関: hypersensitivity pneumonitis

WordNet

characterized by or caused by allergy; "an allergic reaction"
having an allergy or peculiar or excessive susceptibility (especially to a specific factor); "allergic children"; "hypersensitive to pollen" (同)hypersensitive, hypersensitized, hypersensitised, sensitized, sensitised, supersensitive, supersensitized, supersensitised
not forming an essential part of a thing or arising or originating from the outside; "extrinsic evidence"; "an extrinsic feature of the new building"; "that style is something extrinsic to the subject"; "looking for extrinsic aid"
inflammation in the socket of a tooth; sometimes occurs after a tooth is extracted and a blood clot fails to form (同)dry_socket
inflammation of the alveoli in the lungs caused by inhaling dust; with repeated exposure the condition may become chronic

PrepTutorEJDIC

アレルギー性の;(…に)アレルギーを起こす《+『to』+『名』》 / 《補語にのみ用いて》《話》(…に)神経過敏の,(…が)大きらいの《+『to』+『名』(do『ing)』》
固有でない付帯的な;(…にとって)非本質的な《+『to』+『名』》

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/18 00:20:25」(JST)

wiki en

Hypersensitivity pneumonitis (HP; also called extrinsic allergic alveolitis, EAA) is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts. Sufferers are commonly exposed to the dust by their occupation or hobbies.

Pathophysiology

Hypersensitivity pneumonitis involves inhalation of an antigen. This leads to an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity occur in hypersensitivity pneumonitis.^[1]

Symptoms

Hypersensitivity pneumonitis (HP) is categorized as acute, subacute, and chronic based on the duration of the illness.^[2]

Acute

In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.^[3]

Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.^[3]

On chest radiographs, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients." In high-resolution CT scans, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO). Many patients have hypoxemia at rest, and all patients desaturate with exercise.^[3]

Subacute

Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones.^[3] Findings may be present in patients who have experienced repeated acute attacks.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.^[3]

Chronic

In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.^[3]

On chest radiographs, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans.^[3]

Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) associated with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.^[3]

In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise.

Diagnosis

The diagnosis is based upon a history of symptoms after exposure to the allergen and clinical tests. A physician may take blood tests, seeking signs of inflammation, a chest X-ray and lung function tests. The sufferer shows a restrictive loss of lung function.

Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity.^[4]^[5] Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.^[6]

Lung biopsy

Low magnification micrograph of hypersensitivity pneumonitis showing multinucleated giant cells and a centrilobular fibrosis. Trichrome stain.

Lung biopsies are rarely diagnostic, but may help intensify the search for an allergen, as certain characteristics may suggest the diagnosis.

The differential diagnosis of hypersensitivity pneumonitis is, primarily, a group of diseases known as idiopathic interstitial pneumonias.^[7] This group of diseases includes idiopathic pulmonary fibrosis (IPF) (which manifests histologically as usual interstitial pneumonia (UIP)), idiopathic non-specific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia, among others.

Hypersensitivity pneumonitis may manifest, histologically, as usual interstitial pneumonia, i.e. it looks like idiopathic pulmonary fibrosis under the microscope; however, certain features may suggest it is a hypersensitivity pneumonitis. UIP does not typically have multinucleated giant cells, nor does it typically have a centrilobular distribution;^[7] the presence of these features suggest the diagnosis of hypersensitivity pneumonitis.

The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help. This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated. Thus, a lung biopsy, in some cases, may make a decisive difference.

Types

Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen. These include:

