Elevated Serum Glutamic Oxaloacetic Transaminase Research Articles

Risk of Hepatitis to Families of Hemodialysis Patients.

Meeting Abstracts1 May 1971Risk of Hepatitis to Families of Hemodialysis Patients.Sergio Acchiardo, M.D., Richard Garibaldi, M.D., Thomas White Jr., M.D., James G. Johnson, M.D., Kira Stern, M.D., Fred E. Hatch, M.D.Sergio Acchiardo, M.D.Search for more papers by this author, Richard Garibaldi, M.D.Search for more papers by this author, Thomas White Jr., M.D.Search for more papers by this author, James G. Johnson, M.D.Search for more papers by this author, Kira Stern, M.D.Search for more papers by this author, Fred E. Hatch, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-830_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptViral hepatitis is a major risk both to staff and patients in hemodialysis units; only sporadic cases have been diagnosed in the families of dialysis patients. In 421 persons caring for home dialysis patients only 1 case was reported. (National Cooperative Study, 1969).Five of 15 asymptomatic patients had elevations of serum glutamic-oxalacetic transaminase (SGOT) greater than 100 Sigma-Frankel units and positive hepatitis-associated antigen. Secondary spread of hepatitis occurred among the family and contacts of one of these patients. During his home dialysis training his wife sustained a needle puncture and 2 months later developed hepatitis, with a prodromal urticarial... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Memphis, Tenn. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 830-830KeywordsAminotransferasesAntigensHepatitisHepatitis AMedical dialysisSerum glutamic oxaloacetic transaminase Issue Published: 1 May 1971 PDF downloadLoading ...

Diabetic ketosis. Interpretation of elevated serum glutamic-oxaloacetic transaminase (SGOT) by multi-channel chemical analysis.

Multi-channel determination of serum glutamic-oxaloacetic transaminase (SGOT) frequently reveals an elevation in patients with diabetic ketoacidosis. This elevation may represent acetoacetate in the serum and thus be an artifact. It is therefore necessary to include the determination of a serum blank or to utilize a different technic to measure the SGOT in patients with ketonemia.

Acute cholecystitis and serum transaminase activity.

The increment and time course of serum glutamic oxaloacetic transaminase (SGOT) was evaluated in 108 patients with acute cholecystitis, 26 of whom were jaundiced. Seventy-seven percent presented with an elevated SGOT. All of the jaundiced patients had an elevated SGOT and higher values were generally achieved in jaundiced than in nonjaundiced patients. However, 70% of anicteric patients also had an elevated SGOT. Serial enzyme determinations were obtained over a period of at least five days in 38 anicteric and 22 jaundiced patients who presented with elevations. Invariably, the initial SGOT value was the maximal level obtained. When compared to the increment and time course of the SGOT in patients with acute myocardial infarction or hepatocellular disease, the enzyme activity which characterizes an elevated SGOT in patients with acute cholecystitis can be of value in the differential diagnosis of these diseases.

A Clinical Evaluation of Elevated Serum and Urine Amylase

Jensen, H.-E., Nielsen, J. & Amdrup, E. 1970. A Clinical Evaluation of Elevated Serum and Urine Amylase. Scand. J. Gastroent. 5, 543-547.The frequency of elevated serum bilirubin, alkaline phosphatase, and glutamic oxaloacetic transaminase (SGOT), and also albuminuria, was the same in patients with stones in gall bladder and in bile ducts. In patients with elevated amylase but without gall stones the frequency of elevated serumbilirubin and albuminuria was the same as in patients with gall stones, but the incidence of elevated alkaline phosphatase and SGOT was lower. Doubt is raised about the significance of gall stones as an aetiological factor in pancreatitis, and it is also questioned how often elevated amylase betokens primary pancreatic disorder. The similarities between different groups may argue existence of a general toxic state involving liver and kidneys just as much as pancreas.

Health in a Rural Hippie Commune

All cooperating members of a small hippie commune in rural New Mexico were examined carefully for evidence of past or present illness. Current illness was infrequently documented although most had complaints of recent diarrhea, pharyngitis, cough, or gonorrhea, or the finding of an elevated serum glutamic oxaloacetic transaminase level, or abnormal results of an infectious mononucleosis spot test (Monospot). Medical attention was either accepted passively or not at all. No illnesses posing hazards to neighboring communities were apparent and the incidence of hard drug use was low. The observations may be relevant to other groups of young people living in such communes, the numbers of which are now large and probably increasing.

