rheumatology

• リウマチ学

関

rheumatologic、rheumatological

　

WordNet

1. the branch of medicine dealing with the study and treatment of pathologies of the muscles or tendons or joints

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/10/30 17:45:50」(JST)

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Rheumatology

An old fracture with nonunion of the fracture fragments.
System	Musculoskeletal
Subdivisions	Sports, rehabilitation, trauma
Significant diseases	Arthritis, Trauma, Connective tissue disease
Significant tests	Joint aspirate, Rheumatological exam, X-ray
Specialist	Rheumatologist

Rheumatology (Greek ρεύμα, rheuma, river) is a sub-specialty in internal medicine and pediatrics, devoted to diagnosis and therapy of rheumatic diseases. Clinicians who specialize in rheumatology are called rheumatologists. Rheumatologists deal mainly with clinical problems involving joints, soft tissues, autoimmune diseases, vasculitis, and heritable connective tissue disorders.

Many of these diseases are now known to be disorders of the immune system, and rheumatology is increasingly the study of immunology.

Rheumatism

Rheumatism is a colloquial term referring to any painful disorder affecting the loco-motor system including joints, muscles, connective tissues, soft tissues around the joints, and bones. This also includes rheumatic heart disease, which is specific to heart valves but has symptoms similar to rheumatic fever, which typically develops after a streptococcal infection. Rheumatologists are clinicians dealing with arthritis and other rheumatological disorders such as rheumatoid arthritis, ankylosing spondylitis, gout, systemic lupus erythematosus.

One of the major changes in modern rheumatology is the development of new drugs called biologics, or disease modifying agents, which can control severe disease more effectively.

Rheumatologist

Rheumatologist

Occupation
Names	Doctor, Medical Specialist
Activity sectors	Medicine
Description
Education required	Doctor of Medicine (M.D.) or Doctor of Osteopathic Medicine (D.O.)

A rheumatologist is a physician specialized in the field of medical sub-specialty called rheumatology, and holds either a board certification after specialized training after attaining a medical degree (M.D. or D.O.) through fellowship programs in the United States, or specialist registrar positions in the United Kingdom, or DM in India or equivalent programs elsewhere in the world. In the United States, training in this field requires four years undergraduate school, four years of medical school, and then three years of residency, followed by two or three years additional Fellowship training. The requirements may vary in other countries. Rheumatologists are internists or pediatricians who are qualified by additional postgraduate training and experience in the diagnosis and treatment of arthritis and other diseases of the joints, muscles and bones. Many rheumatologists also conduct research to determine the cause and better treatments for these disabling and sometimes fatal diseases. Treatment modalities are based on scientific research, currently, practice of rheumatology is largely evidence based. Clinicians who specialize on this specialty are called Rheumatologists.

Rheumatologists treat arthritis, autoimmune diseases, pain disorders affecting joints, and osteoporosis. There are more than 200 types of these diseases, including rheumatoid arthritis, osteoarthritis, gout, lupus, back pain, osteoporosis, and tendinitis. Some of these are very serious diseases that can be difficult to diagnose and treat. They treat soft tissue problems related to musculoskeletal system sports related soft tissue disorders and the specialty is also interrelated with physiotherapy, physical medicine and rehabilitation of disabled patients. Patient education programs and occupational therapy also go hand in hand with this specialty.

Diseases

Main article: Rheumatism

Diseases diagnosed or managed by the rheumatologist include:

Degenerative arthropathies

• Osteoarthritis

Inflammatory arthropathies

• Rheumatoid arthritis
• spondyloarthropathies
  • Ankylosing spondylitis
  • Reactive arthritis (reactive arthropathy)
  • Psoriatic arthropathy
  • Enteropathic spondylitis
• Juvenile Idiopathic Arthritis (JIA)
• Crystal arthropathies: gout, pseudogout
• Septic arthritis

Systemic conditions and connective tissue diseases

• Lupus
• Sjögren's syndrome
• Scleroderma (systemic sclerosis)
• Polymyositis
• Dermatomyositis
• Polymyalgia rheumatica
• Mixed connective tissue disease
• Polychondritis
• Sarcoidosis
• Vasculitis
  • Microscopic Polyangiitis
  • Churg-Strauss Syndrome
  • Wegener's granulomatosis
  • Polyarteritis nodosa
  • Henoch-Schönlein purpura
  • Serum sickness
  • Giant cell arteritis, Temporal arteritis
  • Takayasu's arteritis
  • Behçet's syndrome
  • Kawasaki's disease (mucocutaneous lymph node syndrome)
  • Buerger's disease (thromboangiitis obliterans)

