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ALCOHOLISM AND HEPATIC CIRRHOSIS
1077
Conferences ALCOHOLISM AND HEPATIC CIRRHOSIS A MEETING on alcoholism and cirrhosis of the liver was held in New York on Nov. 20 and 21 under the presidency of Dr. HANS POPPER (New York) and under the auspices of the National Council on Alcoholism. Cirrhosis is now the fifth commonest cause of death in the United States. It was estimated that one in sixteen of those who take alcohol becomes an alcoholic and about 8% of these will develop cirrhosis. C. H-. BEST (Toronto) believed that the basis of the relation between the two was a nutritional one. A precirrhotic fatty-liver stage could be induced in rats by giving, for about a year, a diet containing 15-30% of calories as alcohol. This change could always b? prevented by choline or methionine. G. KLATSKIN (New Haven) noted that, in rats, alcohol reduced the food intake and increased the requirement for choline. Alcohol could induce fatty change irrespective of calories consumed, and this was reversed by choline. The lesion in the liver of the rat, however, differed from that seen in man: inflammation and degenerative changes in the liver cells were absent. He speculated whether there might not be an additional factor in the human disease, perhaps a direct " toxic effect, perhaps additional infection. The mechanism of fatty liver in alcoholics was further discussed. W. S. HARTROFT (St. Louis), by electron microscopy, had noted that in the fatty liver produced by excess calories the fat was periportal in distribution and situated in little orgastoplasmic saccules, whereas in choline deficiency the fat was centrizonal and the mitochondria were enormous. In choline deficiency the mitochondria might be unable to wrap around- the fat globules with possible interference with oxidative J. H. enzymes on the surface of the mitochondria. QUASTEL (Montreal) had studied the effect of alcohol on isolated liver tissue and found an inhibition of phospholipid production and a stimulation of fatty-acid synthesis. C. S. LIEBER (Boston) had incubated trace amounts of "C-labelled acetate or ethanol with rat liver slices. Both served equally well for fatty-acid synthesis although far more fatty acid was found with ethanol than with He believed that ethanol acted as a donor of acetate. hydrogen ions reducing dipyrridine phosphate (D.P.N.). H. M. MALING (Bethesda) related the acute experimental fatty liver after alcohol to altered fat transport, the fatty acids coming from depot adipose-tissue. The incidence of cirrhosis parallels the consumption of alcohol in a community, but less than 10% of alcoholics develop liver injury. The cause of the individual susceptibility is not known. W. S. HARTROFT emphasised the importance of preceding obesity. F. SCHAFFNER found a four incidence in white times (New York) greater than in the coloured patients seen at Cook County Hospital, Chicago. C. M. LEEVY (Jersey City) observed a higher incidence in those presenting with delirium tremens, 25% of whom showed cirrhosis and 30% fatty
change. The usual cirrhosis in alcoholics is a fine Laennec’s (about 80%). It was agreed, however, that about 8% show a coarse postnecrotic type of lesion and 10% a mixed picture. The association of alcoholism with hsemochromatosis was stressed, 2% of cirrhosis in alcoholics being of this type. The transition of Laennec’s
one
postnecrotic cirrhosis has been described both in animals and by serial needle biopsies in man. This transition is liable to occur if the alcoholic abstains and large nodules regenerate in the liver. The liver cells in alcoholism contain basophilic amorphous material, the Mallory bodies. H. POPPER had seen these in both the Laennec and postnecrotic cirrhosis developing in alcoholics but never in non-alcoholics. P. E. STEINER (Philadelphia), on the basis of studies in Africans, disagreed ; for he found Mallory bodies very frequently in the absence of alcoholism and even of fat in the liver cells. R. M. KARK (Chicago) had seen severe fatty change and ascites disappear in alcoholics given a good diet, and it was generally agreed that this was true of other acute changes in the liver such as polymorph infiltration; fibrosis could diminish. S. SHERLOCK (London) believed that once the architecture of the liver was disturbed anatomical restitution was impossible. C. S. DAVIDSON (Boston) emphasised the distinction between the acute changes (with fat, necrosis, inflammatory cells and Mallory bodies, and clinically liver failure) and the chronic burntout stage (with mainly fibrosis and clinically the development of portal hypertension). The improvement in an alcoholic who gave up alcohol and took a normal diet was so great that every effort should be made both to secure early diagnosis-which may necessitate needle liver biopsy-and to ensure continued abstinence. to
Special Articles MALE HOMOSEXUALITY BY
A MEDICAL PRACTITIONER A TRUE picture of male homosexuality in the community be given if-as in most medical publications-it is based on material drawn only from psychiatric practice, prisons, mental hospitals, and venereal-disease clinics. So long as the only doctors who write on this subject are heterosexual, so long as public opinion is based on emotional prejudice, so long as the law makes it dangerous for the homosexual himself to express an opinion, the present profound ignorance of the subject-both inside and outside the medical profession-will continue. As a general practitioner and a homosexual, I have over the past thirty years discussed the subject intimately in an atmosphere of mutual understanding and confidence with several hundred homosexual men of many nationalities, colours, cultures, and creeds. The following casehistories provide, I believe, a typical cross-section of male homosexuality in the community. cannot
Case-histories Cases 1 and 2.-In 1935 A was a contented married man of about 40 with two children. About this time he introduced into his business, with a view to future partnership, a man B, aged about 25, with capital to invest. B was homosexual and knew it. A bond of friendship, then affection, grew between A and B which later led to overt homosexual practices. A’s marriage disintegrated and his wife and family went to live abroad. After some five years of cohabitation A and B separated amicably, and they are still close friends. A tells me that he had no suspicion that he was homosexually inclined until he met B. He had been reasonably happy. His marital obligations had been fulfilled adequately, but he had
