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Systemic lupus erythematosus(SLE)

MedGen UID:
6146
Concept ID:
C0024141
Disease or Syndrome
Synonyms: DNASE1-Related Susceptibility to Systemic Lupus Erythematosus; SLE
SNOMED CT: SLE - Systemic lupus erythematosus (55464009); Systemic lupus erythematosus (55464009); Disseminated lupus erythematosus (55464009)
Modes of inheritance:
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
 
Genes (locations): CTLA4 (2q33.2); DNASE1 (16p13.3); FCGR2A (1q23.3); FCGR2B (1q23.3); PTPN22 (1p13.2); TREX1 (3p21.31)
Related genes: TLR5, STAT4, PDCD1, IRF5, CR2
 
HPO: HP:0002725
OMIM®: 152700
Orphanet: ORPHA536

Definition

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by production of autoantibodies against nuclear, cytoplasmic, and cell surface molecules that transcend organ-specific boundaries. Tissue deposition of antibodies or immune complexes induces inflammation and subsequent injury of multiple organs and finally results in clinical manifestations of SLE, including glomerulonephritis, dermatitis, thrombosis, vasculitis, seizures, and arthritis. Evidence strongly suggests the involvement of genetic components in SLE susceptibility (summary by Oishi et al., 2008). Genetic Heterogeneity of Systemic Lupus Erythematosus An autosomal recessive form of systemic lupus erythematosus (SLEB16; 614420) is caused by mutation in the DNASE1L3 gene (602244) on chromosome 3p14.3. See MAPPING and MOLECULAR GENETICS sections for a discussion of genetic heterogeneity of susceptibility to SLE. [from OMIM]

Clinical features

From HPO
Nephritis
MedGen UID:
14328
Concept ID:
C0027697
Disease or Syndrome
The presence of inflammation affecting the kidney.
Pericarditis
MedGen UID:
18377
Concept ID:
C0031046
Disease or Syndrome
Inflammation of the sac-like covering around the heart (pericardium).
Psychosis
MedGen UID:
19568
Concept ID:
C0033975
Mental or Behavioral Dysfunction
A mental disorder characterized by personality change, impaired functioning, and loss of touch with reality.
Seizures
MedGen UID:
20693
Concept ID:
C0036572
Sign or Symptom
A seizure is an intermittent abnormality of nervous system physiology characterised by a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
Hemolytic anemia
MedGen UID:
1916
Concept ID:
C0002878
Disease or Syndrome
Anemia resulting from the premature destruction of the peripheral blood red cells. It may be congenital or it may be caused by infections, medications, or malignancies.
Leukopenia
MedGen UID:
6073
Concept ID:
C0023530
Disease or Syndrome
An abnormal decreased number of leukocytes in the blood.
Thrombocytopenia
MedGen UID:
52737
Concept ID:
C0040034
Disease or Syndrome
A reduction in the number of circulating thrombocytes.
Arthritis
MedGen UID:
2043
Concept ID:
C0003864
Disease or Syndrome
Inflammation of a joint.
Pleuritis
MedGen UID:
10807
Concept ID:
C0032231
Disease or Syndrome
Inflammation of the pleura.
Leukopenia
MedGen UID:
6073
Concept ID:
C0023530
Disease or Syndrome
An abnormal decreased number of leukocytes in the blood.
Systemic lupus erythematosus
MedGen UID:
6146
Concept ID:
C0024141
Disease or Syndrome
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by production of autoantibodies against nuclear, cytoplasmic, and cell surface molecules that transcend organ-specific boundaries. Tissue deposition of antibodies or immune complexes induces inflammation and subsequent injury of multiple organs and finally results in clinical manifestations of SLE, including glomerulonephritis, dermatitis, thrombosis, vasculitis, seizures, and arthritis. Evidence strongly suggests the involvement of genetic components in SLE susceptibility (summary by Oishi et al., 2008). Genetic Heterogeneity of Systemic Lupus Erythematosus An autosomal recessive form of systemic lupus erythematosus (SLEB16; 614420) is caused by mutation in the DNASE1L3 gene (602244) on chromosome 3p14.3. See MAPPING and MOLECULAR GENETICS sections for a discussion of genetic heterogeneity of susceptibility to SLE.
Nephritis
MedGen UID:
14328
Concept ID:
C0027697
Disease or Syndrome
The presence of inflammation affecting the kidney.
Pericarditis
MedGen UID:
18377
Concept ID:
C0031046
Disease or Syndrome
Inflammation of the sac-like covering around the heart (pericardium).
Antinuclear antibody positivity
MedGen UID:
101792
Concept ID:
C0151480
Laboratory or Test Result
The presence of autoantibodies in the serum that react against nuclei or nuclear components.
Malar rash
MedGen UID:
75808
Concept ID:
C0277942
Finding
An erythematous (red), flat facial rash that affects the skin in the malar area (over the cheekbones) and extends over the bridge of the nose.
Antiphospholipid antibody positivity
MedGen UID:
866404
Concept ID:
C4019436
Finding
The presence of circulating autoantibodies to phospholipids.
Malar rash
MedGen UID:
75808
Concept ID:
C0277942
Finding
An erythematous (red), flat facial rash that affects the skin in the malar area (over the cheekbones) and extends over the bridge of the nose.
Cutaneous photosensitivity
MedGen UID:
87601
Concept ID:
C0349506
Pathologic Function
An increased sensitivity of the skin to light. Photosensitivity may result in a rash upon exposure to the sun (which is known as photodermatosis). Photosensitivity can be diagnosed by phototests in which light is shone on small areas of skin.

