WordNet

a plane figure with rounded sides curving inward at the top and intersecting at the bottom; conventionally used on playing cards and valentines; "he drew a heart and called it a valentine"
the courage to carry on; "he kept fighting on pure spunk"; "you havent got the heart for baseball" (同)mettle, nerve, spunk
an inclination or tendency of a certain kind; "he had a change of heart" (同)spirit
a playing card in the major suit that has one or more red hearts on it; "he led the queen of hearts"; "hearts were trumps"
the locus of feelings and intuitions; "in your heart you know it is true"; "her story would melt your bosom" (同)bosom
the hollow muscular organ located behind the sternum and between the lungs; its rhythmic contractions move the blood through the body; "he stood still, his heart thumping wildly" (同)pump, ticker
a firm rather dry variety meat (usually beef or veal); "a five-pound beef heart will serve six"
able to perceive sound
an opportunity to state your case and be heard; "they condemned him without a hearing"; "he saw that he had lost his audience" (同)audience
(law) a proceeding (usually by a court) where evidence is taken for the purpose of determining an issue of fact and reaching a decision based on that evidence
the ability to hear; the auditory faculty; "his hearing was impaired" (同)audition, auditory sense, sense of hearing, auditory modality
a session (of a committee or grand jury) in which witnesses are called and testimony is taken; "the investigative committee will hold hearings in Chicago"
receive a communication from someone; "We heard nothing from our son for five years"
examine or hear (evidence or a case) by judicial process; "The jury had heard all the evidence"; "The case will be tried in California" (同)try
perceive (sound) via the auditory sense
an impairment of health or a condition of abnormal functioning
caused by or altered by or manifesting disease or pathology; "diseased tonsils"; "a morbid growth"; "pathologic tissue"; "pathological bodily processes" (同)morbid, pathologic, pathological

PrepTutorEJDIC

〈C〉『心臓』;胸 / 〈C〉(感情の中心をなす)『心』,気持ち / 〈U〉愛情,同情 / 〈U〉『勇気』,元気,熱意 / 《the ~》『中心』,内部,(物事の)本質,核心 / 〈C〉ハート形の物;(カードの)ハートの札
〈U〉『聴力』,聴覚〈U〉〈C〉(…を)『聞くこと』,(…の)聞き取り《+『of』+『名』》・〈C〉聞いてもらう機会,聞いてやること・聴取・聴聞会〈C〉(法廷などでの)尋問,審問,;(刑罰の減免を求める)釈明,意見陳述 / 〈U〉聞こえる距離(範囲)
〈音〉‘が'『聞こえる』,‘を'聞く(進行形にできない) / 〈人の言うこと〉‘に'『耳を傾ける』,‘を'注意深く聞く(listen);(裁判官などが)…の申し立てを聞く / 〈うわさ・ニュースなど〉‘を'『耳にしている』,聞いている / 『耳が聞こえる』 / 《しばしば命令形で》耳を傾ける,注意を向ける / 『うわさ』(『消息』)『を聞く』
(体の)『病気』,疾患 / (精神・道徳などの)病気,病弊
女性の話術芸人 =diseur
病気にかかった / 病的な,不健全な(morbid)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/05/12 16:47:47」(JST)

wiki en

Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis. Believed to be caused by antibody cross-reactivity that can involve the heart, joints, skin, and brain,^[1] the illness typically develops two to three weeks after a streptococcal infection. Acute rheumatic fever commonly appears in children between the ages of 6 and 15, with only 20% of first-time attacks occurring in adults.^[1] The illness is so named because of its similarity in presentation to rheumatism.^[2]

Diagnosis

Rheumatic heart disease at autopsy with characteristic findings (thickened mitral valve, thickened chordae tendineae, hypertrophied left ventricular myocardium).

Modified Jones criteria were first published in 1944 by T. Duckett Jones, MD.^[3] They have been periodically revised by the American Heart Association in collaboration with other groups.^[4] According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase.^[1] Exceptions are chorea and indolent carditis, each of which by itself can indicate rheumatic fever.^[5]^[6]^[7] An April 2013 review article in the Indian Journal of Medical Research stated that echocardiographic and Doppler (E & D) studies, despite some reservations about their utility, have identified a massive burden of rheumatic heart disease, which suggests the inadequacy of the 1992 Jones' criteria. E & D studies have identified subclinical carditis in patients with acute rheumatic fever, as well as in follow-ups of rheumatic heart disease patients who initially presented as having isolated cases of Sydenham's chorea.^[8]

Major criteria

Polyarthritis: A temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
Carditis: Inflammation of the heart muscle (myocarditis) which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
Subcutaneous nodules: Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
Erythema marginatum: A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance. This rash typically spares the face and is made worse with heat.
Sydenham's chorea (St. Vitus' dance): A characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease for at least three months from onset of infection.

