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*LSC develops over the regions which are accessible to scratching.
*LSC develops over the regions which are accessible to scratching.
*The pathogenesis of LSC is unclear, but clinical lesions are due to severe paroxysmal pruritus.  
*The pathogenesis of LSC is unclear, but clinical lesions are due to severe paroxysmal pruritus. The physical and emotional component of the cause are well known, compared to genetic, vascular and neurogenic component.
*Skin with atopic dermatitis and atopic diathesis is most likely to develop lichenification.  
*Skin with atopic dermatitis and atopic diathesis is most likely to develop lichenification.
*There could be a potential relationship between central and peripheral neural tissue and inflammatory mediators in the perception of itch, and leading to changes.  
*There could be a potential relationship between central and peripheral neural tissue and inflammatory mediators in the perception of itch, and leading to changes.
*Emotional disturbances such as anxiety, depression and obsessive-compulsive disorder or other stressors contribute to itching in many cases.
*Emotional disturbances such as anxiety, depression and obsessive-compulsive disorder or other stressors contribute to itching in many cases.
*Transient receptor potential channel A1 ( TRPA1) which is seen in skin, sensory neuron and other tissues has been associated with decreased expression in the lesions of LSC, as per few studies. <ref name="pmid33183050">{{cite journal| author=Qiu Y, Tang N, Zhang W, Xiong JX, Hu L, Cai T| title=Down-regulated expression of transient receptor potential ankyrin 1 in lichen simplex chronicus. | journal=Ann Palliat Med | year= 2020 | volume= 9 | issue= 6 | pages= 3757-3765 | pmid=33183050 | doi=10.21037/apm-20-1712 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33183050  }}</ref>
*Some studies tried to find genetic support to pathology. Like, Serotonin transporter (5HTT) gene polymorphism and dysfunction association to LSC <ref name="pmid18986359">{{cite journal| author=Kirtak N, Inaloz HS, Akçali C, Erdal E, Herken H, Yildirim M | display-authors=etal| title=Association of serotonin transporter gene-linked polymorphic region and variable number of tandem repeat polymorphism of the serotonin transporter gene in lichen simplex chronicus patients with psychiatric status. | journal=Int J Dermatol | year= 2008 | volume= 47 | issue= 10 | pages= 1069-72 | pmid=18986359 | doi=10.1111/j.1365-4632.2008.03821.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18986359  }}</ref>. Transient receptor potential channel A1 ( TRPA1) which is seen in skin, sensory neuron and other tissues has been associated with decreased expression in the lesions of LSC. <ref name="pmid33183050">{{cite journal| author=Qiu Y, Tang N, Zhang W, Xiong JX, Hu L, Cai T| title=Down-regulated expression of transient receptor potential ankyrin 1 in lichen simplex chronicus. | journal=Ann Palliat Med | year= 2020 | volume= 9 | issue= 6 | pages= 3757-3765 | pmid=33183050 | doi=10.21037/apm-20-1712 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33183050  }}</ref> Long interspersed element-1 (LINE-1) pattern changes in epidermis of LSC was found in a study. <ref name="pmid23517394">{{cite journal| author=Yooyongsatit S, Ruchusatsawat K, Supiyaphun P, Noppakun N, Mutirangura A, Wongpiyabovorn J| title=Alterations in the LINE-1 methylation pattern in patients with lichen simplex chronicus. | journal=Asian Pac J Allergy Immunol | year= 2013 | volume= 31 | issue= 1 | pages= 51-7 | pmid=23517394 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23517394  }}</ref>
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*On microscopic histopathological analysis, LSC appears as a hyperkeratotic plaque, with parakeratosis, acanthosis, spongiosis, papillary dermal fibrosis with vertical streaking of collagen bundles, irregularly thickened rete edges, and pseudoepitheliomatous hyperplasia. Electron microscopy shows collagen fibers attached to and above lamina basalis.
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK499991/ |title=Lichen Simplex Chronicus - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}} {{cite web |url=https://emedicine.medscape.com/article/1123423-overview |title=Lichen Simplex Chronicus: Background, Pathophysiology, Etiology |format= |work= |accessdate=}}


==Causes==
==Causes==

Revision as of 05:32, 28 June 2021


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karnik Raju Paila Bangaru, M.B.B.S.[2] Kiran Singh, M.D. [3]

Synonyms and keywords: Neurodermatitis, neurodermatitides, circumscribed neurodermatitis, circumscribed neurodermatitides, localized neurodermatitis, localized neurodermatitides

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Overview

Lichen simplex chronicus (LSC) is a chronic skin condition associated with a persistent itch-scratch cycle, leading to a thick, leathery, dark (lichenified) skin. Similar to many other skin conditions, it may present with associated dryness, scaling or erythema. Commonly affected regions include neck, ankles, extremities, scalp and genital region. The incidence and prevalence of the condition are not well established, but this is observed to be more common in adult female patients. The pathophysiology remains unclear, but its thought to arise from disturbances between central and peripheral neural tissue in the perception of itch, causing the persistent itch-scratch cycle. Several psychological disturbances like anxiety and depression have been associated with this dermatological condition. [1][2][3][4]

