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==Overview== | ==Overview== | ||
The progression of systemic lupus erythematosus involves the immune system. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well. The most prominent events involving immune abnormalities are related to persistent activation of B cells and plasma cells that make auto-antibodies more auto antibodies during disease progression. The most prominent events involving hormonal abnormalities are due to prolactin and estrogen. The most important environmental factors related to disease progression are ultraviolet (UV) light and some infections. On microscopic histopathological analysis, apoptotic keratinocytes, vacuolization of the basement membrane, and dermal mucin deposition are characteristic findings of SLE dermatitis, and active or inactive endocapillary or extracapillary segmental glomerulonephritis are characteristic findings of SLE nephritis. | The progression of systemic lupus erythematosus involves the [[immune system]]. There are other factors like [[genetic]] factors, [[hormonal]] abnormalities, and environmental factors that play some roles as well. The most prominent events involving immune abnormalities are related to persistent activation of [[B cells]] and [[Plasma cell|plasma cells]] that make [[Autoantibody|auto-antibodies]] more auto [[antibodies]] during disease progression. The most prominent events involving hormonal abnormalities are due to [[prolactin]] and [[estrogen]]. The most important environmental factors related to disease progression are [[ultraviolet]] (UV) light and some infections. On microscopic [[histopathological]] analysis, [[apoptotic]] [[Keratinocyte|keratinocytes]], [[vacuolization]] of the [[basement membrane]], and [[dermal]] [[mucin]] deposition are characteristic findings of SLE [[dermatitis]], and active or inactive endocapillary or extracapillary segmental [[glomerulonephritis]] are characteristic findings of SLE nephritis. | ||
==Pathogenesis== | ==Pathogenesis== | ||
The progression of systemic lupus erythematosus involves the immune system. Near all of the | The progression of systemic lupus erythematosus involves the immune system. Near all of the pathological manifestation of SLE are due to [[antibody]] formation and the creation of [[immune complexes]] in different organs of the body. When the [[immune complexes]] designed, they will deposit in different body tissues and vessels, which will lead to more [[complement]] activation and more organ damage. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well. | ||
=== Immune abnormalities === | === Immune abnormalities === | ||
Development of systemic lupus erythematosus (SLE) is the result of different mechanisms that at the end lead to auto-immune response of the body. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their self-antigens and consequently progress an autoimmune disease and develop auto antibodies as a response. During disease progression, B cells and plasma cells that make auto-antibodies are more persistently activated and thus make more auto antibodies. These auto antibodies are targeted predominantly to intracellular nucleoprotein particles | Development of systemic lupus erythematosus (SLE) is the result of different mechanisms that at the end lead to [[auto-immune]] response of the body. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their [[Antigens|self-antigens]] and consequently progress an [[Autoimmunity|autoimmune]] disease and develop auto [[antibodies]] as a response. During disease progression, [[B cell|B cells]] and [[Plasma cell|plasma cells]] that make auto-antibodies are more persistently activated and thus make more auto antibodies. These auto antibodies are targeted predominantly to [[intracellular]] [[nucleoprotein]] particles | ||
8519610 | 8519610 | ||
This increase in auto antibody production and persistence suppose to be down regulated by anti-idiotypic antibodies or regulatory immune cells, but due to immunologic response it is not appropriately been responded. | This increase in auto antibody production and persistence suppose to be down regulated by anti-idiotypic [[antibodies]] or regulatory immune cells, but due to immunologic response it is not appropriately been responded. | ||
The most important immune abnormalities that are related to SLE develop and progression: | The most important immune abnormalities that are related to SLE develop and progression: | ||
* Increase in circulating plasma cells and memory B cells that is associated with SLE activity | * Increase in circulating [[plasma cells]] and memory B cells that is associated with SLE activity | ||