Minor criteria

Fever of 38.2–38.9 °C (100.8–102.0 °F)
Arthralgia: Joint pain without swelling (Cannot be included if polyarthritis is present as a major symptom)
Raised erythrocyte sedimentation rate or C reactive protein
Leukocytosis
ECG showing features of heart block, such as a prolonged PR interval^[9]^[10] (Cannot be included if carditis is present as a major symptom)
Previous episode of rheumatic fever or inactive heart disease

Other signs and symptoms

Abdominal pain
Nose bleeds
Preceding streptococcal infection: recent scarlet fever, raised antistreptolysin O or other streptococcal antibody titre, or positive throat culture.^[10]

Pathophysiology

Pathophysiology of rheumatic heart disease

Micrograph showing an Aschoff body (right of image), as seen in rheumatic heart disease. H&E stain.

Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A Beta hemolytic streptococcal pharyngeal infection. It is believed to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry. Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation. During a Streptococcus infection, mature antigen presenting cells such as B cells present the bacterial antigen to CD4-T cells which differentiate into helper T₂ cells. Helper T₂ cells subsequently activate the B cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus. However the antibodies may also react against the myocardium and joints,^[11] producing the symptoms of rheumatic fever.

Group A Streptococcus pyogenes has a cell wall composed of branched polymers which sometimes contain M protein that are highly antigenic. The antibodies which the immune system generates against the M protein may cross react with cardiac myofiber protein myosin,^[12] heart muscle glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction. However, the only proven cross reaction is with perivascular connective tissue.^{[citation needed]} This inflammation occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils and macrophages. Characteristic Aschoff bodies, composed of swollen eosinophilic collagen surrounded by lymphocytes and macrophages can be seen on light microscopy. The larger macrophages may become Anitschkow cells or Aschoff giant cells. Acute rheumatic valvular lesions may also involve a cell-mediated immunity reaction as these lesions predominantly contain T-helper cells and macrophages.^[13]

In acute rheumatic fever, these lesions can be found in any layer of the heart and is hence called pancarditis. The inflammation may cause a serofibrinous pericardial exudate described as "bread-and-butter" pericarditis, which usually resolves without sequelae. Involvement of the endocardium typically results in fibrinoid necrosis and verrucae formation along the lines of closure of the left-sided heart valves. Warty projections arise from the deposition, while subendocardial lesions may induce irregular thickenings called MacCallum plaques.

Rheumatic heart disease

Chronic rheumatic heart disease (RHD) is characterized by repeated inflammation with fibrinous repair. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion, and shortening and thickening of the tendinous cords.^[13] It is caused by an autoimmune reaction to Group A β-hemolytic streptococci (GAS) that results in valvular damage.^[14] Fibrosis and scarring of valve leaflets, commissures and cusps leads to abnormalities that can result in valve stenosis or regurgitation.^[15] The inflammation caused by rheumatic fever, usually during childhood, is referred to as rheumatic valvulitis. About half of patients with acute rheumatic fever develop inflammation involving valvular endothelium.^[16] The majority of morbidity and mortality associated with rheumatic fever is caused by its destructive effects on cardiac valve tissue.^[15] The pathogenesis of RHD is complex and not fully understood, but it is known to involve molecular mimicry and genetic predisposition that lead to autoimmune reactions.

Molecular mimicry occurs when epitopes are shared between host antigens and GAS antigens.^[17] This causes an autoimmune reaction against native tissues in the heart that are incorrectly recognized as "foreign" due to the cross-reactivity of antibodies generated as a result of epitope sharing. The valvular endothelium is a prominent site of lymphocyte-induced damage. CD4+ T cells are the major effectors of heart tissue autoimmune reactions in RHD.^[18] Normally, T cell activation is triggered by the presentation of GAS antigens. In RHD, molecular mimicry results in incorrect T cell activation, and these T lymphocytes can go on to activate B cells, which will begin to produce self-antigen-specific antibodies. This leads to an immune response attack mounted against tissues in the heart that have been misidentified as pathogens. Rheumatic valves display increased expression of VCAM-1, a protein that mediates the adhesion of lymphocytes.^[19] Self-antigen-specific antibodies generated via molecular mimicry between human proteins and GAS antigens up-regulate VCAM-1 after binding to the valvular endothelium. This leads to the inflammation and valve scarring observed in rheumatic valvulitis, mainly due to CD4+ T cell infiltration.^[19]

