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 retrospectively evaluated the utility of hepatobiliary scintigraphy and various clinical factors in differentiating intrahepatic cholestasis from biliary atresia in 28 consecutive infants with neonatal cholestasis. One millicurie of technetium-labeled diisopropyliminodiacetic acid (DISIDA) was administered intravenously, and images were obtained for up to 24 hours or until gastrointestinal excretion was noted. Nine separate studies in seven infants with biliary atresia were correctly interpreted as showing no gastrointestinal excretion of radionuclide. Of the 21 patients with intrahepatic cholestasis, only nine had gastrointestinal excretion on the first study; in eight without excretion, a second study was done, and five of these showed gut excretion. All infants with either neonatal hepatitis (six) or inspissated bile syndrome (three) had demonstrable gastrointestinal excretion either on the first or second DISIDA study. However, five of six infants with paucity of intrahepatic bile ducts, two of six infants with cholestasis secondary to total parenteral nutrition, and one infant with cholangiolitis did not show evidence of gastrointestinal excretion. The mean birth weight, mean gestational age, and mean weight at study were significantly greater (P less than 0.005) for infants with biliary atresia without excretion than for infants with intrahepatic cholestasis without excretion. The mean direct bilirubin concentration was 6.0 mg/dL for both infants with biliary atresia and infants with intrahepatic cholestasis without excretion; however, infants with excretion had a significantly lower (P less than 0.02) mean direct bilirubin value of 3.4 mg/dL. Excretion was noted in four infants with total bilirubin values greater than 10.0 mg/dL. The absence of gut excretion on the first DISIDA study was 100% sensitive but only 43% specific for biliary atresia. In infants without gut excretion of DISIDA, birth weight greater than 2200 g was 100% sensitive and 92% specific for biliary atresia. We conclude that DISIDA scanning, together with clinical data, is useful in differentiating extrahepatic from intrahepatic cholestasis. The absence of gut excretion on the first DISIDA study does not necessarily indicate extrahepatic obstruction; the study should be repeated if the diagnosis is not clear.
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PMID:Diagnostic utility of hepatobiliary scintigraphy with 99mTc-DISIDA in neonatal cholestasis. 358

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

Our patient had DISIDA scan at 39 days of age to exclude biliary atresia. Gut excretion was seen 18 h after injection and the diagnosis of neonatal hepatitis was made. Because of continued elevated liver function values, liver biopsy was performed and demonstrated findings consistent with biliary atresia. Exploratory laparotomy performed 8 days after the scan showed patent cystic duct, bile duct, and gallbladder, but an atretic common hepatic duct. This case is an example of documented biliary atresia demonstrating gut excretion on the DISIDA scan.
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PMID:Apparent gut excretion of Tc-99m-DISIDA in a case of extrahepatic biliary atresia. 370 1

Lysozyme is a bacteriocidal enzyme which is a major stable secretory product of mononuclear phagocytes, including hepatic sinusoidal macrophages (HSM), and serves as a good marker for these cells. Patients with alcoholic liver disease (ALD) have decreased HSM function which is reflected in reduced clearance of microorganisms and endotoxin derived from the gut. The HSM population in 54 liver biopsies from patients with ALD was studied using immunoperoxidase staining of lysozyme and was compared with 15 histologically normal controls. In both groups lysozyme positive HSM were more numerous in periportal than perivenous parenchyma. In each zone there were significantly fewer positive HSM in cases of ALD than in controls, in alcoholic hepatitis than in ALD without hepatitis, and in cirrhosis than in ALD without cirrhosis. These findings suggest a decreased population of functionally active HSM in ALD which correlates with severity of liver damage. This might be due to decreased lysozyme content of the entire HSM population or to the existence of two populations, one positive and one negative for lysozyme. The observed decrease in HSM function explains many of the phenomena observed in ALD.
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PMID:Hepatic sinusoidal macrophages in alcoholic liver disease. 390 65