* Decrease in cytotoxic T cells and in functions of suppressor T cells and impaired generation of polyclonal T-cell cytolytic activity | * Decrease in [[cytotoxic T cells]] and in functions of [[suppressor T cells]] and impaired generation of polyclonal T-cell cytolytic activity | ||
* Increase in helper T cells and also their function | * Increase in [[T helper cell|helper T cells]] and also their function | ||
* Polyclonal activation of B cells and abnormal B-cell receptor signaling | * [[Polyclonal antibody|Polyclonal]] activation of [[B cell|B cells]] and abnormal B-cell receptor signaling | ||
* Prolonged lives of B cells | * Prolonged lives of [[B cell|B cells]] | ||
* Signaling abnormalities of T and B lymphocytes | * Signaling abnormalities of T and B [[Lymphocyte|lymphocytes]] | ||
** Cellular hyperactivity | ** Cellular hyperactivity | ||
** | ** Hyper responsiveness | ||
** May be due to genetically defects | ** May be due to genetically defects | ||
* Increased expression of IFN-alpha-inducible RNA transcripts by mononuclear cells that lead to elevated levels of IFN-alpha. 15593221 | * Increased expression of IFN-alpha-inducible RNA transcripts by [[Mononuclear cells|mononuclear]] cells that lead to elevated levels of IFN-alpha. 15593221 | ||
* Increase in specific genetic factors expression that may be associated with autoimmunity promotion | * Increase in specific genetic factors expression that may be associated with autoimmunity promotion | ||
* Dysfunctional signaling in T and B cells that may be due to: | * Dysfunctional signaling in T and [[B cell|B cells]] that may be due to: | ||
** Increased calcium responses to antigen stimulation | ** Increased [[calcium]] responses to [[antigen]] stimulation | ||
** Hyperphosphorylation of cytosolic protein substrates | ** [[Hyperphosphorylation]] of cytosolic protein substrates | ||
** Decreased nuclear factor kB | ** Decreased nuclear factor kB | ||
** Abnormal voltage-gated potassium channels: These channels facilitate excessive calcium entry into T cells | ** Abnormal voltage-gated [[potassium]] channels: These channels facilitate excessive calcium entry into T cells | ||
* Increased levels of microparticles (MPs): | * Increased levels of microparticles (MPs): | ||
** Microparticles are small, membrane-bound vesicles enclose DNA, RNA, nuclear proteins, cell-adhesion molecules, growth factors, and cytokines. | ** Microparticles are small, membrane-bound vesicles enclose DNA, RNA, [[nuclear]] proteins, cell-adhesion molecules, [[Growth factor|growth factors]], and [[Cytokine|cytokines]]. | ||
** They are shed from cells during apoptosis or activation | ** They are shed from cells during [[apoptosis]] or activation | ||
** Microparticles can drive inflammation and autoimmunity by their derivatives 23672591 | ** Microparticles can drive inflammation and [[autoimmunity]] by their derivatives 23672591 | ||
* Elevated levels of circulating TNF-alpha correlate with active disease, and TNF is expressed in renal tissue in lupus nephritis | * Elevated levels of circulating [[TNF-alpha]] correlate with active disease, and [[TNF]] is expressed in renal tissue in [[lupus nephritis]] | ||
* | * Abnormally high levels of E-C4d and low levels of E-CR1 are characteristic of SLE, and combined measurement of the 2 molecules has high diagnostic sensitivity and specificity for lupus | ||
* Increased numbers of circulating neutrophils undergoing NETosis, a form of apoptosis specific for neutrophils, releases DNA bound to protein in protein nets, which stimulates anti-DNA and IFN-alpha production | * Increased numbers of circulating [[neutrophils]] undergoing NETosis (NET=eutrophil extracellular traps), a form of [[apoptosis]] specific for neutrophils, releases DNA bound to protein in protein nets, which stimulates anti-DNA and IFN-alpha production | ||
* Increased neutrophil extracellular trap formation: 26658004 | * Increased [[neutrophil]] extracellular trap formation: 26658004 | ||
** It may promote thrombus formation | ** It may promote [[thrombus]] formation | ||
** It is associated with increased disease activity and renal disease and thus can be used even as a disease activity marker. | ** It is associated with increased disease activity and renal disease and thus can be used even as a disease activity marker. | ||
** It can damage and kill endothelial cells and promote inflammation in atherosclerotic plaques, which may contribute to accelerated atherosclerosis in systemic lupus erythematosus | ** It can damage and kill [[endothelial cells]] and promote inflammation in [[Atherosclerosis|atherosclerotic]] plaques, which may contribute to accelerated [[atherosclerosis]] in systemic lupus erythematosus | ||
* As an example of immune abnormalities and their complications, nervous system involvement in SLE is due to: | * As an example of immune abnormalities and their complications, nervous system involvement in SLE is due to: | ||
