OK-432 on IFN-activated immunity. This case suggests that IFN combined with immunotherapy may be effective in some cases of myeloma.
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PMID:[Rapid disappearance of M-protein in multiple myeloma complicated by pneumonia during treatment with HLBI]. 147 92

Malignant pleural or peritoneal effusion-associated lymphoid (EAL) cells from 17 patients with advanced carcinoma were cultured with autologous carcinoma cells in the presence of either recombinant interleukin 2 (rIL 2) or T-cell growth factor (TCGF). Considerable cytolytic activity of the cells against allogeneic tumor cells, such as K562 and Daudi cells was induced by the cultivation. TCGF-activated EAL cells acquired higher anti-Daudi tumor cytotoxicity than rIL 2-activated EAL cells. The resultant TCGF-activated EAL cells from cancer patients significantly exceeded lytic activity of TCGF-activated EAL cells from patients with liver cirrhosis for control (p less than 0.01). Four of 6 cases examined also showed cytotoxic activity against autologous tumor. In facts, viable carcinoma cells co-cultured with EAL cells and TCGF mostly disappeared during 14 days. Similar phenomenon was not observed in rIL 2-activated EAL cells. Thus, it was suggested that more additional lymphokine other than IL 2 was necessary to generate cytotoxic activity against autologous tumor cells. The cell populations responsible for cytolytic activity to allogeneic and/or autologous tumor cells were investigated by two-color flow cytometry. The majority of killer-effector cells against allogeneic cells in rIL 2-activated EAL cells from cancer patients showed CD4+Leu8- phenotype at population level. In contrast, it was suggested that cytolytic activity against allogeneic and/or autologous tumor cells in TCGF-activated EAL cells might be mediated by CD8+ CD11- and CD8+ CD28+ effector cells.
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PMID:Functional and phenotypic characteristics of effusion-associated lymphoid cells cultured in the presence of either recombinant interleukin 2 or T-cell growth factor from malignant pleural and peritoneal effusions in patients with advanced carcinoma. 207 78

We investigated lipopolysaccharide-induced tumor necrosis factor production in vitro by peripheral blood monocytes from patients with various liver diseases. Tumor necrosis factor production was found to be significantly reduced in patients with chronic hepatitis B (n = 17; 135 +/- 30 pg tumor necrosis factor/ml; mean +/- S.E.M.) and patients with chronic non-A, non-B hepatitis (n = 15; 212 +/- 22 pg tumor necrosis factor/ml) compared with healthy control individuals (n = 47; 411 +/- 40 pg tumor necrosis factor/ml; p less than 0.0005 and p less than 0.01, respectively). This reduced tumor necrosis factor production was not only seen with an optimal stimulating concentration of lipopolysaccharide (100 ng/ml) but also with suboptimal concentrations (0.1 ng/ml). In contrast to patients with chronic viral hepatitis, monocytes from patients with alcohol-induced cirrhosis (n = 26; 444 +/- 49 pg tumor necrosis factor/ml), primary biliary cirrhosis (n = 7; 412 +/- 81 pg tumor necrosis factor/ml) and alcohol-induced fatty liver changes (n = 5; 401 +/- 62 pg tumor necrosis factor/ml) produced normal amounts of tumor necrosis factor when stimulated with an optimal concentration of lipopolysaccharide. Lipopolysaccharide (0.1 ng lipopolysaccharide/ml)-stimulated peripheral blood monocytes of patients with chronic hepatitis B (n = 15; 102 +/- 32 pg/ml) or non-A, non-B hepatitis (n = 13; 97+/- 16 pg/ml) could not be induced to produce more tumor necrosis factor either when prestimulated with gamma-interferon (170 +/- 45 pg/ml and 149 +/- 32 pg/ml, respectively), a lymphokine known to activate monocytes, or with the cyclooxygenase inhibitor indomethacin to reduce the suppressive effect of prostaglandin E2 (148 +/- 40 pg/ml and 153 +/- 45 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired lipopolysaccharide-inducible tumor necrosis factor production in vitro by peripheral blood monocytes of patients with viral hepatitis. 212 37