Sixty patients with gut failure were treated with home parenteral nutrition for 2000 patient months. Fifty-one of these 60 patients had either no abnormalities or mild and transient elevations of their liver chemistries and did not have liver biopsies. Nine (15%) of 60 patients had abnormalities of liver tests that persisted from 8 to 95 months (median, 18 months) which prompted one or more liver biopsies per patient. Three patients had prolonged jaundice, one died of hepatic encephalopathy, and another with protracted intrahepatic cholestasis died following a biliary tract exploration. A third patient remains ill with signs and symptoms of chronic liver disease. Steatohepatitis was found in eight of the nine patients and was characterized by centrilobular and midzonal microvesicular and macrovesicular fatty changes with fat cysts, focal necrosis, and mixed inflammatory infiltrates. Centrilobular fibrosis was present in three patients and evidence of nodular regeneration in one. In the three patients demonstrating cholestasis, bile pigment was identified both in hepatocytes and canaliculi. Ceroid pigment in Kupffer cells was a consistent finding and much more severe than expected from the mildness of the hepatitis. Persistent abnormalities of liver chemistries in nine patients and progressive liver disease while receiving home parenteral nutrition in three patients are quite worrisome and suggest that home parenteral nutrition-associated steatohepatitis with or without cholestasis may progress to chronic liver disease.
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PMID:Does long-term home parenteral nutrition in adult patients cause chronic liver disease? 391 94

Fifty-three patients with polyarteritis who were followed up for at least 2 years were defined clinically and studied retrospectively to determine the influence of clinical factors and treatment on the prognosis. There was a spectrum of severity of disease, and the 5-year survival in the group was 55%. A small number of patients had evidence of ongoing immune-complex disease, as indicated by the presence of cryoglobulins or hepatitis Bs antigen or by diminished serum complement. These markers were not associated with distinct clinical features and did not influence prognosis. Organ involvement that most adversely affected prognosis was that of the gut and the kidneys. Six of 8 patients with bowel infarction or serious gastrointestinal bleeding died, and 6 of 10 patients with renal insufficiency died. Hypertension and peripheral neuropathy did not influence the prognosis. Thirty-six patients were treated with corticosteroids alone and 14 with a combination of corticosteroids and cytotoxic agents (3 received no treatment); the outcome was the same in both groups. Twenty-two in the steroid-alone group and six in the combination group were alive when last seen. Early deaths were usually due to complications directly related to the vasculitis, and late deaths were often due to cerebrovascular or cardiovascular complications. At the last follow-up, 18 patients were in remission, and 13 had inactive vasculitic disease and were on maintenance treatment.
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PMID:Clinical features, prognosis, and response to treatment in polyarteritis. 610 26

Since 1976, 16 adult patients with acute leukemia have been treated by chemotherapy, total body irradiation (TBI) and allogeneic bone marrow transplantation (BMT) in the medical school hospital and the satellite hospitals of Nagoya University. The first group of 10 patients were given marrow grafts at the time of leukemic relapse and the second group of six patients were given the grafts in the period of remission of their disease. For the first group (ALL/ANLL 2:8, age (median) 33, M/F 8:2), HLA-identical donor cells (25 x 10(7)/kg [median]) were infused after the patients were conditioned with NSC D 245382 (ACNU) or daunorubicin, cyclophosphamide (CY) and a single shot of 1000 rad of TBI. For the second group (ALL/ANLL 4:2, age (median) 20, M/F 5:1), HLA-identical donor cells (22 x 10(7)/kg [median]) were infused after the patients were conditioned with CY and fractionated (250 rad x 4) TBI. All the patients were isolated in a laminar air flow room (LAF) after gut and skin decontamination. Engraftment of donor cells was confirmed in 15 out of the 16 patients. Febrile periods in LAF and the days required for platelet transfusion were prolonged in the first group. All the patients in the first group died within 12-214 days after BMT because of interstitial pneumonitis (7 patients) or bacterial infection (3 patients). On the other hand, five out of six patients in the second group are alive 84-540 days after BMT. For the surviving patients, the complications of chronic graft versus host disease, viral infections, tuberculosis, hepatitis, hemorrhagic cystitis and recurrence of leukemia are now the problems. It can be stated that the patient's clinical condition at the time of BMT is one of the most essential factors for the success of BMT although the effects of other variables, such a change in the conditioning regimens of the supportive care, must also be carefully analyzed.
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PMID:Sixteen adult patients with acute leukemia treated by chemotherapy, total body irradiation and allogeneic marrow transplantation. 639 11

