HYALINOSIS (hyalinosis; Greek hyalinos transparent, vitreous + - osis; synonym: vitreous degeneration, hyaline dystrophy) — one of types of proteinaceous extracellular dystrophy, at a cut in fabric the homogeneous translucent dense masses reminding a hyaline cartilage are formed.
Can be manifestation of the general disturbances of protein metabolism, however most often it is local focal or system (in vessels) dystrophic process; It is shown as in fiziol., and in patol, conditions.
The concept «hyalinosis» combines various by origin, to the mechanism of development and biol, entities processes. The main G. in development — destruction of fibrous structures of connecting fabric and increase in fabric and vascular permeability in connection with angioneurotic (distsirkulyatorny), metabolic, inflammatory and immuno-patol. processes (see. Plasmorrhagia ). Disturbance of permeability is resulted by treatment of fabric plasma proteins and adsorption of their not changed fibrous structures with the subsequent precipitation. The formed hyalin has various, depending on the nature of a disease, chemical structure (e.g., a hyalin at a diabetic mikroangiopatiya and a hyalin at so-called immune deposit diseases).
Treats extracellular (mesenchymal) disproteinoza. Emergence in cytoplasm of hyaline drops (hyaline and drop dystrophy) or spheres (hyaline spheres) is not connected with G. Gialin is fibrous protein (fig. 1), plasma proteins, in particular fibrin take part in creation to-rogo. At immunogistokhy, a research in a hyalin find not only fibrin, but also components of cell-bound immune complexes (immune globulins, fractions of a complement). Hyaline masses is resistant to effect of acids, alkalis, enzymes, is well painted by acid paints (eosine, magenta acid), pikrofuksiny is painted in yellow or red color; in the mass of a hyalin lipids, salts of calcium can be postponed. Outward of bodies and fabrics at G. depends on a stage of process; more often G. is shown and found nothing only at microscopic examination. When process is expressed sharply, fabrics become pale, dense, translucent., in particular arterioles, can lead to deformation and wrinkling of bodies (e.g., development of an arteriolosklerotichesky nefrotsirroz, valve heart disease).
It is observed in connecting fabric, a stroma of bodies and a wall of vessels (fig. 2) in the result of plasmatic treatment, fibrinoid swelling, a sclerosis, hron, inflammations, a necrosis. In the result of plasmatic treatment there is G. of vessels, is more often in arterial system. G. of small arteries and arterioles is most widespread (see. Arteriolosclerosis ). Of arterioles results from damage of an endothelium, argyrophil membranes and smooth muscle fibers and treatment of vascular walls by proteins of a blood plasma which then are exposed to enzymatic influences, are coagulated and condensed, turning into gialinopodobny dense substance. Hyaline masses pushes aside knaruzh and destroys an elastic plate that leads to thinning of an average cover; as a result of an arteriole turn into reinforced dense tubules with sharply narrowed or completely closed gleam. The of small arteries and arterioles having system character, but which is most expressed in kidneys (fig. 3 and 4), a brain, a retina of an eye, a pancreas, skin (fig. 5) is especially characteristic of an idiopathic hypertensia (hypertensive arteriologialinoz). Quite often system G. of arterioles and small arteries is observed at hron, a vascular glomerulonephritis and symptomatic arterial hypertension of any genesis. Widespread G. of arteries of elastic and elastic and muscular types is constantly observed at atherosclerosis, diabetes and reflects the processes of a plasmorrhagia and insudation characteristic of these diseases. Local G. of arteries as the physiological phenomenon meets in a spleen of adult and elderly people, reflecting functional morfol. features of a spleen as body of deposition of blood.
In the result of the fibrinoid swelling leading to destruction of collagen and treatment of fabric plasma proteins and polysaccharides, connective tissue bunches inflate, lose fibrillation and merge in homogeneous dense chondroid mass; cellular elements are squeezed and atrophies are exposed. The similar mechanism of development of G. of actually connecting fabric and vascular wall is especially often observed at diseases with immune disturbances. So, system G. of connecting fabric and walls of vessels is expressed at collagenic diseases: Of valves of heart, a stroma of a myocardium — at rheumatism, G. of synovial membranes — at a pseudorheumatism, G. of skin — at a scleroderma, G. of walls of vessels — at nodular arteritis and a system lupus erythematosus. Widespread G.'s mechanism of renal balls at an immunocomplex glomerulonephritis is same. In these cases the hyalin is under construction on cell-bound immune complexes that confirms a role immunol, mechanisms in development of. Local G. can complete fibrinoid changes in day hron, stomach ulcers, in fabric of a worm-shaped shoot at appendicitis, and also in the center hron, inflammations.
In the outcome of a sclerosis has generally local character. Such is G. in hems (fig. 6), fibrous commissures of serous cavities, G. of a vascular wall at atherosclerosis, an involutional arteriosclerosis, at the organization of blood clot, G. of the capsule, surrounding any patol, the center, stromas of a tumor. In these cases local metabolic disturbances of connecting fabric are the cornerstone; the similar mechanism has G. of nekrotizirovanny fabrics, fibrinous imposings and other organic substances.
In most cases process is irreversible, but also the rassasyvaniye of hyaline masses is possible. So, a hyalin in hems, so-called. keloids (see), can be exposed to a loosening and a rassasyvaniye. Let's turn G. of a mammary gland, and the rassasyvaniye of hyaline masses occurs in the conditions of hyperfunction of gland. In some cases the hyalinized fabric slimes.
Functional value G. variously depending on localization, degree and prevalence of process. E.g., G. in small skin hems usually does not cause special frustration. Widespread G. leads to considerable functional disturbances as it is observed, e.g., at rheumatism, a scleroderma, a hypertension, diabetes.
See also Proteinaceous dystrophy .
Bibliography: Davydovsky I. V. General pathology of the person, page 58, M., 1969; Rukosuyev V. S. To a question of a hematogenous origin of a hyalin of vessels, Arkh. patol., t. 28, century 6, page 73, 1966, bibliogr.; Saltykov B. B. Morphological and immunoluminescent characteristic of a vascular hyalin, in the same place, t. 36, century 12, page 48, 1974, bibliogr.; In i and at a C.G. and. lake of Renal hyaline, Amer. J. Path., v.44, p. 349, 1964, bibliogr.; Krawczyn-s k at To. Immunohistochemical study of arteriolar (simple) hyalinosis in the spleen, ibid., v. 62, p. 253, 1971, bibliogr.
V. V. Serov.