Type^[8]	Specific antigen	Exposure
Bird fancier's lung Also called bird breeder's lung, pigeon breeder's lung, and poultry worker's lung	Avian proteins	Feathers and bird droppings ^[9]
Bagassosis	Thermophilic actinomycetes^[9]	Moldy bagasse (pressed sugarcane)
Cephalosporium HP	Cephalosporium	Contaminated basements (from sewage)
Cheese-washer's lung	Penicillum casei^[9] or P. roqueforti	Cheese casings
Chemical worker’s lung - Isocyanate HP	Toluene diisocyanate (TDI), Hexamethylene diisocyanate (HDI), or Methylene bisphenyl isocyanate (MDI)	Paints, resins, and polyurethane foams
Chemical worker's lung^[9] - Trimellitic anhydride (TMA) HP	Trimellitic anhydride^[9]	Plastics, resins, and paints
Coffee worker's lung	Coffee bean protein	Coffee bean dust
Compost lung	Aspergillus	Compost
Detergent worker's disease	Bacillus subtilis enzymes	Detergent
Familial HP Also called Domestic HP	Bacillus subtilis, puffball spores	Contaminated walls
Farmer's lung	The molds Thermophilic actinomycetes^[9] Aspergillus species Saccharopolyspora rectivirgula, and Micropolyspora faeni	Moldy hay
Hot tub lung	Mycobacterium avium complex	Mist from hot tubs
Humidifier lung	The bacteria Thermoactinomyces candidus Bacillus subtilis Bacillus cereus, and Klebsiella oxytoca; Thermophilic actinomycetes^[9] the fungi Aureobasidium pullulans;^[9] and the amoebae Naegleria gruberi, Acanthamoeba polyhaga, and Acanthamoeba castellani.	Mist generated by a machine from standing water
Japanese summer house HP Also called Japanese summer-type HP	Trichosporon cutaneum	Damp wood and mats
Laboratory worker's lung	Male rat urine protein	Laboratory rats
Lycoperdonosis	Puffball spores	Spore dust from mature puffballs^[10]
Malt worker's lung	Aspergillus clavatus^[9]	Moldy barley
Maple bark disease	Cryptostroma corticale^[9]	Moldy maple bark
Metalworking fluids HP	Nontuberculous mycobacteria	Mist from metalworking fluids
Miller's lung	Sitophilus granarius (wheat weevil)^[9]	Dust-contaminated grain^[9]
Mollusc shell HP	Aquatic animal proteins	Mollusc shell dust
Mushroom worker's lung	Thermophilic actinomycetes	Mushroom compost
Peat moss worker's lung	Caused by Monocillium sp. and Penicillium citreonigrum	Peat moss
Pituitary snuff taker's lung	Pituitary snuff	Medication
Sauna worker's lung	Aureobasidium, Graphium spp	Contaminated sauna water
Sequoiosis	Aureobasidium, Graphium spp	Redwood bark, sawdust
Streptomyces HP	Streptomyces albus	Contaminated fertilizer
Suberosis	Penicillium glabrum (formerly known as Penicillium frequentans)	Moldy cork dust
Tap water HP	Unknown	Contaminated tap water
Thatched roof disease	Saccharomonospora viridis	Dried grass
Tobacco worker's lung	Aspergillus spp	Moldy tobacco
Wine-grower's lung	Botrytis cinerea mold	Moldy grapes
Woodworker's lung	Alternaria, Penicillium spp	Wood pulp, dust

Of these types, Farmer's Lung and Bird-Breeder's Lung are the most common. "Studies document 8-540 cases per 100,000 persons per year for farmers and 6000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Prevalence varies by region, climate, and farming practices. HP affects 0.4-7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk." ^[3]

Treatment

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.^[11]

Additional images

High magnification micrograph of hypersensitivity pneumonitis showing granulomatous inflammation. Trichrome stain.

References

^ Mohr LC (September 2004). "Hypersensitivity pneumonitis". Curr Opin Pulm Med 10 (5): 401–11. doi:10.1097/01.mcp.0000135675.95674.29. PMID 15316440. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1070-5287&volume=10&issue=5&spage=401.
^ http://www.ucsfhealth.org/adult/medical_services/pulmonary/ild/conditions/hp/signs.html signs and symptoms
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Sharma, Sat. Hypersensitivity Pneumonitis. eMedicine, June 1, 2006.
^ "Lecture 14: Hypersensitivity". http://www-immuno.path.cam.ac.uk/~immuno/part1/lec13/lec13_97.html. Retrieved 2008-09-18.
^ "Allergy & Asthma Disease Management Center: Ask the Expert". http://www.aaaai.org/aadmc/ate/category.asp?cat=1008. Retrieved 2008-09-18.
^ Page 503 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.
^ ^a ^b Ohtani Y, Saiki S, Kitaichi M, et al. (August 2005). "Chronic bird fancier's lung: histopathological and clinical correlation. An application of the 2002 ATS/ERS consensus classification of the idiopathic interstitial pneumonias". Thorax 60 (8): 665–71. doi:10.1136/thx.2004.027326. PMC 1747497. PMID 16061708. http://thorax.bmj.com/cgi/pmidlookup?view=long&pmid=16061708.
^ Enelow, RI (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1161–72. ISBN 0-07-145739-9.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l Kumar 2007, Table 13-5
^ Munson EL, Panko DM, Fink JG. (1997). "Lycoperdonosis: Report of two cases and discussion of the disease". Clinical Microbiology Newsletter 19 (3): 17–24. doi:10.1016/S0196-4399(97)89413-5.
^ [1]

