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References

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Fig. 10.4 Acropustulosis of infancy occurs on the hands and feet of infants. Vesicles rapidly progress to sterile pustules

References

1. Miyamoto D, Santi CG, Aoki V, Maruta CW.Bullous pemphigoid.

An Bras Dermatol. 2019;94(2):133–46. https://doi.org/10.1590/

abd1806- 4841.20199007.

2. Lopez AT, Khanna T, Antonov N, Audrey-Bayan C, Geskin L. A

review of bullous pemphigoid associated with PD-1 and PD-L1

inhibitors. Int J Dermatol. 2018;57(6):664–9. ISSN: 1365-4632

3. Lee SG, Lee HJ, Yoon MS, Kim DH.Association of dipeptidyl pep-

tidase 4 inhibitor use with risk of bullous pemphigoid in patients

with diabetes. JAMA Dermatol. 2019;155(2):172–7. https://doi.

org/10.1001/jamadermatol.2018.4556.

4. Nguyen CN, Kim SJ. Dermatitis herpetiformis: an update on diag-

nosis, disease monitoring, and management. Medicina (Kaunas).

2021;57(8):843. https://doi.org/10.3390/medicina57080843.

5. Bolotin D, Petronic-Rosic V.Dermatitis herpetiformis. Part I. epi-

demiology, pathogenesis, and clinical presentation. J Am Acad

Dermatol. 2011;64:1017–24.

6. Ludwig RJ. Clinical presentation, pathogenesis, diagnosis, and

treatment of epidermolysis bullosa acquisita. ISRN Dermatol.

2013;2013:812029. https://doi.org/10.1155/2013/812029.

7. Hashimoto T, Ishii N, Ohata C, Furumura M.Pathogenesis of epi-

dermolysis bullosa acquisita, an autoimmune subepidermal bullous

disease. J Pathol. 2012 Sep;228(1):1–7. https://doi.org/10.1002/

path.4062.

8. American Osteopathic College of Dermatology (AOCD).

Acropustulosis of infancy. Available at https://www.aocd.org/page/

AcropustulosisInfanc.

9. Infantile acropustulosis--how often is it a sequela of scabies? Pediatr

Dermatol. 1995;12(3):275–6.

Self-Induced andPsychogenic Skin

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Conditions oftheLower Extremity

Some skin conditions are self-induced, albeit unwittingly. A classic example is erythema ab igne which results from prolonged contact with a heat generating device held against the skin. Other skin conditions may have psychogenic undertones such as prurigo nodularis. Tanorexia is a compulsive disorder and delusions of parasitosis is a manifestation of psychosis.

11.1 Erythema Ab Igne

Erythema ab igne (EAI) is an area of localized reticulated erythema and hyperpigmentation that occurs on parts of the body exposed to prolonged infrared radiation. Chronic exposure injures the epidermis and supercial vascular plexus. Initially erythematous, exposed areas subsequently become mottled and acquire brown, blue, or purple colorations. The most common cause is heating pads and the condition predominately affects females aficted with longstanding pain [1]. Most cases are asymptomatic and gradual resolution is anticipated once contact with the inciting agent has been discontinued. Squamous cell carcinomas may rarely arise within affected sites (Fig.11.1) [2].

11.2 Prurigo Nodularis

Prurigo nodularis is a chronic disorder of the skin characterized by rm nodules that range in color from pink to brown. Common locations include the arms, legs, and upper back. The condition occurs primarily in older adults with men and women equally affected. The pathogenesis involves a chronic itch-scratch cycle believed to be a cutaneous inammatory neurogenic response mediated by a variety of peptides [3]. A signicant percentage of patients admit to anxiety, depres-

Fig. 11.1 Erythema ab igne secondary to prolonged use of a heating pad (Courtesy of Ron Hidalgo, DO)

sion, and suicidal ideation [4]. Therapeutic options include topical and systemic steroids, antihistamines, gabapentin, ultraviolet light, and IL 13 and IL 31 inhibitors (Fig.11.2).

11.3 Tanorexia

Tanorexia is a “compulsive need or desire to have and maintain a very dark tan beyond what is typically considered normal” [5]. Chronic excess tanning is now widely considered to be a substance abuse disorder and a true behavioral addiction [6]. Ultraviolet light stimulates production of opioidrelated endorphins in the skin which may factor into pathogenesis. Tanning dependence contributes to premature aging and skin cancer. Of particular risk is indoor tanning

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11 Self-Induced andPsychogenic Skin Conditions oftheLower Extremity

Fig. 11.2 Prurigo nodularis is also referred to as pickers nodules

which delivers a concentrated dose of ultraviolet light and is believed to cause nearly 400,000 cases of skin cancer in the USA each year (Fig.11.3) [7].

11.4 Delusions ofParasitosis

Delusions of parasitosis is a disorder in which affected individuals have an unwavering and erroneous belief that they are infected with bugs, be they parasites, worms, mites, or other living organisms. A related condition, Morgellons disease, substitutes bers for insects. As “proof” patients often transport inanimate objects to the ofce in plastic containers or baggies (“ Ziploc bag sign”) [8]. In keeping with delusional ideation, reasoning or logical discourse is unpersuasive and ineffectual. The oral agent pimozide is the treatment of choice and often induces remission (Fig.11.4) [9].

