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

In 50 patients with different liver diseases (20 with subsided viral hepatitis and 30 with degenerative liver damages) the serum enzyme course of SGOT, SGPT, LDH and CPK was investigated after ergometer load. The enzymes were estimated before as well as 1/2, 2, 4, 24, and 48 hours after load. 48 hours after load additionally the liver biopsy after Menghini was carried out. According to the histological findings the 20 patients with viral hepatitis were subdivided into 13 with still active and 7 with residual hepatitis as well as the 30 patients with degenerative liver damages into 15 with toxical hepatosis, 6 with fatty degeneration of the liver cells and 9 with signs of metabolic activation. Since the significant increases of enzymes could not be proved in any of the fours enzymes 1/2 to 48 hours after load we are of the opinion that the liver, independent on the kind of the lesion, better tolerates physical work. Moreover, it seems that load investigations under ergometry with estimation of the course of the serum enzymes are unsuited for the judgment of the degree of activity and the degree of cure of liver diseases, respectively.
 ...
PMID:[Physical capacity of patients with liver diseases as well as its significance for therapy and evaluation]. 66 3

85 women, 16-43 years of age, were studied for liver damage caused by oral contraceptive (o.c.) use. Laboratory tests were performed, and point biopsies were taken in 76 cases. SGPT levels were consistantly higher than SGOT levels. The transaminase levels were normalized after 14 days in 47 cases and after a longer period in 38 cases. Pathological serum bilirubin levels were observed in 15 women; in 5 cases the patients had experienced hepatosis during pregnancy. Non-cholestatic hepatosis was found in 52 patients and cholestatic hepatosis in 9; in most cases the diagnosis was confirmed by the liver biopsy. Hepatosis in conjunction with reactive hepatitis was more frequent among Ovosiston users. Hepatosis with sinusoid ectasia was more frequent among Non-Ovlon users. Fatty liver in conjunction with hepatosis was observed more often among Gravistat and Non-Ovlon users. Hepatosis with reactive hepatitis and non-cholestatic hepatosis with sinusoid ectasia or fatty liver were associated with elevated transaminase levels. After laboratory test levels were normalized, 50 patients were reintroduced to o.c. use with frequent control check-ups. In those cases where o.c. use could be continued, liver damage was found to have been caused mainly by o.c. use in conjunction with other medications, e.g. analgesics, sedatives, or laxatives. Patients with cholestatic hepatosis redeveloped cholestasis after reintroduction to o.c. use. Blood tests are best taken after reintroduction to o.c. use at the end of the pill-taking period. SGPT tests should be taken at the end of the 2nd cycle of o.c. use and twice a year therafter to determine the effect of o.c.s on the liver.
 ...
PMID:[Liver lesions caused by oral contraceptives. I. Contraceptive-induced hepatosis in 85 women: recommendations for diagnosis and prophylaxis]. 66 3

Twenty infants and young children with hereditary fructose intolerance (HFI) were admitted to hospital. None was diagnosed at admission. Referals were for vomiting of unknown aetiology (16X), pyloric stenosis or hiatus hernia (5X), toxic condition (3X), and hepatomegaly of unknown origin (5X). Feeding difficulties (20X), vomiting (18X), and failure to thrive (16X) were leading symptoms. The most frequent clinical findings were hepatomegaly (18X), pallor (14X), haemorrhages (13X). Ascites, oliguria, tachypnoea, fever, splenomegaly and rickets were less frequent. Laboratory findings were indicative of disturbed hepatic and renal tubular function and also of disturbed intermediary metabolism (hypokaliaemia, hypophosphataemia). However, hypoglycaemia was found in only 4 out of 15 patients tested. Differential diagnosis after hospital admission centered on metabolic disorders such as glycogenoses, galactosaemia, tyrosinosis, or Wilson's disease. Hepatitis, toxic hepatosis, liver tumour, intrauterine infection and sepsis were also considered. Eleven children had first ingested fructose within the first 6 weeks of life. The diagnosis was usually established only many weeks or months after first fructose intake and appearance of symptoms. This documents how difficult the diagnosis of this disease can be both in practice and in hospital. The course was severe in 11 children and lethal in 4. In only 5 patients was the course mild. The 16 survivors are doing well under fructose-exclusion diet. Irreversible visual impairment after intraocular haemorrhage occurred once. In each case HFI could have been suspected immediately, had a detailed nutritional history been taken. Practising paediatricians should know the composition of commonly used infant formulae. They should never prescribe sugared condensed milk for intractable vomiting prior to excluding HFI. Solution for intravenous infusion containing fructose and sorbitol are life-threatening for undiagnosed HFI patients.
 ...
PMID:Hereditary fructose intolerance in early childhood: a major diagnostic challenge. Survey of 20 symptomatic cases. 73