False elevations of serum glutamic-oxalacetic transaminase due to para-aminosalicylic acid.

Para-aminosalicylic acid (PAS) in serum has been shown by in vivo and in vitro studies to induce false elevations in serum glutamic-oxalacetic transaminase (SGOT) level as determined by the colorimetric method commonly used in automated analyzers. This does not appear to reflect any hepatic injury, and no changes have been found in SGOT levels determined by the specific reduced nicotinamide adenine dinucleotide (NADH)-linked method of Karmen, or found in serum glutamic-pyruvic transaminase (SGPT), or in serum lactic acid dehydrogenase (LDH) levels. As the use of multichannel analyzers becomes more widespread more reactions of this type will be observed in patients receiving other drugs.

Carbenicillin: clinical and laboratory experience with a parenterally administered penicillin for treatment of Pseudomonas infections.

Carbenicillin, an alpha carboxybenzyl penicillin, was evaluated in the treatment of pseudomonas, proteus, and enterobacter infections in 41 patients. It was possible to obtain blood and urine concentrations of carbenicillin that were bactericidal for most Pseudomonas and Proteus strains by use of constant intravenous infusions of the drug. Carbenicillin was highly effective in the treatment of urinary tract infections and bacteremia. It was less effective in pulmonary infections, particularly in patients with advanced cystic fibrosis. Klebsiella overgrowth occurred in some patients treated for pulmonary and wound infections. Transient elevations of serum glutamic-oxalacetic transaminase (SGOT) were noted in children. Treatment with 30 g/day did not cause renal, hematologic, or neurologic toxicity. Carbenicillin represents a major advance in the therapy of serious pseudomonas and indole-positive proteus infections.

Diabetic ketosis: elevated serum glutamic-oxaloacetic transaminase (SGOT) and other findings determined by multi-channel chemical analysis.

Twelve-channel chemical analysis (sodium, potassium, chloride, CO2, total protein, albumin, calcium, alkaline phosphatase, total bilirubin, urea nitrogen, glucose, and glutamicoxaloacetic transaminase [SGOT] was performed on sera from fifty-five of sixty-one cases of diabetic ketosis hospitalized over a two-year period. The cases represented consecutive admissions and were not selected for severe ketoacidosis. Abnormalities of the serum sodium, potassium, chloride, CO2, calcium, urea nitrogen and glucose generally conformed to recognized patterns, and abnormalities of the total protein, albumin, alkaline phosphatase, and total bilirubin were noted in a minority of cases. In contrast, the SGOT was elevated in 69 per cent of all cases and in 82 per cent of those in whom the determination was performed on the day of admission. Elevation of the SGOT in ten of eleven patients with hepatomegaly and the relationship between elevations of the SGOT and elevations of the serum glutamic-pyruvic transaminase and lactic dehydrogenase, as well as the recognized occurrence of fatty infiltration of the liver in uncontrolled diabetes, are consistent with an hepatic origin for the elevated SGOT found in patients with diabetic ketosis.

Cirrhosis and the hepatic photoscan.

