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조직구 증식증(희귀병)
Micrograph showing a Langerhans cell histiocytosis with the characteristic reniform Langerhans cells accompanied by abundant eosinophils. H&E stain.
진료과조직구 증식증

랑게르한스 세포 조직증(')LCH)는 [Langerhans cell]s의 클론 증식, [골수]에서 파생된 비정상 [세포(생물학)|세포]와 관련된 희귀한 [[암]이며, 피부에서 [림프 노드]로 옮겨갈 수 있다. 증상은 고립된 뼈 병변에서부터 다계통질환에 이르기까지 다양하다. LCH는 [Histiocytosis|histiocytoses]라고 불리는 신드롬 그룹의 일부로서, [Histiocytoses]s (활성화된 [dendritic cell]s와 [macrophage]s의 고어적 용어)가 비정상적으로 확산되는 것이 특징이다. 이러한 질병들은 [백혈구]나 [림프종]과 같은 다른 형태의 [백혈구] 증식과 관련이 있다.

암은 [손-슐러-기독교병]을 포함한 여러 이름으로 퍼졌다 are related to other forms of abnormal proliferation of white blood cells, such as leukemias and lymphomas.

The cancer has gone by several names, including Hand–Schüller–Christian disease, Abt-Letterer-Siwe disease, Hashimoto-Pritzker disease (a very rare self-limiting variant seen at birth) and histiocytosis X, until it was renamed in 1985 by the Histiocyte Society.[1]

Classification

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Alternative names
Histiocytosis X

Histiocytosis X syndrome

Subordinate terms
Hand-Schüller-Christian disease

Letterer-Siwe disease
Histiocytosis X, unspecified
Eosinophilic Granulomatosis
Langerhans Cell granulomatosis
Langerhans Cell Histiocytosis, Hashimoto-Pritzker Type
Langerhans Cell Histiocytosis of lung
Langerhans Cell Histiocytosis, disseminated (clinical)
Langerhans Cell Histiocytosis, unifocal (clinical)

The disease spectrum results from clonal accumulation and proliferation of cells resembling the epidermal dendritic cells called Langerhans cells, sometimes called dendritic cell histiocytosis. These cells in combination with lymphocytes, eosinophils, and normal histiocytes form typical LCH lesions that can be found in almost any organ.[2] A similar set of diseases has been described in canine histiocytic diseases.

LCH is clinically divided into three groups: unifocal, multifocal unisystem, and multifocal multisystem.[3]

Unifocal

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'[eosinophilic granuloma]' (현재 [misnomer]]로 알려진 더 오래된 용어)라고도 불리는 Unifocal LCH는 랑게르한스 세포가 한 기관에서 확산되어 병변이라 불리는 손상을 일으키는 것이 특징인 질병이다. 그것은 전형적으로 외골격계 관여가 없지만, 피부, 폐, 위에서는 거의 병변을 발견할 수 없다. 장기에 단일 병변으로 나타날 수 있으며, 한 장기에 다량의 병변까지 나타날 수 있다. 여러 병변이 장기 전체에 흩어져 있을 때, 그것은 다초점적인 단조직 품종이라고 불릴 수 있다. 폐에서 발견되면 성인 흡연자에게서 가장 흔히 볼 수 있는 질병의 특별한 범주인 폐 랑게르한스 세포 열혈증과 구별되어야 한다.인용 오류: <ref> 태그가 잘못되었습니다; 잘못된 이름입니다, 예: 너무 많습니다 When found in the skin it is called cutaneous single system Langerhans cell LCH. This version can heal without therapy in some rare cases.[4] This primary bone involvement helps to differentiate eosinophilic granuloma from other forms of Langerhans Cell Histiocytosis (Letterer-Siwe or Hand-Schüller-Christian variant).[5]

Multifocal unisystem

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Seen mostly in children, multifocal unisystem LCH is characterized by fever, bone lesions and diffuse eruptions, usually on the scalp and in the ear canals. 50% of cases involve the pituitary stalk, often leading to diabetes insipidus. The triad of diabetes insipidus, exopthalmos, and lytic bone lesions is known as the Hand-Schüller-Christian triad. Peak onset is 2–10 years of age.