While the mechanisms of genetic predisposition remain unclear, a few genetic factors have been found to increase susceptibility to autoimmune reactions in RHD. The dominant contributors are a component of MHC class II molecules, found on lymphocytes and antigen-presenting cells, specifically the DR and DQ alleles on human chromosome 6.^[20] Certain allele combinations appear to increase RHD autoimmune susceptibility. Human leukocyte antigen (HLA) class II allele DR7 (HLA-DR7) is most often associated with RHD, and its combination with certain DQ alleles is seemingly associated with the development of valvular lesions.^[20] The mechanism by which MHC class II molecules increase a host's susceptibility to autoimmune reactions in RHD is unknown, but it is likely related to the role HLA molecules play in presenting antigens to T cell receptors, thus triggering an immune response. Also found on human chromosome 6 is the cytokine TNF-α which is also associated with RHD.^[20] High expression levels of TNF-α may exacerbate valvular tissue inflammation, contributing to RHD pathogenesis. Mannose-binding lectin (MBL) is an inflammatory protein involved in pathogen recognition. Different variants of MBL2 gene regions are associated in RHD. RHD-induced mitral valve stenosis has been associated with MBL2 alleles encoding for high production of MBL.^[21] Aortic valve regurgitation in RHD patients has been associated with different MBL2 alleles that encode for low production of MBL.^[22] Other genes are also being investigated to better understand the complexity of autoimmune reactions that occur in RHD.

Prevention

Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association suggests that people with a history of bacterial endocarditis may wish to consider long-term antibiotic prophylaxis.^[23]

Treatment

The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics. Aspirin is the drug of choice and should be given at high doses of 100 mg/kg/day. One should watch for side effects like gastritis and salicylate poisoning. In children and teenagers, the use of aspirin and aspirin-containing products can be associated with Reye's syndrome, a serious and potentially deadly condition. The risks, benefits and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Steroids are reserved for cases where there is evidence of involvement of heart. The use of steroids may prevent further scarring of tissue and may prevent development of sequelae such as mitral stenosis. Monthly injections of longacting penicillin must be given for a period of five years in patients having one attack of rheumatic fever. If there is evidence of carditis, the length of therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.

Vaccine

No vaccines are currently available to protect against S. pyogenes infection, although there has been research into the development of one. Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine.^[24]

Infection

Patients with positive cultures for Streptococcus pyogenes should be treated with penicillin as long as allergy is not present. This treatment will not alter the course of the acute disease.

The most appropriate treatment stated in the Oxford Handbook of Clinical Medicine for rheumatic fever is benzathine benzylpenicillin.

Inflammation

Patients with significant symptoms may require corticosteroids. Salicylates are useful for pain.

Heart failure

Some patients develop significant carditis which manifests as congestive heart failure. This requires the usual treatment for heart failure: ACE inhibitors, diuretics, beta blockers, and digoxin. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.

Epidemiology

Disability-adjusted life year for rheumatic heart disease per 100,000 inhabitants in 2004.^[25]

no data

less than 20

20–40

40–60

60–80

80–100

100–120

120–140

140–160

160–180

180–200

200–330

more than 330

Rheumatic fever is common worldwide and responsible for many cases of damaged heart valves. As of 2010 globally it resulted in 345,000 deaths, down from 463,000 in 1990.^[26]

In Western countries, it became fairly rare since the 1960s, probably due to widespread use of antibiotics to treat streptococcus infections. While it has been far less common in the United States since the beginning of the 20th century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a case-fatality rate of 2–5%.^[27]

Rheumatic fever primarily affects children between ages 5 and 17 years and occurs approximately 20 days after strep throat. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The incidence of recurrence with a subsequent untreated infection is substantially greater (about 50%).^[28] The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.

The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode. Heart complications may be long-term and severe, particularly if valves are involved.

Survivors of rheumatic fever often have to take penicillin to prevent streptococcal infection which could possibly lead to another case of rheumatic fever that could prove fatal.

