移植片対宿主病（いしょくへんたいしゅくしゅびょう、graft versus host disease; GVHD）とは臓器移植に伴う合併症のひとつ。
移植片（グラフト）にとって、レシピエント（臓器受給者）の体は異物である。GVHDとはドナー（臓器提供者）の臓器が、免疫応答によってレシピエントの臓器を攻撃することによって起こる症状の総称である。
混同されることがある病態として、いわゆる拒絶反応がある。拒絶反応はレシピエントの免疫応答によってドナーの移植片が攻撃されることによる合併症の総称であり、GVHDとは、攻撃する側と攻撃される側が反対である。
GVHDは様々な他家臓器移植の後に発生するが、特に免疫組織を直接移植する、造血幹細胞移植（骨髄移植）後や輸血後のものが知られている（GVHDの分類と診断）。
目次
- 1 造血幹細胞移植後GVHD
- 1.1 概念
- 1.2 原因
- 1.3 症状
- 1.4 予防
- 1.5 治療と予後
- 2 輸血後GVHD
- 2.1 概念
- 2.2 原因
- 2.3 症状
- 2.4 予防
- 2.5 治療と予後
- 3 脚注
- 4 外部リンク
造血幹細胞移植後GVHD[編集]
概念[編集]
移植による血液提供者の免疫機構が、受血者の全身組織を攻撃、破壊する疾患である。
原因[編集]
原因は確立されていない。 急性期には血液提供者のリンパ球が主因と推測されている。慢性期においては、より多くの免疫機能の働きが関与していると推測されている。
症状[編集]
移植から1～2週間程度で発症する急性GVHDと移植から120日以降に発症する慢性GVHDに分類するが、必ずしも発症時期から分類できる病態ではない。
予防[編集]
急性期には免疫抑制剤やステロイドが有効であるが、慢性期の予防法は確立されていない。
治療と予後[編集]
免疫抑制剤やステロイドの継続投与や増量、パルス状投与が試みられている。 これらの薬剤により免疫機能を一時的に抑制することで炎症を抑えるが、免疫機能の適合性が改善するかは不明である。 急性期には、致命率を改善できているが、コントロールできないケースや、これらの薬剤の副作用で合併症状に至って生命が脅かされる場合も少なくない。
慢性期においても免疫抑制剤やステロイドなど投与が試みられ、症状の一部改善が見られる。 しかし、多くの症例で持続もしくは増悪が見られることから、免疫機能の適合性が薬剤や時間経過で改善できているかは不明である。 一般的に長期生存者のQOLは低い傾向がある。
輸血後GVHD[編集]
詳細は「輸血後移植片対宿主病」を参照
概念[編集]
輸血血液中に含まれる血液提供者のリンパ球が増殖し、受血者の全身組織を攻撃、破壊する疾患である。輸血を伴った術後に激烈なアレルギー様反応を来して死亡する例は昔から知られており「術後紅皮症」とも呼ばれていたが、1980年代から1990年代にかけて原因がほぼ解明され、医療従事者に広く認知されるようになった[1][2][3][4]。
現在では赤血球・血小板など血液の構成成分ごとの輸血が普及し、輸血製剤中のリンパ球は、製剤過程中にほぼ取り除かれているが、それでも少量のリンパ球が製剤中に残存する。通常の場合は輸血血液に含まれるリンパ球と受血者の体組織は、お互いを異物と認識して攻撃し合うが、輸血内のリンパ球は少数であり、前者が後者に勢力で勝ることは通常あり得ない。結局、残存リンパ球は、受血者の免疫応答によって完全に排除される。
しかし、稀に輸血中の残存リンパ球が、受血者の体内で制限を受けず増殖し、ついには受血者の正常な体組織を傷害するに至ることがあり、これを輸血後GVHDと呼ぶ[1][2]。
原因[編集]
原因ははっきりとは確立されていないが、以下のようなことが考えられている。
- HLAが供血者のHLA型がホモ結合で、かつ受血者と半合一致している。
- HLAの一方通行適合(one-way match)と呼ばれる「供血者のリンパ球にとって受血者は異物であるが、受血者にとって供血者の血液を異物として認識できない」状態があり得ることが知られており、このようなケースでは供血者のリンパ球は、受血者の体内で攻撃を受けずに増殖できる。親族間での輸血で発症率が高いことはHLA適合が重要な役割を果たしていることを説明している。[1][2][4]
- 受血者の免疫機能が低下している
