Introduction to the problem of pigment disorders
Brown induration and brown atrophy are two conditions united by an external similarity (the brown hue of the affected organs), but fundamentally different in their pathogenesis. Both processes are associated with impaired metabolism of endogenous pigments, yet these pigments differ: in induration, it is hemosiderin, while in atrophy, it is lipofuscin. Understanding these differences is important for differential diagnosis and for comprehending the general mechanisms of chronic heart failure and regressive tissue changes.
Iron metabolism and hemosiderin formation
Endogenous iron metabolism in the body is associated with the formation of two pigments — ferritin (monomer) and hemosiderin (ferritin polymer). Normally, hemosiderin is deposited in the macrophages of the bone marrow, spleen, and liver; such macrophages are called sideroblasts. Physiological erythrocyte breakdown occurs here with hemoglobin recycling.
During pathological accelerated hemolysis, excess hemosiderin is formed, which is deposited in the cells and stroma of various organs and is no longer utilized as a reserve iron pool. Macrophages that phagocytose pathological hemosiderin are designated as siderophages.
According to their prevalence, the following are distinguished:
- Local hemosiderosis is a consequence of extravascular hemolysis (hemorrhages, local venous congestion).
- Generalized hemosiderosis is a consequence of intravascular hemolysis (hemolytic anemias, intoxications, infections).
Brown induration of the lungs
Brown induration of the lungs is a local hemosiderosis of the lungs developing in chronic heart failure in the stage of decompensation. Venous congestion in the pulmonary circulation leads to diapedetic hemorrhages, destruction of erythrocytes in the alveolar lumens, and accumulation of hemosiderin in macrophage-siderophages. Concurrently, chronic hypoxia stimulates the proliferation of connective tissue.
Macroscopic appearance:
- The lungs are enlarged in size due to venous hyperemia and edema.
- Brown coloration due to hemosiderin deposition.
- Consistent firmness due to developing pneumosclerosis (fibrosis) against the background of chronic ischemia.
- Whitish layers of connective tissue are visible around the bronchi and vessels, as well as diffusely in the parenchyma.
Microscopic appearance: in the lumens of the alveoli, bronchi, and in the stroma, there are clusters of siderophages (brown cells with hemosiderin granules). Alveolar septa are thickened due to fibrosis. A pale pink homogeneous fluid—transudate, characteristic of venous congestion—is detected in the alveolar lumens. Diapedetic hemorrhages are encountered.
Lipofuscin and brown atrophy
Lipofuscin is an insoluble yellow-brown pigment, also known as the aging pigment. It is formed as a product of lipid peroxidation of membranes that is not utilized during an imbalance between oxidative processes and the activity of antioxidant systems. Lipofuscin accumulates in cells with regressive changes.
Main causes of lipofuscinosis:
- Aging of the organism.
- Cachexia and severe exhausting diseases (oncological, infectious).
- Chronic inflammatory processes.
- Prolonged hypoxia and metabolic disorders.
Morphology of brown atrophy
Brown atrophy is most characteristic of the myocardium and liver, and is less frequently detected in skeletal muscles and neurons.
Macroscopic appearance: organs are reduced in size, firm, and acquire a characteristic brown hue. The heart shows tortuous vessels beneath the epicardium and thinned walls; the liver has a sharp anterior margin and reduced mass.
Microscopic appearance: small yellow-brown lipofuscin granules located perinuclearly (at the poles of the nucleus) are revealed in cardiomyocytes and hepatocytes. The cells themselves are reduced in volume—a morphological sign of atrophy.
Comparison of the two conditions
- Pigment: in brown induration, hemosiderin (hemoglobin breakdown product); in brown atrophy, lipofuscin (lipid peroxidation product).
- Etiology: induration—chronic heart failure with venous congestion in the lungs; atrophy—aging, cachexia, debilitating diseases.
- Localization: induration—predominantly the lungs; atrophy—myocardium, liver.
- Organ size: in induration, the lungs are enlarged and firm; in atrophy, the organs are reduced and firm.
- Localization of the pigment within the cell: hemosiderin—in macrophages (siderophages) within alveolar lumens and stroma; lipofuscin—perinuclearly in parenchymal cells.
Key points
- The brown color of the organs in both pathologies is due to the yellow-brown coloration of the pigments, but the nature of the pigments differs.
- Hemosiderin is a ferritin polymer, formed during the breakdown of erythrocytes and accumulates in macrophages.
- Brown induration of the lungs is a manifestation of chronic venous congestion in decompensated CHF with pneumosclerosis.
- In the alveoli during brown induration, siderophages and transudate are found, and septa are thickened.
- Lipofuscin is the aging pigment, a marker of regressive changes and chronic hypoxia.
- Brown atrophy is typical for the myocardium and liver; organs decrease in size and become firm.
- Lipofuscin in cells is located perinuclearly in the form of small granules.
- Differential feature: induration—organ enlargement and siderophages; atrophy—organ reduction and perinuclear granules.