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)

We have recently developed a new colorimetric method, DNA enzyme immunoassay (DEIA), for detecting specific hybrids of complementary nucleic acids. This technology is based on an antibody that selectively recognizes double, but not single-stranded DNA. The molecule does not react with a specific probe immobilized on microwells through an avidin-biotin bridge, nor with non-specific amplified sequences, since they are removed by washing. The antibody reveals the hybridization event, independently of the DNA sequences and, for this reason, the method is broadly applicable and extremely versatile. Although we chose a format based on the immobilization of the probe through an avidin-biotin interaction, DEIA assay can also be applied to other analytical schemes that do not require any modification of the probe. Most importantly, the test has an ELISA format and is rapid and convenient for processing large numbers of samples. This technology has been applied, in our laboratory, to different areas, including virology, genetic and basic immunology. The DEIA assay has been successfully used to detect the presence of hepatitis B (HBV), hepatitis C (HCV) and hepatitis delta virus (HDV) sequences in serum of patients, to discriminate different HLA alleles, to identify mutations in the Cystic Fibrosis gene, and to investigate the role of the T cell receptor in some immunological diseases. The results obtained in all our experiments demonstrated that the advantages offered by the assay do not penalize its analytical performance as compared to conventional Southern blot.
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PMID:Non-radioisotopic methods for DNA probes. 133 35

A male infant presenting with neonatal hepatitis syndrome, characterized by conjugated hyperbilirubinemia and very mild liver function test abnormalities, at 2 weeks of age was found to have no excretion of radioisotope into the intestinal tract on hepatobiliary scan. Liver biopsy revealed severe interlobular bile duct paucity. Other features of Alagille's syndrome were not present; other conditions frequently associated with interlobular bile duct paucity were also excluded. Subsequently, the infant was found to have cystic fibrosis. Cystic fibrosis is thus another disease that may be associated with paucity of interlobular bile ducts presenting as neonatal hepatitis syndrome, and this represents a different pathogenesis of cholestatic jaundice in neonates with cystic fibrosis besides those previously recognized.
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PMID:Neonatal hepatitis syndrome with paucity of interlobular bile ducts in cystic fibrosis. 167 9

We report two cases of children followed for many years with an original diagnosis of non-A/non-B hepatitis. One child developed serious cirrhosis with portal hypertension. Long-term observation of the course of their hepatic disease provided the diagnosis of cystic fibrosis. These cases demonstrate that cystic fibrosis though rarely presenting with initial hepatic signs, can manifest itself with only long-term hepatic symptoms. We therefore strongly recommend analysis of sweat chloride concentration in cases of hepatic disease of unknown origin.
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PMID:False diagnosis of non-A/non-B hepatitis hiding two cases of cystic fibrosis. 212 37

We reviewed the laboratory parameters, clinical information including presence or absence of stool pigmentation, and ultrasonographic findings in 67 patients with neonatal conjugated hyperbilirubinemia and liver biopsies. Hepatobiliary nuclear scintigraphy was done in 14 of the patients. Final diagnoses included extrahepatic biliary atresia, neonatal hepatitis, cystic fibrosis, metabolic liver disease, alpha 1-antitrypsin deficiency, bile duct stenosis, Alagille syndrome (arteriohepatic dysplasia), choledochal cyst, panhypopituitarism, and miscellaneous causes of intrahepatic cholestasis. A single diagnostic criterion is insufficient to distinguish the various causes of neonatal jaundice. Clinical laboratory values varied widely among patients with medical and surgical causes of jaundice. Absence of stool pigmentation was not specific for biliary atresia and was found in patients with medical causes of jaundice. Conversely, two patients with biliary atresia had pigmented stools at presentation. Ultrasonography was diagnostic only for choledochal cyst and bile duct stenosis. Nonvisualization of the gallbladder by either ultrasonography or nuclear hepatobiliary scintigraphy was nonspecific in the discrimination of medical from surgical causes of jaundice. A multidisciplinary approach to the evaluation of neonatal jaundice is necessary, since no single test or imaging modality can reliably define the cause in all cases.
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PMID:Neonatal jaundice: clinical and ultrasonographic findings. 218 86

