FATTY NECROSES (synonym: stearin plaques, necrosis of fatty tissue) — focal necrosis of fatty tissue.
The term is entered in 1882 by W. Balser who described 5 cases of a necrosis of a fatty tissue both in fabric, and in a circle of a pancreas. Similar observations were described earlier by Smith (Smitt, 1818), R. Virkhovy (1852), Ponfiky (E. Ponfick, 1872).
Etiology and pathogeny
Aetiology and pathogeny. N are finally not found out. It is only possible to claim that. N represent a final phase of complex chemical process, in Krom effect of steapsin takes the leading place. Electronic microscopic examinations demonstrate that in certain situations (preferential fatty diet, an alcohol abuse) granules of zymogen eliminirutsya not only in system of output channels of gland, but also in pericellular space. The active lipase current of an intercellular lymph reaches interlobular fatty tissue and nekrotizirut it: there is a so-called remote necrosis. In the centers. the N at gistokhy, a research is marked out high activity of a lipase. Getting to a vascular bed, the active lipase can cause. N in sites of fatty tissue, remote from a pancreas.
Rank amylase and a lecithinase, a phospholipase as the enzymes possessing cytotoxic action on fatty tissue And, a lipase of fatty tissue. Great value in a pathogeny. N attribute to a lipolysis, to-rogo hydrolytic decomposition of triglycerides (neutral fats) on glycerin and fat to - you is the cornerstone. Activity of a lipase is regulated cyclic 3', 5 '-adenosinemonophosphate (3', 5 '-AMF). Contents 3', 5 '-AMF in fabric depends on activity of two enzymes — adenylatecyclases and phosphodiesterases. Adenylatecyclase catalyzes education cyclic 3', 5 '-AMF from ATP. Some hormones (a glucagon and AKTG) stimulate activity of adenylatecyclase and, thus, increase education 3', 5 '-AMF and the subsequent lipolysis of fatty tissue.
Among the processes promoting a lipolysis of fatty tissue, the first place is allocated to acute pancreatitis. At experimental pancreatitis at rats during the first 3 hours the expressed lipolysis was noted, and in 3 — 6 hours in these sites the content of calcium considerably increased. Released at the same time fat to - you are esterified by calcium, and the calcium soaps formed in such way are besieged and represent a basis so-called. N. Insulin with glucose, nicotinic to - that and propranolol (the beta and adrenergic blocking agent) inhibit a lipolysis.
. N represent the centers reminding stearin drops by outward (from here the name «stearin plaques»), rounded shape, a dense consistence, to dia. 1 — 3 mm. Quite often. N, merging, form larger centers to dia, to 1 cm and more. They are localized more often in a pancreas and a fatty tissue of an abdominal cavity (big and an omentulum, a mesentery of a small bowel, retroperitoneal cellulose, cellulose of a small pelvis). In internals (except a pancreas). N are not observed. From other localizations it is necessary to point to hypodermic cellulose of a trunk and extremities, a pericardium, a pleura, a peritoneum, marrow.
For macroscopic diagnosis. N apply Benda's reaction, with the help a cut they are painted in green color.
At microscopic examination in the center. N the cytoplasmic membrane of lipoblasts is indiscernible, kernels of cells are absent and the center is presented by the homogeneous nekrotizirovanny weight (fig). It is microscopically possible to track dynamics of development. the N, edges consists of consecutive development dystrophic, necrobiotic and finally necrotic changes of lipoblasts; in the centers of fatty necroses various crystal inclusions are found. On the periphery of the center. the N is located the demarcation cellular shaft presented by lymphocytes, polymorphonuclear leukocytes, macrophages and plasmocytes. Cellular infiltrate promotes a rassasyvaniye of necrotic masses, and the formed granulyatsionny fabric creates the capsule (encapsulation of the center. N). If in the encapsulated center salts of calcium are laid, then there occurs calcification (calcification).
Wedge, symptomatology. in N it is generally caused by damage of a pancreas (see. Pancreatitis ). Single nepankreatogenny. N (e.g., hypodermic cellulose) can exist asymptomatically and over time obyzvestvlyatsya. Perhaps also their suppuration with development abscess (see). The last can be the reason of peritonitis, pseudocysts of a pancreas or fistulas between an abscess cavity and hollow body (a stomach, a small or large intestine), and also arrosions of walls of vessels with the subsequent bleeding. Extended. the N of a root of a mesentery and side channels of an abdominal cavity considerably complicate the course of pancreatitis, promote development of commissural impassability of intestines (see), and in cases of accession of an infection — diffusion purulent peritonitis.
Because in most cases. N are a consequence of pancreatitis, at the heart of their prevention and treatment measures of the prevention and therapy of this disease lie. For the prevention of abscessing. the N is recommended antibacterial therapy, and in case of the created abscesses — their opening and drainage.
Bibliography: Lobachev S. V. Acute pancreatitis, M., 1953, bibliogr.; Residents of Perm N. K. and Podolsk A. E. O pathogeny of pancreatitis, Surgery, JsTs 9, page 23, 1973; Residents of Perm N. K., Podolsk A. E. of G. P ititov. Ultrastructural analysis of a secretory cycle of a pancreas, M., 1973, bibliogr.; AkgtinS. RudmanD. Relationships between mobilization of free fatty acids from adipose tissue and the concentrations of calcium in the extracellular fluid and in the tissue, Endocrinology, v. 84, p. 926, 1969; E f e n d i 6 S., Aim B. a. L w H. Effect of Ca ++ on lipolysis in human omental adipose tissue in vitro, Horm. Metabol. Res., v. 2, p. 287, 1970; S t about with k G. Fat necrosis in acute pancreatitis, Acta chir. scand., Suppl. 417, 1971; Theve N. O. Fat necrosis, ibid., Suppl. 434, 1972.
H. K. Permyakov.