D-(+)-galactosamine (GalN) induces severe reversible hepatocellular injury in the rat accompanied by lecithin: cholesterol acyltransferase (LCAT) deficiency, defective chylomicron (CM) catabolism, and accumulation of abnormal plasma lipoproteins (Lps), including discoidal high density lipoproteins (HDL). These abnormalities are presumed to result from hepatic injury alone, but the effect of GalN on intestinal Lps has not been studied. To assess possible effects on intestinal Lp formation and secretion, mesenteric lymph fistula rats were injected with GalN or saline. Twenty-four hours later a 2-hr fasting lymph sample was collected; this was followed by an 8-hr duodenal infusion of a lipid emulsion containing 17.7 mM [3H]triolein at 3 ml/hr. Fasting lymph and fat-infused lymph flow rates, 3H, triglyceride, and cholesterol output, residual 3H in intestinal lumen and mucosa, total 3H recovery, and d less than 1.006 g/ml Lp size and lipid composition were unchanged by GalN treatment, but d less than 1.006 g/ml Lps were depleted of apoE and C. Fat-infused lymph phospholipid (PL) output was higher in GalN rats due to PL-enriched d greater than 1.006 g/ml Lps. Electron microscopy of lymph and plasma LDL and HDL revealed spherical Lps in all samples. GalN plasma, fasting lymph, and fat-infused lymph also contained large abnormal LDL and discoidal HDL. Control lymph LDL and HDL did not differ in size from control plasma LDL and HDL. Control lymph LDL contained both apoB240K and B335K. However, spherical LDL and discoidal HDL in fasting lymph from GalN rats differed significantly in size from the corresponding plasma particles and became closer in size to the plasma particles with fat infusion. GalN lymph LDL contained only apoB240K and had a lower PL/CE than GalN plasma LDL. GalN fasting lymph HDL, depleted of apoC and having a PL/CE of 5, became enriched in apoE and the PL/CE increased to 10 with fat infusion to closely resemble GalN plasma HDL. GalN reduces apoE and C (mainly of hepatic origin) in d less than 1.006 g/ml gut Lps, which may contribute to the CM catabolic defect in GalN rats. Lymph LDL and HDL, especially in fasting lymph, may be partially gut-derived with increased filtration of plasma Lps into lymph with fat infusion. GalN fat-infused lymph HDL is enriched in apoE, but unable to transfer apoE to d less than 1.006 g/ml intestinal Lps. We conclude that GalN hepatitis is a model that allows study of intestinal Lps with normal lipid digestion and absorption in the face of severe hepatic injury and LCAT deficiency.
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PMID:Intestinal lipoproteins in the rat with D-(+)-galactosamine hepatitis. 663 Dec 39

A 19-year-old male, suffering from post-hepatitis aplastic anaemia, was transplanted with bone marrow cells from his HLA-identical, MLC non-reactive brother. Haematological recovery ensued, but the patient also developed grade IV graft-versus-host disease (GVHD). In addition to involvement of skin, liver and gut, the kidney seemed affected by GVHD since the patient has hypokalaemia and severe hyperkaluria. Other causes of urinary potassium loss were excluded. The amount of potassium loss correlated well with the severity of the GVH-reaction. Although coagulation disorders prohibited a kidney biopsy, the clinical course suggested GVHD to be the cause of the urinary potassium loss.
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PMID:Extreme potassium loss in a patient with severe graft versus host disease. 700 82

This review aims to outline the nature and origin of free radicals, or oxidants, in biological systems and to summarise their involvement in diseases of interest to anaesthetists, with particular reference to reperfusion injury (of the gut, brain, myocardium and transplanted organs), shock/trauma, inflammation/sepsis and halothane hepatitis. In-vitro and animal studies examining the role of free radicals and antioxidants in the pathophysiology and treatment of these conditions are presented. Some of the evidence from clinical studies supporting the use of antioxidant therapy in patients is also presented.
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PMID:Free radicals in anaesthesia and intensive care. 771 Feb 36


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