HEPATIC photoscanning has been utilized mainly for the detection of space-occupying lesions, but cirrhosis may produce localized scan defects indistinguishable from space-occupying lesions (1–4). Colloidal gold (198Au) has been utilized as the hepatic scanning agent and 2 reports have stated that increased splenic uptake of this material should alert the physician to the probability of cirrhosis as the etiology of the defect on the photoscan (2, 4). 99mTc-S colloid was introduced as an hepatic photoscanning agent by Harper et al. in 1964 (5, 6). The increasing use of this material prompted us to evaluate both agents in patients with proved cirrhosis and localized defects on hepatic photoscans. Methods Fifteen minutes after intravenous injection of 150 µCi of 198,Au colloid or 2 to 3 mCi of 99mTc-S colloid, the photoscan was begun, using a rectilinear photoscanner (Picker-Magnascanner) with a 3-inch Nal crystal and a 19-hole focusing collimator at a speed of 60 cm/min. for 198Au and 90–120 cm/ruin. for 99mTc. Scan parameters varied slightly during the study, but a count rate differential (CRD) of 60 and a density of 50 for 198Au and a CRD of 50 and a density of 18 for 99mTc were customary. Line spacings of 0.35 cm were used. Pulse-height analyzer window settings of 355 to 460 keV and 130 to 155 keV were utilized for 198Au and 99mTc, respectively. Hepatic photoscans were routinely obtained with 198Au colloid. Patients with localized defects and proved or suspected cirrhosis were restudied with 99mTc-S colloid, which was prepared by the method described by Patton et al. (7). Pathological diagnosis in the patients reported was confirmed at surgery or autopsy. Biopsy alone was not sufficient for inclusion in this series. Splenic manometry was performed in 7 patients and portacaval anastomosis in 5 patients in this series. Both preoperative and postoperative photoscans with both agents were obtained in these cases. Hepatic function tests were performed within seven days of the photoscans in all patients. Results Thirteen patients were observed to conform to the described criteria: localized scan defect, cirrhosis, and no evidence of tumor at surgery or autopsy (TABLE I). A review of the liver function tests in these patients revealed almost invariable evidence of active liver disease as manifested by an elevated alkaline phosphatase and SGOT (serum glutamic oxaloacetic transaminase). It was not known whether the abnormal liver function tests were associated with the localized scan defect or merely a reflection of our method in selecting patients for hepatic photoscanning. The initial photoscan in 9 of the 13 patients revealed increased splenic uptake of 198,Au colloid, arbitrarily defined as splenic concentration equal to or greater than the concentration in the left hepatic lobe.

A Screening Test for Detection of Elevated Serum Glutamic Oxalacetic Transaminase Activity

A Screening Test for Detection of Elevated Serum Glutamic Oxalacetic Transaminase Activity

Anicteric Infectious Hepatitis: A Population Study.

s1 October 1964Anicteric Infectious Hepatitis: A Population Study.Frederick W. Sprong, Robert DeForest, James G. Harmeling, Jack T. JonesFrederick W. SprongSearch for more papers by this author, Robert DeForestSearch for more papers by this author, James G. HarmelingSearch for more papers by this author, Jack T. JonesSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-808_4 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe incidence of anicteric infectious hepatitis was studied in 737 military personnel from a group who had been inadvertently exposed to infectious hepatitis by the development of this disease in a food handler in their mess. Each week for 10 weeks, the men were questioned for symptomatology consistent with infectious hepatitis and a blood sample obtained for determination of serum glutamic oxaloacetic transaminase (SGOT). Of the entire group, 76% had an elevated SGOT at some time during the course of the study: 96 of these were admitted to the hospital for further study. All but a few of those admitted... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Frederick W. Sprong; Robert DeForest; James G. Harmeling; Jack T. JonesAffiliations: Newport, R. I. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 808-809KeywordsArmed forcesBloodFoodInfectious diseasesInfectious hepatitisSerum glutamic oxaloacetic transaminase ePublished: 1 December 2008 Issue Published: 1 October 1964 PDF downloadLoading ...

Serum Glutamic-Oxaloacetic Transaminase Levels, Muscular Dystrophy and Certain Hematological Measurements in Chicks and Poults as Influenced by Vitamin E, Selenium and Methionine

STUDIES on muscular dystrophy in chicks have demonstrated that its development depends on a simultaneous deficiency in vitamin E and sulfur-containing amino acids (Dam et al., 1952; Machlin and Shalkop, 1956). Although dietary selenium by itself has been found only partially effective for preventing dystrophy in chicks (Nesheim and Scott, 1961), a synergistic effect between vitamin E and selenium was recently shown (Calvert et al., 1962). In contrast to this, muscular dystrophy in turkey poults can be prevented with dietary selenium as well as vitamin E, whereas the sulfur-containing amino acids are without effect (Walter and Jensen, 1963). Possible synergistic effects of vitamin E and selenium in the prevention of dystrophy in poults have not been tested.An elevated serum glutamic-oxaloacetic transaminase level (GOT) has been suggested as a suitable diagnostic test for muscular dystrophy in lambs and calves (Kuttler and Marble, 1958). Cornelius et al. (1959) reported that inherited…

Experimental Groundnut Poisoning in Pigs

SUMMARY Pigs were poisoned by feeding rations containing 17½–20 per cent toxic groundnut meal. Changes in the livers progressed through steatosis, ductule proliferation and pericellular fibrosis to parenchymal karyomegaly, dissecting fibrosis and finally nodular hyperplasia. The lesions were sometimes accompanied by elevated serum glutamic-oxaloacetic transaminase (SGOT) and alkaline phosphatase levels, increased hepatic concentration of fat, reduced hepatic levels of vitamin A and low thyroid bodyweight ratios.

