Lichen simplex chronicus (LSC) is thickening of the skin with variable scaling that arises secondary to repetitive scratching or rubbing. Lichen simplex chronicus is not a primary process. Rather, a person senses pruritus in a specific area of skin (with or without underlying pathology) and causes mechanical trauma to the point of lichenification.
A proposed variant of lichen simplex chronicus is lichen amyloidosis. Lichen amyloidosis is described as lichen simplex chronicus in which the keratinocytes have necrosed and formed keratinocytic-derived amyloid in the dermis. The initial insult is pruritus with resultant amyloid formation, rather than the reverse.[1, 2]
Lichen simplex chronicus is found on the skin in regions accessible to scratching. Pruritus provokes rubbing that produces clinical lesions, but the underlying pathophysiology is unknown. Some skin types are more prone to lichenification, such as skin that tends toward eczematous conditions (ie, atopic dermatitis, atopic diathesis). A relationship likely exists between central and peripheral neural tissue and inflammatory cell products in the perception of itch and ensuing changes in lichen simplex chronicus. Emotional tensions, such as in patients with anxiety, depression, or obsessive-compulsive disorder, may play a key role in inducing a pruritic sensation, leading to scratching that can become self-perpetuating.[3, 4, 5, 6] The possible interplay among primary lesions, psychic factors, and the intensity of pruritus additively influence the extent and severity of lichen simplex chronicus.
A small study looking at lichen simplex chronicus and the use of P-phenylenediamine (PPD)–containing hair dye showed clinically relevant improvement in symptoms after discontinuation of PPD exposure,[7] thus providing a basis for the role of sensitization and contact dermatitis in the etiology of lichen simplex chronicus.
Atopic dermatitis results in a higher probability of developing lichen simplex chronicus.
Insect bites, scars (eg, traumatic, postherpetic/zoster[8] ), acne keloidalis nuchae,[9] xerosis, venous insufficiency, and asteatotic eczema are common factors.
Neurodermatitis is a term that historically has been used interchangeably with lichen simplex chronicus, given that psychological factors appear to play a role in the development or exacerbation of the condition.[10, 11, 12] A 2014 study demonstrated an increased prevalence of lichen simplex chronicus in patients with underlying anxiety and obsessive-compulsive disorder compared with age- and sex-matched controls.[5] A 2015 study showed that patients with lichen simplex chronicus have increased rates of clinical depression compared with patients without the condition.[6]
Lithium has been linked to lichen simplex chronicus in one reported case. Lichen simplex chronicus was dependent on the administration of lithium as evidenced by the observation that the lichen simplex chronicus remitted when the medication was discontinued and recurred when it was restarted.[13]
A small study looking at lichen simplex chronicus and the use of PPD-containing hair dye showed clinically relevant improvement in symptoms after discontinuation of PPD exposure, thus providing a basis for the role of sensitization and contact dermatitis in the etiology of lichen simplex chronicus.[7] . Several of the patients who cleared after avoiding paraphenylenediamine had widespread, not localized, dermatitis.
Long-term exposure to street traffic exhaust has been associated with an increase in the frequency of childhood skin diseases, including lichen simplex chronicus.[14]
Some reserve the diagnosis of lichen simplex for patients who have no known predisposing skin disorder. The term secondary lichenification has been used if the eruption is initiated by a primary dermatosis.
Exact frequency in the general population is unknown. In one study, 12% of aging patients with pruritic skin had lichen simplex chronicus.
Race
No differences are reported in frequency among races, although prior authors claimed lichen simplex chronicus was more common in Asians and African Americans. The appearance of lesions on darker skin sometimes shows follicular prominence. Secondary pigmentary alterations are also more severe in individuals with darker skin.
Sex
Lichen simplex chronicus is observed more commonly in females than in males. Lichen nuchae is a form of lichen simplex that occurs on the midposterior neck and is observed almost exclusively in women.
Age
Lichen simplex chronicus occurs mostly in mid-to-late adulthood, with highest prevalence in persons aged 30-50 years.
