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generic term for inflammatory conditions of the skin; particularly with vesiculation in the acute stages

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湿疹(しっしん)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/07/31 18:01:16」(JST)

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Eczema herpeticum is a rare but severe disseminated infection that generally occurs at sites of skin damage produced by, for example, atopic dermatitis, burns, long term usage of topical steroids or eczema.^[1] It is also known as Kaposi varicelliform eruption, Pustulosis varioliformis acute and Kaposi-Juliusberg dermatitis.

Some sources reserve the term "eczema herpeticum" when the cause is due to human herpes simplex virus,^[2] and the term "Kaposi varicelliform eruption" to describe the general presentation without specifying the virus.^[3]

This condition is most commonly caused by herpes simplex virus type 1 or 2, but may also be caused by coxsackievirus A16, or vaccinia virus.^[1] It appears as numerous umbilicated vescicles superimposed on healing atopic dermatitis. it is often accompanied by fever and lymphadenopathy. Eczema herpeticum can be life-threatening in babies.

History

Eczema herpeticum was first described by Moriz Kaposi in 1887. Fritz Juliusberg coined the term Pustulosis varioliformis acute in 1898.

Presentation

This infection affects multiple organs, including the eyes, brain, lung, and liver, and can be fatal.

Treatment

It can be treated with systemic antiviral drugs, such as acyclovir or valaciclovir.^[4] Foscarnet may also be used for immunocompromised host with Herpes simplex and acyclovir-resistant Herpes simplex.

References

^ ^a ^b Olson J, Robles DT, Kirby P, Colven R (2008). "Kaposi varicelliform eruption (eczema herpeticum)". Dermatology online journal 14 (2): 18. PMID 18700121.
^ "eczema herpeticum" at Dorland's Medical Dictionary
^ "Kaposi varicelliform eruption" at Dorland's Medical Dictionary
^ Brook I, Frazier EH, Yeager JK (April 1998). "Microbiology of infected eczema herpeticum". Journal of the American Academy of Dermatology 38 (4): 627–9. doi:10.1016/S0190-9622(98)70130-6. PMID 9555806.

External links

Eczema Herpeticum photo library at Dermnet
Images of Eczema herpeticum from Pedoia

UpToDate Contents

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1. 単純ヘルペスウイルス1型感染の臨床症状および診断 clinical manifestations and diagnosis of herpes simplex virus type 1 infection
2. アトピー性皮膚炎（湿疹）の治療 treatment of atopic dermatitis eczema
3. 免疫正常患者における単純ヘルペスウイルス1型感染の治療 treatment of herpes simplex virus type 1 infection in immunocompetent patients
4. 小児における非定型性発疹 atypical exanthems in children
5. 皮膚の水疱を有する患者に対するアプローチ approach to the patient with cutaneous blisters

English Journal

Pathological role of regulatory T cells in the initiation and maintenance of eczema herpeticum lesions.

