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Transcript of FATTY LIVER



Special Articles



AT the second annual meeting of the Association forthe Study of Liver Diseases, held in Chicago on Nov. 1,1951, a panel discussion on fatty liver occupied theafternoon session. The panel comprised Dr. Paul Gyorgyof Philadelphia, Dr. Charles S. Davidson of Boston

(Mass.) and Bethesda, - Dr. W. Stanley Hartroft of

Toronto, and Dr. Victor M. Sborov of Washington, D.C.Dr. Gyorgy summarised their conclusions as follows :We agree that there are various forms of fatty liver ;

the classical form, which is still in the foreground ofour interest, is the so-called dietary fatty liver, easilyproduced experimentally in animals by feeding them ona diet free from choline and its precursors, the methionine-eontaining proteins. The other forms of fatty liverdepend mainly on endocrine factors, the most importanthormones in this respect being insulin (emphasisedespecially by Prof. C. H. Best, F.R.s.), and those ofthe thyroid, pituitary (adipokinine), and adrenal glands.The pathology of the fatty liver varies with its cause-dietary or hormonal-and in many cases histologicaldifferences are seen. The fatty metamorphosis of cholinedeficiency usually starts centrally, while the pituitary-induced type of degeneration commonly extends inwardsfrom the periphery. The old view, which is still generallyheld, was that choline deficiency produces a fatty liverbecause choline is required for the transport of neutralfat from the liver, and neutral fat can only be transportedfrom the liver in the form of phospholipid. This explana-tion cannot be easily reconciled with the well-establishedfact that, on a choline-free diet, fat accumulates in theproximal convoluted tubules of the kidneys as .well asin the liver. It is also hard to explain the fatty liverfound in obese persons and in diabetics. Varioushepatotoxins and bacterial toxins, as yet unidentified,may be responsible.Ethionine, the ethyl homologue of methionine, also

produces a fatty liver, especially in female animals, and’

this is associated with changes in the pancreas, probablycaused by impaired protein synthesis. Protracted feedingwith ethionine finally leads to a sudden reduction in the

’ fat content of the liver to below its normal level.The liver-function tests most commonly affected by

fatty changes are the bromsulphalein and urinaryurobilinogen tests. Glucose tolerance also seems to beimpaired by the degeneration. There is some evidenceto suggest that the fatty liver of obesity may be relatedto pituitary insufficiency. But the pathogenesis of thecondition and the underlying metabolic reactions requirefurther study.

Choline and its precursors have no definite lipotropiceffect on the fatty liver of obesity. Here only a strictreducing diet seems to be effective. The correlationbetween histologically demonstrable fat and biochemi-cally analysed fat seems to be fairly satisfactory providedthat a rather complicated histological technique (freeze-drying, phase miscroscopy, &c.) is followed.

In fatty.liver, especially the dietary type, the fattycysts described by Hartroft are an important stage inthe pathogenesis of the cirrhosis which may follow.When such cysts are present, in experimental as well ashuman cirrhosis, Elias has pointed out that the remainingliver cells may also be damaged. In irreversible liverdamage, even after treatment, the liver cell plates consistof double and not single cells. Regeneration of the fattyliver may proceed until there is no obvious impairmentof function compared with the non-fatty liver.

In alcoholism with uncomplicated fatty liver anyreasonable treatment in hospital will help the patient.The lipotropic drugs are not necessary in the managementof this condition. A normal and even a relativelylow-protein diet, rest in bed, and withdrawal of alcoholwill reverse the fatty changes. On a strict syntheticdiet consisting of glucose, water, and vitamins (withoutcholine), however, even under hospital care and withrestricted exercise, the alcoholic’s fatty liver will showno histological improvement. On such a regime liver-

function tests do not show the improvement which maybe observed even on very low protein diets.

Alcohol may damage the liver in two ways. In smaller,non-intoxicating doses, it seems to promote fatty degen-eration by upsetting the distribution of calories betweenthe dietary constituents. This change is not directlycaused by alcohol ; it may result from variations incarbohydrate and perhaps also in fat intake. In largerdoses alcohol may act as a hepatotoxin. Central necrosisof the liver, following acute alcoholism, may be causedby disturbance of the hepatic circulation. Suddenvascular collapse, rather like traumatic shock, may occurin acute alcoholic intoxication. This carries a highmortality, but at necropsy the usual findings are simplythose of fatty liver. The disturbance in hepatic circula-tion may also explain the broad bands resulting frommassive collapse, found occasionally in alcoholic cirrhosis.After intoxicating doses of alcohol, increased amountsof coproporphyrin may be excreted in the urine ; thisabnormal excretion is suppressed by nikethamide or

nicotinamide.Among chronic alcoholic blood donors with fatty

degeneration or cirrhosis of the liver, even without anyhistory of previous jaundice, several were found to becarriers of the hepatitis virus. The question ariseswhether such a latent hepatitis infection is more commonin patients with fatty liver, alcoholic or otherwise, thanin people with a normal liver.The next meeting of this association is to be held in

Chicago in the autumn, on the day before the meetingof the Central Society for Clinical Research. In theafternoon session there will be a symposium on hepaticcoma, led by Dr. Cecil J. Watson. -

1. Steinberg, H., Lewis, H. E. Brit. med. J. 1951, ii, 465.


RESEARCH into the use of films in instruction wasreviewed at a combined meeting of the Scientific FilmAssociation and the Royal Society of Medicine on Feb. 29.

Dr. H. ELLIs LEWIS described his investigations at

University College Hospital.l Questionaries had beenused in order : (1) to evaluate students’ subjectiveappraisal of the film’s technical and teaching qualities,which was highly favourable ; and (2) to collect

objective evidence of increase in knowledge, which showeda significant increase that was more distinct in respectof minor facts than of basic principle. Dr. Lewisemphasised that this experiment was not designed tocompare the film with any other teaching medium, butmerely to show that it could impart useful knowledgewhich was subsequently maintained.


Mr. J. SHEaR,MAN, of the film section, British TransportCommission, reviewed research at the Pennsylvania StateCollege on behalf of the U.S. Navy, which required amedium of mass instruction in the absence of skilledteachers. Thus they were not asking themselves whetherthe film was the best method of instruction but ratherhow the content of a film could be put over to the bestadvantage. In this investigation, which was larger thanany previously carried out, 15,000 subjects had beenshown films under controlled conditions ; as many as17 versions of one film had been made. Mr. Shearmansaid that so far the results had revealed little thatwas unexpected. Occasionally, however, widely held.opinions-for example, that incorrect methods shouldnot be demonstrated-were contradicted. He questionedwhether some factor was not lost when a film was brokendown into a succession of technical tricks, each of whichwas investigated individually. He felt that researchmust also concern itself with such questions as the effectsof the investigations themselves on the audience, thedesire to learn, conditions of viewing, participation, andso on. He dissociated himself from the view that weshould not make more films until we knew more, and

emphasised that research and the making of films shouldgo hand in hand.