Multifocal multisystem

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Multifocal multisystem LCH, also called Letterer-Siwe disease, is an often rapidly progressing disease in which Langerhans Cell cells proliferate in many tissues. It is mostly seen in children under age 2, and the prognosis is poor: even with aggressive chemotherapy, the five-year survival is only 50%.[6]

Pulmonary Langerhans cell histiocytosis (PLCH)

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Pulmonary Langerhans cell histiocytosis (PLCH) is a unique form of LCH in that it occurs almost exclusively in cigarette smokers. It is now considered a form of smoking-related interstitial lung disease. Some affected people recover completely after they stop smoking, but others develop long-term complications such as pulmonary fibrosis and pulmonary hypertension.[7] PLCH patients, families, and caregivers are encouraged to join the NIH Rare Lung Diseases Consortium Contact Registry. This is a privacy protected site that provides up-to-date information for individuals interested in the latest scientific news, trials, and treatments related to rare lung diseases.

Signs and symptoms

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CT scan showing LCH infiltrating peri-orbital tissue (arrowed).
 
A patient with which is a subtype of Langerhans Cell Histiocytosis.

LCH provokes a non-specific inflammatory response, which includes fever, lethargy, and weight loss. Organ involvement can also cause more specific symptoms.

  • Bone: The most-frequently seen symptom in both unifocal and multifocal disease is painful bone swelling. The skull is most frequently affected, followed by the long bones of the upper extremities and flat bones. Infiltration in hands and feet is unusual. Osteolytic lesions can lead to pathological fractures.[8]
  • Skin: Commonly seen are a rash which varies from scaly erythematous lesions to red papules pronounced in intertriginous areas. Up to 80% of LCH patients have extensive eruptions on the scalp.
  • Bone marrow: Pancytopenia with superadded infection usually implies a poor prognosis. Anemia can be due to a number of factors and does not necessarily imply bone marrow infiltration.
  • Lymph node: Enlargement of the liver in 20%, spleen in 30% and lymph nodes in 50% of Histiocytosis cases.[9]
  • Endocrine glands: Hypothalamic pituitary axis commonly involved.[10] Diabetes insipidus is most common.[11] Anterior pituitary hormone deficiency is usually permanent.[12]
  • Lungs: some patients are asymptomatic, diagnosed incidentally because of lung nodules on radiographs; others suffer from chronic cough and shortness of breath.[13]
  • Less frequently gastrointestinal tract, central nervous system, and oral cavity.[14]

Pathophysiology

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The pathogenesis of Langerhans cell histiocytosis (LCH) is a matter of debate. There are ongoing investigations to determine whether LCH is a reactive (non-cancerous) or neoplastic (cancerous) process. Arguments supporting the reactive nature of LCH include the occurrence of spontaneous remissions, the extensive secretion of multiple cytokines by dendritic cells and bystander-cells (a phenomenon known as cytokine storm) in the lesional tissue, favorable prognosis and relatively good survival rate in patients without organ dysfunction or risk organ involvement.[15][16]

On the other hand, the infiltration of organs by monoclonal population of pathologic cells, and the successful treatment of subset of disseminated disease using chemotherapeutic regimens are all consistent with a neoplastic process.[17][18][19] In addition, a demonstration, using X chromosome–linked DNA probes, of LCH as a monoclonal proliferation provided additional support for the neoplastic origin of this disease.[20] While clonality is an important attribute of cancer, its presence does not prove that a proliferative process is neoplastic. Recurrent cytogenetic or genomic abnormalities would also be required to demonstrate convincingly that LCH is a malignancy.

