PIGMENTATION

By G. Meshchersky · Physiology, Pathology, Dermatology & Venereology

Also known as: Coloration, Pigment Deposition

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

Pigmentation refers to the coloring of tissues and organs in living organisms due to the deposition of coloring substances. This article classifies pigmentation into exogenous and endogenous types, detailing their causes, mechanisms, and pathological manifestations.

Encyclopedia article (1928–1936)

PIGMENTATION, the coloring of tissues and organs of a living organism in a specific color due to the deposition in them of one or another coloring substance. Only rarely does coloring depend on physical causes, i.e., on the fact that the basis of the coloration is the optical phenomenon of light interference, conditioned by the special structure of the object (the plumage of many birds, the scales on butterfly wings, etc.). Such P. can be easily destroyed by mechanical means. According to the nature of deposition, P. is divided into 2 large groups: exogenous and endogenous P. The first arise under the influence of the deposition of coloring substances that have entered the body from outside, the second are caused by the deposition of substances formed in the body itself. Depending on the substrate, endogenous P. in turn are subdivided into hematogenous, the formation of which is related to the breakdown of blood, and autogenous, arising in connection with the metabolic activity of the tissue. Exogenous pigmentations. Their basis is the deposition of coloring substances foreign to the body and penetrating it from outside. This phenomenon thus comes into contact with the areas of professional diseases, poisonings, cosmetics, and experimental in vivo staining. The place of entry of the substance into the body can be the skin, the mucous membrane of the respiratory tract, the digestive tract, the urogenital system, and direct introduction into the blood and lymphatic vessels. The skin is most easily accessible to both voluntary and involuntary external coloring. Among many wild tribes and primitive peoples, the "custom of such coloring, called tattooing, is widely spread. Unintentional P. of the skin occurs as a result of various therapeutic measures (lead ointments, mercury rubs, bismuth powder, cauterization with silver nitrate can cause the deposition of the said metals in the skin and mucous membranes and the corresponding P. of them) and in industries where workers, by the nature of their work, are closely associated with certain dust particles penetrating the skin (grinders, turners, blacksmiths, dyers, etc.). In all these cases, coloring can occur through intact skin. Very often the respiratory tract serve as the entrance gates for exogenous P. The inhalation of all kinds of vegetable (coal), mineral (quartz), and metallic (iron, lead, mercury, copper, etc.) dust creates pictures of anthracosis, siderosis of the lungs. Part of the said dust particles can in this case penetrate into the lymph glands and even into distant internal organs (spleen, kidneys). The entry of coloring substances through the digestive tract is less common. The swallowing of dust particles of course has some significance, but does not lead to intense P. Of greater significance in this sense is the medicinal introduction into the digestive tract of various substances: bismuth during X-ray examination, silver nitrate in stomach ulcers. Chronic consumption of the latter leads to argyria (see). The introduction of coloring substances directly into the blood with subsequent P. of one or another substrates plays a minor role in human pathology. In this sense, the in vivo staining of adipose tissue with Sudan, nerve trunks with methylene blue, and amyloid with congo red deserves attention. The phenomena of in vivo staining are better studied in animals. By means of intravenous injection of ink, solutions of silver, iron, and colloidal dyes of various dispersity (lithium carmine, trypan blue, etc.), it is possible to achieve P. of the skin and internal organs in the corresponding color, and in the main mass the dye is fixed by the reticulo-endothelium and parenchymal elements (see Vital staining). All absorbed substances soluble in the body's juices are excreted from it along with its secretions. In contrast to this, pigments that have precipitated in a granular form in the cytoplasm of cells or in the interstitial substance of connective tissue are removed very slowly. As a result of extensive deposits in the corresponding organs, various persistent morphological and functional changes may occur. The lungs are especially affected. Their saturation with coal pigment can be so great that the tissue necrotizes and disintegrates with the formation of cavities (phthisis atra). The inhalation of quartz dust leads to the proliferation of connective tissue in the lung, to emphysema, to asthma. Endogenous pigmentations. 