in the pathogenesis of chronic active hepatitis the importance of spell out then abbreviate cmi has been emphasized .
the hepatitis b virus is cleared by cytotoxic t - lymphocyte if the clearing is defected , inflammation progresses .
goldyne and goldyne and stobb reported that monocytes play an important role in the regulation of several immunologic responses .
monocytes exert this regulatory function which seems to be due to the production of pge2 is known to suppress various lymphocyte functions ( t - cell cytotoxicity , lymphokine production and cytotoxicity ) .
lymphocyte hyporesponsiveness in cirrhosis has been shown to be mediated by prostaglandins produced by monocytes , as t - cell proliferative response has been depressed in hodgkin s disease and pge2 also plays an important role in the regulation of natural killer cells .
the effect of prostaglandins on the cell is thought to be mediated by their ability to bind to membrane receptors causing an increase in the intracellular cyclic adenosine 5-monophosphate ( camp ) levels .
the authors studied plasma pge2 assay to determine relationship between the plasma pge2 and chronic active hepatitis .
the study group consisted of the patients with chronic active hepatitis and hepatitis b virus carriers who had been hospitalized or visited the internal medicine department , chonbuk national university hospital from jun .
1 ) . group i consisted of 7 normal control subjects who had not been previously exposured to the hepatitis b virus or who were asymptomatic but exposed to hepatitis b virus previously .
gorup ii consisted of 15 patients who had been diagnosed as having chronic active hepatitis by liver biopsy and strongly suggested or had chronic active hepatitis by clinical manifestation .
group iii consisted of 8 patients who were in the recuperative stage or stable stage of chronic hepatitis .
it is based on asymptomatic mild transaminase elevation ( lower than 150 u / l and one - third of the previous level ) which persist for 3 months and as hbeag disappeared , antihbe appeared .
the aqueous layer was then exposed to 3.0 ml of 3:3:1 ethyl acetate : isopropanol : 0.1 mhcl , apparent ph 5.8 and vortexed , and a mixture of 2.0 ml of ethyl acetate and 3.0 ml of water was added .
after further mixing , two phases were separated by centrifugation ( 2000 rpm for 5 min at ambient temperatures ) .
3 ml of the 3.5 ml organic phase were removed by aspiration and dried in air at 55c . after drying 0.5 ml assay buffer ( 0.9 nacl ,
0.01 m edta , 0.3% bovine l - globulin , 0.005% tritonx-100 , 0.05% sodium azide in 50 mm phosphate buffer ph 6.8 ) was added and the two phases were separated by centrifugation , 0.1 ml was removed by aspiration .
the mean plasma pge2 level was 2.650.69 pg / ml in the control group ( table 2 ) .
the mean plasma pge2 level was 9.070.89 pg / ml in 15 patients with chronic active hepatitis and was significantly higher than that of the control group ( p<0.01 ) ( table 3 ) .
the mean plasma pge2 level was 4.65  1.59 pg / ml in 8 patients in the recuperative stage or stable stage of chronic hepatitis and tended to decrease . however , this decrease was significantly different from the control group ( table 4 ) .
the mean plasma pge , level was 3.50.92 pg / ml in 4 hepatitis b carriers and was not significantly different from that of the control group ( p>0.05 ) ( table 5 ) .
the above results suggest that plasma pge2 can be used for the measurement of cell - mediated immunity and follow - up study in patients with chronic active hepatitis and hepatitis b carriers .
chronic hepatitis is defined as a chronic inflammatory reaction in the liver as shown by liver function tests and histologic studies and that continues without improvement for at least 6 months .
a group of european histopathologists and clinicians in zurich in 1968 separated chronic hepatitis into chronic active hepatitis and chronic persistent hepatitis .
chronic active hepatitis is marked by a chronic inflammatory infiltration involving portal zones and extending into the parenchyme with piecemeal necrosis .
the pathogenesis of chronic active hepatitis is till unknown , but the patient having chronic hepatitis b would be expected to have some deficiency of cell mediated immunity .
it also applies to the patients suffering from diseases that depress immunity such as renal failure , malignant disease , and especially those receiving corticosteroids or cancer chemotherapy .