Oxford Handbook of Clinical Medicine

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 過敏性肺臓炎（外因性アレルギー性肺胞炎）の診断 diagnosis of hypersensitivity pneumonitis extrinsic allergic alveolitis
2. 過敏性肺臓炎（外因性アレルギー性肺胞炎）の治療および予後 treatment and prognosis of hypersensitivity pneumonitis extrinsic allergic alveolitis
3. 過敏性肺臓炎（外因性アレルギー性肺胞炎）の疫学および原因 epidemiology and causes of hypersensitivity pneumonitis extrinsic allergic alveolitis
4. 過敏性肺臓炎（外因性アレルギー性肺胞炎）の分類および臨床症状 classification and clinical manifestations of hypersensitivity pneumonitis extrinsic allergic alveolitis
5. 非特異的間質性肺炎 nonspecific interstitial pneumonia

English Journal

New occupational and environmental causes of asthma and extrinsic allergic alveolitis.

Fishwick D.SourceCentre for Workplace Health, Health and Safety Laboratories, The University of Sheffield, Harpur Hill, Buxton, Derbyshire SK17 3JN, UK. Electronic address: d.fishwick@sheffield.ac.uk.
Clinics in chest medicine.Clin Chest Med.2012 Dec;33(4):605-16. doi: 10.1016/j.ccm.2012.07.002.
Asthma and extrinsic allergic alveolitis (EAA) remain prevalent respiratory diseases and the cause of a significant disease burden. This article reviews the recent occupational and environmental causes described for these conditions. Even over the limited time spam addressed by this article, novel a
PMID 23153603

Between-laboratory quality control of automated analysis of IgG antibodies against Aspergillus fumigatus.

van Toorenenbergen AW.SourceDepartment of Clinical Chemistry, Erasmus University Medical Center, Rotterdam, Netherlands. Electronic address: a.w.vantoorenenbergen@erasmusmc.nl.
Diagnostic microbiology and infectious disease.Diagn Microbiol Infect Dis.2012 Nov;74(3):278-81. doi: 10.1016/j.diagmicrobio.2012.07.002. Epub 2012 Aug 25.
Measurement of IgG antibodies against Aspergillus fumigatus is an important criterion for the diagnosis of aspergilloma, allergic bronchopulmonary aspergillosis, and extrinsic allergic alveolitis. In the present study, we compared IgG antibody analysis against A. fumigatus using 2 widely used automa
PMID 22925654

Japanese Journal

Increased Prevalence of High Anti-Cladosporium Antibody Titers in Interstitial Lung Diseases

WATANUKI Zenta,OKADA Shinji,CHIBA Shigeki,KAMEI Katsuhiko,SUZUKI Yasuko,YAMADA Norihiro
Tohoku journal of experimental medicine 226(4), 287-291, 2012-04-01
NAID 10030612920

Increased Prevalence of High Anti-Cladosporium Antibody Titers in Interstitial Lung Diseases

Watanuki Zenta,Okada Shinji,Chiba Shigeki,Kamei Katsuhiko,Suzuki Yasuko,Yamada Norihiro
The Tohoku Journal of Experimental Medicine 226(4), 287-291, 2012
Interstitial lung diseases (ILDs) represent a large group of different diseases, with a large part comprising idiopathic interstitial pneumonias. Differentiating hypersensitivity pneumonitis (HP), es …
NAID 130004459973

Extrinsic allergic alveolitis with eosinophil infiltration induced by 1,1,1,2-tetrafluoroethane (HFC-134a): A case report

Ishiguro Takashi,Yasui Masahide,Nakade Yusuke,Kimura Hideharu,Katayama Nobuyuki,Kasahara Kazuo,Fujimura Masaki
Internal Medicine 46(17), 1455-1457, 2007
… We then determined the patient's diagnosis to be extrinsic allergic alveolits with eosnophil infiltration, caused by HFC134a. …
NAID 130000076070

