移植片対宿主反応

WordNet

(mechanics) the equal and opposite force that is produced when any force is applied to a body; "every action has an equal and opposite reaction"
a response that reveals a persons feelings or attitude; "he was pleased by the audiences reaction to his performance"; "John feared his mothers reaction when she saw the broken lamp"
a bodily process occurring due to the effect of some antecedent stimulus or agent; "a bad reaction to the medicine"; "his responses have slowed with age" (同)response
doing something in opposition to another way of doing it that you dont like; "his style of painting was a reaction against cubism"
an idea evoked by some experience; "his reaction to the news was to start planning what to do"
extreme conservatism in political or social matters; "the forces of reaction carried the election"
be the host of or for; "We hosted 4 couples last night"
an animal or plant that nourishes and supports a parasite; it does not benefit and is often harmed by the association
the owner or manager of an inn (同)innkeeper, boniface
archaic terms for army (同)legion
(medicine) recipient of transplanted tissue or organ from a donor
a person who invites guests to a social event (such as a party in his or her own home) and who is responsible for them while they are there
any organization that provides resources and facilities for a function or event; "Atlanta was chosen to be host for the Olympic Games"
cause to grow together parts from different plants; "graft the cherry tree branch onto the plum tree" (同)engraft, ingraft
the act of grafting something onto something else (同)grafting
(surgery) tissue or organ transplanted from a donor to a recipient; in some cases the patient can be both donor and recipient (同)transplant

PrepTutorEJDIC

{名}(…に対する)『反応』《+『to』+『名』》 / 〈U〉(…に対する)(政治的・社会的な)『反動』,逆コース《+『against』+『名』》 / 〈U〉〈C〉化学反応,化学変化 / 〈U〉〈C〉(物理学で)反作用
(…の)大群,大勢《+『of』+『名』》(multitude)
(客を接待する)『主人』,『主人役』;(…の)主人[役]《+『to』+『名』》 / (旅館の)主人 / 寄生動(植)物の宿主 / 〈晩餐会など〉‘の'主人役を務める,‘を'主催する
(つぎ木の)つぎ穂;つぎ木 / (皮被・内臓・骨などの)移植片 / (木に)〈つぎ穂〉‘を'つぐ,(体に)〈移植片〉‘を'移植する《+『名』+『on』(『upon』,『in』,『into』)+『名』》 / …‘を'結合させる《+『名』+『together』》 / (…に)つぎ木する,移植する《+『on』(『upon』,『in』,『into』)+『名』》
収賄,汚職;贈賄;〈C〉汚職で得たもの / 汚職する,収賄する
(訴訟・競技などで)…対(《略》v.,vs.)(against) / (比較や二者択一において)…に対して
ほう(驚き・賞賛・冷笑などの発声);お‐い(呼びかけ・注意などの発声)
娼婦・売春婦：（whoreの発音をくずしたもの）

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/09/13 00:01:59」(JST)

wiki en

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.

Causes

GVHD pathology

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

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]

Clinical manifestation

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 immune-mediated 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

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

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

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] The use of liver-derived hematopoietic stem cells to reconstitute bone marrow has the highest success rate according to recent studies.
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

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

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]

References

^ ^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. doi:10.4049/jimmunol.166.3.1843. 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. |displayeditors= suggested (help)
^ 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.

UpToDate Contents

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1. 急性移植片対宿主病の臨床症状、診断、および重症度分類 clinical manifestations diagnosis and grading of acute graft versus host disease
2. 移植片対宿主病の予防および治療に使用される免疫抑制剤の概要 overview of immunosuppressive agents used for prevention and treatment of graft versus host disease
3. 慢性移植片対宿主病の臨床症状、診断、および重症度分類 clinical manifestations diagnosis and grading of chronic graft versus host disease
4. 慢性移植片対宿主病の治療 treatment of chronic graft versus host disease
5. 急性移植片対宿主病の治療：臨床試験 treatment of acute graft versus host disease clinical trials

English Journal

High expression of heat shock protein 90 alpha and its significance in human acute leukemia cells.

Tian WL1, He F2, Fu X1, Lin JT3, Tang P1, Huang YM1, Guo R4, Sun L5.Author information 1Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450052, China.2Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450052, China.3Key Laboratory for Medical Tissue Regeneration of Henan Province, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.4Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450052, China. Electronic address: gh7311@aliyun.com.5Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province 450052, China. Electronic address: lingsuncn@126.com.AbstractThis study investigated the expression of heat shock protein 90 alpha (Hsp90α) in acute leukemia cells. The expression of Hsp90α was investigated in leukemia cell lines and human bone marrow mononuclear cells derived from acute leukemia patients and from healthy individuals using polymerase chain reaction, Western blot, and enzyme-linked immunosorbent assay. Compared with cells from healthy individuals, the expression of Hsp90α in the untreated patients was higher. Similarly high levels were observed in remission patients. Significantly higher expression levels were observed in all the tested cell lines, and in cells from refractory and relapsed patients. No obvious relationship was observed between the occurrence of graft versus host disease and the expression of Hsp90α. The untreated patients showing higher expression levels of Hsp90α had lower complete remission rates. During remission of untreated patients, the expression of Hsp90α decreased and reached the lowest level after transplantation, but the expression increased again before relapse. Hsp90α was highly expressed in leukemia cells. The expression level of Hsp90α was associated with leukemia prognosis. However, no obvious relationship was observed between the occurrence of graft versus host disease and the expression of Hsp90α.
Gene.Gene.2014 Jun 1;542(2):122-8. doi: 10.1016/j.gene.2014.03.046. Epub 2014 Mar 25.
This study investigated the expression of heat shock protein 90 alpha (Hsp90α) in acute leukemia cells. The expression of Hsp90α was investigated in leukemia cell lines and human bone marrow mononuclear cells derived from acute leukemia patients and from healthy individuals using polymerase chain
PMID 24680776

Tc1 Clonal T Cell Expansion during Chronic Graft-versus-Host Disease-Associated Hypereosinophilia.