1) Hemoglobinogenic P. are related to the breakdown of blood. The substances causing the coloring of tissues in this case are hemoglobin and its derivatives—hemosiderin and hematoidin (bilirubin). During physiological aging and breakdown of blood, the iron released enters the intermediate metabolism; in organs it is not deposited, not accumulated <i09 and does not give any special coloration to organs. In pathological acute breakdown of blood (hemoglobinuric fever, blood transfusion, poisoning with hydrogen arsenide), the released Hb colors the organs, especially the kidneys, brown. The same appearance is taken by the kidneys also in poisoning with Berthollet's salt from the excretion of methemoglobin. In slow pathological hemolysis, especially intravascular, hemosiderin begins to circulate in the bloodstream; it is absorbed by the reticulo-endothelium, mainly of the spleen, liver, bone marrow, and lymph glands, and due to its brown color gives the organs a rusty color. This phenomenon is called hemosiderosis and is manifested in pernicious anemia, childhood intoxications, liver cirrhosis, hemochromatosis (see) and many other diseases. In some cases, the accumulation of hemosiderin occurs locally, e.g., in the lung with prolonged stagnation in the small circle; the lung also acquires a distinctly rusty tint and becomes dense. Focal P. of the skin and internal organs after bruises and hemorrhages also depends on the appearance of hemosiderin and hematoidin. Upon contact with hydrogen sulfide, hemosiderin turns into iron sulfide, which has a dirty green or black color. This phenomenon is observed in the digestive tract and is known under the name of pseudomelanosis. At the present time, malarial P. (see Malaria) is also included in the blood-forming pigments causing jaundice P. The second blood-forming pigment causing jaundice P. is the bile pigment bilirubin, see Bile, Jaundice, Pathological physiology of the liver. 2) Autogenous pigments, which are products of cell metabolism, are already very common in the normal organism. They are responsible for the coloration of the skin, hair, the pigment layer of the eye, adipose tissue, etc. Their basis is the deposition in the said tissues of pigments: melanin, lipochromes, etc. In certain physiological and pathological conditions of the organism, these P. may weaken or, conversely, intensify. In the first case, for example, the skin may completely lose pigment and become white. An example of this is vitiligo, syphilitic leukoderma, genotypic albinism, etc. The reverse phenomenon—hyperpigmentation, see below P. of the skin and Melanosis. Pigment formation is undoubtedly conditioned by various factors [see Coloration (plants and animals)]. The distribution of pigment in each individual, regardless of the race to which he belongs, follows certain regularities, which can be explained only from the standpoint of genotypicity. In many mammals, for example, and especially in primates, the back and extensor surfaces of the limbs are colored darker than the abdomen and flexor surfaces. This also includes the constancy of color and patterns of bird plumage, the coloration of fur in various animal species, hair in humans (family cases of early graying deserve attention in this sense). It is assumed that the significance of P. for man consists in that it represents a certain protection against light, especially against its ultraviolet rays. With the activation of pigment formation, these rays are absorbed by melanin and thus their penetration into the corium is almost completely prevented. Numerous facts speak in favor of the fact that heavily pigmented skin reacts less to light than unpigmented skin. In this sense, the dark coloration of the skin of peoples living in tropical countries (negroes, Indians, Arabs, etc.) can be regarded as an adaptive act. In addition to this, pigments are also assigned the role of a photocatalyst and a temperature regulator. To the autogenous pigments should also be added lipofuscin, related to melanin. Its accumulation in organs leads to their pigmentation in a brown color. A characteristic example of this process is the brown atrophy of the liver and heart muscle in elderly and marantic subjects. These P. also include ochronosis, in which cartilage, tendons, joint capsules, and vessels are colored black, as well as porphyria, in which all organs and especially bones are pigmented in a reddish-brown color. The nature of the pigment coloring the tumor masses in chloroma in a gray-green color is still completely unknown. Pigmentation with lutein—see Lipochromes.