Pathophysiology

  • LSC develops over the regions which are accessible to scratching.
  • The pathogenesis of LSC is unclear, but clinical lesions are due to severe paroxysmal pruritus. The physical and emotional component of the cause are well known, compared to genetic, vascular and neurogenic component.
  • Skin with atopic dermatitis and atopic diathesis is most likely to develop lichenification.
  • There could be a potential relationship between central and peripheral neural tissue and inflammatory mediators in the perception of itch, and leading to changes.
  • Emotional disturbances such as anxiety, depression and obsessive-compulsive disorder or other stressors contribute to itching in many cases.
  • Some studies tried to find genetic support to pathology. Like, Serotonin transporter (5HTT) gene polymorphism and dysfunction association to LSC [5]. Transient receptor potential channel A1 ( TRPA1) which is seen in skin, sensory neuron and other tissues has been associated with decreased expression in the lesions of LSC. [6] Long interspersed element-1 (LINE-1) pattern changes in epidermis of LSC was found in a study. [7]
  • On microscopic histopathological analysis, LSC appears as a hyperkeratotic plaque, with parakeratosis, acanthosis, spongiosis, papillary dermal fibrosis with vertical streaking of collagen bundles, irregularly thickened rete edges, and pseudoepitheliomatous hyperplasia. Electron microscopy shows collagen fibers attached to and above lamina basalis.
  • "Lichen Simplex Chronicus - StatPearls - NCBI Bookshelf". "Lichen Simplex Chronicus: Background, Pathophysiology, Etiology".

Causes

Disease name] may be caused by [cause1], [cause2], or [cause3].

OR

Common causes of [disease] include [cause1], [cause2], and [cause3].

OR

The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

OR

The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

Differentiating [disease name] from other Diseases

  • [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
  • [Differential dx1]
  • [Differential dx2]
  • [Differential dx3]

Epidemiology and Demographics

  • The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
  • In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].

Age

  • Patients of all age groups may develop [disease name].
  • [Disease name] is more commonly observed among patients aged [age range] years old.
  • [Disease name] is more commonly observed among [elderly patients/young patients/children].

Gender

  • [Disease name] affects men and women equally.
  • [Gender 1] are more commonly affected with [disease name] than [gender 2].
  • The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.

Race

  • There is no racial predilection for [disease name].
  • [Disease name] usually affects individuals of the [race 1] race.
  • [Race 2] individuals are less likely to develop [disease name].

Risk Factors

  • Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Natural History, Complications and Prognosis

  • The majority of patients with [disease name] remain asymptomatic for [duration/years].
  • Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
  • If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
  • Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
  • Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].

Diagnosis

Diagnostic Criteria

  • The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
  • [criterion 1]
  • [criterion 2]
  • [criterion 3]
  • [criterion 4]

History and Symptoms

  • [Disease name] is usually asymptomatic.
  • Symptoms of [disease name] may include the following:
  • [symptom 1]
  • [symptom 2]
  • [symptom 3]
  • [symptom 4]
  • [symptom 5]
  • [symptom 6]

Physical Examination

  • Patients with [disease name] usually appear [general appearance].
  • Physical examination may be remarkable for:
  • [finding 1]
  • [finding 2]
  • [finding 3]
  • [finding 4]
  • [finding 5]
  • [finding 6]

Laboratory Findings

  • There are no specific laboratory findings associated with [disease name].
  • A [positive/negative] [test name] is diagnostic of [disease name].
  • An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
  • Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with [disease name].

OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

OR

[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

There are no MRI findings associated with [disease name].

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References

  1. Juarez, Michelle C.; Kwatra, Shawn G. (2020). "A systematic review of evidence based treatments for lichen simplex chronicus". Journal of Dermatological Treatment: 1–9. doi:10.1080/09546634.2019.1708856. ISSN 0954-6634.
  2. Boozalis, Emily; Tang, Olive; Patel, Shivani; Semenov, Yevgeniy R.; Pereira, Manuel P.; Stander, Sonja; Kang, Sewon; Kwatra, Shawn G. (2018). "Ethnic differences and comorbidities of 909 prurigo nodularis patients". Journal of the American Academy of Dermatology. 79 (4): 714–719.e3. doi:10.1016/j.jaad.2018.04.047. ISSN 0190-9622.
  3. Whang KA, Khanna R, Thomas J, Aguh C, Kwatra SG (2019). "Racial and Gender Differences in the Presentation of Pruritus". Medicines (Basel). 6 (4). doi:10.3390/medicines6040098. PMC 6963580 Check |pmc= value (help). PMID 31569651.
  4. Huang, Amy H.; Canner, Joseph K.; Khanna, Raveena; Kang, Sewon; Kwatra, Shawn G. (2020). "Real-World Prevalence of Prurigo Nodularis and Burden of Associated Diseases". Journal of Investigative Dermatology. 140 (2): 480–483.e4. doi:10.1016/j.jid.2019.07.697. ISSN 0022-202X.
  5. Kirtak N, Inaloz HS, Akçali C, Erdal E, Herken H, Yildirim M; et al. (2008). "Association of serotonin transporter gene-linked polymorphic region and variable number of tandem repeat polymorphism of the serotonin transporter gene in lichen simplex chronicus patients with psychiatric status". Int J Dermatol. 47 (10): 1069–72. doi:10.1111/j.1365-4632.2008.03821.x. PMID 18986359.
  6. Qiu Y, Tang N, Zhang W, Xiong JX, Hu L, Cai T (2020). "Down-regulated expression of transient receptor potential ankyrin 1 in lichen simplex chronicus". Ann Palliat Med. 9 (6): 3757–3765. doi:10.21037/apm-20-1712. PMID 33183050 Check |pmid= value (help).
  7. Yooyongsatit S, Ruchusatsawat K, Supiyaphun P, Noppakun N, Mutirangura A, Wongpiyabovorn J (2013). "Alterations in the LINE-1 methylation pattern in patients with lichen simplex chronicus". Asian Pac J Allergy Immunol. 31 (1): 51–7. PMID 23517394.

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