Sprue

SPRUE [synonyms: aphthae tropicae (van der Burg, 1880), diarrhoea alba, psilosis linguae (Thin, 1897), tropical diarrhoea], a severe chronic disease characterized by cyclic course, diarrhea in the form of abundant pearly white stools, appearance of characteristic ulcers on the oral mucosa and tongue (aphthae tropicae), megaloblastic anemia and severe emaciation. The English name sprue, proposed by Manson (P. Manson, 1870), derives from the Dutch word spruw, meaning saliva, foam, the external resemblance of which to the stools in this disease gave rise to the name. The term spruw was previously used in England and Holland to designate thrush in children. The clinical picture of this disease was noted by physicians practicing in tropical countries more than 150 years ago. - Etiology has not been established with precision, and therefore several theories exist. The fungal theory originates from Colbrugge, de Haan, Le Dantec and others, who found in the stools of patients S. various species of the fungus Monilia. Ashford in 1915 in Puerto Rico found Monilia psilosis, which he considered the etiological factor in S. Later, however, he changed his view, considering the cause of S. to be a disturbance of digestive balance, on the basis of which Monilia psilosis develops. Recent detailed works [Mackie, Chitre (1928) and Yefremov (1932)] have refuted the specificity of intestinal blastomycetes and in particular the importance of the Monilia group. Elders, and then Fischer (1927) and others, and earlier also C. Funk, consider S. as an avitaminosis caused by the absence of vitamins A and B in food. This theory at the present moment is the most probable, especially in regard to the absence of factor B. In view of the fact that this factor is complex, the changes in S. are apparently connected with the absence of one of its fractions. Scott (1924) put forward the hypothesis that S. is caused by a deficiency of calcium salts in the body, since many symptoms of S. are also observed in diseases caused by calcium deficiency in the body (for example tetany, weight loss, edema). S. is widespread mainly in tropical and subtropical countries-British India, Indochina, the Malay Archipelago, China, Korea, Central and South America, USA, West Indies, Morocco, Australia. In the USSR, S. was first discovered in Tashkent in 1922 by A. N. Kryukov, then in 1923 in Transcaucasia in Armenia by P. P. Popov, in Georgia (1923) by Mikeladze, in Azerbaijan (1927) by A. S. Chergeshov (Ganja) and in Baku by K. A. Yegorov, V. A. Tarnogradsky. In the post-war period, Danish and Dutch clinicians have also found S. in the temperate climate of Europe-the so-called "non-tropical sprue". Pathological anatomy of S. Sprue is characterized by severe emaciation, anemia of internal organs and atrophy of the digestive tract mucosa with marked thinning of the intestinal wall and sometimes local erosions. On microscopic examination, there is round-cell infiltration of the villi with their subsequent atrophy. In the submucosal tissue-dilation of blood vessels, round-cell infiltration and fibrosis, especially sharply expressed in the large intestine. The liver is atrophic and often greatly reduced (to half its weight, and sometimes more); atrophy of the heart and adrenal glands. On the tongue, desquamation of the epithelium, especially from the surface, and atrophy mainly of the filiform papillae. Striated muscle is severely atrophic. The nervous system is normal.