Related Pictures

★リンクテーブル★

リンク元	「過敏性肺臓炎」「外因性アレルギー性肺胞炎」「外因性アレルギー性胞隔炎」
関連記事	「allergic」「extrinsic」「allergic alveolitis」

「過敏性肺臓炎」

Hypersensitivity pneumonitis
	Classification and external resources
	; Micrograph of hypersensitivity pneumonitis. Lung biopsy. Trichrome stain.
ICD-10	J67
ICD-9	495
DiseasesDB	4630
MedlinePlus	000109
eMedicine	med/1103 ped/2577
MeSH	D000542

　　[★]

pneumonitis
英: hypersensitivity pneumonitis, HP
同: 過敏性肺炎、外因性アレルギー性肺胞炎 extrinsic allergic alveolitis
関: セコイア症、夏型過敏性肺炎

[show details]

過敏性肺臓炎 : 約 56,300 件
過敏性肺炎 : 約 102,000 件

概念

種々の有機性粉塵を感受性のあるヒトが反復吸入した結果、粉塵中の抗原成分によって惹起される呼吸困難、発熱などをきたす疾患群。
非乾酪性の類上皮細胞性肉芽腫の形成を伴う間質性肺炎である。
肺の炎症性疾患であり、肺胞壁や終末の気道も侵される。
本態はIII型アレルギーおよびIV型アレルギー(慢性期。Th1サイトカインによる肉芽腫形成)である。
外因性アレルギー性胞隔炎extrinsic allergic alveolitisとも呼ばれる。

病型

急性
亜急性
慢性

病因

抗原に感作された人に対する抗原の再暴露により生じる
抗原は種々ある。

病因による分類

夏型過敏性肺臓炎
加湿器肺
空調病
農夫肺
砂糖キビ肺症
鳥飼病
ハト飼病
木屑病
草屋病
キノコ栽培者肺病
毛皮商人肺
コーヒー労働者肺症
チーズ洗い病
楓皮病
コルク肺
麦芽労働者肺
痘苗病
養蚕従事者肺
たたみ職人肺
空洞病
加湿器肺

疫学

IMD

夏型過敏性肺炎：80%。屋内のカビ。日本では8-9月に多い。
農夫肺：8.1%。干草中の真菌。
換気装置肺炎：4.3%
鳥飼病：4.1%

病態

IMD

III型アレルギーの関与

抗原曝露後約4-6時間で発症。抗原除去により6-8時間後に自然消退。
皮内反応：アルサス型
BALF・血清中に抗原特異的IgG・IgAの出現
急性期のBALFには好中球が増加

IV型アレルギーの関与

肺生検において、肉芽腫形成。間質性肺炎(マクロファージ・リンパ球の浸潤)。
BALFにおいて、リンパ球の増加がみられる

病理

病理組織学的には、肺胞壁のリンパ球を主体とした細胞浸潤、肺胞壁とそれに隣接した細気管支領域にみられる類上皮細胞肉芽腫病変が主要所見である。　→　肉芽腫性間質性肺炎

身体所見

両側の下肺野？に捻髪音。
慢性型：ばち指

症状

HIM.1607

急性型：(抗原暴露後6-8時間より)咳、発熱、悪寒、全身倦怠感、呼吸困難
亜急性型：(数週間かけて潜行性に発症)咳、呼吸困難－(次第に悪化)→チアノーゼ、重度の呼吸困難。急性型の病型で、抗原が除去されない場合に亜急性に移行することがある。急性・亜急性型はいずれも抗原除去により数日～数週間～数ヶ月の経過で症状が消失。
慢性型：臨床的に肺線維症と区別できない。不可逆的。

検査

IMD. YN.I-111

原因抗原を確定するために血清中の沈降抗体の証明や、気管支肺胞洗浄液リンパ球の抗原刺激試験が必要

血液検査：(総じて炎症所見)白血球増加、ESR上昇、CRP上昇、リウマチ因子陽性、アンジオテンシン転換酵素(ACE)上昇(類上皮肉芽腫のせい)、γグロブリン上昇、(間質の障害を伴うので)KL-6上昇

好酸球は不変、補体不変

免疫血清学的検査：沈降抗体の検出/リンパ球幼若化反応陽性(Trichosporon asahii, Trichosporon mucoides)