**Small to moderate vessles vasculopathy with perivascular accumulation of mononuclear cells, without destruction of the blood vessel | **Small to moderate vessles vasculopathy with perivascular accumulation of [[mononuclear cells]], without destruction of the blood vessel | ||
**Antiphospholipid antibodies | **[[Antiphospholipid antibodies]] | ||
*These changes promote the production of antinuclear antibodies | *These changes promote the production of [[antinuclear antibodies]] | ||
=== Hormonal abnormalities === | === Hormonal abnormalities === | ||
| Line 56: | Line 56: | ||
* Sexual predilection of females: Shows the relationship of female hormones and the onset of SLE | * Sexual predilection of females: Shows the relationship of female hormones and the onset of SLE | ||
* Significantly increased risk for SLE in:17393454 | * Significantly increased risk for SLE in:17393454 | ||
** Early age of menarche | ** Early age of [[menarche]] | ||
** Early age at menopause or surgical menopause | ** Early age at [[menopause]] or surgical menopause | ||
** Women that are treated with estrogen-containing regimens such as oral contraceptives or postmenopausal hormone replacement therapies | ** Women that are treated with estrogen-containing regimens such as oral contraceptives or postmenopausal hormone replacement therapies | ||
Hormones that are related to SLE disease progression:10503654 | Hormones that are related to SLE disease progression:10503654 | ||
* Gonadotrophins like prolactin | * Gonadotrophins like [[prolactin]] | ||
** Stimulants of immune functions and is elevated in SLE | ** Stimulants of immune functions and is elevated in SLE | ||
* Exogenous estrogen - include oral contraceptive use and post-menopausal hormone replacement therapy: 10503654- 25155581 | * Exogenous [[estrogen]] - include oral contraceptive use and post-menopausal hormone replacement therapy: 10503654- 25155581 | ||
** Stimulates the type 1 IFN pathway | ** Stimulates the type 1 [[IFN]] pathway | ||
** Stimulates thymocytes, CD8+ and CD4+ T cells, B cells, macrophages, the release of certain cytokines (eg, IL-1) | ** Stimulates thymocytes, [[CD8]]+ and [[CD4]]+ [[T cell|T cells]], [[B cell|B cells]], [[Macrophage|macrophages]], the release of certain cytokines (eg, IL-1) | ||
** Prompt maturation of B cells especially those that have a high affinity to | ** Prompt maturation of [[B cell|B cells]] especially those that have a high affinity to anti-DNA antibodies by decreasing the [[apoptosis]] of this self-reactive B-cells 16724801 | ||
** Stimulate expression of HLA and endothelial cell adhesion molecules (VCAM, ICAM) | ** Stimulate expression of [[HLA]] and endothelial cell adhesion molecules (VCAM, ICAM) | ||
** Increases macrophage proto-oncogene expression | ** Increases [[macrophage]] [[proto-oncogene]] expression | ||
** Enhanced adhesion of peripheral mononuclear cells to endothelium | ** Enhanced adhesion of peripheral [[mononuclear cells]] to [[endothelium]] | ||
* Progesterone: | * [[Progesterone]]: | ||
** May inhibit the type 1 [[interferon]] pathway, suggesting that a balance between estrogen and progesterone may be critical for the body to remain healthy | ** May inhibit the type 1 [[interferon]] pathway, suggesting that a balance between [[estrogen]] and [[progesterone]] may be critical for the body to remain healthy | ||
** Downregulates T-cell proliferation and increases the number of CD8 cells | ** Downregulates T-cell proliferation and increases the number of CD8 cells | ||
* Both progesterone and high levels of estrogen promote a Th2 response, which favors autoantibody production | * Both progesterone and high levels of [[estrogen]] promote a [[Th2]] response, which favors [[autoantibody]] production | ||
=== Environmental factors === | === Environmental factors === | ||
* Infections can stimulates some antigen specific cells and lead to SLE disease: | * Infections can stimulates some antigen specific cells and lead to SLE disease: | ||
** Epstein-Barr virus (EBV): | ** [[Epstein Barr virus|Epstein-Barr virus (EBV)]]: May induce anti-DNA antibodies or even lupus-like symptoms. It is associated with higher risk of SLE and also triggering the active course of disease in children | ||
** Trypanosomiasis or mycobacterial infections may have the same effect as EBV | ** [[Trypanosomiasis]] or [[mycobacterial]] infections may have the same effect as EBV | ||
** SLE active disease flares may follow bacterial infections as well | ** SLE active disease flares may follow bacterial infections as well | ||
* Ultraviolet (UV) light: Can stimulates B-cells to produce more antibodies. It can also interfere with antigen processing by activation of macrophages and hence increase the degree of autoimmunity | * [[Ultraviolet|Ultraviolet (UV)]] light: Can stimulates [[B-cells]] to produce more [[antibodies]]. It can also interfere with antigen processing by activation of [[macrophages]] and hence increase the degree of [[autoimmunity]] | ||
