SEARCH RESULTS FOR: Lichen-Sclerosus

Lichen Sclerosus

Lichen Sclerosus (genital manifestation): Pathogenesis and clinical findings Authors: Mina Youakim Reviewers: Elise Hansen Sunawer Aujla Shahab Marzoughi Jori Hardin* * MD at time of publication Histamine receptor binding stimulates sensory nerve endings Pruritus (itching) Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) Chronic inflammation (i.e. chronic infection, chronic toxin exposure) and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) ↑ Activation of CD4+ and CD8+ T cells released from macrophages (white blood cell) in the perineum and genital skin tissue infiltrate into the dermal-epidermal junction T-cells proliferate in a horizontal linear formation Pro-inflammatory response activation Fibroblasts (contributes to the formation of connective tissue) proliferate and persist producing altered collagen under the epidermis Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Sclerotic plaques (localized areas of thickened skin) T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Progressive basal layer degeneration thins the overall skin thickness Mast cells respond to increased need for immune cell flow to area Nitric oxide is released when histamine binds to vascular receptors Localized area appears red Erythema (reddening of the skin) Erosion/ulceration Skin fissures (linear cleavage of skin) Localized histamine release Nitric oxide induces localized vasodilation (↑ blood flow) Normal Skin Lichen Sclerosus Epidermal layer Basal layer Dermal-Epidermal Junction Dermal layer Hypopigmented patches (localized, pale areas of skin) Epidermal atrophy (crinkling paper-type skin appearance) Thinned skin is weakened and prone to physical stress or trauma ↑ fluid in the extracellular space due to capillary leakage from ↑ blood flow Superficial dermal edema (swelling) Fibrotic tissue deposition following healing of damaged tissue Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Dermal layer Scarring Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Mar 25, 2024 on www.thecalgaryguide.com Lichen Sclerosus (genital manifestation): Pathogenesis and clinical findings Authors: Mina Youakim Reviewers: Elise Hansen Sunawer Aujla Shahab Marzoughi Jori Hardin* * MD at time of publication Histamine receptor binding stimulates sensory nerve endings Pruritus (itching) Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) Chronic inflammation (i.e. chronic infection, chronic toxin exposure) and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) ↑ Activation of CD4+ and CD8+ T cells released from macrophages (white blood cell) in the perineum and genital skin tissue infiltrate into the dermal-epidermal junction T-cells proliferate in a horizontal linear formation Pro-inflammatory response activation Fibroblasts (contributes to the formation of connective tissue) proliferate and persist producing altered collagen under the epidermis Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Sclerotic plaques (localized areas of thickened skin) T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Mast cells respond to increased need for immune cell flow to area Nitric oxide is released when histamine binds to vascular receptors ↑ fluid in the extracellular space due to capillary leakage from ↑ blood flow Superficial dermal edema (swelling) Epidermal atrophy (crinkling paper- type skin appearance) Thinned skin is weakened and prone to physical stress or trauma Localized histamine release Nitric oxide induces localized vasodilation (↑ blood flow) Localized area appears red Erythema (reddening of the skin) Erosion/ulceration Skin fissures (linear cleavage of skin) Normal Skin Lichen Sclerosus Epidermal layer Basal layer Dermal-Epidermal Junction Dermal layer Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Dermal layer Progressive basal layer degeneration thins the overall skin thickness Hypopigmented patches (localized, pale areas of skin) Fibrotic tissue deposition following healing of damaged tissue Scarring Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published MONTH, DAY, YEAR on www.thecalgaryguide.com Chronic inflammation (i.e. chronic Reviewers: Dermal layer Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) infection, chronic toxin exposure) and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) Elise Hansen Sunawer Aujla Shahab Marzoughi Jori Hardin* * MD at time of publication ↑ Activation of CD4+ and CD8+ T cells released from macrophages (white blood cell) in the perineum and genital skin tissue infiltrate into the dermal-epidermal junction T-cells proliferate in a horizontal linear formation Pro-inflammatory response activation ↑ Expression of MicroRNA-155 (enhances pro-inflammatory response and ↓ expression of tumor suppression genes) Fibroblasts (contributes to the formation of connective tissue) proliferate and persist producing altered collagen Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Sclerotic plaques (localized areas of thickened skin) T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Mast cells respond to increased need for immune cell flow to area Nitric oxide is released when histamine binds to vascular receptors ↑ fluid in the extracellular space due to capillary leakage from ↑ blood flow Superficial dermal edema (swelling) Epidermal atrophy (crinkling paper- type skin appearance) Thinned skin is weakened and prone to physical stress or trauma Lichen Sclerosus Localized histamine release Nitric oxide induces localized vasodilation (↑ blood flow) Localized area appears red Erythema (reddening of the skin) Erosion/ulceration Skin fissures (linear cleavage of skin) Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Histamine receptor binding stimulates sensory nerve endings Pruritus (itching) Normal Skin Progressive basal layer degeneration thins the overall skin thickness Hypopigmented patches (localized, pale areas of skin) Epidermal layer Basal layer Dermal-Epidermal Junction Fibrotic tissue deposition following healing of damaged tissue Scarring Chronic inflammation (i.e. chronic Reviewers: Dermal layer Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) infection, chronic toxin exposure) and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) Elise Hansen Sunawer Aujla Shahab Marzoughi Jori Hardin* * MD at time of publication ↑ Activation of CD4+ and CD8+ T cells released from macrophages in the perineum and genital skin tissue