動脈血液ガス検査：PaO2低下

ツベルクリン反応：陰性化
肺機能検査：拘束性肺障害、一酸化炭素拡散能低下

胸部単純X線：

急性・亜急性型：(間質性肺炎の像)両側中下肺野を中心にびまん性にすりガラス様陰影や小粒状陰影
慢性型：(肺線維症の像)肺の萎縮、線状影や輪状影。20-30%の症例で上肺野優位。

胸部CT：

急性・亜急性型：肺野濃度の上昇、2-4mm大の境界不鮮明な小円形の粒状影が小葉中心性にびまん性に認められる。
慢性型：辺縁不整な線状影、輪状影

BALF：抗原曝露後24時間以内には多核白血球、以降はリンパ球の増加が認められる。

CD4/CD8低下(Tc優位)：夏型過敏性肺炎、塗装工肺(イソシアネート)
CD4/CD8上昇(Th優位)：農夫肺
CD4/CD8基準範囲内　：換気装置肺炎、鳥飼病　　　←　YN.I-111には鳥飼病ではCD4/CD8↑

経気管支肺生検(TBLB)：

急性型：非乾酪性類上皮性肉芽腫、胞隔炎(リンパ球・マクロファージ)。肺胞内のMasson体
慢性型：肉芽腫病変は稀。

吸入誘発試験：抗原の吸入により咳・呼吸困難を認め、検査上、炎症所見、低酸素血症が認められる。急性・亜急性型で有用。

診断基準

急性過敏性肺炎

(参考1)

a. 臨床像

臨床症状・所見1) ～4) のうちいずれか2つ以上と、検査所見1) ～4) のうち1) を含む2つ以上の項目を同時に満足するもの

1. 臨床症状・所見

1) せき、2) 息切れ　3) 発熱、4) 捻髪音ないし小水疱性ラ音

2. 検査所見

1) 胸部Ｘ線像にてびまん性散布性粒状陰影(またはスリガラス状)
2) 拘束性換気能障害
3) 血沈値亢進、好中球増多、CRP陽性のいずれか一つ)
4) 低酸素血症(安静時あるいは運動後)

b. 発症環境

1) ～6) のうちいずれか1つを満足するもの

1) 夏型過敏性肺炎は夏期(5～10月) に、高温多湿の住宅で起こる
2) 鳥飼病は鳥の飼育や羽毛と関連して起こる
3) 農夫肺は黴びた枯れ草の取り扱いと関連して起こる
4) 空調肺、加湿器肺はこれらの機器の使用と関連して起こる
5) 有機塵挨抗原に曝露される環境での生活歴
6) 特定の化学物質と関連して起こる

注：症状は抗原暴露4～8時間して起こることが多く、環境から離れると自然に軽快する。

c. 免疫学的所見

1) ～3) のうち1つ以上を満足するもの

1) 抗原に対する特異抗体陽性(血清あるもいはBAL*1液中)
2) 特異抗原によるリンパ球増殖反応陽性(末梢瓜あるいはBALリンパ球)
3) BAL所見(リンパ球↑、Tリンパ球↑) *2

d. 吸入誘発

1) ～2) のうち1つ以上を満足するもの

1) 特異抗原吸入にまる臨床像の再現
2) 環境暴露による臨床像の再現

e. 病理学的所見

1) ～3) のうちいずれか2つ以上を満足するもの

1) 肉芽腫形成、2) 胞隔炎、3) Masson体

診断

確実：a、b、dまたはa、b、c、eを満たすもの
強い疑い：aを含む3項目を満たすもの
疑い：aを含む2項目を満たすもの

(*1)bronchoalveolar lavage(気管支肺胞洗浄)

(*2)一般的にリンパ球比率は35％を超える。抗原回避2日以内では好中球増多を示す。

慢性過敏性肺炎

(参考2)

1.　環境誘発あるいは抗原誘発試験で陽性
2.　組織学的の線維化が観察される
3.　HRCTで線維化所見とhoneycombが観察される
4.　肺機能の拘束性障害が1年以上にわたって進行性である
5.　過敏性肺炎と関連した症状が6ヶ月以上続く
6.　当該抗原に対する抗体か、あるいはリンパ球増殖試験が陽性か、両者が陽性