==Genetics== | ==Genetics== | ||
Systemic lupus erythematosus is transmitted in poly-genic inheritance pattern. Genes involved in the pathogenesis of systemic lupus erythematosus include HLA class polymorphism, complement genes, and other genes related to immunologic system as well. | Systemic lupus erythematosus is transmitted in poly-genic [[inheritance]] pattern. Genes involved in the [[pathogenesis]] of systemic lupus erythematosus include [[HLA]] class [[polymorphism]], complement genes, and other genes related to immunologic system as well. | ||
The following evidence is also suggestive of the genetic predisposition of SLE: | The following evidence is also suggestive of the genetic predisposition of SLE: | ||
| Line 111: | Line 111: | ||
CR1 | CR1 | ||
Immunoglobulin Gm and Km | [[Immunoglobulin]] Gm and Km | ||
FcγRIIA (IgG Fc receptor) | FcγRIIA (IgG Fc receptor) | ||
| Line 126: | Line 126: | ||
==Associated Conditions== | ==Associated Conditions== | ||
* Homozygous deficiencies of the components of complement especially C1q are associated with developing immunologic diseases especially SLE or a lupus-like disease : 11564823 | * [[Homozygous]] deficiencies of the components of [[complement]] especially C1q are associated with developing immunologic diseases especially SLE or a lupus-like disease : 11564823 | ||
* The FcγRIIA polymorphism has been associated with nephritis in African Americans and Koreans | * The FcγRIIA [[polymorphism]] has been associated with [[nephritis]] in African Americans and Koreans as well as Hispanic patients. Both FcgammaRIIa and FcgammaRIIIa have low binding [[alleles]] that confer risk for SLE and may act additively in the pathogenesis of disease. 24997134 | ||
* Women that are treated with estrogen-containing regimens such as oral contraceptives or postmenopausal hormone replacement therapies are more predisposed to SLE. | * Women that are treated with [[estrogen]]-containing regimens such as oral contraceptives or postmenopausal hormone replacement therapies are more predisposed to SLE. | ||
* Annular or psoriasiform skin lesions are associated with anti-Ro (SS-A) and anti-La (SS-B) antibodies. | * Annular or psoriasiform skin lesions are associated with anti-Ro (SS-A) and anti-La (SS-B) antibodies. | ||
== Gross Pathology == | == Gross Pathology == | ||
On gross pathology, | On gross pathology of kidney, pallor, and nephromegaly are characteristic findings of systemic lupus erythematosus. | ||
On gross pathology of brain, infarct regions and hemorrhages are characteristic findings of systemic lupus erythematosus. | |||
On gross pathology of cardiac valves, cardiomegaly and valvular vegetations are characteristic findings of systemic lupus erythematosus. | |||
== Microscopic Pathology == | == Microscopic Pathology == | ||
Revision as of 14:24, 30 June 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Raviteja Guddeti, M.B.B.S. [3]
Overview
The progression of systemic lupus erythematosus involves the immune system. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well. The most prominent events involving immune abnormalities are related to persistent activation of B cells and plasma cells that make auto-antibodies more auto antibodies during disease progression. The most prominent events involving hormonal abnormalities are due to prolactin and estrogen. The most important environmental factors related to disease progression are ultraviolet (UV) light and some infections. On microscopic histopathological analysis, apoptotic keratinocytes, vacuolization of the basement membrane, and dermal mucin deposition are characteristic findings of SLE dermatitis, and active or inactive endocapillary or extracapillary segmental glomerulonephritis are characteristic findings of SLE nephritis.
Pathogenesis
The progression of systemic lupus erythematosus involves the immune system. Near all of the pathological manifestation of SLE are due to antibody formation and the creation of immune complexes in different organs of the body. When the immune complexes designed, they will deposit in different body tissues and vessels, which will lead to more complement activation and more organ damage. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well.