Soft Tissue Rheumatism

Local diseases and lesions affecting the joints and structures around the joints including tendons, ligaments capsules, bursae, Stress Fractures, muscles, nerve entrapment, vascular lesions, ganglions, localised Soft tissues disorders. For example:

• Low back pain
• Tennis elbow
• Golfer's elbow
• Olecranon bursitis
• Fibromyalgia

Diseases affecting bones

• Osteoporosis
• Osteomalacia
• Renal osteodystrophy
• Fluorosis
• Rickets

Congenital and familial Disorders affecting Joints

• Hyperextensible joints
• Ehlers-Danlos Syndrome
• Achondroplasia
• Marfan's Syndrome

Diagnosis

Apart from an extensive medical history, there are useful methods of diagnosis both performed easy enough in a physical examination and, on the other hand, more complicated ones, often requiring a rheumatologist or other specialized physicians.

Physical examination

Following are examples of methods of diagnosis able to be performed in a normal physical examination.

• Schober's test tests the flexion of the lower back.
• Multiple joint inspection
• Musculoskeletal Examination
  • Screening Musculoskeletal Exam (SMSE) - a rapid assessment of structure and function
  • General Musculoskeletal Exam (GMSE) - a comprehensive assessment of joint inflammation
  • Regional Musculoskeletal Exam (RMSE) - focused assessments of structure, function and inflammation combined with special testing

Specialized

• Laboratory tests (e.g. Erythrocyte Sedimentation Rate, Rheumatoid Factor, Anti-CCP (Anti-citrullinated protein antibody), ANA (Anti-Nuclear Antibody) )
• X-rays, Ultrasounds, and other imaging methods of affected joints
• Cytopathology and chemical pathology of fluid aspirated from affected joints (e.g. to differentiate between septic arthritis and gout)

Treatment

Most rheumatic diseases are treated with analgesics, NSAIDs (Non-Steroid Anti-Inflammatory Drugs), steroids (in serious cases), DMARDs (Disease-Modifying Anti-Rheumatic Drugs), monoclonal antibodies, such as infliximab and adalimumab, and the soluble TNF receptor etanercept and Methotrexate for moderate to severe Rheumatoid arthritis. Biologic agent Rituximab (Anti-B-Cell Therapy) is now licensed for use in refractory Rheumatoid Arthritis. Physiotherapy is vital in the treatment of many rheumatological disorders. Occupational therapy can help patients finding alternative ways for common movements which would otherwise be restricted by their disease. Patients with rheumatoid arthritis often need a long term, coordinated and a multidisciplinary team approach towards management of individual patients, treatment is often tailored according the individual needs of the individual patient which is also dependent on the response and the tolerability of medications.

Scientific research

Recently, a large body of scientific research deals with the background of autoimmune disease, the cause of many rheumatic disorders. Also, the field of osteoimmunology has emerged to further examine the interactions between the immune system, joints and bones. Epidemiological studies and medication trials are also being conducted. Scientific research on biologics and clinical trials on monoclonal antibody therapies have added a new dimension to the medical treatment of arthritic disorders.

References

External links

• American College of Rheumatology
• Consortium of Rheumatology Researchers of North America, Inc
• British Society for Rheumatology
• Canadian Rheumatology Association
• Association of Rheumatology Health Professionals
• Future Rheumatology journal-Cutting edge commentary and analysis in the field of Rheumatology
• Indian Journal of Rheumatology

UpToDate Contents

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• 1. リウマチ学の最新情報 whats new in rheumatology
• 2. 成人における多関節痛の評価 evaluation of the adult with polyarticular pain
• 3. 関節リウマチの診断および鑑別診断 diagnosis and differential diagnosis of rheumatoid arthritis
• 4. 未分化型の全身性リウマチ性（結合組織）疾患およびオーバーラップ症候群 undifferentiated systemic rheumatic connective tissue diseases and overlap syndromes
• 5. 関節リウマチの管理の一般原則 general principles of management of rheumatoid arthritis

English Journal

• C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration.