After reviewing recent data concerning the pathologic physiology of cystic fibrosis the authors present an anatomoclinical study of 30 infants, of which 13 neonates, with a diagnosis of mucoviscidosiss, emphasizing the clinical and pathohistologic polymorphism of this affection, and, particularly involvement of the liver and intestines. Specific hepatic lesions were encountered in only 10% of the group studied (Bodian biliary cirrhosis and mucus stoppers in the bile ducts). Unspecific hepatic lesions were dominant, common with those of neonatal hepatitis, and hepatic steatosis. Stress is laid on the presence of atrophy of the villi in children with hepatic steatosis, proof of a lesional substrate of malabsorption in this disease. The authors note the early onset of hepatic lesions, the gravity of the cases with an early clinical expression and hepatic biopsy puncture as the only method revealing hepatic affection in cystic fibrosis. In the first semester of life there exists purely digestive forms, hepatic steatosis and oedematous dystrophy in infants at this age being highly suspect of the etiology.
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PMID:[Clinical and histopathologic polymorphism in cystic fibrosis]. 250 62

This article deals with the use of oral contraceptives and IUDs by chronically ill adolescent females. Results of controlled studies of contraceptive choices and problems are reviewed for teenagers with cardiac disease, epilepsy, multiple sclerosis, migraine headaches, asthma, cystic fibrosis, inflammatory bowel disease, hepatitis, diabetes mellitus, thyroid disease, oligomenorrhea and amenorrhea. If oral contraceptives (OC) are prescribed for use in teens with cardiac disease, a contraceptive with 35ug or less of estrogen and the equivalent of 1 mg or less of norethindrone should be used. The low-dose progestin only pill can be prescribed, but should be used in conjunction with a back-up barrier method. Reports to date have failed to reveal increased seizure activity in epileptic pattients on OCs, and there is no significant evidence to date that OCs alter the course of multiple sclerosis. Although the evidence is inconclusive, the physician should use extreme caution in prescribing OCs for teens with prior migraines. Regarding asthmatic patients, no problems have been reported with IUD use except in regard to steroid therapy and its possible effect on reducing IUD effectiveness. No adverse effects 2ndary to the use of OCs in asthmatic patients have been reported. OCs should be avoided or used with extreme caution in the cystic fibrosis patient. Teens with active inflammatory bowel disease should be advised that OCs may be ineffective or dangerous; there are no reports available on the effects of the IUD on the disease. The pill is contraindicated during active liver disease or cirrhosis. The IUD is not highly recommended for contraception in diabetic teenagers, whereas a low-dose combined OC can be used with extreme caution. However, OCs should be avoided in the diabetic patient with nephropathy, vascular complications or retinopathy. There is at present no contraindication for contraceptive use by women with thyroid disease. Finally, patients with prolonged post pill amenorrhea and infertility are generally females with amenorrhea or oligomenorrhea before pill use.
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PMID:Contraceptive use in the chronically ill adolescent female: Part I. 351 58

A retrospective study of 112 infants admitted at Pediatric Clinic of Catania from 1970 to 1985 with diagnosis of "Cholestatic jaundice" shows two prevalent pathologies: neonatal hepatitis and biliary atresia. Some other disease like cystic fibrosis. Hereditary fructose intolerance, Galactosaemia, Paucity of bile duct were found rarely. Some laboratory parameters (Serum direct bilirubin, Alkaline Phosphatase, Alkaline Phosphatase/Transaminase (GOT) show a characteristic pattern. Therefore the analysis of these data could help us to make a probability diagnosis and anticipate the liver biopsy that remain the most sensitive diagnostic instrument. In fact it is known that the earlier diagnosis is very important for the prognosis of these infants.
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PMID:[Neonatal cholestasis : clinical and diagnostic setting]. 378 81

