Hepato-Lienal Diseases
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
Hepato-lienal diseases refer to conditions involving simultaneous damage to the liver and spleen, primarily through cirrhotic processes, with symptoms including cirrhosis, anemia, and sometimes increased hemolysis. The article discusses etiology, pathogenesis, pathology, symptoms, diagnosis, and treatment of these conditions, emphasizing the functional connection between the liver and spleen through their reticuloendothelial tissue.
Encyclopedia article (1928–1936)
HEPATO-LIENAL DISEASES, (from Greek hepar-liver and lien-spleen), a new clinical concept implying parallel damage to the liver and spleen, mainly through cirrhotic processes, with the spleen damage sometimes coming to the forefront; in this case, symptoms of cirrhosis are joined by anemia, sometimes with signs of increased hemolysis and with involvement of the bone marrow. The functional connection and solidarity between the liver and spleen, besides the commonality of blood circulation, is created by the reticulo-endothelial tissue that is part of both organs, playing an important role in the intermediate metabolism of substances, in the process of phagocytosis of various colloidal particles from the blood, and in other complex physiological functions (see Reticulo-endothelial apparatus); in particular, reticulo-endothelial tissue is an important factor in the process of destruction of red blood cells (hemolysis) both under normal and pathological conditions. The great variety and extraordinary diversity of clinical forms of cirrhotic processes (see Cirrhosis of the liver) affecting the liver and spleen do not allow these processes at the present time to be reduced to the three traditional forms associated with the names Laënnec-atrophic cirrhosis, Hanau-hypertrophic cirrhosis, and Banti-splenomegaly form of cirrhosis, and therefore clinical practice resorts to the integral concept of H.-l. d. Etiology. Regarding etiology, it should be noted that H.-l. d. should be considered as the result of a combination of exogenous factors related to the influence of infection, intoxication, environmental conditions and lifestyle, and endogenous factors depending on constitutional peculiarities of the organism. Among infections, syphilis and malaria have the greatest significance (Chiari, Marchand and others). In recent times, mycosis of the spleen has been in the center of attention. Nanta and Pinoy expressed the opinion that the scleropigment nodules of Gandi Gamna contain the mycelium of the fungus Aspergillus. Askanazy kept a preparation with "threads" of the fungus for 15 years, without publishing his discovery and not attaching special importance to it. Emile-Weil found pictures attributable to mycosis of the spleen not only in "Banti's disease" but also in hemolytic jaundice and in two cases of posthemorrhagic anemia. Later, these pictures began to be found in the most diverse processes: leukemia, infarctions of the spleen, arteriosclerosis, etc. Oberling and others came out with criticism of the etiological significance of mycosis in splenomegaly. One could admit that the fungus is not a specific causative agent but only a secondary infection (especially convincing are the cases of posthemorrhagic anemia). Frequent findings of corresponding pictures in hemolytic jaundice, infarctions, etc. become understandable if one recalls Askanazy's statement that some fungi parasitic in the human body absorb iron; with increased hemolysis, they therefore find in the spleen favorable ground for their development. Recently, however, very great doubts have arisen as to whether the pictures described under the name of mycosis really correspond to the fungus (Gamna, Langeron, Abricosov).-Of intoxications, the main role belongs to alcohol and gastrointestinal poisons. Alcohol acts directly on the liver or causes gastrointestinal disorders with subsequent auto-intoxication. According to Simons and Klopstock, 3U cases of cirrhosis of the liver depend on alcoholism. However, one cannot forget that the vast majority of alcoholics do not suffer from cirrhosis (Fahr). Experiments by Lissauer on poisoning rabbits with alcohol led to the development of cirrhosis only in some cases, which apparently depends on constitutional individual peculiarities. Experimentally, cirrhosis of the liver was obtained from poisoning with toluylenediamine, phosphorus, products of protein decay, cholesterol, coal tar, petroleum. Pathogenesis. The liver and spleen absorb toxins and bacterial bodies