An activating somatic mutation of a proto-oncogene in the Raf family, the BRAF gene, was detected in 35 of 61 (57%) LCH biopsy samples with mutations being more common in patients younger than 10 years (76%) than in patients aged 10 years and older (44%).[21] This study documented the first recurrent mutation in LCH samples. Two independent studies have confirmed this finding.[22][23] Presence of this activating mutation could support the notion to characterize LCH as myeloproliferative disorder.

Diagnosis

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Micrograph showing Langerhans Cell Histiocytosis. H&E stain.

Diagnosis is confirmed histologically by tissue biopsy. Hematoxylin-eosin stain of biopsy slide will show features of Langerhans Cell e.g. distinct cell margin, pink granular cytoplasm. Presence of Birbeck granules on electron microscopy and immuno-cytochemical features e. g. CD1 positivity are more specific. Initially routine blood tests e.g. full blood count, liver function test, U&Es, bone profile are done to determine disease extent and rule out other causes. Radiology will show osteolytic bone lesions and damage to the lung. The latter may be evident in chest X-rays with micronodular and interstitial infiltrate in the mid and lower zone of lung, with sparing of the Costophrenic angle or honeycomb appearance in older lesions. MRI and CT may show infiltration in sella turcica. Assessment of endocrine function and bonemarrow biopsy are also performed when indicated.

Treatment

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Guidelines for management of patients up to 18 years with Langerhans cell histiocytosis have been suggested.[30][31][32][33] Treatment is guided by extent of disease. Solitary bone lesion may be amenable through excision or limited radiation, dosage of 5-10 Gy for children, 24-30 Gy for adults. However systemic diseases often require chemotherapy. Use of systemic steroid is common, singly or adjunct to chemotherapy. Local steroid cream is applied to skin lesions. Endocrine deficiency often require lifelong supplement e.g. desmopressin for diabetes insipidus which can be applied as nasal drop. Chemotherapeutic agents such as alkylating agents, antimetabolites, vinca alkaloids either singly or in combination can lead to complete remission in diffuse disease.

예후

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단초점 질환에 탁월하다. 다초점성 질환의 경우 60%가 만성 코스를 갖고 있으며 30%는 완쾌, 사망률은 최대 10%에 이른다.[34]

Prevalence

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LCH usually affects children between 1 and 15 years old, with a peak incidence between 5 and 10 years of age. Among children under the age of 10, yearly incidence is thought to be 1 in 200,000;[35] and in adults even rarer, in about 1 in 560,000.[36] It has been reported in elderly but is vanishingly rare.[37] It is most prevalent in Caucasians, and affects males twice as often as females.[38] In other populations too the prevalence in males is slightly more than in females.[39]

LCH is usually a sporadic and non-hereditary condition but familial clustering has been noted in limited number of cases. Hashimoto-Pritzker disease is a congenital self-healing variant of Hand-Schüller-Christian disease.[40]

대중문화에서

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[집(TV시리즈)] 시즌3 10회에서하우스]]라는 제목의 "'메리 리틀 크리스마스', 주요 환자는 다양한 증상을 보이는 [[드워프리즘]을 가진 소녀로, 궁극적으로 랑게르한스 세포조직증 진단을 받는다.[41]

