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Acute Alcoholic Hepatitis Without Jaundice BRans 580 SEPT. 1, 1962 ACUTE ALCOHOLIC HEPATITIS MEDICAL JOURDNAL Br Med J: first published as 10.1136/bmj.2.5304.580 on 1 September 1962. Downloaded from Investigations.-Hb, 16.9 g./100 ml.; W.B.C, 9.850/ ACUTE ALCOHOLIC HEPATITIS c.mm.; E.S.R. 39 mm. in 1 hour (Westergren). Serum glutamic oxaloacetic-transaminase (S.G.O.T.), 60 units. WITHOUT JAUNDICE Serum total proteins, 7.3 g./100 ml. (albumin 4.6 g., BY globulin 2.7 g.). Total serum bilirubin, 0.9 mg./l100 ml.; serum alkaline phosphatase 10 units/ 100 ml.; thymol A. GORDON BECKETT, B.M., M.R.C.P. turbidity, 1 unit; thymol flocculation negative; colloidal Consultant Physician, New End Hospital, London gold, 0; zinc sulphate turbidity, 2. Prothrombin concentration, 100%. Pyruvate tolerance test within normal A. V. LIVINGSTONE, M.B., M.R.C.P. limits. Liver biopsy (third day after admission): marked Senior Medical Registrar, Royal Free Hospital, London fatty change with cellular degeneration and necrosis and AND with inflammatory activity; stellate scarring; moderate amount of iron pigment intracellularly in the Kupifer cells K. R. HILL, M.D., MIR.C.P., F.R.I.C. and in the portal triads. Professor of Pathology, Royal Free Hospital, London Progress.-On a low-fat diet he rapidly became symptom- free and regained his appetite, being discharged after Acute alcoholic hepatitis with frank jaundice and typical 13 days in hospital. histological changes in the liver is a severe and some- times fatal illness which follows intensified drinking of TABLE II.-Summary of Histological Findings alcohol by the chronic alcoholic (Beckett et al., 1961). 0 A similar less severe illness with the characteristic histo- logical changes may occur without jaundice. This sub- icteric disorder, like the jaundice one, produces anorexia, nausea and vomiting, upper abdominal pain, and fever. Alcoholism may remain unsuspected or even be denied initially by the patient. Recovery occurs spontaneously without specific treatment, as the symptoms temporarily Biopsy 9 0 0 + t+ 0 + 0 + 0 + alcohol. B +y+6 +0+ ++ + + 0 + 0 +- prevent further drinking of 2 .. 1 ++ ++ + + 0 0 + 0 + of this milder subicteric illness have 3 .. 18 0 + + 0 + 0 . + + Five examples 4 .. 10 0 + ++ 0 + 0 + + + been recognized recently. Their details are summarized 5 . 4 0 + + + + 0 i i + in Tables I and I1, and a typical case history is given. 1 1t = IVI^4OSCU1151genange. -1--t = NIoaerTeIiiocase c;nange.Pona.gc _±ncani:J = bcun1y conancnange. Several other patients have been suspected of having 0=Absent.0 Abse this condition, although histological proof is lacking. Histology Some of the cases described here had previously The appearances, details of which are had similar illnesses, which were given, probably histological given in Table II, are similar, though in lesser degree, erroneously, such diagnoses as cholecystitis, dyspepsia, to those found in jaundiced alcoholics (Beckett et al., or " P.U.O." This suggests that the condition may not 1961). Naturally the changes present in any one section be uncommon, and, like the jaundiced illness, be frequently misdiagnosed. will depend on the size of the biopsy, and more parti- http://www.bmj.com/ cularly on the stage of the illness when it was taken. Illustrative Case History The features common to all five biopsies were cellular degeneration and necrosis, with an acute inflammatory A sailor aged 59 (Case 1) had been a heavy drinker for was present 30 years. At the age of 31 he had had an attack of jaundice reaction, and stellate scarring. Fat in of undetermined aetiology, although it had followed a significant amounts in four biopsies out of five. debauch and was accompanied by upper abdominal pain. Mallory's hyaline was present in two biopsies. Only one After protracted celebrations over Christmas, he was patient showed the changes of established cirrhosis. admitted to the Royal Free Hospital at the end of January, on 29 September 2021 by guest. Protected copyright. 1960. with a four-weeks history of intermittent right upper Clinical Commentary abdominal pain. nausea, vomiting, and general malaise. Nothing to suggest jaundice had been noticed. Positive The prominent clinical features of these cases were physical findings were limited to palmar erythema, a non- upper abdominal pain, predominantly right-sided and tender liver enlarged 4 cm. below the costal margin, and a persisting for varying periods of time, anorexia, pyrexia, low-grade fever lasting nine days. nausea, and even vomiting following the imbibing of TABLE I.-Main Presenting Features Duration of Known Liver Ag illness duration of enlargement Upper Prothrombin S.G.O.T. Case Mai Prsnig below pen- No.N. andsex admissionbefore amsyposhospitalpresenting fever in costalRtt meaymegaly TendernessAbdominal Concentration(% (on admission) (days) (days) margin __|__ _ 1 59 M 28 R upper abdominal 9 4 cm. Nil None 100 60 pain Anorexia. Vomiting. Malaise 2 35 F 35 R upper abdominal 7 4 cm. Nil None 43 78 pain. Anorexia. Nauaea. Vomiting. Diarrhoea. 