Fourteen days' culture of human spleen cells with recombinant interleukin-2 (rIL-2) or T-cell growth factor (TCGF) results in the generation of lymphokine-activated killer (LAK) effector cells that have the unique property of lysing natural killer (NK)-resistant human tumor cells, Daudi, and NK-sensitive K562 cells. LAK cells were generated from patients with advanced cancer or liver cirrhosis. The splenic LAK-effector cell types were analyzed by two-color flow cytometry. The rIL-2-induced LAK cells showed an increased proportion of CD8+CD11- and CD57+CD16- and a decreased proportion of CD4+Leu-8- cells. In contrast, TCGF-induced LAK cells revealed a significantly increased proportion of CD8+CD11- and CD4+Leu-8- cells and a decreased proportion of CD57+CD16- cells. Thus, splenic LAK cells with different surface phenotypes were induced by the cultivation with rIL-2 or TCGF. Furthermore, TCGF-induced LAK cell activities in patients with cancer were found to be lower than the rIL-2-induced LAK cell activities. It was noted that the TCGF-activated splenic lymphoid cells did not inhibit the effector process of tumor cell lysis by LAK cells that had been activated by rIL-2. Other mechanisms of lower LAK cell activities of TCGF-activated splenic lymphoid cells from patients with cancer were discussed. The findings suggest that spleens of examined patients with gastric or hepatocellular carcinoma do not seem to be responsible for suppression of cell-mediated antitumor immunity.
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PMID:Functional and phenotypic characteristics of recombinant interleukin-2 or T-cell growth factor-activated splenic lymphoid cells from patients with gastric or hepatocellular carcinoma. 216 47

Hepatocellular carcinoma (HCC) patients can be divided into two groups according to the degree of lymphokine activated killer (LAK) cell activity; a high LAK activity group (H-LAK-HCC) and a low LAK activity group (L-LAK-HCC). Interferon-gamma (IFN-gamma) production is severely defective in L-LAK-HCC but not defective in H-LAH-HCC. IFN-gamma production is suppressed with the addition of anti-Tac in dose dependent manner, though LAK activity is suppressed only in the presence of high concentration of anti-Tac. LAK activity is suppressed with the addition of anti-IFN-gamma, which is most prominent when the antibody is present during the first 12 hr of incubation. LAK generation is enhanced with the addition of recombinant IFN-gamma, which is most prominent when it is present during the first 12 hr of incubation. However, this enhancing effect is less prominent in L-LAK-HCC as compared to normals, liver cirrhosis, and H-LAK-HCC. This enhancement is regarded to depend on the presence of Leu7+ and Leu11+ subset, as this enhancement is abandoned and IFN-gamma production is inhibited when either of these subsets is deleted. These data suggest that IFN-gamma production and the participation of Leu7+ and Leu11+ subsets is important in sufficient LAK generation, and that poor IFN-gamma production and insufficient response to IFN-gamma may be the cause of severely defective LAK generation in L-LAK-HCC.
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PMID:Enhancement of depressed lymphokine activated killer cell activity in patients with hepatocellular carcinoma. 216 82

Lymphokine-activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Maximum lymphokine-activated killer activity was induced at 3 to 5 days of incubation, and lymphokine-activated killer activity tended to increase in a manner dose dependent of recombinant interleukin-2. However, the maximum increase of lymphokine-activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients. Lymphokine-activated killer activity was impaired in hepatocellular carcinoma as compared to that in normal subjects. Hepatocellular carcinoma seemed to consist of two groups: i.e. a high-lymphokine-activated killer activity group and a low-lymphokine-activated killer activity group. Reduction of natural killer activity was also observed in hepatocellular carcinoma as compared with that in normal subjects and patients with liver cirrhosis. No correlation could be demonstrated between natural killer activity and lymphokine-activated killer activity in normal subjects, liver cirrhosis patients and hepatocellular carcinoma patients. With regard to the presence of HBsAg or alpha-fetoprotein concentration in the sera, there was no significant difference in natural killer and lymphokine-activated killer activity in hepatocellular carcinoma patients. Patients with a small mass lesion showed a low lymphokine-activated killer activity, and depressed lymphokine-activated killer activity was not necessarily related to tumor size. In comparison with the high-lymphokine-activated killer group, the low-lymphokine-activated killer group showed a significant decrease in gamma-interferon production and a preserved function of indocyanine green clearance.
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PMID:Defective function of lymphokine-activated killer cells and natural killer cells in patients with hepatocellular carcinoma. 253 90