Fig. 11.3 Tanorexia is a compulsive need to spend time exposed to sun or an ultraviolet light source for maintenance of a tan

Fig. 11.4 Magnied view of a “bug and eggs” brought to the ofce by a patient suffering from delusions

References

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References

1. Kettelhut EA, Traylor J, Roach JP.Erythema ab igne. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2021. Available from: https://www.ncbi.nlm.nih.gov/

books/NBK538250/.

2. Sigmon JR, Cantrell J, Teague D, Sangueza O, Sheehan DJ.Poorly differentiated carcinoma arising in the setting of erythema ab igne. Am J Dermatopathol. 2013;35:676–8.

3. Mullins TB, Sharma P, Riley CA, Sonthalia S.Prurigo Nodularis.

2021. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022.

4. Brenaut E, Halvorsen JA, Dalgard FJ, Lien L, Balieva F, Sampogna F, etal. The self-assessed psychological comorbidities of prurigo in European patients: a multicentre study in 13 countries. J Eur Acad

Dermatol Venereol. 2019;33(1):157–62. https://doi.org/10.1111/

jdv.15145.

5. https://www.merriam- webster.com/dictionary/tanorexia.

6. Petit A, Lejoyeux M, Reynaud M, Karila L.Excessive indoor tanning as a behavioral addiction: a literature review. Curr Pharm Des. 2014;20(25):4070–5. https://doi.org/10.2174/13816128113199990

615.

7. Wehner MR, Chren MM, Nameth D, etal. International prevalence of indoor tanning: a systematic review and meta-analysis. JAMA Dermatol. 2014;150(4):390–400.

8. Reich A, etal. Delusions of parasitosis: an update. Dermatol Ther. 2019;9(4):631–8. https://doi.org/10.1007/s13555- 019- 00324- 3.

9. Brownstone N, Hakimi M, Koo J.Best practices for management of delusions of parasitosis. SKIN J Cutan Med. 2021;5(5):448–52.

https://doi.org/10.25251/skin.5.5.1.

Skin Signs ofSystemic Disease

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andReactive Disorders oftheLower Extremity

A skin condition is on occasion the rst sign of internal disease. Recognizing a disorder that is caused by, or associated with, an internal malady can result in earlier diagnosis and a more favorable clinical outcome. An example is erythema nodosum; recommended work-up may uncover tuberculosis infection or sarcoid. Some reactive processes are uniquely associated with an underlying condition. A prime example is diabetic dermopathy. Other reactive processes may or may not be found in association with underlying illness. Perforating folliculitis can arise in the context of impaired kidney function although most cases are not linked to internal disease.

12.1 Diabetic Dermopathy

Diabetic dermopathy, also referred to as “shin spots,” is the most common cutaneous nding in diabetes, occurring in a signicant number of longstanding diabetic patients older than 50years [1]. The condition presents as smooth, welldened, round to oval atrophic hyperpigmented macules located on the pretibial areas of the lower legs. Lesions are usually bilateral and are distributed in an asymmetric pattern. The condition is asymptomatic.

The cause of diabetic dermopathy is unknown although some cases have been linked to minor trauma. Progression is variable and not related to glycemic control [2]. To date no treatment modality has proven of uniform success and lesions may persist indenitely or spontaneously improve (Fig.12.1).

12.2 Erythema Multiforme

Erythema multiforme is a hypersensitivity reaction that can involve both skin and mucous membranes. The condition may be triggered by herpes simplex viral infections and Mycoplasma pneumonia as well as medications that include

Fig. 12.1 Diabetic dermopathy presents with hyperpigmented macules

nonsteroidal anti-inammatory drugs, antiepileptics, and antibiotics [3]. The disorder is believed to be triggered by a cell-mediated immune reaction.

Patients with cutaneous manifestations of erythema multiforme present with target lesions containing a central blister surrounded by peripheral erythema. These are located in an acral distribution on the palms, back of hands, feet, and extensor surfaces. Lesions are often painless but some patients experience burning sensations. Lesions of the mucosa are also common and may progress to painful erosions. Patients may report fever, malaise, arthralgia, and joint swelling [4].

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Fig. 12.2 Bullous lesions associated with erythema multiforme (Courtesy of Lawrence Schiffman, DO)

12 Skin Signs ofSystemic Disease andReactive Disorders oftheLower Extremity

Treatment depends on the severity of the rash as well as the underlying cause if identied. Lesion resolution may be hastened by use of topical steroids and emollients. Healing occurs spontaneously in 2 to 4weeks. Recurrence is common when linked to herpes infection (Fig.12.2).

12.3 Erythema Nodosum

Erythema nodosum (EN) is a cutaneous inammatory reactive process that most commonly manifests on the lower legs. Characteristic lesions are tender, erythematous to hyperpigmented nodules that are warm to touch and often bilateral. Lesions do not ulcerate and heal without scarring. The condition is most common in women between the ages of 25 and 40 [5]. Diagnosis of EN is usually made clinically. Histopathology of EN reveals a septal panniculitis with varying degrees of supercial and deep perivascular inammatory lymphocytic inltration [6].