Lesions may clear completely. Pruritus may resolve, but some mild scarring and pigmentary changes remain after successful treatment. Relapse is more likely in periods of psychic stress or if previously affected skin is stressed by extremes of heat or humidity or by skin irritants or allergens. In patients who do not comply with the treatment regimen and scratching cessation, lesions will not improve.
No mortality occurs as a result of lichen simplex chronicus. Overall, pruritus of lichen simplex chronicus is mild to moderate, but paroxysms may occur that are relieved by moderate-to-severe rubbing and scratching. Pruritus is usually described as much worse during periods of inactivity, usually at bedtime and during the night.[15] Touch and emotional stress also may provoke pruritus, which is relieved by moderate-to-severe rubbing and scratching.
Lesions cause little direct morbidity; however, occasionally patients report decreased or interrupted sleep, which affects motor and mental functioning.
Lichen simplex chronicus may become secondarily infected after excoriation.
Lichen simplex chronicus is often visible enough to cause patients to seek treatment.
Direct patients to stop scratching. Lichen simplex chronicus is worsened or improved depending on the patient's ability to stop scratching. Discussing individual ways to change habitual scratching is helpful.
Patients with lichen simplex chronicus usually describe stable pruritic plaques on one or more areas; however, thickening of the skin occurs on any location that the patient can reach, including the following:
Scalp[16]
Nape of neck
Extensor forearms and elbows
Vulva and scrotum[6, 17, 18, 19, 20]
Upper medial thighs, knees, lower legs, and ankles
Erythema is noted most in early lesions.
Pruritus is described as worse when patients are still or quiet and as much less or nonexistent when patients are active.
Pruritus is usually intermittent; the resultant scratching provides temporary relief.
Patients may have a past medical history of a chronic skin condition or acute trauma. Patients with atopic dermatitis may have lichen simplex chronicus in areas of former atopic outbreaks. Sites of irritant or allergic contact dermatitis, insect bites, or other past minor skin trauma sometimes demonstrate pruritus and, subsequently, lichen simplex chronicus.
One or more slightly erythematous, scaly, well-demarcated, lichenified, firm, rough plaques with exaggerated skin lines are noted.
Each palm-sized plaque may have 3 zones. A 2- to 3-cm wide peripheral zone that is barely thickened may have isolated papules. The middle zone has lenticular and hemispheric prurigo papules that may be excoriated. The central zone has the greatest thickening and pigmentary alteration.
Pigmentary changes (especially hyperpigmentation) are seen variably as in any dermatitic lesion.
Rubbing plays a key role in lesion formation and is visualized variably by white scratch marks, erosion, and ulceration from deeper scratching.
Lichen simplex chronicus is one of the hyperkeratotic processes from which a cutaneous horn may grow.[21]
Patients may scratch lesions de novo when observed. Some patients may start scratching while discussing the itch or describing the lesions.
Note the images below.
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Lichen simplex chronicus of the dorsal hand and wrist demonstrating increased skin thickness and accentuation of skin markings.
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Plaque of lichen simplex chronicus of the leg with accentuated skin markings and excoriations.
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Plaques of lichen simplex chronicus on the hand.
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Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Der....
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Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbi....
Patients with lichen simplex chronicus have higher rates of diabetes mellitus, hyperlipidemia, hypertension, coronary artery disease, peripheral vascular disease, chronic obstructive pulmonary disease, and chronic kidney disease.[6]
Patients with lichen simplex chronicus are more likely to develop erectile dysfunction than age-matched controls. Physicians should be aware of the association between lichen simplex chronicus and erectile dysfunction and advise or arrange timely sexual consultations.[6]
An elevated serum immunoglobulin E level occasionally supports the diagnosis of an underlying atopic diathesis. Perform potassium hydroxide examination and fungal cultures to exclude tinea cruris or candidiasis in patients with genital lichen simplex chronicus.
Patch testing helps exclude allergic contact dermatitis as an underlying primary dermatosis (eg, allergic contact dermatitis to nickel with secondary lichen simplex chronicus) or as a factor in chronicity (eg, allergic contact dermatitis to topical corticosteroids used to treat lichen simplex chronicus).