circulating in the body, which undergo phagocytosis and extracellular dissolution by special bacteriolysins. The liver is constantly in a state of heightened vital activity due to the absorption of various products from the intestine. Chronic infections and intoxications cause these organs to develop connective tissue and die of parenchyma. To this day, there is a dispute about which organ is primarily affected. Banti, Michel and Storn proved by biopsy that the liver can remain untouched with far-reaching changes in the spleen. Banti, Bleichroder, Leichtenstern and others speak of a "precirrhotic" primary tumor of the spleen; Grawitz, Hartwich and Kretz of primary damage to the liver; Eppinger and Gaukler consider that both organs become sick in parallel. One has to admit different development of the disease in each individual case. The primary damage to one or the other organ depends on etiology. Infectious agents are localized mainly in the spleen due to its anatomical-physiological peculiarities. Toxins, however, first traumatize the liver, which is affected diffusely or partially, depending on which vascular branches of the portal system the poisons are brought by (Ribbert).-Pathological anatomy, see Banti's disease and Cirrhosis of the liver. Symptomatology. The main symptoms are: 1) enlargement of the liver; 2) enlargement of the spleen; 3) signs of stagnation in the vessels of the portal system (portal hypertension); 4) jaundice; 5) anemia; 6) signs of liver insufficiency. The consequence of portal hypertension are: ascites, development of a collateral venous network, gastrointestinal bleeding, hemorrhoids, change in the rhythm of urine excretion (anuria and oliguria). All these symptoms are observed in the late stage of the disease, with marked difficulty in portal circulation. Jaundice occurs as a result of the death of liver cells, and partly due to increased hemolysis, which is connected with the disruption of the function of the reticulo-endothelial apparatus. Ictero-genic forms of the syndrome sometimes directly approach hemolytic jaundice. Anemia occurs, according to Eppinger, in 51% of cases. It is characterized not by anemia due to increased hemolysis, although this is occasionally observed and combined with jaundice, but by anemia due to insufficient erythropoiesis. Anemia rarely combines with enlargement of the liver. It is possible that the liver is an organ not only processing blood pigment but also regulating blood formation. The large insufficiency of the liver is characterized by the phenomena of cholemia. The symptoms of small insufficiency are not strictly outlined, and they cannot always be caught by modern methods of functional diagnostics. According to classical descriptions, the listed symptoms combine into strictly outlined pictures: ascites is combined with a large spleen and atrophy of the liver, jaundice-with enlargement of the liver and spleen, primary splenomegaly-with anemia. The latest observations prove that classical forms are extremely rare, and in everyday practice mixed forms with the most diverse combinations of symptoms are encountered (for example, ascites is observed simultaneously with jaundice, enlargement of the liver and spleen is not accompanied by jaundice, etc.). Diagnosis is based on physical examination of organs and examination of the blood. Besides the study of blood morphology, it is necessary to study hemolysis (osmotic resistance) and pigment metabolism (bilirubin, urobilin, etc.). Functional diagnostics of the liver, spleen and bone marrow is still not sufficiently perfect and gives little diagnostic data. In differential diagnosis, it is necessary to exclude other systemic diseases affecting the liver and spleen; namely: hematopoietic, hemolytic and reticulo-endothelial hepatosplenomegalies.-The course of such processes is usually prolonged. Acute course occurs in exceptional cases.-Prevention consists in careful treatment of chronic infectious diseases (syphilis and malaria) and in the fight against intoxications, mainly against alcoholism.-Treatment. In some cases, only symptomatic treatment is possible (Talma's operation, treatment of anemia). Radical treatment consists in splenectomy. In the presence of splenomegaly without liver damage, the operation gives a brilliant effect. Eppinger proposed splenectomy even for "hypertrophic cirrhosis" and observed in 10 cases good results.
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“Hepato-Lienal Diseases.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/hepato-lienal-diseases/