Term Hierarchy

Conditions with this feature

Systemic lupus erythematosus
MedGen UID:
6146
Concept ID:
C0024141
Disease or Syndrome
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by production of autoantibodies against nuclear, cytoplasmic, and cell surface molecules that transcend organ-specific boundaries. Tissue deposition of antibodies or immune complexes induces inflammation and subsequent injury of multiple organs and finally results in clinical manifestations of SLE, including glomerulonephritis, dermatitis, thrombosis, vasculitis, seizures, and arthritis. Evidence strongly suggests the involvement of genetic components in SLE susceptibility (summary by Oishi et al., 2008). Genetic Heterogeneity of Systemic Lupus Erythematosus An autosomal recessive form of systemic lupus erythematosus (SLEB16; 614420) is caused by mutation in the DNASE1L3 gene (602244) on chromosome 3p14.3. See MAPPING and MOLECULAR GENETICS sections for a discussion of genetic heterogeneity of susceptibility to SLE.
Prolidase deficiency
MedGen UID:
120647
Concept ID:
C0268532
Disease or Syndrome
Prolidase deficiency is characterized by skin lesions (typically severe, chronic, recalcitrant, and painful skin ulcers of the lower extremities and telangiectasias of the face and hands), recurrent infections (particularly of the skin and respiratory tract), dysmorphic facial features, variable intellectual disability, and hepatomegaly with elevated liver enzymes and splenomegaly. Anemia, thrombocytopenia, hypergammaglobulinemia, and hypocomplementemia are common. An association between systemic lupus erythematosus (SLE) and prolidase deficiency has been described.
Limb-girdle myasthenia, autoimmune
MedGen UID:
331795
Concept ID:
C1834635
Disease or Syndrome
Systemic lupus erythematosus 6
MedGen UID:
332086
Concept ID:
C1835919
Finding
Systemic lupus erythematosus (SLE) is a chronic disease that causes inflammation in connective tissues, such as cartilage and the lining of blood vessels, which provide strength and flexibility to structures throughout the body. The signs and symptoms of SLE vary among affected individuals, and can involve many organs and systems, including the skin, joints, kidneys, lungs, central nervous system, and blood-forming (hematopoietic) system. SLE is one of a large group of conditions called autoimmune disorders that occur when the immune system attacks the body's own tissues and organs.\n\nSLE may first appear as extreme tiredness (fatigue), a vague feeling of discomfort or illness (malaise), fever, loss of appetite, and weight loss. Most affected individuals also have joint pain, typically affecting the same joints on both sides of the body, and muscle pain and weakness. Skin problems are common in SLE. A characteristic feature is a flat red rash across the cheeks and bridge of the nose, called a "butterfly rash" because of its shape. The rash, which generally does not hurt or itch, often appears or becomes more pronounced when exposed to sunlight. Other skin problems that may occur in SLE include calcium deposits under the skin (calcinosis), damaged blood vessels (vasculitis) in the skin, and tiny red spots called petechiae. Petechiae are caused by a shortage of cells involved in clotting (platelets), which leads to bleeding under the skin. Affected individuals may also have hair loss (alopecia) and open sores (ulcerations) in the moist lining (mucosae) of the mouth, nose, or, less commonly, the genitals.\n\nPeople with SLE have episodes in which the condition gets worse (exacerbations) and other times when it gets better (remissions). Overall, SLE gradually gets worse over time, and damage to the major organs of the body can be life-threatening.\n\nAbout a third of people with SLE develop kidney disease (nephritis). Heart problems may also occur in SLE, including inflammation of the sac-like membrane around the heart (pericarditis) and abnormalities of the heart valves, which control blood flow in the heart. Heart disease caused by fatty buildup in the blood vessels (atherosclerosis), which is very common in the general population, is even more common in people with SLE. The inflammation characteristic of SLE can also damage the nervous system, and may result in abnormal sensation and weakness in the limbs (peripheral neuropathy); seizures; stroke; and difficulty processing, learning, and remembering information (cognitive impairment). Anxiety and depression are also common in SLE.