Glutamic oxaloacetic transaminase in serum and cerebrospinal fluid in parkinsonism.

INCREASED SERUM ENZYMES have been found in certain neuromuscular diseases, e.g. muscular dystrophy, and glutamic oxaloacetic transaminase (GOT) values of cerebrospinal fluid (CSF) have been found to be elevated in cerebral infarction following cerebrovascular accidents, in brain damage associated with head injury, as well as in some other conditions of nervous system disease. It has been noted that the blood-CSF barrier results in enzyme activities that are relatively independent for serum and cerebrospinal fluid. (A recent study using I 131 in puppies demonstrated the increased permeability of the blood-CSF barrier to GOT after prolonged hypoxia.) For this reason and because of the relative ease of acquiring blood, the clinical study of CSF enzymes and the knowledge of their alterations have been limited. Since this study was completed, increased CSF-GOT values have been found in children with acute paralytic poliomyelitis with no serum-glutamic oxaloacetic transaminase (S-GOT) correlation, and, an elevated S-GOT has

Influenza myocarditis. Report of a case with observations on serum glutamic oxaloacetic transaminase.

This report is the study of a case of acute myocarditis with an associated elevation of influenza A complement fixation titer and complete absence of underlying heart disease. The patient had a 13-day elevation of serum glutamic oxaloacetic transaminase (SGO-T) which was felt to be related to the activity of the myocarditis. The literature concerning influenza myocarditis and SGO-T changes in myocarditis was reviewed. It was concluded that the patient's clinical course and SGO-T changes were compatible with those seen in myocarditis of varied etiology, and that a prolonged elevation of SGO-T may be of some assistance in making the difficult diagnosis of myocarditis. This is the first reported case in which underlying coronary artery disease was excluded by coronary angiography.

Serum enzyme activities following morphine. A study of transaminase and alkaline phosphatase levels in normal persons and those with gallbladder disease.

An increase of serum glutamic oxalacetic transaminase (SGO-T) activity following myocardial infarction was first described by LaDue et al. 1 and subsequently confirmed by numerous investigators. 2-6 Much emphasis has been placed on elevated SGO-T values in substantiating the clinical impression of myocardial infarction, especially when the electrocardiogram reveals equivocal changes, previous infarction, left bundle branch block, or arrhythmia. 7-9 With increased understanding of the ubiquitous nature of GO-T distribution in human tissues, it has become apparent that liver necrosis 10-14 and a host of other disease states 5,6,15-21 can provoke a rise in SGO-T activity. Thus, confusion may still exist when there is elevated SGO-T activity in the absence of electrocardiographic evidence of heart muscle damage. Obstructive biliary tract disease causes a rise in SGO-T activity, 22,23 and this rise may be unrelated to hepatic necrosis. 24 The demonstration of high GO-T activity in bile 25 further serves to

Propionyl Erythromycin Ester Lauryl Sulfate and Jaundice

To the Editor:— In the past 6 months we have received clinical and laboratory data from physicians, indicating that on rare occasions a patient receiving propionyl erythromycin ester lauryl sulfate (Ilosone) may develop sensitivity to the drug manifested by reversible jaundice and liver function test changes of the intrahepatic cholestasis type. Laboratory studies in 7 well-studied patients have been characterized by increased direct-reacting bilirubin levels, negative or weakly positive cephalin flocculation and thymol turbidity tests, elevated serum glutamic oxalacetic transaminase levels (in the range of 100 to 300 units), peripheral eosinophilia, normal cholecystograms, and in some instances elevated alkaline phosphatase levels. In 4 of these 7 patients, symptoms of abdominal distress and jaundice recurred on administration of a second course of the antibiotic, and in one, the symptoms reappeared on readministration of a third course of therapy. A fifth patient developed jaundice following a course of therapy, and then received

The effect of deuterium oxide on ascites tumor growth in mice.