infiltrate into the dermal-epidermal junction T-cells proliferate in a horizontal linear formation Pro-inflammatory response activation ↑ Expression of MicroRNA-155 (short segment of RNA which enhances pro- inflammatory response and ↓ expression of tumor suppression genes) Fibroblasts proliferate and persist producing altered collagen Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Sclerotic plaques (localized areas of thickened skin) T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Progressive basal layer degeneration thins the overall skin thickness Hypopigmented patches (localized, pale areas of skin) Epidermal layer Basal layer Dermal-Epidermal Junction Mast cells respond to increased need for immune cell flow to area Nitric oxide is released when histamine binds to vascular receptors Superficial dermal edema (swelling) Epidermal atrophy (crinkling paper- type skin appearance) Localized histamine release Nitric oxide induces localized vasodilation (↑ blood flow) Localized area appears red Erythema (reddening of the skin) Histamine receptor binding stimulates sensory nerve endings Pruritus (itching) Normal Skin Lichen Sclerosus Skin fissures (linear cleavage of skin) Erosion/ulceration Fibrotic tissue deposition following healing of damaged tissue Scarring Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Reviewers: Dermal layer Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) Chronic inflammation (i.e. chronic infection, chronic toxin exposure) and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) Elise Hansen Sunawer Aujla Shahab Marzoughi Jori Hardin* * MD at time of publication ↑ Activation and infiltration of CD4+ and CD8+ T cells into the dermal-epidermal junction T-cells proliferate in a band (horizontal linear) formation Pro-inflammatory response activation ↑ Expression of MicroRNA-155 (short segment of RNA which enhances pro-inflammatory response and ↓ expression of tumor suppression genes) Fibroblasts proliferate and persist producing altered collagen Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Sclerotic plaques (localized areas of thickened skin) T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Progressive basal layer degeneration thins the epidermis Hypopigmented patches (localized, pale areas of skin) Epidermal layer Basal layer Dermal-Epidermal Junction Mast cells respond to increased need for immune cell flow to area Nitric oxide is released when histamine binds to vascular receptors Superficial dermal edema (swelling) Epidermal atrophy (crinkling paper- type skin appearance) Localized histamine release Histamine receptor binding stimulates sensory nerve endings Pruritus (itching) Skin fissures (linear cleavage of skin) Nitric oxide induces localized vasodilation (↑ blood flow) Localized area appears red Erythema (reddening of the skin) Scarring Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Erosion/ulceration Fibrotic tissue deposition following healing of damaged tissue Normal Skin Lichen Sclerosus Chronic inflammation (i.e. chronic Elise Hansen Unknown triggers Genetic predisposition infection, chronic toxin exposure) Medications (e.g. carbamazepine, (HLA-DQ7 and HLA-DR12) and trauma pembrolizumab, nivolumab, ipilimumab) ↑ Activation and infiltration of CD4+ and CD8+ T cells into the dermal-epidermal junction Sunawer Aujla Shahab Marzoughi Name Name* * MD at time of publication T-cells proliferate in a band (horizontal linear) formation Pro-inflammatory response activation (increase in pro-inflammatory cytokines such as Interleukins 1-alpha and 1-beta) ↑ Expression of MicroRNA-155 (short segment of RNA which enhances pro-inflammatory response and ↓ expression of tumor suppression genes) Fibroblasts proliferate and persist producing altered collagen T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) ↑ Oxidative stress and cell damage Progressive basal layer degeneration thins the epidermis Hypopigmented patches (localized, pale areas of skin) Histamine receptor binding stimulates sensory nerve endings Localized area appears red Localized histamine release Localized vasodilation (↑ blood flow) Superficial dermal edema (swelling) Pruritus Erythema Collagen deposits and hyalinizes (transforms into acellular translucent material) beneath the epidermal layer Normal Skin Sclerotic plaques (localized areas of thickened skin) Epidermal layer Basal layer Dermal-Epidermal Junction Dermal layer Skin fissures (linear cleavage of skin) Bleeding Erosion/Ulceration Epidermal atrophy (crinkling paper- type skin appearance) Lichen Sclerosus Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Dermal layer Fibrotic tissue deposition following healing of damaged tissue Scarring Lichen Sclerosus (genital manifestation): Pathogenesis and clinical findings Authors: Mina Youakim Reviewers: Elise Hansen Sunawer Aujla Shahab Marzoughi Name Name* * MD at time of publication Pruritus Histamine receptor binding stimulates sensory nerve endings Localized area appears red Erythema Unknown triggers Genetic predisposition (HLA-DQ7 and HLA-DR12) Chronic inflammation and trauma Medications (e.g. carbamazepine, pembrolizumab, nivolumab, ipilimumab) ↑ Activation and infiltration of CD4+ and CD8+ T cells into the dermal-epidermal junction T-cells proliferate in a band formation Pro-inflammatory response activation ↑ Expression of MicroRNA-155 (short segment of RNA which enhances pro-inflammatory response and ↓ expression of tumor suppression genes) Fibroblasts proliferate and persist producing altered collagen T cells release of pro-inflammatory cytokines (interleukins and transforming growth factor β) Localized histamine release Localized vasodilation (↑ blood flow) Superficial dermal edema (swelling) Collagen deposits and hyalinizes beneath the atrophic epidermal layer Hypopigmented patches (localized, pale areas of skin) ↑ Oxidative stress and cell damage Progressive basal layer degeneration thins the epidermis Skin fissures Lichen Sclerosus Epidermal atrophy (crinkling paper- type skin appearance) Sclerotic plaques (localized areas of thickened skin) Bleeding Scarring Erosion/Ulceration Normal Skin Epidermal layer Basal layer Dermal-Epidermal Junction Dermal layer Atrophic Epidermal layer Hyalinized collagen deposits Basal layer degeneration Band of T-cell infiltrate Dermal layer Legend: Published MONTH, DAY, YEAR on www.thecalgaryguide.com Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications