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Arthritis

MedGen UID:
2043
Concept ID:
C0003864
Disease or Syndrome
Synonyms: Arthritides
SNOMED CT: Joint inflammation (3723001); Inflammatory arthritis (3723001); Arthritis (3723001)
 
HPO: HP:0001369

Definition

If you feel pain and stiffness in your body or have trouble moving around, you might have arthritis. Most kinds of arthritis cause pain and swelling in your joints. Joints are places where two bones meet, such as your elbow or knee. Over time, a swollen joint can become severely damaged. Some kinds of arthritis can also cause problems in your organs, such as your eyes or skin. Types of arthritis include. -Osteoarthritis is the most common type of arthritis. It's often related to aging or to an injury. -Autoimmune arthritis happens when your body's immune system attacks healthy cells in your body by mistake. Rheumatoid arthritis is the most common form of this kind of arthritis. -Juvenile arthritis is a type of arthritis that happens in children. -Infectious arthritis is an infection that has spread from another part of the body to the joint. -Psoriatic arthritis affects people with psoriasis. -Gout is a painful type of arthritis that happens when too much uric acid builds up in the body. It often starts in the big toe. NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases.  [from MedlinePlus]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVArthritis

Conditions with this feature

Afibrinogenemia
MedGen UID:
7919
Concept ID:
C0001733
Disease or Syndrome
Hereditary deficiency of complement factor I is associated with a propensity to pyogenic infection and follows an autosomal recessive pattern of inheritance (Vyse et al., 1996). See also complement factor H deficiency (609814), which shows overlapping clinical features.
Alkaptonuria
MedGen UID:
1413
Concept ID:
C0002066
Disease or Syndrome
Alkaptonuria is caused by deficiency of homogentisate 1,2-dioxygenase, an enzyme that converts homogentisic acid (HGA) to maleylacetoacetic acid in the tyrosine degradation pathway. The three major features of alkaptonuria are the presence of HGA in the urine, ochronosis (bluish-black pigmentation in connective tissue), and arthritis of the spine and larger joints. Oxidation of the HGA excreted in the urine produces a melanin-like product and causes the urine to turn dark on standing. Ochronosis occurs only after age 30 years; arthritis often begins in the third decade. Other manifestations include pigment deposition, aortic or mitral valve calcification or regurgitation and occasionally aortic dilatation, renal stones, and prostate stones.
Behcet syndrome
MedGen UID:
2568
Concept ID:
C0004943
Disease or Syndrome
Behçet disease is an inflammatory condition that affects many parts of the body. The health problems associated with Behçet disease result from widespread inflammation of blood vessels (vasculitis). This inflammation most commonly affects the mouth, genitals, skin, and eyes.Painful mouth sores called aphthous ulcers are usually the first sign of Behçet disease. These sores occur on the lips and tongue and inside the cheeks. The ulcers look like common canker sores, and they typically heal within one to two weeks. About 75 percent of all people with Behçet disease develop similar ulcers on the genitals. These ulcers occur most frequently on the scrotum in men and on the labia in women.Behçet disease can also cause painful bumps and sores on the skin. Most affected individuals develop pus-filled bumps that resemble acne. These bumps can occur anywhere on the body. Some affected people also have red, tender nodules called erythema nodosum. These nodules usually develop on the legs but can also occur on the face, neck, and arms.An inflammation of the eye called uveitis is found in more than half of people with Behçet disease. Eye problems are more common in younger people with the disease and affect men more often than women. Uveitis can result in blurry vision and an extreme sensitivity to light (photophobia). Rarely, inflammation can also cause eye pain and redness. If untreated, the eye problems associated with Behçet disease can lead to blindness.Less commonly, Behçet disease can affect the joints, gastrointestinal tract, large blood vessels, and brain and spinal cord (central nervous system). Central nervous system abnormalities are among the most serious complications of Behçet disease. Related symptoms can include headaches, confusion, personality changes, memory loss, impaired speech, and problems with balance and movement.The signs and symptoms of Behçet disease usually begin in a person's twenties or thirties, although they can appear at any age. Some affected people have relatively mild symptoms that are limited to sores in the mouth and on the genitals. Others have more severe symptoms affecting many parts of the body, including the central nervous system. The features of Behçet disease typically come and go over a period of months or years. In most affected individuals, the health problems associated with this disorder improve with age.
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.
Pachydermoperiostosis syndrome
MedGen UID:
18210
Concept ID:
C0029411
Disease or Syndrome
Primary hypertrophic osteoarthropathy is a familial disorder characterized by digital clubbing and osteoarthropathy, with variable features of pachydermia, delayed closure of the fontanels, and congenital heart disease. Secondary hypertrophic osteoarthropathy, or pulmonary hypertrophic osteoarthropathy, is a different disorder characterized by digital clubbing secondary to acquired diseases, most commonly intrathoracic neoplasm (Uppal et al., 2008). Touraine et al. (1935) recognized pachydermoperiostosis as a familial disorder with 3 clinical presentations or forms: a complete form characterized by periostosis and pachydermia; an incomplete form with bone changes but without pachydermia; and a 'forme fruste' with pachydermia and minimal skeletal changes. Genetic Heterogeneity PHOAR2 (614441) is caused by mutation in the SLCO2A1 gene (601460) on chromosome 3q22.1-q22.2. Families with an autosomal dominant form of primary hypertrophic osteoarthropathy have also been reported (PHOAD; 167100).
Polyarteritis nodosa
MedGen UID:
14681
Concept ID:
C0031036
Disease or Syndrome
Childhood-onset polyarteritis nodosa is an autosomal recessive systemic vascular inflammatory disorder characterized mainly by involvement of the skin, nervous system, kidney, and gastrointestinal tract. There is considerable variability in the severity and age at onset, although most patients have onset of symptoms in the first decade. Features include recurrent ischemic stroke affecting the small vessels of the brain and resulting in neurologic dysfunction, recurrent fever, elevated acute-phase proteins, myalgias, and livedo racemosa or reticularis with an inflammatory vasculitis on biopsy. Some patients develop hypertension, aneurysms, or ischemic necrosis of the digits (summary by Zhou et al., 2014 and Navon Elkan et al., 2014). Some patients present with clinical immunodeficiency (van Eyck et al., 2014).
Familial Mediterranean fever
MedGen UID:
45811
Concept ID:
C0031069
Disease or Syndrome
Familial Mediterranean fever (FMF) is divided into two phenotypes: type 1 and type 2. FMF type 1 is characterized by recurrent short episodes of inflammation and serositis including fever, peritonitis, synovitis, pleuritis, and, rarely, pericarditis and meningitis. The symptoms and severity vary among affected individuals, sometimes even among members of the same family. Amyloidosis, which can lead to renal failure, is the most severe complication, if untreated. FMF type 2 is characterized by amyloidosis as the first clinical manifestation of FMF in an otherwise asymptomatic individual.
Vertical talus, congenital
MedGen UID:
66821
Concept ID:
C0240912
Congenital Abnormality
Congenital vertical talus (CVT), also known as 'rocker-bottom foot' deformity, is a dislocation of the talonavicular joint characterized by vertical orientation of the talus with a rigid dorsal dislocation of the navicular, equinus deformity of the calcaneus, abduction deformity of the forefoot, and contracture of the soft tissues of the hind- and mid-foot. This condition is usually associated with multiple other congenital deformities and only rarely is an isolated deformity with familial occurrence (summary by Levinsohn et al., 2004). The condition is transmitted in an autosomal dominant pattern of inheritance, and sometimes shows incomplete penetrance and variable expressivity. There may be a broad spectrum of deformities, including flatfoot, talipes equinovarus (TEV or clubfoot), cavus foot, metatarsus adductus, and even hypoplasia of the tibia (summary by Dobbs et al., 2006).
Farber lipogranulomatosis
MedGen UID:
78654
Concept ID:
C0268255
Disease or Syndrome
Farber lipogranulomatosis is an autosomal recessive lysosomal storage disorder characterized by early-onset subcutaneous nodules, painful and progressively deformed joints, and hoarseness by laryngeal involvement. Based on the age of onset, the severity of symptoms, and the difference in organs affected, 6 clinical subtypes due to deficiency of acid ceramidase have been distinguished. The most severe form is subtype 4, a rare neonatal form of the disease with death occurring before 1 year of age (summary by Alves et al., 2013).
Sitosterolemia
MedGen UID:
87466
Concept ID:
C0342907
Pathologic Function