History

References

^ ^a ^b ^c Kumar, Vinay; Abbas, Abul K; Fausto, Nelson; Mitchell, Richard N (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 403–6. ISBN 978-1-4160-2973-1 .
^ "rheumatic fever" at Dorland's Medical Dictionary
^ Jones, T Duckett (1944). "The diagnosis of rheumatic fever". JAMA 126 (8): 481–4. doi:10.1001/jama.1944.02850430015005.
^ Ferrieri, P; Jones Criteria Working, Group (2002). "Proceedings of the Jones Criteria workshop". Circulation (Jones Criteria Working Group) 106 (19): 2521–3. doi:10.1161/01.CIR.0000037745.65929.FA. PMID 12417554.
^ Parrillo, Steven J. "Rheumatic Fever". eMedicine. DO, FACOEP, FACEP. Retrieved 14 July 2007.
^ "Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 update". JAMA (Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association) 268 (15): 2069–73. 1992. doi:10.1001/jama.268.15.2069. PMID 1404745.
^ Saxena, Anita (2000). "Diagnosis of rheumatic fever: Current status of Jones criteria and role of echocardiography". Indian Journal of Pediatrics 67 (4): 283–6. doi:10.1007/BF02758174. PMID 11129913.
^ Kumar, RK; Tandon, R (2013). "Rheumatic fever & rheumatic heart disease: The last 50 years". The Indian Journal of Medical Research 137 (4): 643–658. PMC 3724245.
^ Aly, Ashraf (2008). "Rheumatic Fever". Core Concepts of Pediatrics. University of Texas. Retrieved 6 August 2011.
^ ^a ^b Ed Boon, Davidson's General Practice of Medicine, 20th edition. P. 617.
^ Abbas, Abul K.; Lichtman, Andrew H.; Baker, David L.; et al (2004). Basic immunology: functions and disorders of the immune system (2 ed.). Philadelphia, Pennsylvania: Elsevier Saunders. ISBN 978-1-4160-2403-3.
^ Faé KC, da Silva DD, Oshiro SE, et al. (May 2006). "Mimicry in recognition of cardiac myosin peptides by heart-intralesional T cell clones from rheumatic heart disease". J. Immunol. 176 (9): 5662–70. PMID 16622036.
^ ^a ^b Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0187-1.
^ Kaplan, MH; Bolande, R; Rakita, L; Blair, J (1964). "Presence of Bound Immunoglobulins and Complement in the Myocardium in Acute Rheumatic Fever. Association with Cardiac Failure". The New England journal of medicine 271 (13): 637–45. doi:10.1056/NEJM196409242711301. PMID 14170842.
^ ^a ^b Brice, Edmund A. W; Commerford, Patrick J. (2005). "Rheumatic Fever and Valvular Heart Disease". In Rosendorff, Clive. Essential Cardiology: Principles and Practice. Totowa, New Jersey: Humana Press. pp. 545–563. doi:10.1007/978-1-59259-918-9_30. ISBN 978-1-59259-918-9.
^ Caldas, AM; Terreri, MT; Moises, VA; Silva, CM; Len, CA; Carvalho, AC; Hilário, MO (2008). "What is the true frequency of carditis in acute rheumatic fever? A prospective clinical and Doppler blind study of 56 children with up to 60 months of follow-up evaluation". Pediatric cardiology 29 (6): 1048–53. doi:10.1007/s00246-008-9242-z. PMID 18825449.
^ Guilherme, L; Kalil, J; Cunningham, M (2006). "Molecular mimicry in the autoimmune pathogenesis of rheumatic heart disease". Autoimmunity 39 (1): 31–9. doi:10.1080/08916930500484674. PMID 16455580.
^ Kemeny, E; Grieve, T; Marcus, R; Sareli, P; Zabriskie, JB (1989). "Identification of mononuclear cells and T cell subsets in rheumatic valvulitis". Clinical immunology and immunopathology 52 (2): 225–37. doi:10.1016/0090-1229(89)90174-8. PMID 2786783.
^ ^a ^b Roberts, S; Kosanke, S; Terrence Dunn, S; Jankelow, D; Duran, CM; Cunningham, MW (2001). "Pathogenic mechanisms in rheumatic carditis: Focus on valvular endothelium". The Journal of infectious diseases 183 (3): 507–11. doi:10.1086/318076. PMID 11133385.
^ ^a ^b ^c Stanevicha, V; Eglite, J; Sochnevs, A; Gardovska, D; Zavadska, D; Shantere, R (2003). "HLA class II associations with rheumatic heart disease among clinically homogeneous patients in children in Latvia". Arthritis Research & Therapy 5 (6): R340–R346. doi:10.1186/ar1000. PMC 333411.
^ Schafranski, MD; Pereira Ferrari, L; Scherner, D; Torres, R; Jensenius, JC; De Messias-Reason, IJ (2008). "High-producing MBL2 genotypes increase the risk of acute and chronic carditis in patients with history of rheumatic fever". Molecular immunology 45 (14): 3827–31. doi:10.1016/j.molimm.2008.05.013. PMID 18602696.
^ Ramasawmy, R; Spina, GS; Fae, KC; Pereira, AC; Nisihara, R; Messias Reason, IJ; Grinberg, M; Tarasoutchi, F; Kalil, J; Guilherme, L. (2008). "Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology". Clinical and Vaccine Immunology : CVI 15 (6): 932–936. doi:10.1128/CVI.00324-07. PMC 2446618.
^ "What About My Child and Rheumatic Fever?" (PDF). American Heart Association. Retrieved 23 February 2014.
^ "Initiative for Vaccine Research (IVR) - Group A Streptococcus". World Health Organization. Retrieved 15 June 2012.
^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.
^ Lozano, R; Naghavi, M; Foreman, K; Lim, S; Shibuya, K; Aboyans, V; Abraham, J; Adair, T; Aggarwal, R (15 December 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2095–128. doi:10.1016/S0140-6736(12)61728-0. PMID 23245604.
^ "Rheumatic fever". Medline Plus Medical Encyclopedia. NLM/NIH .
^ Porth, Carol (2007). Essentials of pathophysiology: concepts of altered health states. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7087-4.