- 輸血後GVHDは、老人や免疫不全時、手術時に高頻度で発生する。ただし以前は受給者が免疫不全状態にある場合にのみ発症すると考えられていたが、現在では免疫正常者にも発症することが知られている。そのため、HLAが類似しない供血者からの輸血時に起こるGVHDはこちらが原因だと考えることができる[1][2]。
症状[編集]
輸血から約1～2週間後に発熱や赤斑が現れ、やがて赤斑は全身に及ぶ。さらに下の症状が起こる。
- 発熱
- 発疹
- 下痢
- 肝機能障害
- 顆粒球減少と、それに伴う重篤な日和見感染症
- 血小板減少
- 貧血
- 多臓器不全
これらの症状は激烈かつ難治性であり、ほとんどの場合、骨髄無形成をきたして程なく死亡に至る。多くの症状があるが、急性GVHDの標的は皮膚、消化管、肝臓、慢性GVHDの標的は多臓器に及ぶというイメージで推定は可能である[1][2]。
予防[編集]
「ガンマ線滅菌」も参照
-
- リンパ球を失活させる方法であり、非常に有効。輸血用製剤はリンパ球除去を行っていても完全に排除することは困難なので採血後2週間以内の非照射血液製剤では輸血後GVHDは起こりえる。
- 自己血輸血を行う
- 近親者間での輸血を避ける
- 輸血を行わない（詳細は無輸血手術）
なお輸血製剤中の分裂能を有するリンパ球は時間とともに減少することから、一般的に新鮮な血液ほどリスクが高いとされる。血液製剤に放射線照射を行えない場合は、新鮮血は避ける[1][2][4]。
治療と予後[編集]
輸血後GVHDは、ひとたび発症すると致死率が非常に高いことで知られ、ほぼ全例が死亡する。増殖したリンパ球が組織内に侵入するため、血漿交換も意味がなく、治療は非常に困難である。シクロスポリンAや骨髄移植で命を救ったわずかな例が報告されているにすぎない[1]。蛋白分解酵素阻害剤が輸血後GVHDに有効であったとの症例報告もある [4]。
脚注[編集]
- ^ a b c d e f g 浅野茂隆、池田康夫、内山卓 監修 『三輪血液病学』文光堂、2006年、ISBN 4-8306-1419-6、pp.709-710
- ^ a b c d e f 遠山 博、他、編著『輸血学』改訂第3版、中外医学社、2004年、ISBN 4-498-01912-1、pp.636-644
- ^ 小川 聡 総編集 『内科学書』Vol.6 改訂第7版、中山書店、2009年、ISBN 978-4-521-73173-5、p.54
- ^ a b c d 徳島大学医学部附属病院輸血部 廣瀬政雄, 輸血後移植片対宿主病 2000年10月4日改訂 大阪大学大学院医学系研究科・医学部HP寄稿記事
外部リンク[編集]
- 造血幹細胞など生体移植の拒絶反応を防ぐ仕組みを発見－マウスの移植片対宿主病の制御機構を世界で初めて証明－ 理化学研究所
| Graft-versus-host disease |
| Classification and external resources |
| ICD-10 |
T86.0 |
| ICD-9 |
279.50 |
| DiseasesDB |
5388 |
| MedlinePlus |
001309 |
| eMedicine |
med/926 ped/893 derm/478 |
| MeSH |
D006086 |
Graft-versus-host disease (GVHD) is a common complication following an allogeneic tissue transplant. It is commonly associated with stem cell or bone marrow transplant but the term also applies to other forms of tissue graft. Immune cells (white blood cells) in the tissue (the graft) recognize the recipient (the host) as "foreign". The transplanted immune cells then attack the host's body cells. GVHD can also occur after a blood transfusion if the blood products used have not been irradiated.
