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

It is generally accepted that the bile acids are responsible for pathologies as a result of deficiency or by toxic action. Quantitative deficiency is difficult to evaluate but the normal pool of bile acids is generally considered to be between 2 and4 grams. Daily loss and replacement by synthesis is thought to be between 500 and 700 mg. There is experimental evidence to demonstrate the toxic action of certain bile acids on metabolic structures and processes. There is no doubt that alterations in the metabolism of bile acids give rise to certain pathologic aspects in some diseases of the gastrointestinal tract or the hepatobiliary system. There are other conditions, on the other hand, in which the study of these acids may reveal significant physiopathologic implications. The first group includes terminal ileopathy, blind loop syndrome, gastric ulcer, gastritis, cholestasis, cirrhosis of the liver, and cholelithiasis. In the second group are such diverse conditions as acute pancreatitis, cancer of the colon, endocrine disturbances, some hyperlipidemias, and others. Much of the present day understanding of the physiopathology of the bile acids will probably have to be revised in the nex few years, in view of the rapid advances being made in this field.
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PMID:[Bile acids II. Physiopathologic and clinical aspects (author's transl)]. 47 Apr 97

12 g of albumin are synthesized daily by the bound polyribosomes of all human liver cells together, corresponding to 10% of the intravascular albumin mass. The cell is producing a precursor albumin. During secretion albumin is liberated by splitting of a small peptide. Only 40% of the total body albumin is located intravascularly. 12g of albumin are degraded or excreted daily, 30% of it by the liver, the kidneys and the gastrointestinal tract. The main site of albumin catabolism is unknown. Albumin with a half-life of about 20 days is degraded at a constant fractional catabolic rate. The absolute rate of degradation varies depending on the plasma content. This mechanism allows an effective regulation of the serum albumin level. The fractional catabolic rate, however, is not completely fixed. It is slowly reduced if the serum albumin content is markedly reduced as in protein deficiency, the blind loop syndrome, cirrhosis, nephrosis, and diseases of the gastrointestinal tract. Infusion of albumin increases the fractional catabolic rate slowly. This must be taken in consideration substitution albumin in chronic diseases. The shift from the extravascular to the intravascular compartment is a short-term regulatory mechanism. The regulation of synthesis and degradation are independent from each other. The molecular mechanism of regulation of synthesis and degradation are unknown, partially due to inadequate methods.
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PMID:[The regulation of serum albumin in physiological and pathological conditions (author's transl)]. 87 Jul 44

The experimental study on 30 patients of the Blood Stasis Syndrome of liver diseases was discussed in this paper. Two characteristics were found. One was the pathological feature which manifested as follows: (1) DIAGNOSIS: the Blood Stasis Syndrome of liver disease was mainly diagnosed in the chronic active hepatitis and the early stage of cirrhosis of liver, while that of non-Blood Stasis was mainly observed in the chronic persistent hepatitis (P less than 0.01); (2) Pathological change: The histological changes such as piecemeal necrosis, bridging necrosis, the destruction of limiting plate, eosinophilic change, etc. It was more obvious in the Blood Stasis group than that with non-Blood Stasis Syndrome (P less than 0.01), (3) The manifestation of Blood Stasis Syndrome was not in parallel with the severity of the liver disease. The another characteristic was the changes of liver function, which expressed more markedly in the Blood Stasis group with higher level of SGPT, lower ratio of A/G and increased globulin, they were more obvious than that in non-Blood Stasis group (P less than 0.01).
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PMID:[Characteristics of clinical pathology and changes of liver function in blood stasis syndrome in liver diseases]. 149 40

Anatomical abnormalities of the small bowel that cause intestinal stagnation result in bacterial overgrowth and a blind loop syndrome (BLS). Bacterial breakdown of bile salts and deamination of protein lead to malabsorption, steatorrhea, and fat-soluble vitamin deficiencies. Four children developed BLS as a complication of necrotizing enterocolitis, jejunal atresia, gastroschisis, and biliary atresia. BLS was suggested by abdominal pain, feculent vomiting, steatorrhea, and hypoalbuminemia. Dilated, stagnant bowel loops were demonstrated in each instance by upper gastrointestinal contrast study. Positive intestinal bacterial aspirates were confirmatory. Antibiotic treatment in two patients improved symptomatology but all children ultimately required surgery. Surgical procedures consisted of blind loop resection, intestinal plication, and catheterization of the bilioenteric conduit. All patients are now asymptomatic but one child suffers from parenteral nutrition-related cirrhosis and another requires chronic antibiotic therapy.
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PMID:The blind loop syndrome in children. 240 46

Many patients with chronic hepatitis B (CHB) seek help from traditional Chinese medicine (TCM). TCM treatment is based on syndrome differentiation. This study aimed to investigate the syndrome distribution in populations of CHB patients. The pre-specific search strategy was set, and 93 studies (20,106 participants) were identified by electronic and hand searches. The methodological quality of included studies was assessed. Data on syndrome distribution and correlations between syndromes and severity of CHB, were extracted and analyzed. Forty-seven syndromes were identified under 24 different syndrome diagnosis systems for CHB. The majority of included studies reported Liver Depression and Spleen Deficiency (LDSD) (52.54% of studies) or Liver-Gallbladder Dampness Heat (LGDH)/Dampness-Heat Obstructing Middle Energizer (DHME) (32.20%) as the major syndromes in CHB patients without cirrhosis. Pooled analysis revealed that LDSD and LGDH/DHME accounted for 61.19% of participants without cirrhosis. In addition, Liver-Kidney Yin Deficiency (LKYinD) (40.99%) and Spleen-Kidney Yang Deficiency (SKYangD) (40.43%) syndromes were common in patients with severe CHB. The percentage of patients with Blood Stasis syndrome increased as the disease progressed to cirrhosis (32.09%). To conclude, LDSD and LGDH/DHME syndromes are found in a significant majority of CHB patients, particularly in the early stages. LKYinD, SKYangD and Blood Stasis dominate in patients at more advanced stages. More epidemiological studies of high methodological quality on syndrome distribution in CHB and standardization of syndrome differentiation for CHB are required to confirm the trends indicated by the studies reviewed here; confirming these trends can increase the efficacy of treatment and give guidance to doctors.
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PMID:Traditional Chinese medicine syndrome distribution in chronic hepatitis B populations: a systematic review. 2208 81