External links

Rheumatic fever information from Seattle Children's Hospital Heart Center
Jones major criteria, Mnemonic
Rheumatic Heart Disease Network

UpToDate Contents

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1. リウマチ性心疾患の自然史、スクリーニング、およびマネージメント natural history screening and management of rheumatic heart disease
2. 急性リウマチ熱の臨床症状および診断 clinical manifestations and diagnosis of acute rheumatic fever
3. 急性リウマチ熱の治療および予防 treatment and prevention of acute rheumatic fever
4. 僧帽弁狭窄症の臨床症状および診断 clinical manifestations and diagnosis of mitral stenosis
5. 急性リウマチ熱の疫学および病因 epidemiology and pathogenesis of acute rheumatic fever

English Journal

The heart and pediatric rheumatology.

Vogel T, Kitcharoensakkul M, Fotis L, Baszis K.Author information Division of Rheumatology, Department of Pediatrics, Washington University School of Medicine, Box 8116, One Children's Place, St Louis, MO 63110, USA; Division of Rheumatology, Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA.AbstractRecent advances in Kawasaki disease have included attempts to define genes involved in its pathogenesis. There have been recent advances in the studies of rheumatic carditis, leading to a better understanding of the mechanism of the disease. Histologic evaluation of patients with neonatal lupus erythematosus has revealed fibrosis with collagen deposition and calcification of the atrioventricular node. Therapy for cardiac involvement in systemic juvenile idiopathic arthritis should involve treatment of the underlying disease and systemic inflammatory state, and typically includes nonsteroidal antiinflammatory drugs, corticosteroids, disease-modifying drugs, and biologic therapies targeting tumor necrosis factor-alpha, interleukin-1, and interleukin-6.
Rheumatic diseases clinics of North America.Rheum Dis Clin North Am.2014 Feb;40(1):61-85. doi: 10.1016/j.rdc.2013.10.008.
Recent advances in Kawasaki disease have included attempts to define genes involved in its pathogenesis. There have been recent advances in the studies of rheumatic carditis, leading to a better understanding of the mechanism of the disease. Histologic evaluation of patients with neonatal lupus eryt
PMID 24268010

The heart in vasculitis.