Frequently, skin biopsy is performed to exclude other disorders, particularly psoriasis or mycosis fungoides (cutaneous T-cell lymphoma) in elderly patients.[22]
Histologic examination demonstrates hyperkeratosis, acanthosis, spongiosis, and patches of parakeratosis in the epidermis. Epidermal thickening of all layers is noted, with elongation of rete ridges and with pseudoepitheliomatous hyperplasia. Papillary dermal fibrosis with vertical streaking of collagen bundles is characteristic.
A characteristic finding of lichen simplex chronicus that is noted on electron microscopy is frequent collagen fibers attached to and just above the lamina basalis.
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H and E biopsy of lichen simplex chronicus from forearm skin viewed at 40x magnification. Note the characteristic hyperkeratosis, hypergranulosis, ps....
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H and E biopsy of lichen simplex chronicus from forearm skin viewed at 100x magnification. Note the characteristic hyperkeratosis, hypergranulosis, p....
Treatment is aimed at reducing pruritus and minimizing existing lesions because rubbing and scratching cause lichen simplex chronicus. Location, lesion morphology, and extent of the lesions influence treatment. For example, a thick psoriasiform plaque of lichen simplex chronicus on a limb is commonly treated with a highly potent topical corticosteroid or intralesional corticosteroids, whereas vulvar lesions are more commonly treated with a mild topical corticosteroid or a topical calcineurin inhibitor. Widespread lesions are more likely to require systemic treatment or total body phototherapy.
Topical steroids are the current treatment of choice because they decrease inflammation and itch while concurrently softening the hyperkeratosis.[23, 24, 25] Because lesions are by nature chronic, treatment most likely is lifelong. On larger and more active lesions, a midpotency steroid may be used to treat acute inflammation. Occasionally, occlusion is used to increase potency and enhance delivery of the agent. Occlusion also provides a physical barrier to the scratching. Midpotency topical steroids are not recommended for thin skin (eg, vulva, scrotum, axilla, face). Direct long-term therapy more at daily use of low-potency nontrophogenic topical corticosteroids. High-potency topical corticosteroids may be used for 3-week courses on thicker-skinned areas.
Intralesional injection of corticosteroids is useful for refractory lesions. A 2018 report describes the use of a transcutaneous pneumatic injection device for lesions refractory to 1 month of treatment with a potent topical steroid. Triamcinolone injected into the lesions at 2-cm intervals led to significant improvement.[26]
Oral antianxiety medications and sedation may be considered in certain patients. According to individual need, treatment can be scheduled throughout the day, at bedtime, or both. Antihistamines such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) are common. Doxepin (Sinequan) and clonazepam (Klonopin) may be considered in appropriate cases.
For infected lesions, a topical or oral antibiotic can be considered.
Other topical medications reported to decrease pruritus include doxepin cream[27] and capsaicin cream.[28]
One study suggests that topical aspirin/dichloromethane is effective in patients with lichen simplex chronicus who have not responded to topical corticosteroids.[29]
For topical corticosteroid unresponsive patients or those with lesions on thin skin, a few case reports and small studies have shown efficacy of topical immunomodulators tacrolimus and pimecrolimus.[30]
A more investigational treatment for patients who fail conventional therapy is local botulinum toxin injections.[31, 32]
Transcutaneous electrical nerve stimulation (TENS) has been reported as a possible effective treatment in a small, open trial of cases of lichen simplex chronicus resistant to topical corticosteroid treatment.[33]
Direct patients to stop scratching. Lichen simplex chronicus is worsened or improved depending on the patient's ability to stop scratching. Discussing individual ways to change habitual scratching is helpful.
Extremes of temperature and/or humidity, psychic stress, and exposure of previously affected or predisposed areas to cutaneous irritants and allergens provoke relapse.
Periodically examine patients with lichen simplex chronicus in an outpatient dermatology clinic to evaluate lesions for changes. Perform follow-up examinations more frequently in patients being treated with potent class I topical corticosteroids or oral agents.
Clinical Context:
Clobetasol is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.
Clinical Context:
Betamethasone dipropionate cream 0.05% is for inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells.
Clinical Context:
Fluocinolone is a medium potency topical corticosteroid that inhibits cell proliferation; it also is immunosuppressive, antiproliferative, and anti-inflammatory. Flurandrenolide tape (4 mcg/cm2; Cordran tape) combines a topical steroid with the benefits of occlusion and is classified as a group I (potency) preparation.