Contents
- 1 Causes
- 2 Types
- 3 Clinical manifestation
- 4 Transfusion-associated GVHD
- 5 In thymus transplantation
- 6 Prevention
- 7 Treatment of GVHD
- 8 Investigational therapies for graft-versus-host disease
- 9 See also
- 10 Further reading
- 11 References
Causes[edit source | edit]
Billingham Criteria, 3 criteria must be met in order for GVHD to occur.[1]
- An immuno-competent graft is administered, with viable and functional immune cells.
- The recipient is immunologically disparate - histo-incompatible.
- The recipient is immuno-compromised and therefore cannot destroy or inactivate the transplanted cells.
After bone marrow transplantation, T cells present in the graft, either as contaminants or intentionally introduced into the host, attack the tissues of the transplant recipient after perceiving host tissues as antigenically foreign. The T cells produce an excess of cytokines, including TNF-α and interferon-gamma (IFNγ). A wide range of host antigens can initiate graft-versus-host-disease, among them the human leukocyte antigens (HLAs). However, graft-versus-host disease can occur even when HLA-identical siblings are the donors. HLA-identical siblings or HLA-identical unrelated donors often have genetically different proteins (called minor histocompatibility antigens) that can be presented by Major histocompatibility complex (MHC) molecules to the donor's T-cells, which see these antigens as foreign and so mount an immune response.[citation needed]
While donor T-cells are undesirable as effector cells of graft-versus-host-disease, they are valuable for engraftment by preventing the recipient's residual immune system from rejecting the bone marrow graft (host-versus-graft). In addition, as bone marrow transplantation is frequently used to treat cancer, mainly leukemias, donor T-cells have proven to have a valuable graft-versus-tumor effect. A great deal of current research on allogeneic bone marrow transplantation involves attempts to separate the undesirable graft-vs-host-disease aspects of T-cell physiology from the desirable graft-versus-tumor effect.[citation needed]
Types[edit source | edit]
In the clinical setting, graft-versus-host-disease is divided into acute and chronic forms.
- The acute or fulminant form of the disease (aGVHD) is normally observed within the first 100 days post-transplant,[2] and is a major challenge to transplants owing to associated morbidity and mortality.[3]
- The chronic form of graft-versus-host-disease (cGVHD) normally occurs after 100 days. The appearance of moderate to severe cases of cGVHD adversely influences long-term survival.[4]
This distinction is not arbitrary: Acute and chronic graft-versus-host-disease appear to involve different immune cell subsets, different cytokine profiles, somewhat different host targets, and respond differently to treatment.[citation needed] Acute GVHD is likely caused by alloreactive memory T-cells pre-existent in the graft. The mechanisms by which chronic GVHD develops are as yet ill-defined.[citation needed]
Clinical manifestation[edit source | edit]
In the classical sense, acute graft-versus-host-disease is characterized by selective damage to the liver, skin (rash), mucosa, and the gastrointestinal tract. Newer research indicates that other graft-versus-host-disease target organs include the immune system (the hematopoietic system, e.g., the bone marrow and the thymus) itself, and the lungs in the form of idiopathic pneumonitis. Biomarkers can be used to identify specific causes of GVHD, such as elafin in the skin.[5] Chronic graft-versus-host-disease also attacks the above organs, but over its long-term course can also cause damage to the connective tissue and exocrine glands.[citation needed]
Acute GVHD of the GI tract can result in severe intestinal inflammation, sloughing of the mucosal membrane, severe diarrhea, abdominal pain, nausea, and vomiting. This is typically diagnosed via intestinal biopsy. Liver GVHD is measured by the bilirubin level in acute patients. Skin GVHD results in a diffuse maculopapular rash, sometimes in a lacy pattern.[citation needed]
Mucosal damage to the vagina can result in severe pain and scarring, and appears in both acute and chronic GVHD. This can result in an inability to have sexual intercourse.[1]
Acute GVHD is staged as follows: overall grade (skin-liver-gut) with each organ staged individually from a low of 1 to a high of 4. Patients with grade IV GVHD usually have a poor prognosis. If the GVHD is severe and requires intense immunosuppression involving steroids and additional agents to get under control, the patient may develop severe infections as a result of the immunosuppression and may die of infection.[citation needed]