Miloslavsky E, Unizony S.Author information Rheumatology Unit, Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Yawkey 2, 55 Fruit Street, Boston, MA 02114, USA.AbstractAll primary vasculitides can target the heart, but this complication is more frequent in TAK, PAN, and EGPA. Although pericarditis is seen in virtually all forms of vasculitis, it rarely becomes a significant clinical problem. Myocarditis is more prevalent in EGPA and TAK, and coronary angiitis is most common in TAK, PAN, and BD. In addition, AI is a classic complication of TAK-induced aortitis, and intracavitary cardiac thrombus formation mainly affects patients with BD. Myocarditis, coronary arteritis, and valvular disease can lead to congestive heart failure and represent poor prognostic factors that require aggressive therapy. Imaging and pathology studies have found that subclinical involvement is common (e.g., TAK, PAN, EGPA, GPA, and BD). Management differs depending on the cardiac structure involved and the activity of the disease.Although pericarditis can be treated with NSAIDs, colchicine, or-low dose prednisone, myocarditis and coronary vasculitis require high doses of CS and frequently cytotoxic agents. Valvular lesions, coronary arteriopathy, and ventricular thrombosis often need surgical intervention. In the face of active disease, clinical judgment is important to help weigh the risks and benefits of delaying surgery versus operating in possibly inflamed tissues. As in other rheumatic diseases, risks factors for atherosclerosis (eg, hypertension, dyslipidemia) should be identified and corrected. Finally, heart failure–and ischemia-targeted therapies are important components of the treatment strategy when indicated.
Rheumatic diseases clinics of North America.Rheum Dis Clin North Am.2014 Feb;40(1):11-26. doi: 10.1016/j.rdc.2013.10.006.
All primary vasculitides can target the heart, but this complication is more frequent in TAK, PAN, and EGPA. Although pericarditis is seen in virtually all forms of vasculitis, it rarely becomes a significant clinical problem. Myocarditis is more prevalent in EGPA and TAK, and coronary angiitis is m
PMID 24268007

The heart in inflammatory myopathies.

Van Gelder H, Charles-Schoeman C.Author information Division of Rheumatology, Department of Internal Medicine, Olive View-UCLA Medical Center, Los Angeles, CA, USA.AbstractSystemic autoimmune diseases are becoming increasingly linked to accelerated risks of cardiovascular disease and events. What is apparent from the above review is that the IIM are not an exception to this growing pattern. Although not always clinically apparent, there seems to be a large percentage of patients who have subclinical CV involvement. Many of the traditional risk factors for CAD, such as hypertension and hyperlipidemia, are associated with developing cardiac involvement in patients with IIM. At this time, it is unclear how much of the atherosclerotic CV morbidity and mortality in IIM patients is driven by traditional CV risk factors versus the effects of chronic systemic inflammation from the underlying IIM. The effects of immunosuppression on cardiac disease and events in IIM patients requires further investigation in carefully controlled studies. IIM patients with cardiac involvement are at increased risk for overall mortality when compared with IIM patients without CV disease. The risk of severe cardiac and vascular disease complications seems to be higher than that of the general population. Treatments can be focused on preventing traditional cardiovascular risk factors including avoidance of corticosteroids when possible, although this task remains challenging in IIM as is true of other rheumatic diseases. Once complications do develop, they should be managed similarly to patients without IIM. The use of statins for hyperlipidemia and atherosclerosis in IIM is an area that is in need of further investigation, although initial work suggests that their use is not uncommon by IIM specialists. Further work is needed to determine whether aggressive immunosuppressive treatment of patients with subclinical cardiac disease will lead to better outcomes. Work is also needed in the area of better laboratory, imaging, and serologic testing to identify patients at risk for the worst cardiovascular complications. At this point, based on the body of evidence reviewed here and elsewhere, it is imperative that physicians treating IIM patients performa routine cardiovascular risk assessment at the onset of diagnosis. Appropriate diagnostic and monitoring studies should be performed on those patients who screening history or examination is suggestive of cardiac involvement.
Rheumatic diseases clinics of North America.Rheum Dis Clin North Am.2014 Feb;40(1):1-10. doi: 10.1016/j.rdc.2013.10.002.
Systemic autoimmune diseases are becoming increasingly linked to accelerated risks of cardiovascular disease and events. What is apparent from the above review is that the IIM are not an exception to this growing pattern. Although not always clinically apparent, there seems to be a large percentage
PMID 24268006

Japanese Journal

3. 弁膜症(<特集>日本の心臓・大血管外科レベルは欧米を超えているか?)

橋本和弘
日本外科学会雑誌 113(3), 278-282, 2012-05-01
NAID 110009445213

Mitral Valve Repair in a Patient with Myelodysplastic Syndrome

OMOTO Tadashi,HIROTA Masanori,ISHIKAWA Noboru,TEDORIYA Takeo
Annals of thoracic and cardiovascular surgery 17(6), 614-617, 2011-12-01
… Open heart operations for patients with myelodysplastic syndrome (MDS) are associated with infective and bleeding complications. … We report a 67-year-old woman with rheumatic, severe mitral regurgitation and mitral stenosis associated with MDS who underwent a mitral valve (MV) repair. … Although the feasibility of MV repair is low in patients with restrictive pathology due to rheumatic disease, MV repair may be preferred in patients with MDS. …
NAID 10030235581

Progression of Isolated Tricuspid Regurgitation Late After Left-Sided Valve Surgery : Clinical Features and Mechanisms