Clinical Context:
Triamcinolone topical is for inflammatory dermatoses responsive to steroids; it decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.
Clinical Context:
Hydrocortisone valerate cream is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects, resulting in anti-inflammatory activity.
Clinical Context:
Fluocinonide is a high-potency topical corticosteroid that inhibits cell proliferation. It has immunosuppressive and anti-inflammatory properties.
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.They decrease pruritus, thin lichenification, and reduce inflammation.
Clinical Context:
Clonazepam is for anxiety associated with pruritus. It binds receptors at several sites within the CNS, including the limbic system and reticular formation. Its effects may be mediated through the GABA receptor system.
Clinical Context:
Pramoxine topical blocks nerve conduction and impulses by inhibiting the depolarization of neurons. It is a hypoallergenic topical anesthetic. It contains 0.5% menthol and 0.5% camphor, which are nonstaining agents that provide a subjective cooling effect to the skin and are much preferred to rubbing or scratching the skin.
Clinical Context:
Doxepin inhibits histamine and acetylcholine activity. Widespread topical use produces sedation, as does its use in areas of high percutaneous absorption (eg, genitals). Many individuals develop an allergy to topical doxepin. It is marketed orally as an antidepressant but is used for its antihistamine/antipruritic effects also.
Oral agents may control itching by blocking effects of endogenously released histamine. They may decrease the sense of pruritus, sedate/calm patients, and induce sleep. Topical agents stabilize neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing local anesthetic action.
Clinical Context:
Tacrolimus ointment's mechanism of action in LSC is unknown. It reduces itching and inflammation by suppressing the release of cytokines from T cells. It also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, it may inhibit the release of preformed mediators from skin mast cells and basophils and down-regulate the expression of FCeRI on Langerhans cells. It can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. It is available as ointment in concentrations of 0.03 and 0.1%. It is indicated only after other treatment options have failed.
Clinical Context:
Pimecrolimus is derived from ascomycin, a natural substance produced by the fungus Streptomyces hygroscopicus var ascomyceticus. It selectively inhibits the production and release of inflammatory cytokines from activated T cells by binding to the cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids. It is indicated only after other treatment options have failed.
Clinical Context:
OnabotulinumtoxinA is one of several toxins produced by Clostridium botulinum. It blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; botulinum toxin type A (BTA) binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or conduction of electrical signals along the nerve fiber. It prevents calcium-dependent release of acetylcholine and produces a state of denervation at the neuromuscular junction and postganglionic sympathetic cholinergic nerves in the sweat glands.
Typically, a 24- to 72-hour delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 months.
This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.
BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution, each 0.1 mL results in 5-U dose. The patient should receive 5-10 injections per visit.
OnabotulinumtoxinA must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative using the manufacturer's instructions to provide injection volume of 0.1 mL; it must be used within 4 hours of storage in the refrigerator at 2-8°C.
Preconstituted dry powder must be stored in the freezer at colder than 5°C.
Injections of BTA must be repeated at varying intervals to maintain long-term results.