Immune abnormalities
Development of systemic lupus erythematosus (SLE) is the result of different mechanisms that at the end lead to auto-immune response of the body. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their self-antigens and consequently progress an autoimmune disease and develop auto antibodies as a response. During disease progression, B cells and plasma cells that make auto-antibodies are more persistently activated and thus make more auto antibodies. These auto antibodies are targeted predominantly to intracellular nucleoprotein particles
8519610
This increase in auto antibody production and persistence suppose to be down regulated by anti-idiotypic antibodies or regulatory immune cells, but due to immunologic response it is not appropriately been responded.
The most important immune abnormalities that are related to SLE develop and progression:
- Increase in circulating plasma cells and memory B cells that is associated with SLE activity
- Decrease in cytotoxic T cells and in functions of suppressor T cells and impaired generation of polyclonal T-cell cytolytic activity
- Increase in helper T cells and also their function
- Polyclonal activation of B cells and abnormal B-cell receptor signaling
- Prolonged lives of B cells
- Signaling abnormalities of T and B lymphocytes
- Cellular hyperactivity
- Hyper responsiveness
- May be due to genetically defects
- Increased expression of IFN-alpha-inducible RNA transcripts by mononuclear cells that lead to elevated levels of IFN-alpha. 15593221
- Increase in specific genetic factors expression that may be associated with autoimmunity promotion
- Dysfunctional signaling in T and B cells that may be due to:
- Increased calcium responses to antigen stimulation
- Hyperphosphorylation of cytosolic protein substrates
- Decreased nuclear factor kB
- Abnormal voltage-gated potassium channels: These channels facilitate excessive calcium entry into T cells
- Increased levels of microparticles (MPs):
- Microparticles are small, membrane-bound vesicles enclose DNA, RNA, nuclear proteins, cell-adhesion molecules, growth factors, and cytokines.
- They are shed from cells during apoptosis or activation
- Microparticles can drive inflammation and autoimmunity by their derivatives 23672591
- Elevated levels of circulating TNF-alpha correlate with active disease, and TNF is expressed in renal tissue in lupus nephritis
- Abnormally high levels of E-C4d and low levels of E-CR1 are characteristic of SLE, and combined measurement of the 2 molecules has high diagnostic sensitivity and specificity for lupus
- Increased numbers of circulating neutrophils undergoing NETosis (NET=eutrophil extracellular traps), a form of apoptosis specific for neutrophils, releases DNA bound to protein in protein nets, which stimulates anti-DNA and IFN-alpha production
- Increased neutrophil extracellular trap formation: 26658004
- It may promote thrombus formation
- It is associated with increased disease activity and renal disease and thus can be used even as a disease activity marker.
- It can damage and kill endothelial cells and promote inflammation in atherosclerotic plaques, which may contribute to accelerated atherosclerosis in systemic lupus erythematosus
- As an example of immune abnormalities and their complications, nervous system involvement in SLE is due to:
- Small to moderate vessles vasculopathy with perivascular accumulation of mononuclear cells, without destruction of the blood vessel
- Antiphospholipid antibodies
- These changes promote the production of antinuclear antibodies
Hormonal abnormalities
The following evidence is suggestive of the hormonal predisposition of SLE:
- Sexual predilection of females: Shows the relationship of female hormones and the onset of SLE
- Significantly increased risk for SLE in:17393454
Hormones that are related to SLE disease progression:10503654
- Gonadotrophins like prolactin
- Stimulants of immune functions and is elevated in SLE
- Exogenous estrogen - include oral contraceptive use and post-menopausal hormone replacement therapy: 10503654- 25155581
- Stimulates the type 1 IFN pathway
- Stimulates thymocytes, CD8+ and CD4+ T cells, B cells, macrophages, the release of certain cytokines (eg, IL-1)
- Prompt maturation of B cells especially those that have a high affinity to anti-DNA antibodies by decreasing the apoptosis of this self-reactive B-cells 16724801
- Stimulate expression of HLA and endothelial cell adhesion molecules (VCAM, ICAM)
- Increases macrophage proto-oncogene expression
- Enhanced adhesion of peripheral mononuclear cells to endothelium
- Progesterone:
- May inhibit the type 1 interferon pathway, suggesting that a balance between estrogen and progesterone may be critical for the body to remain healthy
- Downregulates T-cell proliferation and increases the number of CD8 cells
- Both progesterone and high levels of estrogen promote a Th2 response, which favors autoantibody production
Environmental factors
- Infections can stimulates some antigen specific cells and lead to SLE disease:
- Epstein-Barr virus (EBV): May induce anti-DNA antibodies or even lupus-like symptoms. It is associated with higher risk of SLE and also triggering the active course of disease in children
- Trypanosomiasis or mycobacterial infections may have the same effect as EBV
- SLE active disease flares may follow bacterial infections as well
- Ultraviolet (UV) light: Can stimulates B-cells to produce more antibodies. It can also interfere with antigen processing by activation of macrophages and hence increase the degree of autoimmunity
Genetics
Systemic lupus erythematosus is transmitted in poly-genic inheritance pattern. Genes involved in the pathogenesis of systemic lupus erythematosus include HLA class polymorphism, complement genes, and other genes related to immunologic system as well.