In the oral cavity, chronic graft-versus-host-disease manifests as lichen planus with a higher risk of malignant transformation to oral squamous cell carcinoma in comparison to the classical oral lichen planus. Graft-versus-host-disease-associated oral cancer may have more aggressive behavior with poorer prognosis, when compared to oral cancer in non-hematopoietic stem cell transplantation patients.[6]
Transfusion-associated GVHD[edit source | edit]
Main article: Transfusion-associated graft versus host disease
This type of GVHD is associated with transfusion of un-irradiated blood to immunocompromised recipients. It can also occur in situations in which the blood donor is homozygous and the recipient is heterozygous for an HLA haplotype. It is associated with higher mortality (80-90%) due to involvement of bone marrow lymphoid tissue, however the clinical manifestations are similar to GVHD resulting from bone marrow transplantation. Transfusion-associated GVHD is rare in modern medicine. It is almost entirely preventable by controlled irradiation of blood products to inactivate the white blood cells (including lymphocytes) within[7]
In thymus transplantation[edit source | edit]
Thymus transplantation may be said to be able to cause a special type of GVHD because the recipients thymocytes would use the donor thymus cells as models when going through the negative selection to recognize self-antigens, and could therefore still mistake own structures in the rest of the body for being non-self. This is a rather indirect GVHD because it is not directly cells in the graft itself that causes it but cells in the graft that make the recipient's T cells act like donor T cells. It can be seen as a multiple-organ autoimmunity in xenotransplantation experiments of the thymus between different species.[8] Autoimmune disease is a frequent complication after human allogeneic thymus transplantation, found in 42% of subjects over 1 year post transplantation.[9] However, this is partially explained by the fact that the indication itself, that is, complete DiGeorge syndrome, increases the risk of autoimmune disease.[10]
Prevention[edit source | edit]
- DNA-based tissue typing allows for more precise HLA matching between donors and transplant patients, which has been proven to reduce the incidence and severity of GVHD and to increase long-term survival.[11]
- The T-cells of umbilical cord blood (UCB) have an inherent immunological immaturity,[12] and the use of UCB stem cells in unrelated donor transplants has a reduced incidence and severity of GVHD.[13]
- Methotrexate, ciclosporin and tacrolimus are common drugs used for GVHD prophylaxis.[citation needed]
- Graft-versus-host-disease can largely be avoided by performing a T-cell-depleted bone marrow transplant. However, these types of transplants come at a cost of diminished graft-versus-tumor effect, greater risk of engraftment failure, or cancer relapse,[14] and general immunodeficiency, resulting in a patient more susceptible to viral, bacterial, and fungal infection. In a multi-center study, disease-free survival at 3 years was not different between T cell-depleted and T cell-replete transplants.[15]
Treatment of GVHD[edit source | edit]
Intravenously administered glucocorticoids, such as prednisone, are the standard of care in acute GVHD[3] and chronic GVHD.[16] The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the host tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect.[citation needed]
Investigational therapies for graft-versus-host disease[edit source | edit]
There are a large number of clinical trials either ongoing or recently completed in the investigation of graft-versus-host disease treatment and prevention.[17]
On May 17, 2012, Osiris Therapeutics announced that Canadian health regulators approved Prochymal, its drug for acute graft-versus host disease in children who have failed to respond to steroid treatment. Prochymal is the first stem cell drug to be approved for a systemic disease.[18]
See also[edit source | edit]
- Organ transplant
- Immunology
- Cancer
Further reading[edit source | edit]
- Ferrara JLM, Deeg HJ, Burakoff SJ. Graft-Vs.-Host Disease: Immunology, Pathophysiology, and Treatment. Marcel Dekker, 1990 ISBN 0-8247-9728-0
- Polsdorfer, JR Gale Encyclopedia of Medicine: Graft-vs.-host disease
References[edit source | edit]
- ^ a b Spiryda, L; Laufer, MR; Soiffer, RJ; Antin, JA (2003). "Graft-versus-host disease of the vulva and/or vagina: Diagnosis and treatment". Biology of Blood and Marrow Transplantation 9 (12): 760–5. doi:10.1016/j.bbmt.2003.08.001. PMID 14677115.
