Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 55-year-old female was admitted to our hospital because of high fever, nonproductive cough and dyspnea. Initially she had been treated with cephem antibiotics by a local doctor. However, acute respiratory failure due to severe pneumonia developed. The partial pressure of oxygen in arterial blood was 55.5 Torr. Her chest X-ray revealed wide-spread infiltrates with air bronchograms throughout the entire left lung, and pleural effusions were also present in the chest CT scan. Because the patient had a history of the contact with birds, we suspected psittacosis and administered Minocycline immediately. As a result, her clinical condition improved and the abnormal shadow on the chest X-ray film improved markedly in three days. Because the serum titer of a complement fixation test against Chlamydia rose to 1:512, we made the diagnosis of psittacosis. In addition, femoral muscle pain, and a high level of serum GOT, GPT, CK, Aldolase and Myoglobin indicated hepatitis and myositis. In the lung tissue specimens obtained by TBLB performed on the 10th hospital day, slight interstitial pneumonia and intracellular inclusion bodies were found by light microscopy and Chlamydial agents were found electron microscopically.
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PMID:[A case of fulminant psittacosis showing Chlamydia in TBLB specimens]. 204 Dec 51

A radioimmunoassay specific for human aldolase A was used to measure human aldolase A levels in human tissue and serum of patients with various liver diseases. The method was a double-antibody technique using radio-iodinated purified aldolase A, chicken antibody to aldolase A, and rabbit antibody to chicken immunoglobulin G. Normal liver tissue contains only a small amount of aldolase A. In contrast, aldolase A predominates in liver cell carcinoma tissue. Aldolase A levels in the sera of normal subjects were 171 +/- 39 ng/ml (mean +/- 2 SD). In almost all of the nonmalignant liver diseases, the aldolase A levels remained less than 210 ng/ml. The serum aldolase A levels increased remarkable only in fulminant hepatitis. in contrast, 32 of 34 patients with liver cell carcinoma and all of 29 patients with metastatic liver carcinoma showed clearly increased serum aldolase A levels. More patients with primary liver cell carcinoma had increased serum aldolase A levels than elevations of serum alpha-fetoprotein. These results suggest that the determination of aldolase A by radioimmunoassay may be useful to differentiate malignant form nonmalignant liver diseases.
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PMID:Aldolase A isoenzyme levels in serum and tissues of patients with liver diseases. 618 64

Radioimmunoassays specific for fructose-1, 6-diphosphate aldolase isozymes were developed for the quantification of human aldolase A, B and C. The method is a double-antibody radioimmunoassay using radioiodinated purified aldolase A, B and C as ligand, chicken antibodies to aldolase A, B and C, and rabbit antibodies to chicken IgG. The Iodogen method was used for the iodination of aldolase A, B and C in this study. Aldolase A was predominantly high in concentration in muscle, aldolase B was high in normal adult liver, and aldolase C was high in adult brain. Aldolase A was elevated in hepatoma tissue and hepatoma cell lines, where aldolase B was distinctly low. Normal serum levels for the three isozymes were determined. The aldolase A levels in serum obtained from 41 normal subjects were 170 +/- 39 ng/ml. Serum aldolase A levels were increased in many patients with cancer and muscle diseases, but were not increased in patients with hepatitis or other benign diseases. Serum aldolase B levels obtained from 11 normal subjects were 28.5 +/- 9.2 ng/ml. Serum aldolase B levels were increased in patients with hepatitis and correlated well with serum GPT levels. Serum aldolase C levels obtained from 12 normal subjects were 2.4 +/- 0.7 ng/ml. The determination of aldolase A, B and C by radioimmunoassay may be a valuable tool in biochemical and clinical studies of aldolase isozymes.
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PMID:Subunit-specific radioimmunoassay for aldolase A, B, and C subunits: clinical significance. 632 58

A radioimmunoassay was developed for the direct quantification of aldolase B in human serum and tissues. The method is a double antibody radioimmunoassay technique using radioiodinated aldolase B homopolymer as ligand, chicken antibodies to aldolase B and rabbit antibodies to chicken IgG. This radioimmunoassay was shown to be specific for the aldolase B subunit, with no cross-reactivity with either human aldolase A subunit or homopolymeric human aldolase C (C4). The lowest measurable amount by this method was 2 ng/ml. Aldolase B is predominantly found in normal liver tissue, with relatively high aldolase B levels also observed in kidney. Aldolase B levels in the serum obtained from 11 normal subjects ranged from 23 to 38 ng/ml, with a mean of 28.5 +/- 9.2 (S.D.) ng/ml. Almost all of patients with hepatitis had serum aldolase B levels greater than 30 ng/ml. In cancer patients, serum aldolase B was slightly elevated in patients with metastatic liver cancer and primary lever cell carcinoma, whereas no elevation of serum aldolase B was shown in patients without liver metastasis.
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PMID:Human aldolase B subunit-specific radioimmunoassay. 682 89

Hereditary fructose intolerance is an autosomal recessive disorder that is caused by a deficiency in fructose-1-phosphate aldolase (Aldolase B). Children can present with hypoglycemia, jaundice, elevated liver enzymes and hepatomegaly after intake of dietary fructose. Long-term intake of fructose in undiagnosed patients can result in hepatic failure or renal failure. We experienced a case of hereditary fructose intolerance presenting as recurrent hepatitis-like episodes. Detailed evaluation of her dietary habits revealed her avoidance of sweetened foods and fruits. Genetic analysis of ALDOB revealed that she is a homozygote for a novel frameshifting mutation c[758_759insT]+[758_759insT] (p.[val25 3fsX24]+[val253fsX24]). This report is the first of a Korean patient diagnosed with hereditary fructose intolerance using only molecular testing without undergoing intravenous fructose tolerance test or enzyme assay.
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PMID:A Novel Frameshift Mutation of the ALDOB Gene in a Korean Girl Presenting with Recurrent Hepatitis Diagnosed as Hereditary Fructose Intolerance. 2237 83