Interleukin-2 has proved to be effective for the intralesional treatment of tumors of the bladder. There are examples in literature of hepatocellular carcinoma (HCC) treatment with lymphokine-activated killer (LAK) cells infused in the hepatic artery. We decided to check the effects of echo-guided intralesional injection of these cells in this disease. We treated 5 patients with inoperable hepatocellular carcinoma, following cirrhosis; in 4 cases the mass had a diameter less than 3 cm (small HCC) while in the remaining case it measured 7 cm. Tumor size remained unchanged in 3 of the 4 small HCC, and increased only slightly in the other (over a period of 10 months). This would appear to indicate that treatment halted neoplasm growth or at least slowed it down. The echo pattern of the lesions changed, with a constant reduction in echogenicity. Finally, in multiple control biopsies, fibrosis, present in only one case before treatment, was found fairly constantly after treatment. There were no significant side effects, apart from slight water retention in one patient. On the basis of our preliminary results, we consider it worthwhile continuing this study to establish the most suitable IL-2 doses and analyze in more detail the modifications induced in the neoplasm.
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PMID:Intratumoral echo-guided injection of interleukin-2 and lymphokine-activated killer cells in hepatocellular carcinoma. 255 85

To investigate whether disordered immune function, as shown by abnormalities in lymphokine production, is present in alcoholic liver disease, interleukin-1 and interleukin-2 activity were assayed in a group of patients with acute alcoholic hepatitis in the absence of underlying cirrhosis, and a group of patients with inactive alcoholic cirrhosis. Activities of both IL-1 and IL-2 in alcoholic hepatitis were similar to those of normal individuals, although in abstinent patients with alcoholic cirrhosis, IL-1 activity was increased and IL-2 activity decreased. Lymphocyte transformation in response to PHA in patients with alcoholic hepatitis was significantly impaired when compared with normal controls, and addition of exogenous IL-2 did not correct this impaired response over a wide range of concentrations of both PHA and IL-2. These observations suggest the underlying defects in cell mediated immunity in acute alcoholic hepatitis, as assessed by blast transformation, could be fundamentally different from those of alcoholic cirrhosis and could be secondary to the metabolic effects of acetaldehyde or altered redox potentials on the behaviour of proliferating cells.
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PMID:Contrasts in interleukin-1 and interleukin-2 activity in alcoholic hepatitis and cirrhosis. 262 42

Abnormalities of lymphocyte proliferation in chronic hepatitis B virus infection are well documented, although the underlying mechanisms are poorly understood. To determine whether these defects may be secondary to disordered lymphokine production, we have simultaneously assayed interleukin-1 and interleukin-2 production in 31 chronic carriers of the hepatitis B virus. Supernatants from mononuclear cells cultured both in the presence and absence of lipopolysaccharide contained significantly increased quantities of interleukin-1 activity in patients compared with normal controls (p less than 0.01). Lysates of monocytes from patients also contained more interleukin-1 than those of controls (p less than 0.05) in the presence of lipopolysaccharide or silica, or both. These results indicate that interleukin-1 production is markedly elevated in patients with chronic hepatitis B virus infection, whereas in contrast, interleukin-2 production was found to be reduced in these patients (p less than 0.01). As one of the biological properties of interleukin-1 is to stimulate fibroblasts to produce collagen, the relationship between fibrosis in the liver biopsy specimen and interleukin production was examined. There was a highly significant correlation (p less than 0.001) between interleukin-1 production and the severity of fibrosis, suggesting that this lymphokine may be closely related to the development of cirrhosis in such patients.
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PMID:Interleukin-1 and interleukin-2 activity in chronic hepatitis B virus infection. 325 34

Continuing hepatic injury despite cessation of ethanol intake has suggested a potential role for altered humoral and cellular immunity in the pathogenesis of alcoholic liver disease. Variation of cell-mediated response has been observed most commonly in patients with alcoholic hepatitis. These alterations include decreased mitogen response in vitro, reduction of circulating T-cell numbers with a corresponding increase of intrahepatic T-cells, lymphokine production in vitro in response to isolated alcoholic hyalin (Mallory bodies), and in vitro evidence of increased spontaneous cell-mediated cytotoxicity. Fewer immunologic alterations are detected in patients with alcoholic fatty liver or cirrhosis. At present, these observations have not established a definite causal relationship between ethanol-induced liver injury and immunologic mechanisms. Studies utilizing in vitro correlates of cellular immunity in alcoholics are carried out after development of hepatic injury. To establish the role of humoral and cellular immune events in the pathogenesis of alcoholic liver injury will require development of a suitable animal model.
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PMID:Immunologic aspects of alcoholic liver disease. 616 11


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