같이 보기

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각주

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  1. ↑ The Writing Group of the Histiocyte Society (1987). “Histiocytosis syndromes in children. Writing Group of the Histiocyte Society”. 《Lancet》 1 (8526): 208–9. doi:10.1016/S0140-6736(87)90016-X. PMID 2880029. 
  2. ↑ Makras P, Papadogias D, Kontogeorgos G, Piaditis G, Kaltsas G (2005). “Spontaneous gonadotrophin deficiency recovery in an adult patient with Langerhans cell Histiocytosis (LCH)”. 《Pituitary》 8 (2): 169–74. doi:10.1007/s11102-005-4537-z. PMID 16379033. 
  3. ↑ Cotran, Ramzi S.; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Robbins, Stanley L. (2005). 《Robbins and Cotran pathologic basis of disease》. St. Louis, Mo: Elsevier Saunders. 701–쪽. ISBN 978-0-8089-2302-2. 
  4. ↑ Afsar, Fatma Sule; Ergin, Malik; Ozek, Gulcihan; Vergin, Canan; Karakuzu, Ali; Seremet, Sila (2017). “Histiocitose de Células de Langerhans Autolimitada e de Início Tardio: Relato de Uma Entidade Raríssima”. 《Revista Paulista de Pediatria》 35 (1): 115–119. doi:10.1590/1984-0462/;2017;35;1;00015. ISSN 0103-0582. PMC 5417814. PMID 28977321. 
  5. ↑ Ladisch, Stephan (2011). 〈Histiocytosis Syndromes of Childhood〉. Kliegman, Robert M.; Stanton, Bonita F.; St. Geme, Joseph; Schor, Nina; Behrman, Richard E. 《Nelson Textbook of Pediatrics》 19판. Saunders. 1773–7쪽. ISBN 978-1-4377-0755-7. 
  6. ↑ Langerhans Cell Histiocytosis - eMedicine
  7. ↑ Juvet, Stephen C; Hwang, David; Downey, Gregory P (2010). “Rare lung diseases III: pulmonary Langerhans' cell histiocytosis”. 《Canadian Respiratory Journal》 17 (3): e55–62. doi:10.1155/2010/216240. PMC 2900147. PMID 20617216. 
  8. ↑ Stull, MA; Kransdorf, MJ; Devaney, KO (July 1992). “Langerhans cell histiocytosis of bone”. 《Radiographics》 12 (4): 801–23. doi:10.1148/radiographics.12.4.1636041. PMID 1636041. 
  9. ↑ “Langerhans Cell Histiocytosis - Patient UK”. 2007년 5월 10일에 확인함. 
  10. ↑ Kaltsas, GA; Powles, TB; Evanson, J; Plowman, PN; Drinkwater, JE; Jenkins, PJ; Monson, JP; Besser, GM; Grossman, AB (April 2000). “Hypothalamo-pituitary abnormalities in adult patients with langerhans cell histiocytosis: clinical, endocrinological, and radiological features and response to treatment”. 《The Journal of Clinical Endocrinology and Metabolism》 85 (4): 1370–6. doi:10.1210/jcem.85.4.6501. PMID 10770168. 
  11. ↑ Grois, N; Pötschger, U; Prosch, H; Minkov, M; Arico, M; Braier, J; Henter, JI; Janka-Schaub, G; Ladisch, S; Ritter, J; Steiner, M; Unger, E; Gadner, H; DALHX- and LCH I and II Study, Committee (February 2006). “Risk factors for diabetes insipidus in langerhans cell histiocytosis”. 《Pediatric Blood & Cancer》 46 (2): 228–33. doi:10.1002/pbc.20425. PMID 16047354. 
  12. ↑ Broadbent, V; Dunger, DB; Yeomans, E; Kendall, B (1993). “Anterior pituitary function and computed tomography/magnetic resonance imaging in patients with Langerhans cell histiocytosis and diabetes insipidus”. 《Medical and Pediatric Oncology》 21 (9): 649–54. doi:10.1002/mpo.2950210908. PMID 8412998. 
  13. ↑ Sholl, LM; Hornick, JL; Pinkus, JL; Pinkus, GS; Padera, RF (June 2007). “Immunohistochemical analysis of langerin in langerhans cell histiocytosis and pulmonary inflammatory and infectious diseases”. 《The American Journal of Surgical Pathology》 31 (6): 947–52. doi:10.1097/01.pas.0000249443.82971.bb. PMID 17527085. 
  14. ↑ Cisternino A, Asa'ad F, Fusco N, Ferrero S, Rasperini G (Oct 2015). “Role of multidisciplinary approach in a case of Langerhans cell histiocytosis with initial periodontal manifestations”. 《Int J Clin Exp Pathol》 8 (10): 13539–45. PMC 4680515. PMID 26722570. 
  15. ↑ Broadbent, V.; Davies, E.G.; Heaf, D.; Pincott, J.R.; Pritchard, J.; Levinsky, R.J.; Atherton, D.J.; Tucker, S. (1984). “Spontaneous remission of multi-system histiocytosis X”. 《Lancet》 1 (8371): 253–4. doi:10.1016/S0140-6736(84)90127-2. PMID 6142997. 
  16. ↑ Filippi, Paola; De Badulli, Carla; Cuccia, Mariaclara; Silvestri, Annalisa; De Dametto, Ennia; Pasi, Annamaria; Garaventa, Alberto; Prever, Adalberto Brach; del Todesco, Alessandra; Trizzino, Antonino; Danesino, Cesare; Martinetti, Miryam; Arico, Maurizio (2006). “Specific polymorphisms of cytokine genes are associated with different risks to develop single-system or multi-system childhood Langerhans cell histiocytosis”. 《British Journal of Haematology》 132 (6): 784–7. doi:10.1111/j.1365-2141.2005.05922.x. PMID 16487180. 
  17. ↑ Steen, A.E.; Steen, K.H.; Bauer, R.; Bieber, T. (2001년 7월 1일). “Successful treatment of cutaneous Langerhans cell histiocytosis with low-dose methotrexate”. 《British Journal of Dermatology》 145 (1): 137–140. doi:10.1046/j.1365-2133.2001.04298.x. PMID 11453923. 
  18. ↑ Allen CE, Flores R, Rauch R, Dauser R, Murray JC, Puccetti D, Hsu DA, Sondel P, Hetherington M, Goldman S, McClain KL (2010). “Neurodegenerative central nervous system Langerhans cell histiocytosis and coincident hydrocephalus treated with vincristine/cytosine arabinoside”. 《Pediatr Blood Cancer》 54 (3): 416–23. doi:10.1002/pbc.22326. PMC 3444163. PMID 19908293. 
  19. ↑ Minkov, M.; Grois, N.; Broadbent, V.; Ceci, A.; Jakobson, A.; Ladisch, S. (1999년 11월 1일). “Cyclosporine A therapy for multisystem Langerhans cell histiocytosis”. 《Medical and Pediatric Oncology》 33 (5): 482–485. doi:10.1002/(SICI)1096-911X(199911)33:5<482::AID-MPO8>3.0.CO;2-Y. PMID 10531573. 
  20. ↑ Willman, Cheryl L.; Busque, Lambert; Griffith, Barbara B.; Favara, Blaise E.; McClain, Kenneth L.; Duncan, Marilyn H.; Gilliland, D. Gary (1994년 7월 21일). “Langerhans'-Cell Histiocytosis (Histiocytosis X) -- A Clonal Proliferative Disease”. 《New England Journal of Medicine》 331 (3): 154–160. doi:10.1056/NEJM199407213310303. PMID 8008029. 
  21. ↑ Badalian-Very G, Vergilio JA, Degar BA, MacConaill LE, Brandner B, Calicchio ML, Kuo FC, Ligon AH, Stevenson KE, Kehoe SM, Garraway LA, Hahn WC, Meyerson M, Fleming MD, Rollins BJ (2010). “Recurrent BRAF mutations in Langerhans cell histiocytosis”. 《Blood》 116 (11): 1919–23. doi:10.1182/blood-2010-04-279083. PMC 3173987. PMID 20519626. 