以上1か6、および2か3、および4か5の3項目以上を満足させれば慢性過敏性肺炎と診断する

付記

1.　環境誘発試験は陰性のこともあるが、抗原誘発試験は陽性となる。この場合、症状の発現は弱くても白血球数、CRP、PaO2、DLCOなどの検査所見だけでも陽性と判定する。

2. 病理学的所見では肉芽腫はほとんどみられず、限局性のhoneycomb、リンパ球主体の肺隔炎とリンパ球の集族がみられる

3.　症状は抗原吸入を持続しても軽くなることが多い。労作時呼吸困難が主な症状である。

4.　抗体が陰性で抗原添加リンパ球増殖試験だけが陽性例もみられる

5.　KL-6、SP-Dは高値

6.　慢性過敏性肺炎の発症環境として、カビの多い住宅や仕事場、羽毛布団使用、隣人の鳩飼育、公園・神社・駅の野鳩、野鳥の集団棲息などがある

治療

抗原の隔離
薬物療法：ステロイド(呼吸困難例)、ステロイドパスル療法(呼吸困難の重症例、急性増悪例)
支持療法：在宅酸素療法

予後

抗原から隔離されれば予後良好

予防

抗原からの隔離

参考

まとめ

http://www.naoru.com/kabinseihaien.htm

慢性過敏性肺炎

http://www.geocities.jp/kokyukika/document/ChronicHP.html

急性過敏性肺臓炎

http://www.ibaraisikai.or.jp/treasure/chisivew/chisi-03.html

国試

104I067、103A049、103E045

「外因性アレルギー性肺胞炎」

　　[★]

英: extrinsic allergic alveolitis
関: 外因性アレルギー性胞隔炎、過敏性肺臓炎

「外因性アレルギー性胞隔炎」

　　[★]

英: extrinsic allergic alveolitis
関: 過敏性肺臓炎、外因性アレルギー性肺胞炎

「allergic」

　　[★]

adj.

アレルギーの、アレルギー性の、アレルギー型の

関: allergy、hypersensitivity

「extrinsic」

　　[★]

adj.

外因性の、外的な

関: exogenous

「allergic alveolitis」

　　[★] アレルギー性肺胞炎

[pmid15316440-1] Mohr LC (September 2004). "Hypersensitivity pneumonitis". Curr Opin Pulm Med 10 (5): 401–11. doi:10.1097/01.mcp.0000135675.95674.29. PMID 15316440. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1070-5287&volume=10&issue=5&spage=401.

[2] ttp://www.ucsfhealth.org/adult/medical_services/pulmonary/ild/conditions/hp/signs.html signs and symptoms

[Sharma-3] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Sharma, Sat. Hypersensitivity Pneumonitis. eMedicine, June 1, 2006.

[4] "Lecture 14: Hypersensitivity". http://www-immuno.path.cam.ac.uk/~immuno/part1/lec13/lec13_97.html. Retrieved 2008-09-18.

[5] "Allergy & Asthma Disease Management Center: Ask the Expert". http://www.aaaai.org/aadmc/ate/category.asp?cat=1008. Retrieved 2008-09-18.

[Kumar503-6] Page 503 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 1-4160-2973-7.

[pmid16061708-7] Ohtani Y, Saiki S, Kitaichi M, et al. (August 2005). "Chronic bird fancier's lung: histopathological and clinical correlation. An application of the 2002 ATS/ERS consensus classification of the idiopathic interstitial pneumonias". Thorax 60 (8): 665–71. doi:10.1136/thx.2004.027326. PMC 1747497. PMID 16061708. http://thorax.bmj.com/cgi/pmidlookup?view=long&pmid=16061708.

[Fishman-8] Enelow, RI (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1161–72. ISBN 0-07-145739-9.

[Kumar13-5-9] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l Kumar 2007, Table 13-5

[Munson1997-10] Munson EL, Panko DM, Fink JG. (1997). "Lycoperdonosis: Report of two cases and discussion of the disease". Clinical Microbiology Newsletter 19 (3): 17–24. doi:10.1016/S0196-4399(97)89413-5.

[11] [1]

Hypersensitivity pneumonitis
Classification and external resources
Micrograph of hypersensitivity pneumonitis. Lung biopsy. Trichrome stain.
ICD-10	J67
ICD-9	495
DiseasesDB	4630
MedlinePlus	000109
eMedicine	med/1103 ped/2577
MeSH	D000542

匿名

検索

案内

extrinsic allergic alveolitis