Spondyloenchondrodysplasia with immune dysregulation
MedGen UID:
375009
Concept ID:
C1842763
Disease or Syndrome
Spondyloenchondrodysplasia with immune dysregulation (SPENCDI) is an immunoosseous dysplasia combining the typical metaphyseal and vertebral bone lesions of spondyloenchondrodysplasia (SPENCD) with immune dysfunction and neurologic involvement. The skeletal dysplasia is characterized by radiolucent and irregular spondylar and metaphyseal lesions that represent islands of chondroid tissue within bone. The vertebral bodies show dorsally accentuated platyspondyly with disturbance of ossification. Clinical abnormalities such as short stature, rhizomelic micromelia, increased lumbar lordosis, barrel chest, facial anomalies, and clumsy movements may be present (Menger et al., 1989). Central nervous system involvement includes spasticity, mental retardation, and cerebral calcifications, and immune dysregulation ranges from autoimmunity to immunodeficiency. Neurologic and autoimmune manifestations have been observed in different combinations within a single family, suggesting that this disorder may be defined by specific radiographic features but has remarkably pleiotropic manifestations (Renella et al., 2006). Briggs et al. (2016) also noted variability in skeletal, neurologic, and immune phenotypes, which was sometimes marked between members of the same family. Classification of the Enchondromatoses In their classification of the enchondromatoses, Spranger et al. (1978) called Ollier disease and Maffucci syndrome types I and II enchondromatosis, respectively; metachondromatosis (156250), type III; and spondyloenchondrodysplasia (SPENCD), also called spondyloenchondromatosis, type IV; enchondromatosis with irregular vertebral lesions, type V; and generalized enchondromatosis, type VI. Halal and Azouz (1991) added 3 tentative categories to the 6 in the classification of Spranger et al. (1978). Pansuriya et al. (2010) suggested a new classification of enchondromatosis (multiple enchondromas).
Complement component 4, partial deficiency of
MedGen UID:
343867
Concept ID:
C1852700
Disease or Syndrome
Pulmonary nodular lymphoid hyperplasia, familial
MedGen UID:
401226
Concept ID:
C1867419
Disease or Syndrome
Pulmonary nodular lymphoid hyperplasia (PNHL) is a reactive lymphoid proliferation manifesting as solitary or multiple nodules in the lung.
Complement component 2 deficiency
MedGen UID:
461625
Concept ID:
C3150275
Disease or Syndrome
Complement component 2 deficiency is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as bacteria and viruses. People with complement component 2 deficiency have a significantly increased risk of recurrent bacterial infections, specifically of the lungs (pneumonia), the membrane covering the brain and spinal cord (meningitis), and the blood (sepsis), which may be life-threatening. These infections most commonly occur in infancy and childhood and become less frequent in adolescence and adulthood.\n\nComplement component 2 deficiency is also associated with an increased risk of developing autoimmune disorders such as systemic lupus erythematosus (SLE) or vasculitis. Autoimmune disorders occur when the immune system malfunctions and attacks the body's tissues and organs. Between 10 and 20 percent of individuals with complement component 2 deficiency develop SLE. Females with complement component 2 deficiency are more likely to have SLE than affected males, but this is also true of SLE in the general population.\n\nThe severity of complement component 2 deficiency varies widely. While some affected individuals experience recurrent infections and other immune system difficulties, others do not have any health problems related to the disorder.