  22. ↑ Satoh T, Smith A, Sarde A, Lu HC, Mian S, Mian S, Trouillet C, Mufti G, Emile JF, Fraternali F, Donadieu J, Geissmann F (2012). “B-RAF mutant alleles associated with Langerhans cell histiocytosis, a granulomatous pediatric disease”. 《PLOS ONE》 7 (4): e33891. doi:10.1371/journal.pone.0033891. PMC 3323620. PMID 22506009. 
  23. ↑ Peters, Tricia L.; Tsz-Kwong Chris Man; Price, Jeremy; George, Renelle; Phaik Har Lim; Kenneth Matthew Heym; Merad, Miriam; McClain, Kenneth L.; Allen, Carl E. (2011년 12월 10일). “1372 Frequent BRAF V600E Mutations Are Identified in CD207+ Cells in LCH Lesions, but BRAF Status does not Correlate with Clinical Presentation of Patients or Transcriptional Profiles of CD207+ Cells”. Oral and Poster Abstracts presented at 53rd ASH Annual Meeting and Exposition 
  24. ↑ 가 나 Wilson, AJ; Maddox, PH; Jenkins, D (January 1991). “CD1a and S100 antigen expression in skin Langerhans cells in patients with breast cancer”. 《The Journal of Pathology》 163 (1): 25–30. doi:10.1002/path.1711630106. PMID 2002421. 
  25. ↑ Coppola, D; Fu, L; Nicosia, SV; Kounelis, S; Jones, M (May 1998). “Prognostic significance of p53, bcl-2, vimentin, and S100 protein-positive Langerhans cells in endometrial carcinoma”. 《Human Pathology》 29 (5): 455–62. doi:10.1016/s0046-8177(98)90060-0. PMID 9596268. 
  26. ↑ McLelland, J; Chu, AC (October 1988). “Comparison of peanut agglutinin and S100 stains in the paraffin tissue diagnosis of Langerhans cell histiocytosis”. 《The British Journal of Dermatology》 119 (4): 513–9. doi:10.1111/j.1365-2133.1988.tb03255.x. PMID 2461216. 
  27. ↑ Ye, F; Huang, SW; Dong, HJ (November 1990). “Histiocytosis X. S-100 protein, peanut agglutinin, and transmission electron microscopy study”. 《American Journal of Clinical Pathology》 94 (5): 627–31. doi:10.1093/ajcp/94.5.627. PMID 2239828. 
  28. ↑ Valladeau J, Ravel O, Dezutter-Dambuyant C, Moore K, Kleijmeer M, Liu Y, Duvert-Frances V, Vincent C, Schmitt D, Davoust J, Caux C, Lebecque S, Saeland S (2000). “Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules”. 《Immunity》 12 (1): 71–81. doi:10.1016/S1074-7613(00)80160-0. PMID 10661407. 
  29. ↑ Lau, SK; Chu, PG; Weiss, LM (April 2008). “Immunohistochemical expression of Langerin in Langerhans cell histiocytosis and non-Langerhans cell histiocytic disorders”. 《The American Journal of Surgical Pathology》 32 (4): 615–9. doi:10.1097/PAS.0b013e31815b212b. PMID 18277880. 
  30. ↑ Haupt, Riccardo; Minkov, Milen; Astigarraga, Itziar; Schäfer, Eva; Nanduri, Vasanta; Jubran, Rima; Egeler, R. Maarten; Janka, Gritta; Micic, Dragan; Rodriguez-Galindo, Carlos; Van Gool, Stefaan; Visser, Johannes; Weitzman, Sheila; Donadieu, Jean (February 2013). “Langerhans cell histiocytosis (LCH): Guidelines for diagnosis, clinical work-up, and treatment for patients till the age of 18 years”. 《Pediatric Blood & Cancer》 60 (2): 175–184. doi:10.1002/pbc.24367. PMC 4557042. PMID 23109216. 