• Tang Y, Huang XR, Lv J1, Chung AC, Zhang Y2, Chen JZ1, Szalai AJ3, Xu A1, Lan HY.Author information 1*Department of Nephrology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.2†Li Ka Shing Institute of Health Sciences and Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.3§Division of Clinical Immunology and Rheumatology, The University of Alabama at Birmingham, Birmingham, AL, U.S.A.AbstractCRP (C-reactive protein) is regarded as an inflammatory biomarker in AKI (acute kidney injury), but its exact role in AKI remains unclear. Thus we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP levels were found to associate closely with increased serum creatinine and urea levels (P<0.01) in patients with AKI, which then fell after recovery from AKI. To determine the role of CRP in AKI, an ischaemia/reperfusion mouse model of AKI was developed using Tg (transgenic) mice that express human CRP. Compared with the WT (wild-type) mice, CRP Tg mice developed more severe renal injury at 24 h after ischaemia as determined by significantly increased serum creatinine and tubular necrosis. This was associated with an impaired TEC (tubular epithelium cell) regeneration as shown by an over 60% reduction in PCNA+ (proliferating-cell nuclear antigen) and BrdU+ (bromodeoxyuridine) TECs in CRP Tg mice with AKI. In vitro, the addition of CRP to a human TEC line (HK-2) also largely suppressed the proliferation of TECs. The functional role of CRP in AKI was demonstrated further by the blocking of CRP binding to the FcγRII (Fcγ receptor II) with a neutralizing anti-CD32 antibody, which restored TEC proliferation and prevented AKI in CRP Tg mice. Moreover, we found that impaired G1/S transition by suppression of the phosphorylation of CDK2 (cyclin-dependent kinase 2) and expression of cyclin E may be a key mechanism by which CRP inhibits TEC regeneration during the AKI repair process. In conclusion, CRP plays a pathogenic role in AKI by inhibiting G1/S-dependent TEC regeneration. The results of the present study suggest that targeting CRP signalling may offer a new therapeutic potential for AKI.
• Clinical science (London, England : 1979).Clin Sci (Lond).2014 May 1;126(9):645-59. doi: 10.1042/CS20130471.
• CRP (C-reactive protein) is regarded as an inflammatory biomarker in AKI (acute kidney injury), but its exact role in AKI remains unclear. Thus we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP levels were found to associate closely with increased serum creatinine and u
• PMID 24206243

• TNFR2 increases the sensitivity of ligand-induced activation of the p38 MAPK and NF-κB pathways and signals TRAF2 protein degradation in macrophages.

• Ruspi G1, Schmidt EM1, McCann F1, Feldmann M1, Williams RO1, Stoop AA2, Dean JL3.Author information 1Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Old Road Campus, Roosevelt Drive, Headington, Oxford OX3 7FY, United Kingdom.2Innovation Biopharm Discovery Unit, Biopharm R&D, GlaxoSmithKline, Cambridge CB4 0WG, United Kingdom.3Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Old Road Campus, Roosevelt Drive, Headington, Oxford OX3 7FY, United Kingdom. Electronic address: jonathan.dean@kennedy.ox.ac.uk.AbstractTumour necrosis factor (p55 or p60) receptor (TNFR) 1 is the major receptor that activates pro-inflammatory signalling and induces gene expression in response to TNF. Consensus is lacking for the function of (p75 or p80) TNFR2 but experiments in mice have suggested neuro-, cardio- and osteo-protective and anti-inflammatory roles. It has been shown in various cell types to be specifically required for the induction of TNFR-associated factor-2 (TRAF2) degradation and activation of the alternative nuclear factor (NF)-kappaB pathway, and to contribute to the activation of mitogen-activated protein kinases (MAPK) and the classical NF-kappaB pathway. We have investigated the signalling functions of TNFR2 in primary human and murine macrophages. We find that in these cells TNF induces TRAF2 degradation, and this is blocked in TNFR2(-/-) macrophages. TRAF2 has been previously reported to be required for TNF-induced activation of p38 MAPK. However, TRAF2 degradation does not inhibit TNF-induced tolerance of p38 MAPK activation. Neither TNF, nor lipopolysaccharide treatment, induced activation of the alternative NF-kappaB pathway in macrophages. Activation by TNF of the p38 MAPK and NF-kappaB pathways was blocked in TNFR1(-/-) macrophages. In contrast, although TNFR2(-/-) macrophages displayed robust p38 MAPK activation and IkappaBα degradation at high concentrations of TNF, at lower doses the concentration dependence of signalling was weakened by an order of magnitude. Our results suggest that, in addition to inducing TRAF2 protein degradation, TNFR2 also plays a crucial auxiliary role to TNFR1 in sensitising macrophages for the ligand-induced activation of the p38 MAPK and classical NF-kappaB pro-inflammatory signalling pathways.
• Cellular signalling.Cell Signal.2014 Apr;26(4):683-90. doi: 10.1016/j.cellsig.2013.12.009. Epub 2013 Dec 27.
• Tumour necrosis factor (p55 or p60) receptor (TNFR) 1 is the major receptor that activates pro-inflammatory signalling and induces gene expression in response to TNF. Consensus is lacking for the function of (p75 or p80) TNFR2 but experiments in mice have suggested neuro-, cardio- and osteo-protecti
• PMID 24378531

