Superior Index Go to the next: Chapter 12
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DETWEILER WRITES regarding portal cirrhosis: "It is by no means uncommon for portal cirrhosis to exist unsuspected during life and only be found after death from accident, intercurrent infection, or other diseases. The early recognition of the disease, therefore, may be extremely difficult. Sometimes careful examination reveals loss of appetite, loss of weight, nausea, flatulence and occasional vomiting."66
In malignancy of the liver or in the intestinal tract, the symptoms are described: "The onset is very insidious and is manifested in weakness, loss of appetite, and failure in general health ... there is usually progressive loss of weight and increasing secondary anemia (characteristic of any chronic or degenerative disease)."67
"Symptoms referable to the liver itself may be absent, but a sense of fullness and disconfort in the hepatic region is often noted. Jaundice, ascites and pain are absent in simple cases. Vague gastro-intestinal disturbances may occur."68
Three different systems closely connected with each other are in the liver:
"The liver performs various detoxication processes, but it is not known exactly where and how these take place."69 The same is true with reference to various enzyme systems, vitamins and minerals (copper, cobalt, manganese, iron, potassium, etc.). Enzymes and vitamins are combined, stored and reactivated mostly in the liver. Albumin is also formed in the liver, probably in the Kupffer cells, while globulin is formed in the lymphocytes, but is increased when the liver is impaired. The reason has not yet been found. The ratio of [albumin/globulin] is therefore lowered in the liver diseases and used for one of the tests.
Neoplasia: About 1:200 malignant tumors arise primarily in the liver. Most malignancies are metastatic in origin and are derived from the intestinal organs.
Fifty patients with various types of cancer of the general intestinal tract presented pronounced hepatic dysfunctions.70 After removal of the tumors the liver recovered to a certain degree for some time, but the changes showed that the deterioration is reversible. May I anticipate here that the described treatment does the same: removal of the tumor-mass, glands, etc. and an overcoming of the dysfunction of the liver. According to Greenstein, "There seems to be little doubt that hepatic insufficiency is a concomitant phenomenon with cancer and, as the authors emphasize, such damaged livers impose an addittional hazard to those normally accompanying operative procedures."71
During the first stage - development and appearance of the disease - the liver dysfunction is undetectable. During the second stage - tumor growth and some metastases in glands - one finds the liver mostly hypertrophic and, as we see in some cases, also hypertrophy or edema of other organs. In the third stage - an almost entire ruling (autonomy) of the cancer - with rapid poisoning, destruction and later dissolution of the organs, including liver, which can no longer maintain its substance and functions. In the first stage the tumor-protein would seem to be supported by the food - in the second stage most probably a part of the protein is supported by the muscle tissue and at that time there is considerable hyperlipemia present which stays there till the reserves of the body's lipids are consumed.
In the third (or terminal) stage there is an acute loss of muscle and liver substance and all resistance is lost. How the tumor produces such a condition is unknown. Greenstein assumes "the production by the tumor of a circulating toxin which accelerates the catabolism of the body tissues."72 Rudolf Keller thought that the progressive loss of K-and K-group minerals are responsible for it by losing the electrical potentials and defense of muscle cytoplasma. The stimulation of the visceral nervous system by the loss of K and the tumor poisons seems also to be contributing to this deleterious effect.
The newer labeled examination with C14 glycine by Norberg and D. M. Greenberg proved that the liver and plasma of tumor-bearing animals have an increased protein metabolism.73
The same effect also occurs in pregnancy (measured by glycine C14 and P32 as in the liver of tumor-bearing animals) reflecting a quicker growth somewhere else in the body. That means that this process is not specific for cancer and is not caused by specific toxins.
The beneficial influence of large amounts of carbohydrates in the diet has been recognized. Besides the protective action of glycogen upon the liver cell, further benefit is derived from carbohydrate by virtue of its protein-sparing action. The protective value of carbohydrate appears to be twice that of protein when sufficient protein is already present in the diet to provide plenty and necessary amino acids for reparative purposes. An isocaloric amount of carbohydrate cannot be substituted for proteins without deterioration of the clinical and biochemical state. Fifty-eight grams may be spared by conversion to carbohydrate when 100 grams of protein are fed if the carbohydrate intake is enough to satisfy the immediate need for sugar. Nevertheless, the additional requirement of high "biologic value" protein in patients with liver disease are not known, the indications are that there is a great protein wastage. Anorexia, hypoproteinemia, and loss of weight are positive evidence of protein depletion. Uncompensated liver cell protein catabolism also implies rapid loss of enzyme proteins of all types. Protein repletion may help, therefore, in restoring the necessary enzymes. There is little risk of protein surfeit even if the patient consumes protein beyond satiety. This reassurance is welcome since there is some reluctance in some quarters to overload the insuficient liver. Dock has demonstrated that the liver differs from the kidney in the capacity to handle protein excess. The hepatic artery circulation can take up the increased demand for oxygen when the protein content of the diet is increased to 74 per cent.
A dietary formula which patients accept even with marked anorexia consists of 350 to 500 grams of carbohydrate, 100 to 120 grams of protein, and 50 to 80 grams of fat. This composition of diet is recommended by Snell, Stare and Thorn, Patek, Patek and Post, Fleming and Snell; Ingelfinger and Holt follow this general formula with minor variations. Morrison prescribed a maximum protein regimen which comprises a daily diet of 2500 to 4000 calories with 200 to 300 grams of protein, 300 to 500 grams of carbohydrates and 50 to 100 grams of fat. Goodman and Garvin succeeded in administering a diet with a caloric value of 5000 calories derived from 150 to 250 grams of protein, 600 to 800 grams of carbohydrate and 150 to 200 grams of fat to 18 cases with acute hepatitis. Hourly feedings supplemented three regular meals. An almost "electric" response in the patients' physical and mental appearance was noted. Diets planned in excess of these amounts are not likely to be consumed in their entirety. It is a better policy to offer a diet which is acceptable regularly and consistently. The major problem is not to prescribe a diet of a particular composition but to insure the ingestion of a maximal amount of nutritious food. Missing a meal is a serious handicap in serious liver trouble. It is best replaced promptly by an intravenous infusion of glucose, several authors think.