Takahashi R, Sato Y, Kurata M, Yamazaki Y, Kimishima M, Shiohara T.Author information Division of Flow Cytometry, Kyorin University Graduate School of Medicine, Mitaka, Tokyo 181-8611, Japan.AbstractIt remains unknown why the occurrence of eczema herpeticum (EH) caused by an extensive disseminated cutaneous infection with HSV-1 or HSV-2 is associated with the exacerbation of atopic dermatitis lesions after withdrawal of treatment. Although regulatory T cells (Tregs) limit the magnitude of HSV-specific T cell responses in mice, their role in the induction and resolution of EH has not been defined. We initially investigated the frequencies, phenotype, and function of Tregs in the peripheral blood of atopic dermatitis with EH (ADEH) patients at onset and after clinical resolution, atopic dermatitis patients without EH, and healthy controls. Tregs with the skin-homing phenotype and the activated/induced phenotype were expanded at onset and contracted upon resolution. Treg-suppressive capacity was retained in ADEH patients and, the expanded Tregs suppressed IFN-γ production from HSV-1-specific CD8(+) and CD4(+) T cells. The increased frequency of CD14(dim)CD16(+) proinflammatory monocytes (pMOs) was also observed in the blood and EH skin lesions. Thus, pMOs detected in ADEH patients at onset were characterized by an increased ability to produce IL-10 and a decreased ability to produce proinflammatory cytokines, unlike their normal counterparts. Our coculture study using Tregs and pMOs showed that the pMOs can promote the expansion of inducible Tregs. Tregs were detected frequently in the vicinity of HSV-expressing and varicella zoster virus-expressing CD16(+) monocytes in the EH lesions. Expansions of functional Tregs, together with pMOs, initially required for ameliorating excessive inflammation occurring after withdrawal of topical corticosteroids could, in turn, contribute to the initiation and progression of HSV reactivation, resulting in the onset of EH.
Journal of immunology (Baltimore, Md. : 1950).J Immunol.2014 Feb 1;192(3):969-78. doi: 10.4049/jimmunol.1300102. Epub 2013 Dec 30.
It remains unknown why the occurrence of eczema herpeticum (EH) caused by an extensive disseminated cutaneous infection with HSV-1 or HSV-2 is associated with the exacerbation of atopic dermatitis lesions after withdrawal of treatment. Although regulatory T cells (Tregs) limit the magnitude of HSV-s
PMID 24379126

Herpesviruses and the microbiome.

Dreyfus DH.Author information Department of Pediatrics, Clinical Faculty, Yale School of Medicine, New Haven, and the Center for Allergy, Asthma, and Immunology, Waterbury, Conn. Electronic address: dhdreyfusmd@gmail.com.AbstractThe focus of this article will be to examine the role of common herpesviruses as a component of the microbiome of atopic patients and to review clinical observations suggesting that atopic patients might be predisposed to more severe and atypical herpes-related illness because their immune response is biased toward a TH2 cytokine profile. Human populations are infected with 8 herpesviruses, including herpes simplex virus HSV1 and HSV2 (also termed HHV1 and HHV2), varicella zoster virus (VZV or HHV3), EBV (HHV4), cytomegalovirus (HHV5), HHV6, HHV7, and Kaposi sarcoma-associated herpesvirus (termed KSV or HHV8). Herpesviruses are highly adapted to lifelong infection of their human hosts and thus can be considered a component of the human "microbiome" in addition to their role in illness triggered by primary infection. HSV1 and HSV2 infection and reactivation can present with more severe cutaneous symptoms termed eczema herpeticum in the atopic population, similar to the more severe eczema vaccinatum, and drug reaction with eosinophilia and systemic symptoms syndrome (DRESS) is associated with reactivation of HSV6 and possibly other herpesviruses in both atopic and nonatopic patients. In this review evidence is reviewed that primary infection with herpesviruses may have an atypical presentation in the atopic patient and conversely that childhood infection might alter the atopic phenotype. Reactivation of latent herpesviruses can directly alter host cytokine profiles through viral expression of cytokine-like proteins, such as IL-10 (EBV) or IL-6 (cytomegalovirus and HHV8), viral encoded and secreted siRNA and microRNAs, and modulation of expression of host transcription pathways, such as nuclear factor κB. Physicians caring for allergic and atopic populations should be aware of common and uncommon presentations of herpes-related disease in atopic patients to provide accurate diagnosis and avoid unnecessary laboratory testing or incorrect diagnosis of other conditions, such as drug allergy or autoimmune disease. Antiviral therapy and vaccines should be administered promptly when indicated clinically.
The Journal of allergy and clinical immunology.J Allergy Clin Immunol.2013 Dec;132(6):1278-86. doi: 10.1016/j.jaci.2013.02.039. Epub 2013 Apr 20.
The focus of this article will be to examine the role of common herpesviruses as a component of the microbiome of atopic patients and to review clinical observations suggesting that atopic patients might be predisposed to more severe and atypical herpes-related illness because their immune response
PMID 23611298