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Related to lichen amyloidosis: lichen planus, macular amyloidosis


Deposition of amyloid in one or more organs of the body.



or amyloid dystrophy, a disorder of protein metabolism accompanied by the formation within tissues of a specific protein polysaccharide complex known as amyloid. The progress of the disease is associated with distortion of the protein-synthesizing function of the reticuloendothelial system and with accumulation of anomalous proteins in the blood plasma which act as autoantigens and also stimulate the formation of autoantibodies. As a result of antigen-antibody interaction, there is deposition of widely dispersed proteins which figure in the formation of amyloid. Once deposited in tissues, such as vascular and gland walls, the amyloid displaces functionally specialized elements of the organ; this process leads to the destruction of the organ.

Several types of amyloidosis are recognized: primary, secondary, and senile amyloidosis; amyloidosis with multiple myeloma; and localized tumorlike amyloidosis. Primary amyloidosis has no connection with any other disease; it affects mainly the cardiovascular system, alimentary tract, muscles, and skin. Secondary amyloidosis develops subsequent to other diseases which are accompanied by prolonged suppuration and tissue breakdown, such as tuberculosis, syphilis, and rheumatoid arthritis. It most often affects the spleen, liver, kidneys, adrenal glands, and intestines. Senile amyloidosis usually involves the heart. Amyloidosis may be either general or localized. Im-munodepressive and hepatic preparations are used in its treatment.


References in periodicals archive ?
Three diabetics had lichen amyloidosis and one had macular amyloidosis.
Among the 20 clinically lichen amyloidosis patients, 85% had used scrubs.
When small focal deposits were seen in the papillary dermis, macular amyloidosis was diagnosed and wherever globular amyloid deposits were seen, which displaced the rete ridges, a diagnosis of lichen amyloidosis was made.
Hyperkeratosis and acanthosis were more prominent in lichen amyloidosis compared to macular amyloidosis.
5 It is suggested that amyloid deposition in macular amyloidosis and lichen amyloidosis is primarily caused by epidermal keratinocyte degeneration, any relationship between systemic amyloidosis has not been detected.
14 There are not many reports about the usage of topical calcineurin inhibitors, however Cazares et al reported improvement in lichen amyloidosis using treatment with 0.
Patients with lichen amyloidosis were treated with UVB or topical PUVA on one limb and moderate to potent topical corticosteroids on the other limb.