The weights of the spleens of series of patients with various disorders of children dating from birth or early infancy and causing splenomegaly, with or without cirrhosis of the liver, were analyzed. The linear regression equation for spleen weight versus age in months for each disease was derived, and the rate constants from these equations were adjusted for the age range of the patients in each group. The original data of Coppoletta and Wolbach were used for normal values. The rates of splenic growth of appropriate entities for which the regression equation could be computed fell into three groups, with adjusted rate constants (growth of spleen in grams per month) of 6.53-6.95 (biliary atresia, thalassemia, and cirrhosis following neonatal hepatitis), 2.30-2.62 (cirrhosis of alpha-1-antitrypsin deficiency, infantile polycystic disease, and spherocytosis), and 1.06-1.11 (cystic fibrosis and idiopathic thrombocytopenic purpura). These classes of splenic growth rates are approximately 10, 3.7, and 1.6 times the normal growth rate (0.67 g/mo). Rate constants could not be computed for the categories cirrhosis following viral hepatitis and hemolytic anemia other than spherocytosis and sickle cell anemia, and the numbers of patients with splenic vein obstruction, cirrhosis with the cholestatic syndrome of parenteral alimentation, hypoplastic anemia with hemosiderosis, tyrosinemia, Byler's disease, congenital hepatic fibrosis, and Wilson's disease were too few for analysis. The significance of the finding of classes or "quantum groups" of splenic growth rates in disorders of children, dating from birth or early infancy and causing splenomegaly, is uncertain. Comparable data on adequate series of patients with other appropriate disorders will be necessary.
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PMID:Splenic growth rates in cirrhotic and other splenomegalic diseases of childhood. 384 62

During the past 6 years, 25 consecutive patients with esophageal variceal hemorrhage were treated by esophageal endosclerosis (direct injection of varices with a sclerosing agent). The primary disease in the 25 children was portal vein thrombosis (11 patients), biliary atresia (nine patients), and hepatic cirrhosis from cystic fibrosis (three patients), alpha 1-antitrypsin deficiency (one patient), and neonatal hepatitis (one patient). Thirteen patients were treated during acute, major variceal hemorrhage. Esophageal endosclerosis was repeated at regular intervals until all esophageal varices were obliterated. Twenty-one patients completed therapy. Four patients died: one of a complication of therapy and three of the primary disease. Other than the one death, complications were minor. Recurrent esophageal variceal hemorrhage has not been encountered in follow-up from 9 months to 6 years after completion of therapy.
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PMID:Esophageal endosclerosis in children. 387 48

74 patients with cystic fibrosis aged 1-19 years were assessed prospectively for 1-7 years for evidence of liver involvement. 20 of these patients were referred primarily because of hepatic problems. 3 of 4 with neonatal hepatitis recovered. Chronic active hepatitis developed in a further child but resolved spontaneously. 6 patients had abnormal liver-function tests without clinical evidence of liver disease. In 18 cirrhosis was detected at age 4-13 years. Liver disease was stable in these except terminally in 3 with cor pulmonale. The principal hepatic problem was variceal bleeding, which occurred in 6 patients. 50% of bleeds followed aspirin ingestion. This drug therefore should be avoided in such patients. 13 had hypersplenism. 2 had severe splenic pain necessitating splenectomy with lienorenal shunt, which was performed also in 2 patients who had bled. 3 remain well up to 5 years later. In 3 patients seen in the past 3 years injection sclerotherapy has controlled bleeding. This technique was well tolerated without the pain associated with, or intensive physiotherapy necessary after, shunt surgery; and this may be the method of choice for controlling variceal bleeding in cystic fibrosis.
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PMID:Hepatic complications of cystic fibrosis. 611 50


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