Every effort is made to make food attractive. Fat and meat add to palatability. For this reason Hoagland recently questioned the wisdom of restricting fat. It appears that patients actually have little difficulty in digesting fats in spite of theoretical considerations. The fact should not be lost from sight that the protective effects of choline and methionine can be reversed by excess fat supplements. Ample fat, however, improves the efficiency of utilization of carbohydrate and protein in the diet. The objectives of improved appetite and increased caloric intake are readily achieved by a liberalized menu. A self-selected fare is a step forward in this direction. The dietitian and physician are invariably guided by matters of available food stocks and principies of diet; the patient knows his personal likes and dislikes better than anyone else. A single unappetizing item in a meal may completely abolish a capricious appetite. Appearance or odor may decide a patient against taking food.
Interest in the diet must not lag for a single meal; the anoretic patient is only too willing to skip the next feeding. Once a meal is consumed, there appears to be no difficulty in handling foodstuffs. Under constant goading, anoretic patients consume prodigious meals regularly, yet suffer no unusual distress. The dietary plan must be flexible enough, however, to permit variations depending on changes in the condition of the patient. For instance, with increasing ascites, cirrhotics find it difficult to swallow large meals. Small concentrated feeds are preferred. Regular-sized meals are resumed after paracentesis. In the average case of liver disease where food intake is a problem, the mid-day repast is usually the "best meal," and the evening meal the worst. It is advisable therefore to offer a light supper supplemented by a generous snack later in the evening. Abdominal distention tends to increase in the latter part of the afternoon and subside after supper. This may influence daily variations in appetite.
It is not a good policy to gorge the patient during one meal only to cope with a disinclination to eat several meals thereafter. Large helpings of fatty foods, although they temporarily improve the appetite, may only pay a limited dividend. Fats delay gastric emptying. Encroachment upon the next meal may prove a net loss in total daily caloric intake.
The protein, fat, and carbohydrate rations are discussed in detail below. The indications and contraindications for parenteral glucose, plasma, whole blood, purified human albumin, protein hydrolysates, synthetic amino acid mixtures and vitamins are reviewed. Diet, however, appeared to have no influence on liver tumors in rats produced by 2-acetylaminofluorene.74 The manner in which diet produces its procarcinogenic or anticarcinogenic effect is unknown.75 Chemical differences between mitochondria of normal liver and mouse liver hepatoma has been reported by Hogeboom and Schneider.
Some interesting observations in regard to the influence of diet on the development of spontaneous hepatomas in inbred CH3 mice were made by Tannenbaum and Silverstone. These investigators have shown that increase of fat in the diet from two per cent to 20 per cent increased the rate of hepatoma formation from 37 per cent to 53 per cent. Low riboflavin intake resulted in a decrease of hepatoma formation. This can be attributed to the lowered caloric intake, which has been shown to inhibit growth of hepatomas in this species. It has likewise been shown that, contrary to the experiences in the induced hepatomas in rats, the spontaneous tumors in mice are not accelerated by a rice diet but, on the contrary, are accelerated by increased casein content. Methionine has likewise been shown to accelerate the development of these tumors in mice. The conclusion is drawn that the sulphur-containing amino acids, which are necessary for normal growth, are also necessary for growth and development of these neoplasms. Again a startling indication of the similarity between physiological growth and neoplasia!
Concerning lipotropic substances, Spellberg held that the object of the treatment is to remove the fat from the liver and to reinstitute the normal hepatic histology and physiology. With the tremendous amount of experimental work done on lipotropic agents, and their effectiveness in dietary fatty liver in animals, it is only natural that clinicians should turn to these substances in the treatment of fatty liver; however, the only type of fatty liver that choline (the most important of the lipotropic substances) can cure is the one due to choline deficiency. It is likely that at least some of the fatty livers in man are due to choline deficiency, but in the fatty livers of prolonged infection or those due to toxins, no deficiency of choline in the diet can be postulated, and therefore, no beneficial effect from choline can be expected.76
With regard to diet, Spellberg has said that the diet should be high in proteins of good quality, such as meat and fish. A protein intake of 150 gm. a day should be aimed at. The bulk of the calories should be provided by carbohydrates and, therefore, this should be close to 350 gm. a day. The dietary fat should be kept to a minimum. Since a palatable natural diet high in protein cannot be devised fat free, at least 70 gm. of fat must be included. I cannot see how one can condonc a high fat diet, especially in the case of fatty liver. What is the logic of supplying more of the substance that we are trying to remove from the liver? When some of this exogenous fat reaches the liver, it requires more lipotropic substances and makes the object of therapy more difficult. The diet should be low in salt if there is evidence of edema or ascites.77
"This is principally symptomatic but the diet is of great importance. It should consist entirely of milk and sugar or other carbohydrates. Animal proteins should be reduced to a minimum, as the liver has lost to a great extent, if not entirely, its detoxicating function. Intestinal antisepsis by means of bismuth, salol or calomel may be attempted but without much hope of success. The fluid intake must be maintained at two liters or more a day. The vomiting is best treated by giving fluids half hourly in small quantities but if persistent all foods by mouth should be stopped and intravenous, rectal or subcutaneous administration of glucose saline substituted."78