- ^ "Improved Management of Graft-Versus-Host Disease". National Marrow Donor Program.
- ^ a b Goker, H; Haznedaroglu, IC; Chao, NJ (2001). "Acute graft-vs-host disease Pathobiology and management". Experimental Hematology 29 (3): 259–77. doi:10.1016/S0301-472X(00)00677-9. PMID 11274753.
- ^ Lee, Stephanie J.; Vogelsang, Georgia; Flowers, Mary E.D. (2003). "Chronic graft-versus-host disease". Biology of Blood and Marrow Transplantation 9 (4): 215–33. doi:10.1053/bbmt.2003.50026. PMID 12720215.
- ^ Paczesny, S.; Levine, J.E.; Hogan, J.; Crawford, J.; Braun, T.M.; Wang, H.; Faca, V.; Zhang, Q. et al. (2009). "Elafin is a Biomarker of Graft Versus Host Disease of the Skin". Biology of Blood and Marrow Transplantation 15 (2): 13–4. doi:10.1016/j.bbmt.2008.12.039. PMC 2895410. PMID 20371463.
- ^ Elad, Sharon; Zadik, Yehuda; Zeevi, Itai; Miyazaki, Akihiro; De Figueiredo, Maria A. Z.; Or, Reuven (2010). "Oral Cancer in Patients After Hematopoietic Stem-Cell Transplantation: Long-Term Follow-Up Suggests an Increased Risk for Recurrence". Transplantation 90 (11): 1243–4. doi:10.1097/TP.0b013e3181f9caaa. PMID 21119507.
- ^ Moroff, G; Leitman, SF; Luban, NL (1997). "Principles of blood irradiation, dose validation, and quality control". Transfusion 37 (10): 1084–92. doi:10.1046/j.1537-2995.1997.371098016450.x. PMID 9354830.
- ^ Xia, G; Goebels, J; Rutgeerts, O; Vandeputte, M; Waer, M (2001). "Transplantation tolerance and autoimmunity after xenogeneic thymus transplantation". Journal of immunology 166 (3): 1843–54. PMID 11160231.
- ^ Markert, M. Louise; Devlin, Blythe H.; McCarthy, Elizabeth A.; Chinn, Ivan K.; Hale, Laura P. (2008). "Thymus Transplantation". In Lavini, Corrado; Moran, Cesar A.; Morandi, Uliano et al. Thymus Gland Pathology: Clinical, Diagnostic, and Therapeutic Features. pp. 255–67. doi:10.1007/978-88-470-0828-1_30. ISBN 978-88-470-0827-4.
- ^ Markert, M. L.; Devlin, B. H.; Alexieff, M. J.; Li, J.; McCarthy, E. A.; Gupton, S. E.; Chinn, I. K.; Hale, L. P. et al. (2007). "Review of 54 patients with complete DiGeorge anomaly enrolled in protocols for thymus transplantation: Outcome of 44 consecutive transplants". Blood 109 (10): 4539–47. doi:10.1182/blood-2006-10-048652. PMC 1885498. PMID 17284531.
- ^ Morishima, Y.; Sasazuki, T; Inoko, H; Juji, T; Akaza, T; Yamamoto, K; Ishikawa, Y; Kato, S et al. (2002). "The clinical significance of human leukocyte antigen (HLA) allele compatibility in patients receiving a marrow transplant from serologically HLA-A, HLA-B, and HLA-DR matched unrelated donors". Blood 99 (11): 4200–6. doi:10.1182/blood.V99.11.4200. PMID 12010826.
- ^ Grewal, S. S.; Barker, JN; Davies, SM; Wagner, JE (2003). "Unrelated donor hematopoietic cell transplantation: Marrow or umbilical cord blood?". Blood 101 (11): 4233–44. doi:10.1182/blood-2002-08-2510. PMID 12522002.
