Urobilinuria

UROBILINURIA, the excretion of urobilin in the urine, acquires the significance of a pathological symptom only in cases of noticeably increased urobilin content in the urine. A small amount of urobilin and urobilinogen can be found in the urine frequently, perhaps even always. Although the boundary between normal and pathological excretion has not been established with precise figures, judgment in this regard usually encounters no special difficulties. Like all pigments, urobilin is excreted in the urine in small quantities; in the most severe cases, one can speak of decigrams. Excretion increases with fatty food and meat diet. Fasting can also give an increase in urobilin, as can slight intestinal atony. All the regularities concerning urobilin excretion are not very strict. Urobilinuria is a capricious symptom, changing, not absolutely linked to any specific disease, and therefore often misleading, but hardly ever decisive for diagnosis. Simultaneously with urobilin, other dark pigments often appear in the urine, the significance of which is similar to that of urobilin. A sharp increase in urobilin in the urine is encountered first of all in various diseases of the liver. Often, at the same time, the bile pigment is also found in the urine. There is no parallelism in the excretion of these pigments. Rather, one can think that where a lot of bilirubin appears, urobilin is excreted only in small quantities, and conversely—cases with obvious liver damage can proceed without bile pigment in the urine, but with sharp urobilinuria. When the bile duct is completely closed, urobilin disappears from the urine. If, in this way, there is jaundice without urobilinuria and urobilinuria without clinically detectable jaundice, nevertheless these two phenomena are close to each other. We often see that before jaundice appears, increased excretion of urobilin begins, or, conversely, urobilinuria is established when jaundice passes. The concept of urobilin jaundice arising on the basis of clinical observations was explained in the sense that in these cases jaundice occurs from the bile pigment, and urobilin, although excreted in the urine, does not participate in the jaundice coloration. Moreover, since the introduction of tests for bile pigment in the blood into clinical practice, it has been discovered that hidden bilirubinemia also occurs, which does not cause jaundice coloration of the skin, and usually the amount of urobilin in the urine increases. Just as jaundice and bilirubinemia first make one think of liver disease, the same is said by urobilinuria. Considering all the above, one must admit that urobilinuria can be a more subtle liver symptom than jaundice and the content of bile pigment in the blood. If gross anatomical damage to the liver and such obvious liver signs as jaundice are not always associated with the appearance of urobilin in the urine, this in no way speaks against urobilinuria as a liver symptom: functional symptoms often diverge from anatomical ones and from each other. Being a subtle liver symptom, urobilinuria sometimes appears in diseases in which the liver does not have a predominant significance in the clinical picture. Thus, in heart decompensations, sharp urobilinuria appears, in which jaundice can often be seen, and sometimes also enlargement and hardening of the liver. The same can be said about lobar pneumonia, which gives besides urobilinuria also jaundice and tenderness and changes in the liver. (Clinical considerations allow and often the increased urobilinuria in fever to be attributed to the liver, since infectious damage to the liver is certain.) The second extensive group of diseases in which a lot of urobilin is excreted links urobilin with the blood pigment. If in the group of hepatogenous urobilinuria the intestine is often poor in pigments and the feces become pale, then in so-called hemolytic processes, on the contrary, the feces are sharply colored. Quantitative determination of urobilin, despite its inaccuracy and approximation, gives clear indications of increased pigment excretion both in the urine and in the feces. In anemias caused by blood loss, urobilin excretion falls, and the urine becomes pale. This is not the case in cases where the disintegration of erythrocytes occurs inside the organism. Here urobilin excretion grows, and especially great attention must be paid to the pigment of the feces. Most authors do not attach exceptional importance to the absolute value of urobilin excretion and, as a sign of pigment turnover and blood wear and tear, propose various coefficients, into which in addition to the amount of excreted urobilin, the amount of Hb is introduced. The simplest coefficient is the amount of urobilin divided by the total amount of Hb. Its value in the norm fluctuates from 10 to 30. All influences favorable for anemia are reflected in a decrease in urobilin. Thus, the removal of the spleen in hemolytic jaundice acts, and so does hepatotherapy in malignant anemia. Not only in these two diseases can we speak of hemolytic processes. A number of pharmacological poisons (hemolytic poisons, lead) causes a completely certain increase in urobilin excretion. Two groups of urobilinuria, which can be called hepatogenous and hemolytic, are not always easy to distinguish. On the one hand, so-called hemolytic poisons appear harmful not exclusively to erythrocytes, but also act on the liver; on the other hand, there are many clinical pictures in which the symptoms of hemolysis and the symptoms of hepatogenous disease are closely intertwined. So-called hepatosplenic syndromes represent a instructive example in this regard. The connection of various diseases with urobilinuria is established by direct observation at the patient's bedside. The mechanism of formation and excretion of urobilin has not yet been fully analyzed. All existing chemical and clinical observations unanimously speak of a connection between urobilin and other animal pigments. Urobilinuria is therefore correctly considered a feature of general pigment metabolism, which ultimately comes down to a deviation of the metabolism of pyrrole derivatives. Whether increased formation and excretion of urobilin always occurs by one path or by several, still needs clarification. Special caution is needed in this regard because there are many substances with the properties of urobilin (urobilinogen). The lineage of urobilin can be traced only starting from bilirubin. If one follows various cases of jaundice, it turns out that with the complete absence of bile in the intestine, urobilin disappears from the urine altogether. If bile is injected into the bile-free intestine, urobilinuria resumes. From this it was concluded that urobilin is formed from bilirubin in the intestine and only in the intestine. However, the persuasiveness of this experiment is disputed by some authors on the grounds that acholia is almost never encountered at all and, moreover, the bile used for the experiment always contains urobilinogen. The theory is sometimes proposed to be corrected in the sense that after absorption urobilin falls under the action of the liver and, with sufficient function, returns again to the general pigment metabolism. Another theory, based on clinical data, proposes to consider urobilin exclusively as a product of the liver cell. Then it is not clear why, with normal relations, urobilinuria is not observed and why urobilin excretion decreases precisely in the most diverse jaundices. A very great difficulty in explaining the origin of urobilinuria arises from the question of how urobilin reaches the kidney: urobilin is not easily detected in the blood plasma, and in most cases its detection here is unsuccessful. Therefore, the point of view is sometimes supported that urobilin of the urine is formed only in the kidneys from the bilirubin delivered here. This assumption does not explain why, in severe jaundices, the excretion of urobilin from bilirubin ceases. Finally, it is sometimes stated that urobilin is formed not in the kidneys and not in the liver, but generally in the tissues, from where, remaining elusive (?) in the blood, it is transported to the kidneys and excreted (histogenous theory). What is the connection between hemoglobin and urobilin in hemolysis, does it go through bilirubin or are both substances connected with each other, as in the chemical experiment, through other intermediates—is not clarified. The often emerging connection of jaundice and hemolysis speaks rather for the first assumption. Until the indicated difficulties are removed, urobilinuria remains a bright but incomprehensible symptom, which can be used only with caution to confirm and strengthen the diagnosis established on the basis of other considerations. On methods for determining urobilin in the urine—see Urine.