Sitosterolemia is characterized by: Tendon xanthomas or tuberous (i.e., planar) xanthomas that can occur in childhood and in unusual locations (heels, knees, elbows and buttocks); Premature atherosclerosis which can lead to angina, aortic valve involvement, myocardial infarction, and sudden death; Hemolytic anemia, abnormally shaped erythrocytes (stomatocytes), and large platelets (macrothrombocytopenia). On occasion, the abnormal hematologic findings may be the initial presentation. The phenotypic spectrum of sitosterolemia is probably not fully appreciated due to underdiagnosis and the fact that clinical findings in infants are likely to be highly dependent on diet.
Hyperimmunoglobulin D with periodic fever
MedGen UID:
140768
Concept ID:
C0398691
Disease or Syndrome
Mevalonate kinase deficiency is a condition characterized by recurrent episodes of fever, which typically begin during infancy. Each episode of fever lasts about 3 to 6 days, and the frequency of the episodes varies among affected individuals. In childhood the fevers seem to be more frequent, occurring as often as 25 times a year, but as the individual gets older the episodes occur less often.Mevalonate kinase deficiency has additional signs and symptoms, and the severity depends on the type of the condition. There are two types of mevalonate kinase deficiency: a less severe type called hyperimmunoglobulinemia D syndrome (HIDS) and a more severe type called mevalonic aciduria (MVA).During episodes of fever, people with HIDS typically have enlargement of the lymph nodes (lymphadenopathy), abdominal pain, joint pain, diarrhea, skin rashes, and headache. Occasionally they will have painful sores called aphthous ulcers around their mouth. In females, these may also occur around the vagina. A small number of people with HIDS have intellectual disability, problems with movement and balance (ataxia), eye problems, and recurrent seizures (epilepsy). Rarely, people with HIDS develop a buildup of protein deposits (amyloidosis) in the kidneys that can lead to kidney failure. Fever episodes in individuals with HIDS can be triggered by vaccinations, surgery, injury, or stress. Most people with HIDS have abnormally high levels of immune system proteins called immunoglobulin D (IgD) and immunoglobulin A (IgA) in the blood. It is unclear why people with HIDS have high levels of IgD and IgA. Elevated levels of these immunoglobulins do not appear to cause any signs or symptoms. Individuals with HIDS do not have any signs and symptoms of the condition between fever episodes and typically have a normal life expectancy.People with MVA have signs and symptoms of the condition at all times, not just during episodes of fever. Affected children have developmental delay, progressive ataxia, progressive problems with vision, and failure to gain weight and grow at the expected rate (failure to thrive). Individuals with MVA typically have an unusually small, elongated head. In childhood or adolescence, affected individuals may develop eye problems such as inflammation of the eye (uveitis), a blue tint in the white part of the eye (blue sclera), an eye disorder called retinitis pigmentosa that causes vision loss, or clouding of the lens of the eye (cataracts). Affected adults may have short stature and may develop muscle weakness (myopathy) later in life. During fever episodes, people with MVA may have an enlarged liver and spleen (hepatosplenomegaly), lymphadenopathy, abdominal pain, diarrhea, and skin rashes. Children with MVA who are severely affected with multiple problems may live only into early childhood; mildly affected individuals may have a normal life expectancy.
Severe immunodeficiency, autosomal recessive, T-cell negative, B-cell negative, NK cell-positive
MedGen UID:
321935
Concept ID:
C1832322
Disease or Syndrome
Severe combined immunodeficiency refers to a genetically and clinically heterogeneous group of disorders with defective cellular and humoral immune function. Patients with SCID present in infancy with recurrent, persistent infections by opportunistic organisms, including Candida albicans, Pneumocystis carinii, and cytomegalovirus, among many others. Laboratory analysis shows profound lymphopenia with diminished or absent immunoglobulins. The common characteristic of all types of SCID is absence of T cell-mediated cellular immunity due to a defect in T-cell development. Without treatment, patients usually die within the first year of life. The overall prevalence of all types of SCID is approximately 1 in 75,000 births (Fischer et al., 1997; Buckley, 2004). SCID can be divided into 2 main classes: those with B lymphocytes (B+ SCID) and those without (B- SCID). Presence or absence of NK cells is variable within these groups. The most common form of SCID is X-linked T-, B+, NK- SCID (300400) caused by mutation in the IL2RG gene (308380) on chromosome Xq13.1. Autosomal recessive SCID includes T-, B+, NK- SCID (600802) caused by mutation in the JAK3 gene (600173) on 19p13.1; T-, B+, NK+ SCID (608971) caused by mutation in the IL7R gene (146661) on 5p13, the CD45 gene (151460) on 1q31-q32, or the CD3D gene (186790) on 11q23; T-, B-, NK- SCID (102700) caused by mutation in the ADA (608958) gene on 20q13.11; T-, B-, NK+ SCID with sensitivity to ionizing radiation caused by mutation in the Artemis gene on 10p; and T-, B-, NK+ SCID caused by mutation in the RAG1 and RAG2 genes on 11p13 (Kalman et al., 2004). Approximately 20 to 30% of all SCID patients are T-, B-, NK+, and approximately half of these patients have mutations in the RAG1 or RAG2 genes (Schwarz et al., 1996; Fischer et al., 1997).