- ^ Laughlin, Mary J.; Barker, Juliet; Bambach, Barbara; Koc, Omer N.; Rizzieri, David A.; Wagner, John E.; Gerson, Stanton L.; Lazarus, Hillard M. et al. (2001). "Hematopoietic Engraftment and Survival in Adult Recipients of Umbilical-Cord Blood from Unrelated Donors". New England Journal of Medicine 344 (24): 1815–22. doi:10.1056/NEJM200106143442402. PMID 11407342.
- ^ Hale, G; Waldmann, H (1994). "Control of graft-versus-host disease and graft rejection by T cell depletion of donor and recipient with Campath-1 antibodies. Results of matched sibling transplants for malignant diseases". Bone marrow transplantation 13 (5): 597–611. PMID 8054913.
- ^ Wagner, John E; Thompson, John S; Carter, Shelly L; Kernan, Nancy A; Unrelated Donor Marrow Transplantation Trial (2005). "Effect of graft-versus-host disease prophylaxis on 3-year disease-free survival in recipients of unrelated donor bone marrow (T-cell Depletion Trial): A multi-centre, randomised phase II–III trial". The Lancet 366 (9487): 733–41. doi:10.1016/S0140-6736(05)66996-6. PMID 16125590.
- ^ Menillo, S A; Goldberg, S L; McKiernan, P; Pecora, A L (2001). "Intraoral psoralen ultraviolet a irradiation (PUVA) treatment of refractory oral chronic graft-versus-host disease following allogeneic stem cell transplantation". Bone Marrow Transplantation 28 (8): 807–8. doi:10.1038/sj.bmt.1703231. PMID 11781637.
- ^ search of clinicaltrials.gov for Graft-versus-host disease
- ^ "World’s First Stem-Cell Drug Approval Achieved in Canada". The National Law Review. Drinker Biddle & Reath LLP. 2012-06-12. Retrieved 2012-07-01.
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Organ transplantation
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| Types |
- Allotransplantation
- Autotransplantation
- Xenotransplantation
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| Organs and tissues |
- Bone
- Bone marrow
- Brain
- Corneal
- Face
- Hand
- Head
- Heart
- Heart–lung
- Kidney
- Liver
- Lung
- Pancreas
- Penis
- Skin
- Spleen
- Thymus
- Uterus
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| Medical grafting |
- Bone grafting
- Skin grafting
- Vascular grafting
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| Organ donation |
- Non-heart-beating donation
- Organ harvesting
- Organ trade
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| Complications |
- Graft-versus-host disease
- Post-transplant lymphoproliferative disorder
- Transplant rejection
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| Organizations |
- Anthony Nolan
- DKMS Americas
- Eurotransplant
- Halachic Organ Donor Society
- Human Tissue Authority
- National Marrow Donor Program
- National Transplant Organization
- NHS Blood and Transplant
- United Network for Organ Sharing
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| Countries |
- Organ transplantation in different countries
- Organ transplantation in China
- Organ transplantation in Israel
- Organ transplantation in Japan
- Organ theft in Kosovo
- Gurgaon kidney scandal
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| People |
|
Heart
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- Christiaan Barnard
- Adrian Kantrowitz
- Richard Lower
- Norman Shumway
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Kidney
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- J. Hartwell Harrison
- John P. Merrill
- Joseph Murray
- Michael Woodruff
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Liver
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Lung
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- Joel D. Cooper
- Vladimir Demikhov
- James Hardy
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Other
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- Alexis Carrel
- Jean-Michel Dubernard
- Donna Mansell
- Bruce Reitz
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- List of organ transplant donors and recipients