C1q deficiency
MedGen UID:
462252
Concept ID:
C3150902
Disease or Syndrome
C1q deficiency is a rare autosomal recessive disorder characterized by recurrent skin lesions, chronic infections, and an increased risk of autoimmune diseases, particularly systemic lupus erythematosus (SLE; see 152700) or SLE-like diseases. It has also been associated with chronic glomerulonephritis and renal failure. C1q deficiency presents in 2 different forms, absent C1q protein or presence of a dysfunctional molecule (summary by Topaloglu et al., 1996 and Vassallo et al., 2007).
Complement component 3 deficiency, autosomal recessive
MedGen UID:
462421
Concept ID:
C3151071
Disease or Syndrome
C3 glomerulopathy (C3G) is a complex ultra-rare complement-mediated renal disease caused by uncontrolled activation of the complement alternative pathway (AP) in the fluid phase (as opposed to cell surface) that is rarely inherited in a simple mendelian fashion. C3G affects individuals of all ages, with a median age at diagnosis of 23 years. Individuals with C3G typically present with hematuria, proteinuria, hematuria and proteinuria, acute nephritic syndrome or nephrotic syndrome, and low levels of the complement component C3. Spontaneous remission of C3G is uncommon, and about half of affected individuals develop end-stage renal disease (ESRD) within ten years of diagnosis, occasionally developing the late comorbidity of impaired visual acuity.
Complement component c1s deficiency
MedGen UID:
462428
Concept ID:
C3151078
Disease or Syndrome
Type I complement component 8 deficiency
MedGen UID:
462431
Concept ID:
C3151081
Disease or Syndrome
Patients with deficiency of C8 suffer from recurrent neisserial infections, predominantly with meningococcus infection of rare serotypes. Most such patients are discovered among those having their first episode of meningitis at ages older than 10 years (Ross and Densen, 1984). Two kinds of inherited C8 deficiency have been reported in man: type I, in which only C8 alpha and C8 gamma are deficient, and type II (613789), in which only C8 beta (C8B; 120960) is deficient (Marcus et al., 1982; Tedesco et al., 1983). The 2 types are clinically indistinguishable (Ross and Densen, 1984).
MASP2 deficiency
MedGen UID:
462435
Concept ID:
C3151085
Disease or Syndrome
MASP2 deficiency, classically defined as MASP2 protein level of less than 100 ng/ml, occurs in about 4% of Caucasians and up to 18% of some African populations. Some MASP2-deficient individuals have increased risk of infection or autoimmune disease, but most are asymptomatic. MASP2 plays a role in activation of the lectin pathway of the complement system; deficiency may thus lead to defects in the complement system (summary by Thiel et al., 2007 and Sokolowska et al., 2015). For a discussion of genetic heterogeneity of lectin complement activation pathway defects, see LCAPD1 (614372).
C4a deficiency
MedGen UID:
482272
Concept ID:
C3280642
Finding
A reduced level of the complement component C4a in circulation.
Systemic lupus erythematosus 16
MedGen UID:
482372
Concept ID:
C3280742
Disease or Syndrome