Necrotizing encephalomyelopathy, subacute, of Leigh, adult
MedGen UID:
331718
Concept ID:
C1834340
Disease or Syndrome
Leukoencephalopathy, arthritis, colitis, and hypogammaglobulinema
MedGen UID:
324768
Concept ID:
C1837329
Disease or Syndrome
Uric acid concentration, serum, quantitative trait locus 1
MedGen UID:
330702
Concept ID:
C1841837
Finding
Gout is a common disorder resulting from tissue deposition of monosodium urate crystals as a consequence of hyperuricemia. Patients with gout experience very painful attacks caused by precipitation of urate in joints, which triggers subsequent inflammation. Elevated serum uric acid concentration is a key risk factor for gout (summary from Matsuo et al., 2009 and Woodward et al., 2011). Genetic Heterogeneity of Serum Uric Acid Concentration Quantitative Trait Loci See also UAQTL2 (see 612076), conferred by variation in the SLC2A9 gene (606142) on chromosome 4p; UAQTL4 (612671), conferred by variation in the SLC17A3 gene (611034) on chromosome 6p21; UAQTL5 (614746), associated with a SNP on chromosome 19q13; and UAQTL6 (614747), associated with a SNP on chromosome 1.
Familial mediterranean fever, autosomal dominant
MedGen UID:
341987
Concept ID:
C1851347
Disease or Syndrome
Pyogenic arthritis, pyoderma gangrenosum and acne
MedGen UID:
346801
Concept ID:
C1858361
Disease or Syndrome
An autoinflammatory disease caused by mutations in the PSTPIP1 gene. It is characterized by episodes of destructive arthritis, ulcerative skin lesions and cystic acne.
Camptodactyly arthropathy coxa vara pericarditis syndrome
MedGen UID:
349226
Concept ID:
C1859690
Disease or Syndrome
The camptodactyly-arthropathy-coxa vara-pericarditis syndrome is an autosomal recessive condition characterized by the association of congenital or early-onset camptodactyly and noninflammatory arthropathy with synovial hyperplasia. Progressive coxa vara deformity and/or noninflammatory pericardial or pleural effusions are found in some patients (summary by Faivre et al., 2000).
Blau syndrome
MedGen UID:
348835
Concept ID:
C1861303
Disease or Syndrome
Blau syndrome is characterized by the triad of granulomatous arthritis, uveitis, and dermatitis. First described in 1985, it was considered to be distinct from sarcoidosis due to the early age of onset and autosomal dominant inheritance pattern. Published reports of sporadic cases of children with 'early-onset sarcoidosis' (EOS) with granulomatous involvement of different organs, primarily affecting joints, eyes, and skin, were suspected to represent the same disorder because the patients' characteristics were nearly identical. Subsequently, identical NOD2 mutations were identified in patients with Blau syndrome as well as in patients diagnosed with EOS, confirming earlier suspicions that they represented the same disease (summary by Borzutzky et al., 2010). Unlike older children diagnosed with sarcoidosis, these patients have no apparent pulmonary involvement; however, the disease is progressive and may result in severe complications such as blindness and/or joint destruction (Shetty and Gedalia, 1998).
Spondyloepiphyseal dysplasia tarda autosomal dominant
MedGen UID:
355785
Concept ID:
C1866717
Disease or Syndrome
Psoriasis susceptibility 1
MedGen UID:
357279
Concept ID:
C1867449
Disease or Syndrome
Psoriasis (psoriasis vulgaris; PV) is a chronic inflammatory dermatosis that affects approximately 2% of the population. It is characterized by red, scaly skin patches that are usually found on the scalp, elbows, and knees, and may be associated with severe arthritis. The lesions are caused by abnormal keratinocyte proliferation and infiltration of inflammatory cells into the dermis and epidermis. The usual age of onset of psoriasis is between 15 and 30 years, although it can present at any age (summary by Matthews et al., 1996). Generalized pustular psoriasis (GPP) is a life-threatening disease characterized by sudden, repeated episodes of high-grade fever, generalized rash, and disseminated pustules, with hyperleukocytosis and elevated serum levels of C-reactive protein (123260) (summary