3 54 M 5 R upper abdominal 6 4 cm. Nil None 100 - pain. Anorexia. Oedema of lees 4 65 M 28 An.rexia Lower cen- 6 Nil Nil None 100 42 tral chest pain. Loss (Oth day after of wrlaht. Diarrhoea admison) 5 59 M 7 R. upper abdominal 2 Nil Nil None 100 35 pain. Anorexia. Nausea. Vomiting BRITISH 581 SEPT. 1, 1962 ACUTE ALCOHOLIC HEPATITIS 581 1, MEDICAL JOURNAL Br Med J: first published as 10.1136/bmj.2.5304.580 on 1 September 1962. Downloaded from excessive quantities of alcohol. A history of alcoholism factor, but also suggested that lack of exercise, over- was not readily forthcoming in two patients. The eating, and tropical diseases might play a part. Hurst prospect of surgical intervention in such cases is con- (1941) made almost identical observations, again speci- siderable, though a fruitless operation would be less fying the European in tropical climates as being prone harmful than in those with jaundice or ascites. to alcoholism and suggesting the other possible factors Three patients had themselves correlated upper mentioned above. He thought clinical recovery was the abdominal pain with excessive drinking on several rule provided teetotalism was practised thereafter, and previous occasions. Two of them had been told else- he recognized that the patient with established cirrhosis where that the gall-bladder was the source of their pain - came into a different category, but admitted that no one had had a cholecystectomy for symptoms which histological proof existed for his beliefs. persisted unchanged, as did his habits thereafter, while As Hurst's patients either recovered or much later the other, notably reticent about being an alcoholic, had appeared as cases of established portal cirrhosis, no evaded this operation only by failure to accept admission further progress in the understanding of their illnesses, for it on two occasions. Surprisingly none of the histologically or otherwise, could be made at that time. patients described had tenderness of the liver. Now that needle biopsy of the liver is a safe procedure With the exception of a slightly raised serum bilirubin in skilled hands, it is possible to establish the presence initially in Case 3 and a low serum albumin with reduced and nature of the structural changes. Indeed, as no prothrombin concentration in Case 2, the standard tests test of liver function, other than the recently introduced of liver function were within normal limits in all cases. serum enzyme tests such as the transaminases, constantly The S.G.O.T. was raised in three of the four cases in indicates liver cell damage, biopsy is the only way of which it was estimated (in one only marginally so). making an accurate diagnosis. In contrast to jaundiced cases, no abnormality in the The histological abnormalities in this acute illness are total or differential white-cell count and no anaemia liver-cell degeneration and necrosis surrounded by acute was encountered (although one was known to have had inflammatory cells, together with inflammatory changes a macrocytic anaemia during a previous similar episode in the portal tracts. Mallory's alcoholic hyaline, prob- elsewhere). ably the result of liver-cell degeneration, may be seen. Some conclusive diagnostic biochemical test in addi- Fatty change is almost universal, as is some degree of tion to the serum transaminases would be of great stellate scarring of the portal tracts in the more value, but clinical awareness of the illness is essential if prolonged cases. In addition to these changes, there these and needle biopsy of the liver, at present the only will also-be evidence of any pre-existing disease. It certain method of diagnosis, are to be undertaken. must be stressed that established cirrhosis is not an of this and indeed was seen The important differential diagnosis from acute essential part illness, only alcoholic hepatitis without jaundice is probably once in the present series. pancreatitis, acute recurrent or chronic, to which The illness discussed here does not appear to have alcoholics appear to have an increased susceptibility been described adequately before, although Neame and Joubert (1961), in a of following (Shallenberger and Kapp, 1958; Bartholomew and Cain, study hypoglycaemia http://www.bmj.com/ 1961 ; Howard and Ehrlich, 1961), although this is alcoholic bouts in non-jaundiced Africans and Indians, denied by others. Pancreatitis, not thought to have suggested that the hypoglycaemia was caused by an acute produced the symptoms in the present series, is probably toxic hepatitis due to alcohol. The report of their liver a more severe illness, at least in the earlier attacks, biopsies made no reference to cellular degeneration and affecting particularly alcoholics below the age of 40, and necrosis or to acute inflammatory changes; 14 of the has a poor prognosis (Howard and Ehrlich, 1961).
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