About a third of people with SLE develop kidney disease (nephritis). Heart problems may also occur in SLE, including inflammation of the sac-like membrane around the heart (pericarditis) and abnormalities of the heart valves, which control blood flow in the heart. Heart disease caused by fatty buildup in the blood vessels (atherosclerosis), which is very common in the general population, is even more common in people with SLE. The inflammation characteristic of SLE can also damage the nervous system, and may result in abnormal sensation and weakness in the limbs (peripheral neuropathy); seizures; stroke; and difficulty processing, learning, and remembering information (cognitive impairment). Anxiety and depression are also common in SLE.\n\nPeople with SLE have episodes in which the condition gets worse (exacerbations) and other times when it gets better (remissions). Overall, SLE gradually gets worse over time, and damage to the major organs of the body can be life-threatening.\n\nSLE may first appear as extreme tiredness (fatigue), a vague feeling of discomfort or illness (malaise), fever, loss of appetite, and weight loss. Most affected individuals also have joint pain, typically affecting the same joints on both sides of the body, and muscle pain and weakness. Skin problems are common in SLE. A characteristic feature is a flat red rash across the cheeks and bridge of the nose, called a "butterfly rash" because of its shape. The rash, which generally does not hurt or itch, often appears or becomes more pronounced when exposed to sunlight. Other skin problems that may occur in SLE include calcium deposits under the skin (calcinosis), damaged blood vessels (vasculitis) in the skin, and tiny red spots called petechiae. Petechiae are caused by a shortage of cells involved in clotting (platelets), which leads to bleeding under the skin. Affected individuals may also have hair loss (alopecia) and open sores (ulcerations) in the moist lining (mucosae) of the mouth, nose, or, less commonly, the genitals.\n\nSystemic lupus erythematosus (SLE) is a chronic disease that causes inflammation in connective tissues, such as cartilage and the lining of blood vessels, which provide strength and flexibility to structures throughout the body. The signs and symptoms of SLE vary among affected individuals, and can involve many organs and systems, including the skin, joints, kidneys, lungs, central nervous system, and blood-forming (hematopoietic) system. SLE is one of a large group of conditions called autoimmune disorders that occur when the immune system attacks the body's own tissues and organs.
Myeloproliferative/lymphoproliferative neoplasms, familial (multiple types), susceptibility to
MedGen UID:
895780
Concept ID:
C4225174
Finding
Familial myeloproliferative/lymphoproliferative neoplasms is an autosomal dominant cancer predisposition syndrome characterized by adult-onset of hematologic malignancies mainly affecting the myeloid line. Most patients present with myelodysplastic syndrome (MDS; 614286) and/or acute myeloid leukemia (AML; 601626). Rare lymphoid malignancies, including lymphoma, can also occur. Some mutation carriers, even if unaffected by a hematologic malignancy, may have evidence of immune dysregulation disorders, including asthma, eczema, or juvenile arthritis. The disorder shows incomplete penetrance (summary by Lewinsohn et al., 2016). Patients may show a favorable response to treatment with lenalidomide (summary by Polprasert et al., 2015).
Epilepsy, progressive myoclonic, 11
MedGen UID:
1716712
Concept ID:
C5394362
Disease or Syndrome
Progressive myoclonic epilepsy-11 (EPM11) is a neurodegenerative disorder characterized by onset of developmental regression and various types of seizures around 2 years of age after relatively normal early development. The seizures are usually refractory to treatment and are associated with multiple abnormalities on EEG. During the first and second decades, affected individuals develop additional neurologic signs and symptoms, including pyramidal, extrapyramidal, and cerebellar signs such as spasticity, loss of independent ambulation, myoclonus, tremor, and ataxia. Cognitive impairment is severe, and patients can speak only a few words or are non-verbal (summary by Hamanaka et al., 2020). For discussion of genetic heterogeneity of progressive myoclonic epilepsy, see EPM1A (254800).