The growth of Krebs-2A ascites tumors in mice was appreciably depressed by the presence of deuterium in the body fluids in concentrations ranging from 13 to 32%. Measurement of the glutamic oxalacetic transaminase (GO-T) levels revealed that with increasing deuteration there was a prcgressive elevation of serum GO-T in tumor-bearing mice and an even more rapid rise of ascitic plasma GO- T. These data suggest that deuteration of the organism leads to tumor-cell injury with resulting release of GO-T into the ascitic fiuid, whence it is carried into the general circulation. The notion that deuterium injures and possibly destroys mouse ascites tumor cells is supported, in part, by the terminal increase in the incidence of eosin-stainable tumor cells and, in part, by the absence of any striking difference in mitotic index of deuterated and nondeuterated tumor cells. These conclusions also apply to transplantable mouse ascites tumors. (auth)

Serum glutamic oxalacetic transaminase (SGO-T) in conngestive heart failure: clinical study and review of the literature.

Article1 May 1960SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGO-T) IN CONGESTIVE HEART FAILURE: CLINICAL STUDY AND REVIEW OF THE LITERATURERONALD G. FRAGGE, M.D., FREDRIC B. KOPEL, M.D., ARNOLD IGLAUER, M.D., F.A.C.P.RONALD G. FRAGGE, M.D.Search for more papers by this author, FREDRIC B. KOPEL, M.D.Search for more papers by this author, ARNOLD IGLAUER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-52-5-1042 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONConsiderable confusion has arisen in the interpretation of serum glutamic oxalacetic transaminase (SGO-T) levels as the number of clinical conditions to which this determination has been applied has increased. This refers in particular to congestive heart failure. Numerous series have been reported in which the levels of SGO-T have varied widely. Some observers have reported that acute congestive heart failure with liver engorgement may be associated with significant SGO-T elevation. Another author has stated that right heart failure does not ordinarily affect significantly the level of SGO-T activity.PROCEDURERecords of patients with congestive heart failure were surveyed from...Bibliography1. KarmenWróblewskiLaDue AFJS: Transaminase activity in human blood, J. Clin. Investigation 34: 126-133 (Jan.) 1955. CrossrefMedlineGoogle Scholar2. Sherlock S(a) : Diseases of the liver, edited by L. Schiff, 1956, J. B. Lippincott Co., Philadelphia, pp. 529-533. (b) Popper, H., and Schaffner, E.: Liver: structure and function, 1957, The Blakiston Co., pp. 473-478. Google Scholar3. MolanderWróblewskiLaDue DWFJS(a) : Serum glutamic oxalacetic transaminase as an index of hepatocellular integrity, J. Lab. and Clin. Med. 46: 831-839 (Dec.) 1955. (b) Wróblewski, F., Jervis, G., and LaDue, J. S.: The diagnostic, prognostic and epidemiologic significance of serum glutamic oxalacetic transaminase (SGO-T) alteration in acute hepatitis, Ann. Int. Med. 45: 782-800 (Nov.) 1956. MedlineGoogle Scholar4. ShieldsShannon LARE(a) : Acute hepatic congestion as a factor in elevated serum glutamic oxalacetic transaminase titers above 400 units, Am. J. M. Sc. 236: 438-446 (Oct.) 1958. (b) Dewar, H. A., Rowell, M. B., and Smith, A. J.: Serum glutamic oxalacetic transaminase in acute myocardial infarction, Brit. M. J. 2: 1121-1125 (Nov. 8) 1958. (c) Hanson, H., and Biorck, G.: Glutamic oxalacetic transaminase in the diagnosis of myocardial infarction, Acta med. scandinav. 157: 493-502 (June) 1957. CrossrefMedlineGoogle Scholar5. LiebermanLaskyDulkinLobstein JIISIOE: Serum glutamic oxalacetic transaminase activity in conditions associated with myocardial infarction, Ann. Int. Med. 46: 497-505 (Mar.) 1957. LinkGoogle Scholar6. ChinskySchmagranoffSherry MGLS(a) : Serum transaminase activity: observations in a large group of patients, J. Lab. and Clin. Med. 47: 108-118 (Jan.) 1956. (b) Chinsky, M., Wolff, R. J., and Sherry, S.: Serum transaminase activity. A comparison of pyruvic and oxalacetic transaminase, Am. J. M. Sc. 233: 400-408 (Apr.) 1957. (c) Denney, J. L., McAuley, C. B., Martin, H. E., Ware, A. G., and Segalove, M.: Evaluation of the serum glutamic oxalacetic aminopherase (transaminase) test, J. A. M. A. 161: 614-616 (June 16) 1956. (d) Dutoit, C. H., quoted by Conrad, F. B.: Transaminase, New England J. Med. 256: 602-607, 1957. (e) Kessler, G., and Phelps, A.: Serum glutamic oxaloacetic transaminase, J. Albert Einstein M. Center 4: 91-94 (June) 1956. (f) Ratner, J. T., and Sacke, H. J.: Transaminase in coronary artery disease, Canad. M. A. J. 76: 720-725 (May) 1957. MedlineGoogle Scholar7. Friedberg CK: Diseases of the heart, 2nd Ed., 1956, W. B. Saunders Co., Philadelphia, p. 511. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cincinnati, Ohio*Received for publication October 8, 1959.From the Department of Internal Medicine, the Jewish Hospital Association, Cincinnati.†Present address: Brooklyn Jewish Hospital, Brooklyn, N. Y.Requests for reprints should be addressed to Ronald G. Fragge, M.D., Bellevue Hospital, Twenty-sixth Street and First Avenue, New York, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCardiac HepatopathyHypoxic hepatitisExtreme Elevation of Transaminase Levels in Acute Heart Disease-a Problem in Differential Diagnosis?LATE RISE IN SGPT AFTER ACUTE MYOCARDIAL INFARCTIONSerumenzyme nach ElektroregularisationTHE VALUE OF SERUM CREATINE PHOSPHOKINASE ESTIMATIONS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTIONMyokinasebestimmungen in der Diagnostik des HerzinfarktsSerum α-hydroxybutyric dehydrogenase (HBD) in myocardial infarctionCardiac Failure Simulating Viral Hepatitis Three Cases with Serum Transaminase Levels above 1,000ROBERT G. LOGAN, M.D., FRANK M. MOWRY, M.D., RICHARD D. JUDGE, M.D.Alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes 1 May 1960Volume 52, Issue 5Page: 1042-1050KeywordsAminotransferasesClinical chemistryEdemaElectrocardiographyEmphysemaHeart failureHospital medicineLongitudinal studiesResearch laboratoriesTechnicians ePublished: 1 December 2008 Issue Published: 1 May 1960 PDF downloadLoading ...