What is lichen simplex chronicus (LCS)?What is the relationship between lichen simplex chronicus (LCS) and lichen amyloidosis?What is the pathophysiology of lichen simplex chronicus (LCS)?What is the role of P-phenylenediamine (PPD) in the pathophysiology of lichen simplex chronicus (LCS)?How does atopic dermatitis affect the probability of developing lichen simplex chronicus?What are other common causes of lichen simplex chronicus?What is the role of neurodermatitis in lichen simplex chronicus?Which medications can trigger lichen simplex chronicus?Can PPD in hair dye cause lichen simplex chronicus?What is the role of long-term exposure to street traffic exhaust in lichen simplex chronicus?What is secondary lichenification in lichen simplex chronicus?How common is lichen simplex chronicus (LCS)?What are the race-related demographics of lichen simplex chronicus (LCS)?Is lichen simplex chronicus (LCS) more common in men or women?What are the age-related demographics of lichen simplex chronicus (LCS)?What is the prognosis of lichen simplex chronicus (LCS)?What is the mortality of lichen simplex chronicus (LCS)?What is the morbidity of lichen simplex chronicus (LCS)?What causes secondary infection in lichen simplex chronicus (LCS)?How clinically apparent is lichen simplex chronicus (LCS)?How are patients educated about lichen simplex chronicus (LCS)?Where does thickening of the skin typically occur in lichen simplex chronicus (LCS)?When is erythema noted in lichen simplex chronicus (LCS)?How is pruritus characterized in patients with lichen simplex chronicus (LCS)?What is the role of chronic skin conditions in lichen simplex chronicus (LCS)?How are plaques characterized in lichen simplex chronicus (LCS)?How are pigmentary changes characterized in the plaques of lichen simplex chronicus?How does rubbing the skin contribute to lesion formation in lichen simplex chronicus?What is the relationship between lichen simplex chronicus and cutaneous horns?What behaviors may a patient exhibit during an exam for lichen simplex chronicus?Which noncutaneous conditions are associated with lichen simplex chronicus?What are the differential diagnoses for Lichen Simplex Chronicus?Which lab studies are used in the workup of lichen simplex chronicus?How is patch testing used in the workup of lichen simplex chronicus?Which procedures are used in the workup of lichen simplex chronicus?What histologic findings are associated with lichen simplex chronicus?What is the goal of lichen simplex chronicus treatment?What is the treatment of choice for lichen simplex chronicus?How are oral antianxiety medications and sedation used in the treatment of lichen simplex chronicus?When are antibiotics indicated in the treatment of lichen simplex chronicus?When is topical aspirin/dichloromethane indicated in the treatment of lichen simplex chronicus?Which medications may be useful in the treatment of lichen simplex chronicus in patients who do not respond to topical corticosteroids?What is the role of botulinum toxin injections in the treatment of lichen simplex chronicus?What is the role of transcutaneous electrical nerve stimulation (TENS) in the treatment of lichen simplex chronicus?When is consultation with a dermatologist indicated in the treatment of lichen simplex chronicus?When is consultation with an allergist indicated in the treatment of lichen simplex chronicus?When is consultation with a psychiatrist indicated in the treatment of lichen simplex chronicus?How does the prevention of scratching help the treatment of lichen simplex chronicus?How do extreme temperatures, humidity, and stress affect the treatment of lichen simplex chronicus?What is the long-term monitoring in patients with lichen simplex chronicus?What are the goals of drug treatment for lichen simplex chronicus?Which medications in the drug class Neuromuscular Blocker Agent, Toxin are used in the treatment of Lichen Simplex Chronicus?Which medications in the drug class Immune Modulator are used in the treatment of Lichen Simplex Chronicus?Which medications in the drug class Immunosuppressant Agent are used in the treatment of Lichen Simplex Chronicus?Which medications in the drug class Antipruritic agents are used in the treatment of Lichen Simplex Chronicus?Which medications in the drug class Corticosteroids are used in the treatment of Lichen Simplex Chronicus?
Jason Schoenfeld, MD, Resident Physician, Department of Dermatology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences
Disclosure: Nothing to disclose.
Coauthor(s)
Thomas N Helm, MD, Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory
Disclosure: Nothing to disclose.
Specialty Editors
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center
Disclosure: Nothing to disclose.
James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
Disclosure: Nothing to disclose.
Siobahn M Hruby, MD, Internal Medicine Physician, Boys Town National Research Hospital
Lichen simplex chronicus of the dorsal hand and wrist demonstrating increased skin thickness and accentuation of skin markings.
Plaque of lichen simplex chronicus of the leg with accentuated skin markings and excoriations.
Plaques of lichen simplex chronicus on the hand.
Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 40x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 100x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.
Plaques of lichen simplex chronicus on the hand.
Lichen simplex chronicus of the dorsal hand and wrist demonstrating increased skin thickness and accentuation of skin markings.
Plaque of lichen simplex chronicus of the leg with accentuated skin markings and excoriations.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 40x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
H and E biopsy of lichen simplex chronicus from forearm skin viewed at 100x magnification. Note the characteristic hyperkeratosis, hypergranulosis, pseudoepitheliomatous hyperplasia, and papillary dermal fibrosis.
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