Anthracosis, lipofuscin, hemosiderin and melanin accumulation

1. Overview of Pigments

• Exogenous (from outside): coal/carbon, silica, tattoo ink.
• Endogenous (made in body): lipofuscin, melanin, hemosiderin.

2. Exogenous — Carbon (Anthracosis)

• Inhaled carbon/coal (pollution, smoking) → phagocytosed by alveolar macrophages → carried to lung lymph nodes → black pigmentation; usually no clinical consequence.
• Coal workers’ pneumoconiosis / silicosis: coal mixed with silica (toxic) → kills macrophages → lysosomal enzyme release → necrosis → fibrotic nodules → ↑lung resistance → cor pulmonale (right heart failure).

3. Lipofuscin (Wear-and-Tear Pigment)

• Insoluble brown-yellow lipid-protein granules, perinuclear; from free-radical lipid peroxidation.
• Harmless itself — a marker of past oxidative injury / aging.
• Accumulates in heart, liver, brain → brown atrophy (e.g. shrunken heart in elderly/cachectic patients).

4. Hemosiderin (Iron Storage Pigment)

• Hb-derived yellow-brown aggregates of ferritin micelles; iron stored with apoferritin (free iron is toxic → peroxidation). Prussian blue positive.
• Hemosiderosis = accumulation in phagocytes (local or systemic); no parenchymal damage unless iron becomes free.

Local

• Bruise: Hb breakdown → color change blue→brown → macrophage clearance.
• Brown induration of lung: left heart failure / mitral stenosis → pulmonary congestion → microhemorrhage → heart failure cells (hemosiderin-laden macrophages) in alveoli/sputum.

Systemic

• Hemolysis / repeated transfusions → systemic hemosiderosis (all organs brown).
• Hereditary hemochromatosis: HFE/hepcidin mutation → ↓hepcidin → uncontrolled iron absorption → parenchymal iron overload → liver cirrhosis, pancreatic fibrosis (bronze diabetes), cardiomyopathy, skin pigmentation; ~200× risk of HCC; M:F 7:1; Rx phlebotomy/chelation.

5. Melanin & Melanocyte Disorders

• Melanin = brown-black pigment from tyrosine → (tyrosinase) → melanin, made by melanocytes in the basal epidermis; transferred to keratinocytes.

Condition	Mechanism	Key feature
Ephelis (freckle)	↑melanin transfer (no hyperplasia)	Sun-induced; commonest pigmented lesion in children
Melasma	↑transfer, hormonal	Facial; pregnancy; resolves after
Vitiligo	Autoimmune loss of melanocytes	Depigmented patches
Albinism	Tyrosinase mutation	Generalized absence of melanin
Melanocytic nevus	Melanocyte hyperplasia	Junctional / compound / intradermal

💡 High-yield: Distinguish pigments by source + stain + site — carbon (lung, anthracosis), lipofuscin (aging/brown atrophy), hemosiderin (Prussian blue, iron overload → hemochromatosis), melanin (tyrosinase; nevus = hyperplasia, freckle/melasma = ↑transfer only).