Clinical picture, differential diagnosis. The incubation period in S. is unknown. The onset is always insidious. Clinically, S. is characterized by the presence of the following symptoms: 1) ulcers on the tongue and oral mucosa, 2) dyspeptic disorders, 3) characteristic pearly white diarrhea, mainly at night or early in the morning, 4) anemia and changes in the blood and 5) severe emaciation. The entire course is accompanied by periods of exacerbation and remission. The tongue is first inflamed, raspberry-red; then along its edges, on the tip and on the frenulum, on the buccal mucosa, hard and soft palate, small vesicles with turbid content appear, which burst, forming superficial irregularly bounded erosions. After some time (days, weeks) these phenomena on the tongue and oral mucosa disappear, and after some time they appear again (see separate table to the article Streptococci, fig. 7). After several exacerbations, the filiform papillae on the dorsum of the tongue atrophy, as a result of which the fungiform papillae, hidden in healthy individuals, begin to protrude in the form of reddish swollen points. Changes in the tongue in S. are best observed early in the morning before eating. Increased salivation is characteristic of S. The strength of the ptyalin reaction of saliva i-Lp remains unchanged, as does taste, increased only for sour and salty. Subsequently, the tongue becomes completely smooth (psilosis linguae) and decreases in volume. Dyspeptic phenomena in S. consist of a number of subjective sensations: feeling of heaviness, fullness, burning in the oral cavity and along the esophagus, bloating, rumbling, nausea, and sometimes vomiting occurring some time after eating food. Diarrhea in S. is very distinctive and characteristic: appearing insidiously and being at the beginning of the disease not prolonged, they occur at night or early in the morning. The amount of stool is not large, and initially they are normally colored, then become paler and paler. Tenesmata are absent in uncomplicated cases; the stools do not contain pus, blood, or mucus, but contain a lot of gas, so they appear voluminous and as if fermenting; their smell is sourish; on microscopic examination, in addition to bacteria, fungi and desquamated epithelial cells, they contain a large amount of fatty acid crystals (in S. 20% to 50% of fat is not absorbed). Such alternation of exacerbations of diarrhea and remissions subsequently leads to severe emaciation, physical weakness and reluctance to work. Weight drops sharply, the skin becomes hard, and the mucous membranes become pale.--Very strong changes in S. are observed in the blood, where usually hyperchromic megaloblastic anemia is noted, resembling pernicious anemia. Hemoglobin rarely falls below 50%. The number of red blood cells usually fluctuates within 3₂-3 million. The color index is usually above one. In the bone marrow of the sternum, megaloblastic blood formation is observed. The number of platelets in S. in most cases does not deviate from the norm, less often-decreased. Usually there is leukopenia with relative increase in lymphocytes and shift to the right in leukocytes (increase in the number of segments to G, 8, 9). The blood serum always gives an indirect reaction to bilirubin. Calcium, sugar and blood cholesterol are significantly reduced. In the urine in S., an increase in urobilin is noted. Gastric juice: more often a decrease in HCl is observed, sometimes anaciditas. The pepsin content fluctuates. The pancreatic enzyme is sometimes absent. Differential diagnosis. S. is easily distinguished from pellagra by the presence of skin manifestations in the latter (see Pellagra); from amebiasis-absence of Entamoeba histolytica (see Amoebae, Dysentery, amebic dysentery), although mixed cases may occur; from bacillary dysentery-absence of the bacilli Shiga-Kruse, Flexner's, Strong's and the cyclic course, involvement of the tongue, characteristic changes in stool and blood; from Bimer's pernicious anemia-absence of specific diarrhea, severe exhaustion; in the morphological picture of blood-mainly the difference in the average diameter of red blood cells during remission: in pernicious anemia it approaches normal, while in S. it always fluctuates between 8-9 μ. From chronic pancreatitis S. differs by the presence of symptoms from the mouth and tongue and megaloblastic anemia. From cancer of the pancreas, proceeding with jaundice and constipation, it differs by the absence of jaundice, diarrhea, etc. Treatment of S. Since the introduction of liver therapy by Minot and Murphy, the latter has been widely applied with very good results also in the treatment of S. In cases where there is severe impairment of absorption, protein-free concentrated liver extracts are administered orally, subcutaneously and intravenously with equal effect. Along with liver, preparations of pig stomach and brewer's yeast (autolysates) are used with great success. The justification for the success of this therapy is the high content in the aforementioned products of complex vitamin B, the absence of which in food is etiologically linked to the development of S. Of medications, large doses of Natr. bicarbon. (Castellan i), Pancreatin 0.6-3 times a day after meals, Parathyreoidin, Yatren 0.5-1.0-3 times a day are used. Calcium preparations per os or intravenously give good effect.-Prevention of S. is little developed, since the causes causing it have not yet been established with precision at the present time. Proceeding from the premise of avitaminosis etiology, it is recommended to care in the warm climate for adequate, easily digestible nutrition, with sufficient content of complex factor B in it.