E. Gertsenberg. P. of the skin, coloring it in various shades from yellow or gray to coal-black, unwashable and not removable by rubbing, is a physiological phenomenon caused by the presence in the basal cells of the epidermis of the pigment melanin produced by them, the abundance of which determines the color of the skin of both individual races and individuals of the same race. Works from the clinic of Bloch (Vg. V loch) indicated on the frequently observed ability of basal cells of the mucous membrane, especially of the oral cavity, to produce pigment. The amount of skin pigment, negligible in fair-skinned individuals at birth, rapidly increases under the influence of sunlight, reaching a certain norm for a given subject; it particularly increases P. "with age. P. is not the same over the entire surface of the skin: the skin of the palms, soles, and nail bed is poor in pigment; it is more abundant on the exposed parts, external genitalia, armpits, outer sides of the forearms, in the epigastric region and especially on the nipples and their areola. Repeated prolonged insolation makes the skin swarthy. Prolonged residence of a person of a colored race in the north softens the shade of his skin. Pregnancy is often accompanied by darkening of certain areas of the skin. Pathological P. of the skin (hyperchromia, or melanosis) are in their main features reduced either to an abnormal abundance of melanin in the epidermis with the usual presence of chromatophores in the dermis, or to the deposition of hemosiderin in the dermis (intra- and extra-cellular) (see). In the first case, a cotton swab when rubbing the skin surface becomes colored, in the second--this is not observed. Hyperchromia should be distinguished from cases where only the horny layer is pigmented, the removal of which reveals normally pigmented skin. These include: black ichthyosis, so-called black seborrhea, pityriasis versicolor, senile warts, Darier's disease. Dermatoses in which P. as a constant symptom is caused by the persistent content of hemosiderin can be called cutaneous sideroses (M. Diss). These include: 1) progressive pigmented disease of Schamberg; 2) its subspecies--annular telangiectatic purpura of Majocchi; 3) varicose dermatitis of the legs or pigmented purpuric dermatitis of the Lyon dermatological school. Experimentally, hemosiderin P. cannot be reproduced: the blood pigment introduced into the dermis quickly dissolves and disappears. Evidently, for its persistent retention by the dermis, it is necessary to lower the biological properties of histiocytes, possibly the loss of the ability to free themselves from phagocytized pigment. Examples of universal P. of the skin (so-called melanodermias) by blood pigment are melanoderma in chronic malaria, in which the pigment is contained even in the endothelium of blood and lymphatic vessels. In dermatoses where there are various lesions of the vascular wall (Kaposi's sarcoma, all types of purpura, radiodermatitis, atrophic acrodermatitis, syphilids, etc.), only isolated grains of hemosiderin can be found in the dermis. Melanin hyperchromias are divided into congenital and acquired. The former include pigmented nevi, early and late, including freckles, diffuse P. in Recklinghausen's disease and lentigo, both juvenile and senile (lentigo maligna). The latter is a melanotic precancerous dermatosis. For pathological accumulation of melanin, see Melanosis. In the clinical picture of other dermatoses, hyperchromia enters as a concomitant symptom along with others. These include scleroderma, acanthosis nigricans, pellagrous erythema in the withering stage, pediculous melanoderma, Riehl's melanosis with its subspecies--Hoffman's toxic melanodermatitis, apparently caused by intoxication with acridine compounds+the action of ultraviolet rays. Reticular type melanoses with limited localization are usually caused by the local action of heat (compresses, hot-water bottles, stoves, etc.) in individuals with acrocyanosis and marbled skin, while with widespread distribution (poikiloderma, rare reticular forms of arsenobenzol dermatitis, Riehl's and E. Hoffman's melanodermatoses)--by general intoxication or possibly auto-intoxication. Melanoses of accessible mucous membranes, especially of the oral cavity, in the form of spots or bands of various sizes are observed both in isolation and in melanodermias. Their etiology is reduced either to racial properties--Malays, Gypsies, Romanians, Algerian Arabs, etc., or to a partial manifestation of diffuse melanosis of the skin, most often in Addisonian or pediculous melanodermias, less often in tuberculous, arsenical, bronze diabetes (M. Labbe, Bith). According to Milian, the main cause of pigmented spots of the mucous membrane is syphilis. Consecutive temporary P. at the site of a former dermatosis, repeating the localization, form and size of the preceding elements, is a banal phenomenon, especially in Duhring's dermatitis, pemphigus, lichen planus, syphilids, etc. To establish the etiology of pathological P., in addition to studying its morphology and evolution, a detailed clinical examination of the patient is usually required. Only sharply defined band-like, correctly angular or correctly rounded hyperchromias give the right to speak of P. artificial.

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“PIGMENTATION.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/pigmentation/