IZUMI Chisato,MIYAKE Makoto,TAKAHASHI Shuichi,MATSUTANI Hayato,HASHIWADA Sumiyo,KUWANO Kazuyo,HAYASHI Hidetaka,NAKAJIMA Seiko,NISHIGA Masataka,HANAZAWA Koji,SAKAMOTO Jiro,KONDO Hirokazu,TAMURA Toshihiro,KAITANI Kazuaki,YAMANAKA Kazuo,NAKAGAWA Yoshihisa
Circulation journal : official journal of the Japanese Circulation Society 75(12), 2902-2907, 2011-11-25
… Background: Severe tricuspid regurgitation (TR) sometimes develops late after left-sided valve surgery without left heart failure, pulmonary hypertension or rheumatic tricuspid valve. … Conclusions: Severe isolated TR developing late after mitral valve surgery is not uncommon, thus it is important to recognize this disease entity. …
NAID 10030033699

「rheumatic valvular disease」

Rheumatic fever
	Classification and external resources
	Streptococcus pyogenes bacteria (Pappenheim's stain). Rheumatic fever is an autoimmune disease in which the body's own antibodies to strep attack different parts of a person's body such as the heart valves, the brain's basal ganglia, and the joints.
ICD-10	I00-I02
ICD-9	390–392
DiseasesDB	11487
MedlinePlus	003940
eMedicine	med/3435 med/2922 emerg/509 ped/2006
MeSH	D012213

　　[★]

関: rheumatic heart disease
同: RHD

「リウマチ性心疾患」

　　[★]

英: rheumatic heart disease
関

「disease」

　　[★]

n.

疾患：illnessより厳密な概念。「ある臓器に明確な障害が確認され、それによって症状が出ているとはっきり説明できる場合」 (PSY.9)

特定の原因、病態生理、症状、経過、予後、病理組織所見が全てそろった場合 (PSY.9)

something that is very wrong with people's attitudes, way of life or with society.

関: ail、ailment、disease entity、disorder、ill、illness、malady、sick、sickness

注意

disease ≠ illness ≠ disorder

「hearing」

　　[★]

n。

聴力、聴覚。聞くこと、聴取。聞こえる距離/範囲。聞いてやること、傾聴。聞いてもらうこと、発言の機会。(委員会などの)聴聞会、ヒアリング。(法)審問、尋問。

「rheumatic」

　　[★]

adj.

リウマチ性の、リウマチの

関: rheumatica、rheumatism、rheumatoid

「hear」

　　[★]

v.

聞く、聞こえる

「heart」

　　[★] 心臓

[Robbins-1] Kumar, Vinay; Abbas, Abul K; Fausto, Nelson; Mitchell, Richard N (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 403–6. ISBN 978-1-4160-2973-1 .

[2] "rheumatic fever" at Dorland's Medical Dictionary

[3] Jones, T Duckett (1944). "The diagnosis of rheumatic fever". JAMA 126 (8): 481–4. doi:10.1001/jama.1944.02850430015005.

[4] Ferrieri, P; Jones Criteria Working, Group (2002). "Proceedings of the Jones Criteria workshop". Circulation (Jones Criteria Working Group) 106 (19): 2521–3. doi:10.1161/01.CIR.0000037745.65929.FA. PMID 12417554.

[5] Parrillo, Steven J. "Rheumatic Fever". eMedicine. DO, FACOEP, FACEP. Retrieved 14 July 2007.

[6] "Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 update". JAMA (Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association) 268 (15): 2069–73. 1992. doi:10.1001/jama.268.15.2069. PMID 1404745.

[7] Saxena, Anita (2000). "Diagnosis of rheumatic fever: Current status of Jones criteria and role of echocardiography". Indian Journal of Pediatrics 67 (4): 283–6. doi:10.1007/BF02758174. PMID 11129913.

[8] Kumar, RK; Tandon, R (2013). "Rheumatic fever & rheumatic heart disease: The last 50 years". The Indian Journal of Medical Research 137 (4): 643–658. PMC 3724245.

[9] Aly, Ashraf (2008). "Rheumatic Fever". Core Concepts of Pediatrics. University of Texas. Retrieved 6 August 2011.

[davidson617-10] Ed Boon, Davidson's General Practice of Medicine, 20th edition. P. 617.

[11] Abbas, Abul K.; Lichtman, Andrew H.; Baker, David L.; et al (2004). Basic immunology: functions and disorders of the immune system (2 ed.). Philadelphia, Pennsylvania: Elsevier Saunders. ISBN 978-1-4160-2403-3.

