| Caused by hepatic fatty degeneration associated with inheritance,environment and metabolism, fatty liver disease (FLD) is a clinical pathologicalsyndrome characterized as fat weight over 5% of total liver weight or more than30% hepatic cells contain lipid drops in histo-pathological slides due to excessivefat deposit (mainly triglyceride).With the improvement of living standard,morbidity of FLD steps up year by year and presents a low age status. Sometimesassociated with viral hepatitis, FLD may lead to hepatic cirrhosis, hepatic cellularcancer and liver function failure. Besides, FLD has close relationship to the type 2diabetes and angio-sclerosis heart-cerebral vessels event. Hence, FLD has drawninterest of clinicians. According to the presence or absence of excessive alcoholintake history, FLD is classified into two types: alcohol liver disease (ALD) andnon-alcoholic fatty liver disease (NAFLD). These two types are hard to bedifferentiated according to pathological findings, yet both include a serial ofhepatic injuries like simplex adipose degeneration, fatty hepatitis, advancedhepatic fibrosis and hepatic cirrhosis. Lipid deposition especially triglyceridedeposition in hepatic cells caused by IR is key factor of NAFLD. Twice hit theoryinterprets common mechanism of the ALD and NAFLD. In the theory, alcohol,fatness and diabetes serve as the first hit, which causes imbalance of triglyceridesynthesis and metabolism within hepatic cells, leads to fat deposit and formationof simplex fatty liver. The second hit refers to the oxygen related lipidperoxidation and inflammatory factors that cause hepatic cells to inflammate,necrose and fibrose. The difference of ALD and NAFLD lies in that morbidity ofALD is caused by ethanol and its metabolic products, while that of NAFLD isassociated with resistance of insulin. Treatments of FLD include basic treatment,drug treatment direct to hepatic diseases, and prevention and treatment towardconcomitant diseases. The principles of early stage interference, long terminsistence and combination of entirety treatment and individual treatment shouldbe followed. Change life style, treating concomitant diseases and relativedangerous factors are the basic prerequisite of whole treatment. Successful basictreatment can reverse simplex adipose degeneration and relative pathologicalsystemic changes, strengthen effects of drug treatment directed to fatty hepatitisand prevent recurrence of FLD after liver transplantation. Applicable to all kindsof FLD patients, basic treatment means remodeling life style through healtheducation, psychological and behavior modification and sometimes even withcombination of abstinence medicine and weight reduction medicine. Restrainingalcohol, avoiding liver-poison substances and caution of applying liver-poisonmedicine are rules to be followed. Primary goal of ALD treatment is life longabstinence of alcohol. On the cases that basic treatment alone is not effective,adjuvant medicine directed to principal contradiction of each individual should beconsidered. There is no random controlled big sample clinical study till now. Theclinical observations were different at starting point, laboratory test to be observedand ending point, so there is no recommended treatment to FLD. The medicinecan be used to deal with FLD with complication of type 2 diabetes or abnormalglucose tolerance include insulin agonist and peroxisome vegetation activatedreceptor (PPAR gamma) agonist. But some researches revealed that with theelongation of treating, liver dysfunction might recurrence and high serum lacticacid might present. Moreover, there was no significant histological improvement.Jifeiluoqi, activator of PPAR alpha, has effect of reducing blood fat. Patients withcomplication of hyperlipemia who have two or more dangerous factors can betreated with Jifeiluoqi or pravastatin with caution to lower blood fat to safety level.After using Jifeiluoqi, blood fat of the patients decreased notably, yet there is noimprovement regarding to liver lipid deposition, inflammation and fibrosis. Liverprotectant is an important component of medicine interventions. Aim at protectinghepatic cells, liver protectant has antagonism effect against oxidative stress / lipidperoxidation. Also it has anti-inflammatory, anti-apoptosis and anti-fibrosis effects.That is why liver protectant can protect simplex fatty hepatisis liver from thesecond hit, can avoid liver and gall complication that might be induced by weightreduction medicine and blood fat reduction medicine, can amend or even reverseinflammation, necrosis and fibrosis in fatty hepatitis. Nowadays, it is impossibleto apply medicine intervention to all patients due to following reasons. First of all,natural course of FLD is not clear. Secondly, many dangerous factors indicatingprogression of FLD are yet to be discovered. Finally, liver protectant has limitedeffects and cost of long-term-treatment is hard to afford. Being a precursor ofVitaminB15, Gan-le (dichloroacetic acid diisopropylamine DIPA) decompose todiisopropylamine and dichloroacetic acid in vivo. The latter metabolize intoglycine, then into methyl-tetra-hydrofolic acid after interaction with the glycinelysase. Over 90% DIPA participate in biochemical reaction in hepatic cells, so it isa typical targeted medicine.115 cases of FLD were included in this study, which was divided intotreatment group and control randomly. There was no significant differenceregarding to age, sex, height, weight, alcohol intake status, course of the disease,history of the past illness, clinical symptoms, extend of liver functional damage,level of blood glucose & blood fat and B type ultrasonic findings in the bothgroups. Being hospitalized, all patients were properly rested, strictly abstainedfrom alcohol, restricted to low fat diet with fixed time and quantity. Control groupwas given Gan-li-xin 150mg/day in 250ml 0.9%NaCl intravenously. Treatmentgroup was given Gan-le 120mg in 0.9%NaCl 250ml/d on the basis of Gan-li-xin.Course of treatment was 28 days. Follow-up observation was preceded 4 weeksafter treatment. In the course of treatment, other liver pertectants, fat-reductionmedicine and hormones were excluded in both groups. Liver function, totalbilirubin, blood glucose blood fat, kidney function, blood routine examination,urine routine examination, electrocardiogram, abdominal B type ultrasonic werechecked on 1 day before and after treatment respectively. Clinical symptoms andsigns including hypodynamia, anorexia, fullness of abdomen, sickness, vomit andswelling of liver and spleen before and after treatment were also recorded. Eightweeks after treatment, total effective rate of treatment group was 94.1%, whilethat of control group was 73.0%;rate of ALT restore to normal of treatment groupwas 91.7%, while that of control group was 74.5%;total effective rate of blood fatof treatment group was 93.3%, while that of control group was 72.7%;totaleffective rate of B type ultrasonic of treatment group was 40.0%, while that ofcontrol group was 23.6%. All the above data has statistical differences between 2groups. Our research discovered that DIPA had an effect of lowering ALT andblood glucose, improving disorder of lipid metabolism and reducing fat depositionin hepatic cells. Functioning at multi-points, DIPA can eliminate liver lipid andblood fat fundamentally;reverse lipid to energy;provide energy for hepatic cells;restore damaged hepatic cells;enhance metabolism of hepatic cells. All in all,DIPA is an ideal medicine for FLD.
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