by Marrakchi et al., 2011). GPP often presents in patients with existing or prior psoriasis vulgaris; however, GPP can develop without a history of PV (Sugiura et al., 2013). Palmoplantar pustulosis and acrodermatitis continua of Hallopeau represent acral forms of pustular psoriasis that have historically been grouped with GPP (summary by Setta-Kaffetzi et al., 2013). Nestle et al. (2009) provided a detailed review of the pathogenesis and genetics of psoriasis. Genetic Heterogeneity of Psoriasis and Psoriasis Susceptibility PSORS2 (602723) is caused by mutation in the CARD14 gene (607211) on chromosome 17q25, and PSORS14 (614204) is caused by mutation in the IL36RN gene (605507) on chromosome 2q13. Psoriasis susceptibility loci include PSORS1 on 6p21.3; PSORS3 (601454) on 4q; PSORS4 on 1q21; PSORS5 (604316) on 3q21; PSORS6 (605364) on 19p; PSORS7 (605606) on 1p; PSORS8 (610707) on 16q; PSORS9 (607857) on 4q31; PSORS10 (612410) on 18p11; PSORS11 (612599) on 5q31-q33; PSORS12 (612950) on 20q13; PSORS13 (614070), conferred by variation in the TRAF3IP2 gene (607043) on 6q21; and PSORS15 (616106), conferred by variation in the AP1S3 gene (615781) on 2q36. An additional putative psoriasis candidate locus has been reported on 20p (Nair et al., 1997).
Sarcoidosis 1
MedGen UID:
394568
Concept ID:
C2697310
Finding
Idiopathic scoliosis is a structurally fixed lateral curvature of the spine with a rotatory component. There is at least a 10 degree curvature as demonstrated by upright spine roentgenograms by the Cobb method (Weinstein, 1994).
Roifman-Chitayat syndrome
MedGen UID:
442377
Concept ID:
C2750068
Disease or Syndrome
Diarrhea 5, with tufting enteropathy, congenital
MedGen UID:
413031
Concept ID:
C2750737
Disease or Syndrome
Congenital tufting enteropathy (CTE) is a rare inherited intractable diarrhea of infancy characterized by villous atrophy and absence of inflammation, with intestinal epithelial cell dysplasia manifesting as focal epithelial tufts in the duodenum and jejunum. CTE presents in the first few months of life with chronic watery diarrhea and failure to thrive, and most affected individuals require parenteral nutrition for normal growth and development (summary by Sivagnanam et al., 2008). Semiquantitative assessment of the epithelial surface in CTE patients revealed that 80 to 90% contained tufts, compared to only 16% in patients with celiac disease and less than 10% in normal jejunum (Reifen et al., 1994). For a discussion of phenotypic and genetic heterogeneity of congenital diarrhea, see DIAR1 (214700).
Complement component c1r/c1s deficiency
MedGen UID:
461624
Concept ID:
C3150274
Disease or Syndrome
Lack of production of either functional C1r or C1s protein, due to a genetic defect. Approximately 60% of patients with a C1r/C1s deficiency will develop a severe systemic lupus erythematosus at an early age. Patients also present with frequent sinopulmonary infections often with Streptococcus pneumoniae.
Common variable immunodeficiency 8, with autoimmunity
MedGen UID:
766426
Concept ID:
C3553512
Disease or Syndrome
Common variable immunodeficiency-8 with autoimmunity is an autosomal recessive disorder of immune dysregulation. Affected individuals have early childhood onset of recurrent infections, particularly respiratory infections, and also develop variable autoimmune disorders, including idiopathic thrombocytopenic purpura, autoimmune hemolytic anemia, and inflammatory bowel disease. The presentation and phenotype are highly variable, even within families (summary by Lopez-Herrera et al., 2012 and Alangari et al., 2012). Immunologic findings are also variable and may include decreased B cells, hypogammaglobulinemia, and deficiency of CD4+ T regulatory (Treg) cells (Charbonnier et al., 2015). For a general description and a discussion of genetic heterogeneity of common variable immunodeficiency, see CVID1 (607594).
Autoimmune disease, multisystem, infantile-onset, 1
MedGen UID:
799886
Concept ID:
CN207828
Disease or Syndrome
Infantile-onset multisystem autoimmune disease-1 is characterized by early childhood onset of a spectrum of autoimmune disorders affecting multiple organs. Common manifestations include insulin-dependent diabetes mellitus and autoimmune enteropathy, or celiac disease, and autoimmune hematologic disorders. Other features include short stature and nonspecific dermatitis. More variable features include hypothyroidism, autoimmune arthritis, and delayed puberty. Some patients may show recurrent infections. The disorder results from an inborn error of cytokine signaling (summary by Flanagan et al., 2014 and Milner et al., 2015). Genetic Heterogeneity of Infantile-Onset Multisystem Autoimmune Disease See also ADMIO2 (617006), caused by mutation in the ZAP70 gene (176947) on chromosome 2q12.