hepatitis b virus is cleared by cytotoxic t - lymphocyte from infected liver cell , but in patients with a depressed cell activity , the virus is not cleared and can develope into chronic hepatitis . thereafter , a plasma pge2 assay in patients with chronic active hepatitis and hepatitis b carriers performed for the evaluation of the origin of deficiency of cmi . in 1980 goldyne , goldyne , stobb , galanard reported that pge2 from macrophages ragulated the t - cell activity .
monocytes have a receptor to prostaglandin , so pge2 suppress the lymphocyte function & natural killer cell activity .
fisher reported that the pathogenesis of the depressed t - cell proliferative response in hodgkin s disease is monocyte - mediated suppression via prostaglandins and hydrogen peroxide .
other evidence of cmi suppression due to pge2 such as reduced monocyte function is found in cirrhosis but in the presence of indomethacine there is a significantly increased the lymphocyte response to pha - p in patients with cirrhosis .
lymphocyte hyporesponsiveness in cirrhosis has been shown to be mediated by prostaglandins produced by monocytes .
the mechanism of immunoregulation of prostaglandins is that the human leukocyte posses specific and separate receptors for endogenous hormones including -adrenergics , histamine prostaglandins .
this receptor has a high affinity for pge2 which increases the camp levels which cause inhibition of release of lymphokine , lymphotoxin , interleukin-2 ( il-2 ) for the t - cell proliferation .
thereafter immunoregulatory action was performed by a decreased amount il-2 and lymphokine due to increased plasma pge2 levels .
the proliferation of cells from spleen , lymph node , bone marrow may be inhibited by prostaglandin e2 .
the sensitivity of various cell populations , the quantities of prostaglandins and augmentation by indomethacin suggested that prostaglandin may modulate cell function in the bone marrow and thymus .
natural killer cells are a subpopulation of lymphocytes that are cytotoxic to a variety of malignant and normal cells .
droller reported that spontaneous cytotoxicity of human peripheral blood lymphocyte against tumor cells can be inhibited . in patients associated with depressed natural killer activity ,
so prostaglandins suppress immune reactivities and may be an important set of regulators of natural killer cell activity .
because the above described mechanisms of immunoregulatory action of prostaglandin e2 , the increased pge2 level which suppress the t , t cell proliferation , cytotoxicity was decreased . under this state , infected hepatitis b virus can not be cleared by cytotoxic t - lymphocyte and progressed into chronic active hepatitis .
we tried the plasma pge2 level in patients with chronic active hepatitis and hepatitis b carrier because these disease seems to have defect of cmi .
the results were that the plasma pge2 level in patients with chronic active hepatitis is significantly higher than that of the control group .
this fact suggest that plasma pge2 level has a close reversed relationship with cmi . because we do nt have a specific methods to predict the prognosis of chronic active hepatitis , plasma pge2 level will be helpful in evaluating the prognosis of hepatitis patient .
 prostaglandin e2 ( pge2 ) , one of the major prostaglandins synthesized in human monocyte and macrophage , is able to modulate t lymphocyte reactivity , such as lymphokine secretion and cytotoxicity . some immunologic abnormalities such as alteration in the synthesis of pge2 by monocyte and macrophage or in the response of t lymphocytes to pge2 can be found in clinical disease.we measured the plasma pge2 level in the control group and patients with chronic liver disease.the results were obtained as follows . 
 
 the mean plasma pge2 level was 2.65  0.69 pg / ml in the control group.the mean plasma pge2 level was 9.07  5.89 pg / ml in 15 patients with chronic active hepatitis and was significantly higher than that of the control group ( p<0.01).the plasma mean pge2 level was 4.65  1.59 pg / ml in 8 patients in the healing stage or stable stage of chronic hepatitis and was tend to decrease 
 . however , this decrease is significantly different from that of the control group.the plasma pge2 level was 3.5  0.92 pg / ml in 4 hepatitis b carriers and was not significantly different from that of the control group ( p<0.05).this results suggest that plasma pge2 can be used for the measurement of cell - mediated immunity and follow - up study in patients with chronic active hepatitis and hepatitis b carriers . 