• Importance of adherence in the outcome of juvenile idiopathic arthritis.

• Len CA, Miotto E Silva VB, Terreri MT.Author information Pediatric Rheumatology Unit, Allergy, Immunology and Rheumatology Division, Department of Pediatrics, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM-UNIFESP), São Paulo, Brazil, claudiolen@gmail.com.AbstractMedical treatment of juvenile idiopathic arthritis (JIA) has advanced in the last decade, and improved prognosis is a reality in daily clinical practice. Despite this improvement in the quality of treatment, the outcome can still be compromised by modifiable factors, including delayed referral to a specialist, delayed drug treatment, poor adherence to treatment, and early interruption of drug treatment. In this review we discuss the most relevant aspects related to adherence to treatment in JIA, with emphasis on: factors that affect adherence to treatment; effect of poor adherence to treatment on JIA prognosis; when to suspect and how to assess poor adherence to treatment; and strategies to promote adherence to treatment, with an emphasis on information-reinforcement education. Besides presenting the findings of other authors, we also try to report our experience of this subject, which is still a challenge for health professionals.
• Current rheumatology reports.Curr Rheumatol Rep.2014 Apr;16(4):410. doi: 10.1007/s11926-014-0410-2.
• Medical treatment of juvenile idiopathic arthritis (JIA) has advanced in the last decade, and improved prognosis is a reality in daily clinical practice. Despite this improvement in the quality of treatment, the outcome can still be compromised by modifiable factors, including delayed referral to a
• PMID 24504596

Japanese Journal

• 宮崎県下の成人喘息患者に対して10年間連続して行った実態調査 : 宮崎県気管支喘息フォーラムでの検討

• 関 良二,長友 安弘,山口 哲朗,松本 紫朗
• アレルギー 63(6), 794-804, 2014-06-01
• 【目的】宮崎県気管支喘息フォーラムを通して,喘息ガイドラインに沿った治療の普及を行い,宮崎県の喘息死を減らすことを目的とした.【方法】県内の成人喘息患者を対象に, 1999年から10年間のほぼ同時期に,患者自己記入式アンケート調査を行った.【結果】県内の医療機関から, 10年間で延べ7899人分のアンケートを回収した,治療内容では10年間の経過で長期管理薬である吸入ステロイド薬,長時間作用性吸入β …
• NAID 110009818445

• 成人喘息におけるThymic stromal lymphopoietin (TSLP) 遺伝子多型とアトピー状態及び肺機能の関連

• 守口 知,内海 裕,佐々木 信人,中村 豊,小林 仁
• 岩手医学雑誌 66(2), 47-55, 2014-06-01
• NAID 110009807827

• TNFα, PDGF, and TGFβ synergistically induce synovial lining hyperplasia via inducible PI3Kδ

• Shibuya Hideyuki,Yoshitomi Hiroyuki,Murata Koichi,Kobayashi Shio,Furu Moritoshi,Ishikawa Masahiro,Fujii Takayuki,Ito Hiromu,Matsuda Shuichi
• Modern rheumatology
• Published by Informa Healthcare for the Japan Rheumatism AssociationObjectives. To determine the mechanism underlying hypertrophic synovium in rheumatoid arthritis (RA). Methods. We examined micromass …
• NAID 120005465740

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