Recent clinical studies

Etiology

Sepúlveda-Delgado J, Vera-Lastra OL, Trujillo-Murillo K, Canseco-Ávila LM, Sánchez-González RA, Gómez-Cruz O, Lugo-Trampe A, Fernández-Salas I, Danis-Lozano R, Contreras-Contreras A, Mendoza-Torres A, Domínguez-Arrevillaga S, Mena-Vela BA, Ocaña-Sibilla M, Ramirez-Valdespino JC, Jara LJ
Clin Rheumatol 2017 Mar;36(3):695-699. Epub 2016 Sep 28 doi: 10.1007/s10067-016-3419-2. PMID: 27680539
Patterson KK, Sibley KM
BMC Neurol 2016 Jul 26;16:114. doi: 10.1186/s12883-016-0636-x. PMID: 27456977Free PMC Article
Alves CH, Farrell E, Vis M, Colin EM, Lubberts E
Clin Rev Allergy Immunol 2016 Aug;51(1):27-47. doi: 10.1007/s12016-015-8522-7. PMID: 26634933Free PMC Article
Pinheiro LC, Callahan LF, Cleveland RJ, Edwards LJ, Reeve BB
J Rheumatol 2016 Jan;43(1):131-7. Epub 2015 Dec 1 doi: 10.3899/jrheum.150432. PMID: 26628600
Lo T, Parkinson L, Cunich M, Byles J
Expert Rev Pharmacoecon Outcomes Res 2016 Jun;16(3):383-91. Epub 2015 Nov 2 doi: 10.1586/14737167.2016.1096199. PMID: 26523846

Diagnosis

Xu X, Liu L, Xie W, Zhang Y, Zeng H, Zhang F, Reis C, Cao X, Zhao Y
Medicine (Baltimore) 2017 Mar;96(13):e6496. doi: 10.1097/MD.0000000000006496. PMID: 28353598Free PMC Article
Barbour KE, Helmick CG, Boring M, Brady TJ
MMWR Morb Mortal Wkly Rep 2017 Mar 10;66(9):246-253. doi: 10.15585/mmwr.mm6609e1. PMID: 28278145
Sepúlveda-Delgado J, Vera-Lastra OL, Trujillo-Murillo K, Canseco-Ávila LM, Sánchez-González RA, Gómez-Cruz O, Lugo-Trampe A, Fernández-Salas I, Danis-Lozano R, Contreras-Contreras A, Mendoza-Torres A, Domínguez-Arrevillaga S, Mena-Vela BA, Ocaña-Sibilla M, Ramirez-Valdespino JC, Jara LJ
Clin Rheumatol 2017 Mar;36(3):695-699. Epub 2016 Sep 28 doi: 10.1007/s10067-016-3419-2. PMID: 27680539
Patterson KK, Sibley KM
BMC Neurol 2016 Jul 26;16:114. doi: 10.1186/s12883-016-0636-x. PMID: 27456977Free PMC Article
Pinheiro LC, Callahan LF, Cleveland RJ, Edwards LJ, Reeve BB
J Rheumatol 2016 Jan;43(1):131-7. Epub 2015 Dec 1 doi: 10.3899/jrheum.150432. PMID: 26628600