High serum transaminase activity in heart disease. Circulatory failure and hepatic necrosis.

A survey of all patients with very high serum glutamic oxalacetic transaminase activity encountered during a 30-month period at The New York Hospital revealed 17 patients with cardiac disease who had 1 or more serum glutamic oxalacetic transaminase (SGOT) determinations exceeding 500 units. None had clinical evidence of primary liver or gallbladder disease. Eleven were admitted with acute myocardial infarction, 6 with severe heart failure. All 17 developed hypotension or shock and all but 1 right heart failure prior to high SGOT activity. Several patients had abnormalities of liver function when SGOT activity was very high. In 4 there was an excessive increase in prothrombin time following administration of anticoagulants. In the 8 patients who came to autopsy there was histologic evidence of acute hepatic central necrosis. In 4 there was necrosis of both heart and liver, in 4 necrosis of liver alone. Clinical and autopsy data from a control series of patients with heart disease selected without regard for the level of SGOT activity corroborate the association between hypotension, central necrosis of the liver, and increased SGOT activity. Increase in venous pressure in the absence of hypotension was not associated with acute central necrosis or elevated SGOT activity. It is concluded that very high SGOT activity (>500 units) in patients with heart disease is at least in part caused by acute hepatic central necrosis secondary to a drop in cardiac output and reduced hepatic blood flow. Caution is urged in the interpretation of increased blood activity of intracellular enzyme systems as evidence for myocardial necrosis. Acute circulatory changes may result in hepatic necrosis and increased blood enzyme activity without myocardial infarction.