Conferences ALCOHOLISM AND HEPATIC CIRRHOSIS A MEETING on alcoholism and cirrhosis of the liver was held in New York on Nov. 20 and 21 under the presidency of Dr. HANS POPPER (New York) and under the auspices of the National Council on Alcoholism. Cirrhosis is now the fifth commonest cause of death in the United States. It was estimated that one in sixteen of those who take alcohol becomes an alcoholic and about 8% of these will develop cirrhosis. C. H-. BEST (Toronto) believed that the basis of the relation between the two was a nutritional one. A precirrhotic fatty-liver stage could be induced in rats by giving, for about a year, a diet containing 15-30% of calories as alcohol. This change could always b? prevented by choline or methionine. G. KLATSKIN (New Haven) noted that, in rats, alcohol reduced the food intake and increased the requirement for choline. Alcohol could induce fatty change irrespective of calories consumed, and this was reversed by choline. The lesion in the liver of the rat, however, differed from that seen in man: inflammation and degenerative changes in the liver cells were absent. He speculated whether there might not be an additional factor in the human disease, perhaps a direct " toxic effect, perhaps additional infection. The mechanism of fatty liver in alcoholics was further discussed. W. S. HARTROFT (St. Louis), by electron microscopy, had noted that in the fatty liver produced by excess calories the fat was periportal in distribution and situated in little orgastoplasmic saccules, whereas in choline deficiency the fat was centrizonal and the mitochondria were enormous. In choline deficiency the mitochondria might be unable to wrap around- the fat globules with possible interference with oxidative J. H. enzymes on the surface of the mitochondria. QUASTEL (Montreal) had studied the effect of alcohol on isolated liver tissue and found an inhibition of phospholipid production and a stimulation of fatty-acid synthesis. C. S. LIEBER (Boston) had incubated trace amounts of "C-labelled acetate or ethanol with rat liver slices. Both served equally well for fatty-acid synthesis although far more fatty acid was found with ethanol than with He believed that ethanol acted as a donor of acetate. hydrogen ions reducing dipyrridine phosphate (D.P.N.). H. M. MALING (Bethesda) related the acute experimental fatty liver after alcohol to altered fat transport, the fatty acids coming from depot adipose-tissue. The incidence of cirrhosis parallels the consumption of alcohol in a community, but less than 10% of alcoholics develop liver injury. The cause of the individual susceptibility is not known. W. S. HARTROFT emphasised the importance of preceding obesity. F. SCHAFFNER found a four incidence in white times (New York) greater than in the coloured patients seen at Cook County Hospital, Chicago. C. M. LEEVY (Jersey City) observed a higher incidence in those presenting with delirium tremens, 25% of whom showed cirrhosis and 30% fatty
change. The usual cirrhosis in alcoholics is a fine Laennec’s (about 80%). It was agreed, however, that about 8% show a coarse postnecrotic type of lesion and 10% a mixed picture. The association of alcoholism with hsemochromatosis was stressed, 2% of cirrhosis in alcoholics being of this type. The transition of Laennec’s
one
postnecrotic cirrhosis has been described both in animals and by serial needle biopsies in man. This transition is liable to occur if the alcoholic abstains and large nodules regenerate in the liver. The liver cells in alcoholism contain basophilic amorphous material, the Mallory bodies. H. POPPER had seen these in both the Laennec and postnecrotic cirrhosis developing in alcoholics but never in non-alcoholics. P. E. STEINER (Philadelphia), on the basis of studies in Africans, disagreed ; for he found Mallory bodies very frequently in the absence of alcoholism and even of fat in the liver cells. R. M. KARK (Chicago) had seen severe fatty change and ascites disappear in alcoholics given a good diet, and it was generally agreed that this was true of other acute changes in the liver such as polymorph infiltration; fibrosis could diminish. S. SHERLOCK (London) believed that once the architecture of the liver was disturbed anatomical restitution was impossible. C. S. DAVIDSON (Boston) emphasised the distinction between the acute changes (with fat, necrosis, inflammatory cells and Mallory bodies, and clinically liver failure) and the chronic burntout stage (with mainly fibrosis and clinically the development of portal hypertension). The improvement in an alcoholic who gave up alcohol and took a normal diet was so great that every effort should be made both to secure early diagnosis-which may necessitate needle liver biopsy-and to ensure continued abstinence. to
Special Articles MALE HOMOSEXUALITY BY
A MEDICAL PRACTITIONER A TRUE picture of male homosexuality in the community be given if-as in most medical publications-it is based on material drawn only from psychiatric practice, prisons, mental hospitals, and venereal-disease clinics. So long as the only doctors who write on this subject are heterosexual, so long as public opinion is based on emotional prejudice, so long as the law makes it dangerous for the homosexual himself to express an opinion, the present profound ignorance of the subject-both inside and outside the medical profession-will continue. As a general practitioner and a homosexual, I have over the past thirty years discussed the subject intimately in an atmosphere of mutual understanding and confidence with several hundred homosexual men of many nationalities, colours, cultures, and creeds. The following casehistories provide, I believe, a typical cross-section of male homosexuality in the community. cannot
Case-histories Cases 1 and 2.-In 1935 A was a contented married man of about 40 with two children. About this time he introduced into his business, with a view to future partnership, a man B, aged about 25, with capital to invest. B was homosexual and knew it. A bond of friendship, then affection, grew between A and B which later led to overt homosexual practices. A’s marriage disintegrated and his wife and family went to live abroad. After some five years of cohabitation A and B separated amicably, and they are still close friends. A tells me that he had no suspicion that he was homosexually inclined until he met B. He had been reasonably happy. His marital obligations had been fulfilled adequately, but he had