7 individual cases of hepatocellular damage caused by the use of oral hormonal contraceptives are examined. 3 different morphological patterns of damage were observed: reactive hepatitis, intrahepatic cholestasis, and subacute hepatitis. Discussion of the pathenogenesis of this damage revolves around the theory of competitive effect of sex hormones on the metabolism and transport of bilirubin, the theory of hypersensitivity, and theoretical toxic actions of contraceptive hormones. The reversibility of hepatocellular damage in 3 cases in the form of gestational hepatosis perhaps advocates the theory of hypersensitivity to endogenous and exogenous hormones. 1 case of subacute hepatitis had a lethal outcome, which suggests the possibility of direct toxic effects of hormonal contraceptives.
 ...
PMID:[Types of hepatocellular damage caused by contraceptives]. 90 63

A series of 107 patients with hepatosis of pregnancy and 61 controls with normal pregnancy is reported. The delivery and the condition of the infant were the main objects of investigation. The hepatosis group was also examined for liver function, glucose tolerance, and daily urinary oestrogen. The duration of the first stage of delivery was found to be slightly shortened in the hepatosis group. Two cases (1.9%) of intrauterine death occurred in the hepatosis series, and the Apgar scores at 1 and 15 minutes were somewhat lower than in the control group. Birthweight was slightly lower in the hepatosis series, corresponding to the earlier date of delivery. 11.9% of the infants weighed less than 2.5 kg at birth. The absolute and relative weights of the placenta showed no differences. The histological examination of the placenta made on part of the series revealed maturing defects in 35%. The liver function tests confirmed the cholestatic nature of hepatosis observed earlier, yielding elevated values especially for aminotransferases, alkaline phosphatase and bilirubin. The thymol turbidity test was within the normal limits, which means that hepatitis could be excluded. Neither glucose tolerance, nor daily urinary oestrogen differed significantly from the normal. The fetal survival rate has been improved considerably by intensive care of hepatosis of pregnancy.
 ...
PMID:Hepatotis of pregnancy. A clinical study of 107 patients. 113 35

The results of the experiments with use of isoniazid and its metabolites showed that in the liver of rats isoniazid induced albuminous degeneration with stroma inflammation and hepatocyte necrosis, monoacetylhydrazine induced fatty hepatosis, acetylisoniazid induced fatty hepatosis with stroma inflammation and hepatocyte necrosis and isonicotinic acid induced granular degeneration. Piracetam proved to be efficient in fatty hepatosis. Riboxin and dibunol were efficient in hepatitis. The drugs used clinically as liver protectors, i.e. cobamamide, pyridoxal phosphate and methionine had no protective action in liver affections induced by isoniazid whereas catergen, lipamide, dipromonium and methindione even aggravated such affections.
 ...
PMID:[Drug prophylaxis of liver lesions induced by isoniazid and its metabolites]. 274 56

This is a broad review (140 literature citations) of the possible effects of oral contraceptives on the liver. The oral contraceptives considered consist of combined preparations of estrogens and progestogens although the so-called "minipills" contain only a progestogen. The effects are divided into 1) decrease in excretory liver function; 2) influence on bile acid formation, including cholesterol metabolism; 3) increased synthesis of various transport proteins (ceruloplasmin, transferrin, thyroxine-binding protein, and cortisol-binding protein); 4) the effects of increased tissue circulation caused by sexual hormones and anabolic steroids as a cause for more frequent cavernous angiomas and peliosis hepatis; 5) interference with the metabolism of other drugs by the competitive action of the hepatic metabolites of steroid hormones. This includes the increased formation of delta amino levulinic-acid synthetase, the key enzyme for porphyrin synthesis. The gestagen component of oral contraceptives is responsible for enzyme induction in the smooth endoplasmic reticulum. Morphological liver changes caused by oral contraceptives include parenchyma changes, hepatosis, reactive hepatitis, hepatitis resembling viral hepatitis, vascular changes, sinusoid ectasia, Budd-Chiari syndrome, hyperplasias and neoplasias, focal nodular hyperplasia, adenoma and liver cell carcinoma.
 ...
PMID:[Effects of oral contraceptives on liver function and structure]. 332 30