Therapy

Xu X, Liu L, Xie W, Zhang Y, Zeng H, Zhang F, Reis C, Cao X, Zhao Y
Medicine (Baltimore) 2017 Mar;96(13):e6496. doi: 10.1097/MD.0000000000006496. PMID: 28353598Free PMC Article
Carter K, Lahiri M, Cheung PP, Santosa A, Rome K
J Foot Ankle Res 2016;9:29. Epub 2016 Aug 17 doi: 10.1186/s13047-016-0161-6. PMID: 27540415Free PMC Article
Patterson KK, Sibley KM
BMC Neurol 2016 Jul 26;16:114. doi: 10.1186/s12883-016-0636-x. PMID: 27456977Free PMC Article
Barber CE, Marshall DA, Mosher DP, Akhavan P, Tucker L, Houghton K, Batthish M, Levy DM, Schmeling H, Ellsworth J, Tibollo H, Grant S, Khodyakov D, Lacaille D; Arthritis Alliance of Canada Performance Measurement Development Panel.
J Rheumatol 2016 Mar;43(3):530-40. Epub 2016 Jan 15 doi: 10.3899/jrheum.150839. PMID: 26773106
Alves CH, Farrell E, Vis M, Colin EM, Lubberts E
Clin Rev Allergy Immunol 2016 Aug;51(1):27-47. doi: 10.1007/s12016-015-8522-7. PMID: 26634933Free PMC Article

Prognosis

Sepúlveda-Delgado J, Vera-Lastra OL, Trujillo-Murillo K, Canseco-Ávila LM, Sánchez-González RA, Gómez-Cruz O, Lugo-Trampe A, Fernández-Salas I, Danis-Lozano R, Contreras-Contreras A, Mendoza-Torres A, Domínguez-Arrevillaga S, Mena-Vela BA, Ocaña-Sibilla M, Ramirez-Valdespino JC, Jara LJ
Clin Rheumatol 2017 Mar;36(3):695-699. Epub 2016 Sep 28 doi: 10.1007/s10067-016-3419-2. PMID: 27680539
Carter K, Lahiri M, Cheung PP, Santosa A, Rome K
J Foot Ankle Res 2016;9(1):37. Epub 2016 Sep 2 doi: 10.1186/s13047-016-0169-y. PMID: 27594920Free PMC Article
Albrecht K, Callhoff J, Buttgereit F, Straub RH, Westhoff G, Zink A
Arthritis Care Res (Hoboken) 2016 Mar;68(3):400-5. doi: 10.1002/acr.22667. PMID: 26275790
Popma JW, Snel FW, Haagsma CJ, Brummelhuis-Visser P, Oldenhof HG, van der Palen J, van de Laar MA
J Rheumatol 2015 Oct;42(10):1865-8. Epub 2015 Aug 1 doi: 10.3899/jrheum.141630. PMID: 26233499
Duquenne C, Cornec D, Marhadour T, Jousse-Joulin S, Cantagrel A, Pavy S, Devauchelle-Pensec V, Saraux A
Joint Bone Spine 2015 Dec;82(6):417-22. Epub 2015 Jul 14 doi: 10.1016/j.jbspin.2015.02.012. PMID: 26184529

Clinical prediction guides

Sepúlveda-Delgado J, Vera-Lastra OL, Trujillo-Murillo K, Canseco-Ávila LM, Sánchez-González RA, Gómez-Cruz O, Lugo-Trampe A, Fernández-Salas I, Danis-Lozano R, Contreras-Contreras A, Mendoza-Torres A, Domínguez-Arrevillaga S, Mena-Vela BA, Ocaña-Sibilla M, Ramirez-Valdespino JC, Jara LJ
Clin Rheumatol 2017 Mar;36(3):695-699. Epub 2016 Sep 28 doi: 10.1007/s10067-016-3419-2. PMID: 27680539
Barden AE, Moghaddami M, Mas E, Phillips M, Cleland LG, Mori TA
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