Recent clinical studies

Etiology

Yudhishdran J, Sivakumar J, Navinan MR, Bandapatti S
J Med Case Rep 2021 Jul 8;15(1):339. doi: 10.1186/s13256-021-02950-y. PMID: 34233732Free PMC Article
Al-Riyami N, Salman B, Al-Rashdi A, Al-Dughaishi T, Al-Haddabi R, Hassan B
Sultan Qaboos Univ Med J 2021 May;21(2):e244-e252. Epub 2021 Jun 21 doi: 10.18295/squmj.2021.21.02.013. PMID: 34221472Free PMC Article
Cuen-Ojeda C, Pascual-Ramos V, Contreras-Yáñez I, Anaya-Ayala JE, Elenes-Sanchez E, Rosas-Rios C, Mendez-Sosa MA, Lozano-Corona R, Hinojosa CA
Vascular 2021 Feb;29(1):126-133. Epub 2020 Jun 26 doi: 10.1177/1708538120936407. PMID: 32588786
Kwon OC, Kim YG, Park JH, Park MC
Lupus 2020 Jun;29(7):697-704. Epub 2020 Apr 11 doi: 10.1177/0961203320917748. PMID: 32279583
Miguel DF, Terreri MT, Pereira RMR, Bonfá E, Silva CAA, Corrente JE, Magalhaes CS; Brazilian Childhood-onset Systemic Lupus Erythematosus Group.
Adv Rheumatol 2020 Feb 1;60(1):10. doi: 10.1186/s42358-020-0114-4. PMID: 32005292

Diagnosis

Yudhishdran J, Sivakumar J, Navinan MR, Bandapatti S
J Med Case Rep 2021 Jul 8;15(1):339. doi: 10.1186/s13256-021-02950-y. PMID: 34233732Free PMC Article
Cuen-Ojeda C, Pascual-Ramos V, Contreras-Yáñez I, Anaya-Ayala JE, Elenes-Sanchez E, Rosas-Rios C, Mendez-Sosa MA, Lozano-Corona R, Hinojosa CA
Vascular 2021 Feb;29(1):126-133. Epub 2020 Jun 26 doi: 10.1177/1708538120936407. PMID: 32588786
Gasser EK, Schell-Chaple HM
AACN Adv Crit Care 2020 Sep 15;31(3):296-307. doi: 10.4037/aacnacc2020355. PMID: 32866257
Kwon OC, Kim YG, Park JH, Park MC
Lupus 2020 Jun;29(7):697-704. Epub 2020 Apr 11 doi: 10.1177/0961203320917748. PMID: 32279583
Miguel DF, Terreri MT, Pereira RMR, Bonfá E, Silva CAA, Corrente JE, Magalhaes CS; Brazilian Childhood-onset Systemic Lupus Erythematosus Group.
Adv Rheumatol 2020 Feb 1;60(1):10. doi: 10.1186/s42358-020-0114-4. PMID: 32005292

Therapy

Yudhishdran J, Sivakumar J, Navinan MR, Bandapatti S
J Med Case Rep 2021 Jul 8;15(1):339. doi: 10.1186/s13256-021-02950-y. PMID: 34233732Free PMC Article
Al-Riyami N, Salman B, Al-Rashdi A, Al-Dughaishi T, Al-Haddabi R, Hassan B
Sultan Qaboos Univ Med J 2021 May;21(2):e244-e252. Epub 2021 Jun 21 doi: 10.18295/squmj.2021.21.02.013. PMID: 34221472Free PMC Article
Cuen-Ojeda C, Pascual-Ramos V, Contreras-Yáñez I, Anaya-Ayala JE, Elenes-Sanchez E, Rosas-Rios C, Mendez-Sosa MA, Lozano-Corona R, Hinojosa CA
Vascular 2021 Feb;29(1):126-133. Epub 2020 Jun 26 doi: 10.1177/1708538120936407. PMID: 32588786
Zhao X, Zhang J, Liang Y, Li J, Ding S, Wang Y, Chen Y, Liu J
Curr Med Chem 2021;28(6):1251-1268. doi: 10.2174/0929867327666200625150408. PMID: 32586244
Gasser EK, Schell-Chaple HM
AACN Adv Crit Care 2020 Sep 15;31(3):296-307. doi: 10.4037/aacnacc2020355. PMID: 32866257