Drugs are exogenous substances often requiring metabolic transformation to be therapeutically effective. This occurs primarily in the liver, the most important metabolic organ and a structure able to adapt to this burden. Should its adaptive potential be exceeded, damage can occur, affecting principally the liver parenchyma. Such damage manifests itself as disturbed secretory function and as reversible or irreversible structural alteration of the liver cells. The constellation of toxic-degenerative lesions is referred to as hepatosis (toxic hepatosis, toxic hepatopathy). A variety of patterns of damage (lipidosis, necrosis, cholestasis etc.) occur alone or in combination. Depending on the severity and extent of these alterations a secondary inflammatory reaction may result. These changes are manifest as cellular infiltration and proliferation with formation of reticulo-histiocytic nodules or minifocal epitheloid cell reactions and non-caseous epitheloid cell granulomas. The eosinophilic component is striking. In the face of continued toxic exposures, changes resembling those of chronic aggressive hepatitis may develop following the acute changes. Other drug-related liver damage may present as vascular lesions the afferent or efferent venous systems as well as in the sinusoids (i.e. peliosis hepatis, Budd-Chiari syndrome). Moreover there may be neoplastic alterations such as focal nodular hyperplasia or liver cell adenomas. Pathognomonic histologic criteria for drug-induced liver damage have as yet to be recognized, particularly in the case of facultative toxins. Morphologic indications can only suggest that a prior pharmaceutical agent was the likely cause of the damage. Histologic changes must however be viewed in the context of the medical history, clinical and laboratory findings, as well as results of other studies before the conclusion is drawn that the observed liver changes represent drug-induced injury.
 ...
PMID:[Morphological reaction patterns of the liver induced by drugs]. 383 9

Morphologically identical liver damage may be caused by dihydralazine (Depressan, Nepresol) and propranolol (Obsidan, Dociton). Among 24 patients with clinical manifestations of drug-induced hepatitis associated with Depressan or Obsidan treatment, liver biopsies in 15 showed drug hepatitic changes with confluent necrosis. In five of these cases this finding was combined with cholangiolitis, in four there was a drug-induced hepatopathy resembling the picture of viral hepatitis. In 20 cases of Ketazon-induced liver damage the biopsy demonstrated toxic hepatosis with or without cholestasis, reactive hepatitis or cholangiolitis. A drug-related hepatitis with central lobular necrosis was observed in one patient with Ketazon-induced liver damage. In 28 patients a lymphocyte proliferation test was undertaken to confirm a causal relationship between the use of either Depressan, Obsidan or Ketazon and the morphologically demonstrated liver damage. The test was positive in 25 cases (18 with Depressan, 2 with Obsidan and 5 with Ketazon). In several uncertain cases, for example, exposure to both Depressan and Obsidan or to Ketazon and Rewodina, the morphologic picture could be attributed to a specific medication by the use of the lymphocyte proliferation test. The results of the lymphocyte proliferation test and the morphologic findings emphasize the role of cell-mediated immune reactions in the pathogenesis of liver damage from dihydralazine, propranolol, and ketophenylbutazone.
 ...
PMID:[Morphology and pathogenesis of liver injury produced by dihydralazine , propranolol and ketophenylbutazone]. 384 42

Serum enzymes are sensitive tools for demonstration of injury to different organs of the body, including lesions that are side effects of drugs or the application of certain compounds for diagnostic purposes. It has been reported that tuberculosis therapy can cause liver damage of the unpredictable drug-induced liver lesion-type. The liver lesions due to tuberculostatics resemble an unspecific or viral hepatitis. Oral contraceptives can also cause hepatic lesions, some of them being quite serious. They have been known to cause hepatosis with or without cholestasis, drug-induced hepatitis, circulatory disturbances such as hepatic peliosis and Budd-Chiari syndrome, and benign and malignant tumors. Therapy control should be instituted in these cases. Enzymes can be used as indicators. A considerable increase of coeruloplasmin (or serum copper) is a useful marker for monitoring contraceptive medication; the aminotransferases initially show a slight increase while later, they may be decreasing to subnormal values. The appearance of serious morphological findings may necessitate delineation of normal ranges and alarm ranges. Serial enzyme determinations are suggested in: 1) high risk patients who have been suffering from hepatitis or intrahepatic cholestasis due to pregnancy or drugs, and 2) in persons complaining of signs or symptoms suggestive of liver involvement. The kidney is another organ which might be influenced by certain drugs leaving the organism via the urinary tract. The presence of enzymes in urine can serve as sensitive indicators of a proximal tubular lesion. The effects of certain hormones on the kidneys are discussed.
 ...
PMID:A review of enzyme changes in serum and urine due to treatment with drugs (tuberculostatics, contraceptive medication, diagnostics and drugs in real diseases). 626 69


1 2 Next >>