Clave E1, Xhaard A2, Douay C1, Adès L3, Cayuela JM4, Peffault de Latour R2, Robin M2, Toubert A5, Socié G6.Author information 1Departement d'Immunologie, INSERM UMRS-940, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Paris, France.2Service d'Hématologie-Greffe, AP-HP Hôpital Saint Louis, Paris, France.3Service d'Hématologie, AP-HP Hôpital Avicenne, Paris, France.4Service d'Hématologie Biologique, AP-HP Hôpital Saint Louis, Paris, France.5Departement d'Immunologie, INSERM UMRS-940, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Paris, France; Service d'Immunologie, AP-HP Hôpital Saint Louis, Paris, France.6Departement d'Immunologie, INSERM UMRS-940, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Paris, France; Service d'Hématologie-Greffe, AP-HP Hôpital Saint Louis, Paris, France. Electronic address: gerard.socie@sls.aphp.fr.AbstractAlthough hypereosinophilia (HE) associated with chronic graft-versus-host disease (GVHD) has long been recognized, biological data on this phenomenon are scarce. Here we compare patients with chronic GVHD with HE together with a clonal T cell expansion and control patients with acute or chronic GVHD but without HE. These clonal expansions share a CD8(+) TC1 phenotype rather than a CD4(+) Th2 profile. In contrast to the drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, these allogeneic CD8(+) clones do not recognize the epitopes of herpesviruses. Furthermore, these TC1 clones do not produce IL-17 as described in the DRESS syndrome.
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation.Biol Blood Marrow Transplant.2014 May;20(5):739-42. doi: 10.1016/j.bbmt.2014.01.023. Epub 2014 Jan 24.
Although hypereosinophilia (HE) associated with chronic graft-versus-host disease (GVHD) has long been recognized, biological data on this phenomenon are scarce. Here we compare patients with chronic GVHD with HE together with a clonal T cell expansion and control patients with acute or chronic GVH
PMID 24468638

Selective organ specific inflammation in offspring harbouring microchimerism from strongly alloreactive mothers.

Leveque L1, Hodgson S2, Peyton S3, Koyama M4, Macdonald KP4, Khosrotehrani K2.Author information 1The University of Queensland, UQ Centre for Clinical Research, Experimental Dermatology Group, Brisbane, Australia; QIMR Berghofer Medical Research Institute, Brisbane, Australia. Electronic address: lucie.leveque@uq.edu.au.2The University of Queensland, UQ Centre for Clinical Research, Experimental Dermatology Group, Brisbane, Australia.3Pathology Queensland, Royal Brisbane Hospital, Brisbane, Australia.4QIMR Berghofer Medical Research Institute, Brisbane, Australia.AbstractThe origins of autoimmunity are not yet understood despite significant advances in immunology. The trafficking of maternal cells to the offspring represents the very first immunological event in foetal life and is reinforced during lactation. The persistence of maternal cells in offspring's tissues and circulation has been associated with several autoimmune disorders. However a direct causal effect has never been demonstrated. Maternal T cells specifically targeting foetal insulin producing cells have been shown to generate islet inflammation without directly participating in this process. Our objective was to evaluate if alloreactive maternal cells could directly trigger a graft-versus host like reaction or indirectly influence the development of the offspring's regulatory T cells favouring autoimmunity. We adopted a breeding strategy comparing genetically identical offspring from either strongly alloreactive transgenic mothers compared to immunodeficient mothers. We detected maternal alloreactive T cells in the offspring and early signs of inflammation in small intestine of 6 weeks old offspring. Interestingly, CD4(+) Foxp3(+) regulatory T cell frequency was diminished in mesenteric lymph nodes from eight months old offspring born of alloreactive mothers compared to offspring of immunodeficient mothers. Our study favours a hypothesis where highly alloreactive maternal cell microchimerism indirectly predisposes offspring to autoimmunity.
Journal of autoimmunity.J Autoimmun.2014 May;50:51-8. doi: 10.1016/j.jaut.2013.10.005. Epub 2013 Nov 20.
The origins of autoimmunity are not yet understood despite significant advances in immunology. The trafficking of maternal cells to the offspring represents the very first immunological event in foetal life and is reinforced during lactation. The persistence of maternal cells in offspring's tissues
PMID 24268809

Japanese Journal

関節リウマチ・悪性関節リウマチに対するアフェレシス療法(<特集>血管炎症候群とアフェレシス)

日本アフェレシス学会雑誌 34(2), 131-136, 2015-05-31
NAID 110009964088

Successful Secondary Umbilical Cord Blood Transplantation for Graft Failure in Acute Myelogenous Leukemia, Treated with Modified One-Day Conditioning Regimen, and Graft-Versus-Host Disease Prophylaxis Consisting of Mycophenolate and Tacrolimus

Journal of Clinical and Experimental Hematopathology 55(2), 89-96, 2015
NAID 130005104661

血縁HLA半合致移植（ハプロ移植）の現状と今後

臨床血液 56(3), 289-297, 2015
NAID 130005065336

Related Pictures

★リンクテーブル★

リンク元	「移植片対宿主反応」「GVHR」
関連記事	「versus」「graft」「grafting」「reaction」「host」

「移植片対宿主反応」

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