The following evidence is also suggestive of the genetic predisposition of SLE:
- Increase of disease occurrence in identical twins
- The increase in frequency of SLE among first degree relatives
- The increased risk of developing the disease in siblings of SLE patients
| Gene class | Gene subtype |
| HLA genes | DR2, DR3, DR4, DR7, DR8, DRw12, DQw2, DQA1,
DQB1, DQ6, DQw6, DQ7, DQw7, DQw8, DQw9, B61, B8 |
| Complement genes | C2, C4, C1q |
| Non-HLA genes | Mannose binding lectin polymorphisms
Tumour necrosis factor α T cell receptor Interleukin 6 CR1 Immunoglobulin Gm and Km FcγRIIA (IgG Fc receptor) FcγRIIIA (IgG Fc receptor) PARP (poly-ADP ribose polymerase) Heat shock protein 70 Humhr 3005 |
- 10768211
Associated Conditions
- Homozygous deficiencies of the components of complement especially C1q are associated with developing immunologic diseases especially SLE or a lupus-like disease : 11564823
- The FcγRIIA polymorphism has been associated with nephritis in African Americans and Koreans as well as Hispanic patients. Both FcgammaRIIa and FcgammaRIIIa have low binding alleles that confer risk for SLE and may act additively in the pathogenesis of disease. 24997134
- Women that are treated with estrogen-containing regimens such as oral contraceptives or postmenopausal hormone replacement therapies are more predisposed to SLE.
- Annular or psoriasiform skin lesions are associated with anti-Ro (SS-A) and anti-La (SS-B) antibodies.
Gross Pathology
On gross pathology of kidney, pallor, and nephromegaly are characteristic findings of systemic lupus erythematosus.
On gross pathology of brain, infarct regions and hemorrhages are characteristic findings of systemic lupus erythematosus.
On gross pathology of cardiac valves, cardiomegaly and valvular vegetations are characteristic findings of systemic lupus erythematosus.
Microscopic Pathology
On microscopic histopathological analysis, apoptotic keratinocytes, vacuolization of the basement membrane, and dermal mucin deposition are characteristic findings of SLE dermatitis, and active or inactive endocapillary or extracapillary segmental glomerulonephritis are characteristic findings of SLE nephritis.
Skin histo-pathology:
Common shared histopathologic features among all different subtypes of cutaneous lupus include:
- Hyperkeratosis
- Epidermal atrophy
- Dermal mucin deposition
- Liquefactive degeneration of the basal layer of the epidermis and vacuolization
- Thickening of the basement membrane
- Pigment incontinence
- Mononuclear cell infiltration at dermo-epidermal junction
- Superficial, perivascular, and perifollicular areas (due to mononuclear cell inflammatory infiltrate)
| SLE dermatitis subtype | Specific microscopic findings |
|---|---|
| Acute cutaneous lupus erythematosus |
|
| Subacute cutaneous lupus erythematosus |
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| Chronic cutaneous lupus erythematosus |
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Glomerulonephritis histo-pathology:
| SLE nephritis subtype | Light microscopy findings | Electron microscopy/Immunofluorescence findings |
|---|---|---|
| Minimal mesangial lupus nephritis (class I) | - |
|
| Mesangial proliferative lupus nephritis (class II) |
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| Focal lupus nephritis (class III) |
|
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| Diffuse lupus nephritis (class IV) |
|
|
| Lupus membranous nephropathy (class V) |
|
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| Advanced sclerosing lupus nephritis (class VI) |
|
|
Synovial histopathology
- Nonspecific histopathologic findings
- Superficial fibrin-like material
- Local or diffuse synovial cell lining proliferation
- Vascular changes:
- Perivascular mononuclear cells
- Lumen obliteration
- Enlarged endothelial cells
- Thrombi
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