Prognosis

Al-Riyami N, Salman B, Al-Rashdi A, Al-Dughaishi T, Al-Haddabi R, Hassan B
Sultan Qaboos Univ Med J 2021 May;21(2):e244-e252. Epub 2021 Jun 21 doi: 10.18295/squmj.2021.21.02.013. PMID: 34221472Free PMC Article
Cuen-Ojeda C, Pascual-Ramos V, Contreras-Yáñez I, Anaya-Ayala JE, Elenes-Sanchez E, Rosas-Rios C, Mendez-Sosa MA, Lozano-Corona R, Hinojosa CA
Vascular 2021 Feb;29(1):126-133. Epub 2020 Jun 26 doi: 10.1177/1708538120936407. PMID: 32588786
Guo X, Lai J, Wang H, Tian Z, Zhao J, Li M, Fang Q, Fang L, Liu Y, Zeng X
Hypertension 2020 Oct;76(4):1161-1168. Epub 2020 Aug 10 doi: 10.1161/HYPERTENSIONAHA.120.15682. PMID: 32772648
Kwon OC, Kim YG, Park JH, Park MC
Lupus 2020 Jun;29(7):697-704. Epub 2020 Apr 11 doi: 10.1177/0961203320917748. PMID: 32279583
Sohrabian A, Parodis I, Carlströmer-Berthén N, Frodlund M, Jönsen A, Zickert A, Sjöwall C, Bengtsson AA, Gunnarsson I, Rönnelid J
Arthritis Res Ther 2019 Nov 29;21(1):259. doi: 10.1186/s13075-019-2056-y. PMID: 31783909Free PMC Article

Clinical prediction guides

Al-Riyami N, Salman B, Al-Rashdi A, Al-Dughaishi T, Al-Haddabi R, Hassan B
Sultan Qaboos Univ Med J 2021 May;21(2):e244-e252. Epub 2021 Jun 21 doi: 10.18295/squmj.2021.21.02.013. PMID: 34221472Free PMC Article
Charoenngam N, Ponvilawan B, Wongtrakul W, Ungprasert P
Clin Rheumatol 2021 Feb;40(2):529-536. Epub 2020 Jul 7 doi: 10.1007/s10067-020-05279-x. PMID: 32638252
Cuen-Ojeda C, Pascual-Ramos V, Contreras-Yáñez I, Anaya-Ayala JE, Elenes-Sanchez E, Rosas-Rios C, Mendez-Sosa MA, Lozano-Corona R, Hinojosa CA
Vascular 2021 Feb;29(1):126-133. Epub 2020 Jun 26 doi: 10.1177/1708538120936407. PMID: 32588786
Kwon OC, Kim YG, Park JH, Park MC
Lupus 2020 Jun;29(7):697-704. Epub 2020 Apr 11 doi: 10.1177/0961203320917748. PMID: 32279583
Miguel DF, Terreri MT, Pereira RMR, Bonfá E, Silva CAA, Corrente JE, Magalhaes CS; Brazilian Childhood-onset Systemic Lupus Erythematosus Group.
Adv Rheumatol 2020 Feb 1;60(1):10. doi: 10.1186/s42358-020-0114-4. PMID: 32005292

Recent systematic reviews

Charoenngam N, Ponvilawan B, Wongtrakul W, Ungprasert P
Clin Rheumatol 2021 Feb;40(2):529-536. Epub 2020 Jul 7 doi: 10.1007/s10067-020-05279-x. PMID: 32638252
Constantin A, Năstase D, Tulbă D, Bălănescu P, Băicuș C
Lupus 2020 Oct;29(12):1509-1519. Epub 2020 Aug 5 doi: 10.1177/0961203320948181. PMID: 32757735
Bae SC, Lee YH
Lupus 2019 Nov;28(13):1571-1576. Epub 2019 Oct 25 doi: 10.1177/0961203319884653. PMID: 31653192
Quilter MC, Hiraki LT, Korczak DJ
Lupus 2019 Jun;28(7):878-887. doi: 10.1177/0961203319853621. PMID: 31188723
Matusik PS, Matusik PT, Stein PK
Lupus 2018 Jul;27(8):1225-1239. Epub 2018 Apr 26 doi: 10.1177/0961203318771502. PMID: 29697012

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