  31. ↑ Girschikofsky, Michael; Arico, Maurizio; Castillo, Diego; Chu, Anthony; Doberauer, Claus; Fichter, Joachim; Haroche, Julien; Kaltsas, Gregory A; Makras, Polyzois; Marzano, Angelo V; de Menthon, Mathilde; Micke, Oliver; Passoni, Emanuela; Seegenschmiedt, Heinrich M; Tazi, Abdellatif; McClain, Kenneth L (2013). “Management of adult patients with Langerhans cell histiocytosis: recommendations from an expert panel on behalf of Euro-Histio-Net”. 《Orphanet Journal of Rare Diseases》 8 (1): 72. doi:10.1186/1750-1172-8-72. PMC 3667012. PMID 23672541. 
  32. ↑ “Langerhans cell histiocytosis - Histiocyte Society Evaluation and Treatment Guidelines”. April 2009. 
  33. ↑ “Langerhans Cell Histiocytosis Treatment (PDQ®)”.  and 1
  34. ↑ Komp D, El Mahdi A, Starling K, Easley J, Vietti T, Berry D, George S (1980). “Quality of survival in Histiocytosis X: a Southwest Oncology Group study”. 《Med. Pediatr. Oncol.》 8 (1): 35–40. doi:10.1002/mpo.2950080106. PMID 6969347. 
  35. ↑ “MedlinePlus Medical Encyclopedia: Histiocytosis”. 2007년 5월 10일에 확인함. 
  36. ↑ “Histiocytosis Association of Canada”. 2007년 5월 14일에 원본 문서에서 보존된 문서. 2007년 5월 16일에 확인함. 
  37. ↑ Gerlach, Beatrice; Stein, Annette; Fischer, Rainer; Wozel, Gottfried; Dittert, Dag-Daniel; Richter, Gerhard (1998). “Langerhanszell-Histiozytose im Alter” [Langerhans cell histiocytosis in the elderly]. 《Der Hautarzt》 (독일어) 49 (1): 23–30. doi:10.1007/s001050050696. PMID 9522189. 
  38. ↑ Sellari-Franceschini, S.; Forli, F.; Pierini, S.; Favre, C.; Berrettini, S.; Macchia, P.A. (1999). “Langerhans' cells histiocytosis: a case report”. 《International Journal of Pediatric Otorhinolaryngology》 48 (1): 83–7. doi:10.1016/S0165-5876(99)00013-0. PMID 10365975. 
  39. ↑ Aricò, M.; Girschikofsky, M.; Généreau, T.; Klersy, C.; McClain, K.; Grois, N.; Emile, J.-F.; Lukina, E.; De Juli, E.; Danesino, C. (2003). “Langerhans cell histiocytosis in adults: Report from the International Registry of the Histiocyte Society”. 《European Journal of Cancer》 39 (16): 2341–8. doi:10.1016/S0959-8049(03)00672-5. PMID 14556926. 
  40. ↑ Kapur, Payal; Erickson, Christof; Rakheja, Dinesh; Carder, K. Robin; Hoang, Mai P. (2007). “Congenital self-healing reticulohistiocytosis (Hashimoto-Pritzker disease): Ten-year experience at Dallas Children's Medical Center”. 《Journal of the American Academy of Dermatology》 56 (2): 290–4. doi:10.1016/j.jaad.2006.09.001. PMID 17224372. 
  41. ↑ [하우스(시즌 3)|"하우스" (시즌 3)] CSI 시즌 15편 4편에서 한 학생이 LCH를 가지고 있다. 또한 '굿 닥터' 시즌1 5회에서는 머피 박사가 이전에 골육종 진단을 받은 소년에게서 랑게르한스 세포조직증을 진단하려고 한다.틀:Citation 필요} 브룩 로러(Brooke Rohrer)는 '[Mystery Divich]' '핑크를 본 여인'의 한 에피소드에서 복통 증세를 경험하고 있는 랑게르한스 세포 조직증후군 진단을 받았다

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    랑게르한스 세포 조직증은 권위 있는 교과서에서도 가끔 "랑게르한" 또는 "랑게르한" 세포 조직체로 잘못 표기된다. 그러나 그 이름은 발견자인 폴 랑게르한스에서 유래되었다.ref>Jolles, S. (April 2002). “Paul Langerhans”. 《Journal of Clinical Pathology》 55 (4): 243. doi:10.1136/jcp.55.4.243. PMC 1769627. PMID 11919207. 

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