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| Related topics |
- Biomedical tissue
- Edmonton protocol
- Eye bank
- Immunosuppressive drugs
- Lung allocation score
- Machine perfusion
- Total body irradiation
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Consequences of external causes (T66–T78, 990–995)
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| Temperature/radiation |
- elevated temperature
- Hyperthermia
- Heat syncope
- reduced temperature
- Hypothermia
- Immersion foot syndromes
- Trench foot
- Tropical immersion foot
- Warm water immersion foot
- Chilblains
- Frostbite
- Aerosol burn
- Cold intolerance
- Acrocyanosis
- Erythrocyanosis crurum
- radiation
- Radiation poisoning
- Radiation burn
- Chronic radiation keratosis
- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy
- Radiation acne
- Radiation cancer
- Radiation recall reaction
- Radiation-induced erythema multiforme
- Radiation-induced hypertrophic scar
- Radiation-induced keloid
- Radiation-induced morphea
|
|
| Air |
- Hypoxia/Asphyxia
- Barotrauma
- Aerosinusitis
- Decompression sickness
- High altitude
- Altitude sickness
- Chronic mountain sickness
- HAPE
- HACE
|
|
| Food |
|
|
| Maltreatment |
- Physical abuse
- Sexual abuse
- Psychological abuse
|
|
| Travel |
- Motion sickness
- Seasickness
- Airsickness
- Space adaptation syndrome
|
|
| Adverse effect |
- Hypersensitivity
- Anaphylaxis
- Angioedema
- Allergy
- Arthus reaction
|
|
| Other |
- Electric shock
- Drowning
- Lightning injury
|
|
Ungrouped
skin conditions
resulting from
physical factors |
- Dermatosis neglecta
- Pinch mark
- Pseudoverrucous papules and nodules
- Sclerosing lymphangiitis
- Tropical anhidrotic asthenia
- UV-sensitive syndrome
- environmental skin conditions
- Electrical burn
- frictional/traumatic/sports
-
- Black heel and palm
- Equestrian perniosis
- Jogger's nipple
- Pulling boat hands
- Runner's rump
- Surfer's knots
- Tennis toe
- Vibration white finger
- Weathering nodule of ear
- Wrestler's ear
- Coral cut
- Painful fat herniation
- Uranium dermatosis
- iv use
-
- Skin pop scar
- Skin track
- Slap mark
- Pseudoacanthosis nigricans
- Narcotic dermopathy
|
|
|
Immune disorders: hypersensitivity and autoimmune diseases (279.5–6)
|
|
Type I/allergy/atopy
(IgE) |
|
Foreign
|
Atopic dermatitis · Allergic urticaria · Hay fever · Allergic asthma · Anaphylaxis · Food allergy (Milk, Egg, Peanut, Tree nut, Seafood, Soy, Wheat), Penicillin allergy
|
|
|
Autoimmune
|
none
|
|
|
Type II/ADCC
(IgM, IgG) |
|
Foreign
|
Pernicious anemia · Hemolytic disease of the newborn
|
|
|
Autoimmune
|
|
Cytotoxic
|
Autoimmune hemolytic anemia · Idiopathic thrombocytopenic purpura · Bullous pemphigoid · Pemphigus vulgaris · Rheumatic fever · Goodpasture's syndrome
|
|
|
"Type 5"/receptor
|
Graves' disease · Myasthenia gravis
|
|
|
|
Type III
(Immune complex) |
|
Foreign
|
Henoch–Schönlein purpura · Hypersensitivity vasculitis · Reactive arthritis · Farmer's lung · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
|
|
|
Autoimmune
|
Systemic lupus erythematosus · Subacute bacterial endocarditis · Rheumatoid arthritis
|
|
|
Type IV/cell-mediated
(T-cells) |
|
Foreign
|
Allergic contact dermatitis · Mantoux test
|
|
|
Autoimmune
|
Diabetes mellitus type 1 · Hashimoto's thyroiditis · Guillain–Barré syndrome · Multiple sclerosis · Coeliac disease · Giant-cell arteritis
|
|
|
GVHD
|
Transfusion-associated graft versus host disease
|
|
|
Unknown/
multiple |
|
Foreign
|
Hypersensitivity pneumonitis (Allergic bronchopulmonary aspergillosis) · Transplant rejection · Latex allergy (I+IV)
|
|
|
Autoimmune
|
Sjögren's syndrome · Autoimmune hepatitis · Autoimmune polyendocrine syndrome (APS1, APS2) · Autoimmune adrenalitis · Systemic autoimmune disease
|
|
|
|
|
cell/phys/auag/auab/comp, igrc
|
|
|
|
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