[12] Faé KC, da Silva DD, Oshiro SE, et al. (May 2006). "Mimicry in recognition of cardiac myosin peptides by heart-intralesional T cell clones from rheumatic heart disease". J. Immunol. 176 (9): 5662–70. PMID 16622036.

[RobbinsPath-13] Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0187-1.

[14] Kaplan, MH; Bolande, R; Rakita, L; Blair, J (1964). "Presence of Bound Immunoglobulins and Complement in the Myocardium in Acute Rheumatic Fever. Association with Cardiac Failure". The New England journal of medicine 271 (13): 637–45. doi:10.1056/NEJM196409242711301. PMID 14170842.

[essential-15] Brice, Edmund A. W; Commerford, Patrick J. (2005). "Rheumatic Fever and Valvular Heart Disease". In Rosendorff, Clive. Essential Cardiology: Principles and Practice. Totowa, New Jersey: Humana Press. pp. 545–563. doi:10.1007/978-1-59259-918-9_30. ISBN 978-1-59259-918-9.

[16] Caldas, AM; Terreri, MT; Moises, VA; Silva, CM; Len, CA; Carvalho, AC; Hilário, MO (2008). "What is the true frequency of carditis in acute rheumatic fever? A prospective clinical and Doppler blind study of 56 children with up to 60 months of follow-up evaluation". Pediatric cardiology 29 (6): 1048–53. doi:10.1007/s00246-008-9242-z. PMID 18825449.

[17] Guilherme, L; Kalil, J; Cunningham, M (2006). "Molecular mimicry in the autoimmune pathogenesis of rheumatic heart disease". Autoimmunity 39 (1): 31–9. doi:10.1080/08916930500484674. PMID 16455580.

[18] Kemeny, E; Grieve, T; Marcus, R; Sareli, P; Zabriskie, JB (1989). "Identification of mononuclear cells and T cell subsets in rheumatic valvulitis". Clinical immunology and immunopathology 52 (2): 225–37. doi:10.1016/0090-1229(89)90174-8. PMID 2786783.

[Roberts-19] Roberts, S; Kosanke, S; Terrence Dunn, S; Jankelow, D; Duran, CM; Cunningham, MW (2001). "Pathogenic mechanisms in rheumatic carditis: Focus on valvular endothelium". The Journal of infectious diseases 183 (3): 507–11. doi:10.1086/318076. PMID 11133385.

[Stanevicha-20] Stanevicha, V; Eglite, J; Sochnevs, A; Gardovska, D; Zavadska, D; Shantere, R (2003). "HLA class II associations with rheumatic heart disease among clinically homogeneous patients in children in Latvia". Arthritis Research & Therapy 5 (6): R340–R346. doi:10.1186/ar1000. PMC 333411.

[21] Schafranski, MD; Pereira Ferrari, L; Scherner, D; Torres, R; Jensenius, JC; De Messias-Reason, IJ (2008). "High-producing MBL2 genotypes increase the risk of acute and chronic carditis in patients with history of rheumatic fever". Molecular immunology 45 (14): 3827–31. doi:10.1016/j.molimm.2008.05.013. PMID 18602696.

[22] Ramasawmy, R; Spina, GS; Fae, KC; Pereira, AC; Nisihara, R; Messias Reason, IJ; Grinberg, M; Tarasoutchi, F; Kalil, J; Guilherme, L. (2008). "Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology". Clinical and Vaccine Immunology : CVI 15 (6): 932–936. doi:10.1128/CVI.00324-07. PMC 2446618.

[aha-23] "What About My Child and Rheumatic Fever?" (PDF). American Heart Association. Retrieved 23 February 2014.

[24] "Initiative for Vaccine Research (IVR) - Group A Streptococcus". World Health Organization. Retrieved 15 June 2012.

[25] "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.

[Loz2012-26] Lozano, R; Naghavi, M; Foreman, K; Lim, S; Shibuya, K; Aboyans, V; Abraham, J; Adair, T; Aggarwal, R (15 December 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2095–128. doi:10.1016/S0140-6736(12)61728-0. PMID 23245604.

[27] "Rheumatic fever". Medline Plus Medical Encyclopedia. NLM/NIH .

[28] Porth, Carol (2007). Essentials of pathophysiology: concepts of altered health states. Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7087-4.

リンク元	「rheumatic valvular disease」「リウマチ性心疾患」
関連記事	「disease」「hearing」「rheumatic」「hear」「heart」

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案内

案内

rheumatic heart disease