Although many cases of EN are idiopathic, the disorder may be triggered by contagious disorders including streptococcal infection, tuberculosis, and leprosy [7]. EN has also been associated with inammatory bowel disease, sarcoid, and malignancies as well as with oral contraceptives. EN is usually self-limited but requires work-up for identiable causality (Fig.12.3).

12.4 Granuloma Annulare

Granuloma annulare (GA) is a benign, noninfectious, selflimited disorder. The condition is most common in women and middle-aged to older individuals [8]. There are several forms of GA including localized, generalized, and subcutaneous [9]. The localized subtype usually presents on the dorsal or lateral surfaces of the hands and feet. The classic appearance is that of an annular esh colored to erythematous patch or plaque with a slightly elevated border. Generalized GA usually affects adult females and manifests

Fig. 12.3 Painful leg nodules indicative of erythema nodosum

as multiple erythematous to light brown papules and patches. The trunk and upper thighs are primarily involved. Subcutaneous or deep GA usually occurs in children and is characterized by rm asymptomatic nodules. Most cases of GA are diagnosed clinically. Biopsy reveals palisading granulomatous inammation accompanied by dermal collagen degeneration admixed with macrophages, neutrophils, and multinucleated giant cells.

GA may be triggered by trauma and has been associated with a number of systemic abnormalities including thyroid disease, malignancy, diabetes, and HIV infection [10]. Treatment options for localized disease include topical and intralesional steroids and cryosurgery. Many cases resolve spontaneously within 2years of onset (Fig.12.4).

12.5 Idiopathic Guttate Hypomelanosis

Idiopathic guttate hypomelanosis is an acquired benign leukoderma that presents as discrete annular hypopigmented macules ranging in size from 2 to 6mm [11]. The condition most commonly arises in elderly, fair-skinned persons with equal distribution in males and females. Relation to sun exposure as well as to hereditary predisposition has been proposed but not universally accepted. The majority of cases

12.7 Lipodermatosclerosis

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Fig. 12.4 A discolored plaque with raised borders characterizes granuloma annulare

are diagnosed clinically. Histopathology reveals a diminished number of melanocytes unlike vitiligo where melanocytes are absent.

A number of modalities have been utilized for treatment including cryosurgery, lasers, microdermabrasion, microneedling, and topical retinoids and calcineurin inhibitors. All should be used cautiously to avoid worsening of the leukoderma or inducement of postinammatory hyperpigmentation (Fig.12.5).

12.6 Leukocytoclastic Vasculitis

Leukocytoclastic vasculitis is a small vessel inammatory process targeting venules and capillaries. Approximately 50% of cases are idiopathic; identiable causes include medications, infections, autoimmune disease, and underlying malignancy [12]. The condition involves the lower legs and is usually asymptomatic. Palpable purpura is the classic presentation. Lesions are erythematous to violaceous in hue, bilaterally distributed, and often appear in crops. Diagnosis is made by biopsy which reveals neutrophil inltration within small vessel walls accompanied by brinoid necrosis.

Fig. 12.5 Idiopathic guttate hypomelanosis presents with hypopigmented macules

Direct immunouorescence is often positive [13]. Baseline work-up includes complete blood count, urinalysis, sedimentation rate, and measurement of liver and kidney status.

Most cases of leukocytoclastic vasculitis are self-limited. Supportive therapy includes leg elevation and bed rest. If drug induced, removal of the offending medication results in clearance. Symptomatic or persistent cases may respond to colchicine or dapsone [14]. High dose corticosteroids may be required for adequate control (Fig.12.6).

12.7 Lipodermatosclerosis

Lipodermatosclerosis is an inammatory skin condition of the lower extremities that usually occurs in the setting of venous insufciency. Unlike stasis dermatitis in which inammatory changes are more supercial, lipodermatosclerosis is a panniculitis with involvement of subcutaneous fat [15]. The disorder is painful in the acute phase and may resemble cellulitis or erythema nodosum. The prevalence is highest in middle-aged to elderly women [16].

Clinically, lipodermatosclerosis is characterized by the appearance of rm, indurated plaques. Pigmentation may be

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Fig. 12.6 The hallmark of leukocytoclastic vasculitis is palpable purpura

12 Skin Signs ofSystemic Disease andReactive Disorders oftheLower Extremity

marked and increases over time. The pattern on the legs has been likened to an “inverted champagne bottle.” Therapies that may prove of value include compression stockings and intralesional triamcinolone (Fig.12.7) [17].

12.8 Necrobiosis Lipoidica

Necrobiosis lipoidica is an inammatory granulomatous disorder of the skin that most commonly presents on the shins of type 1 diabetics (referred to as necrobiosis lipoidica diabeticorum) [18]. The lesions appear as yellow-red plaques associated with central atrophy, telangiectasias, and raised violaceous borders. The condition predominates in female patients typically between 30 and 40years of age. Lesions are asymptomatic but can become ulcerated, especially after trauma. The etiology is unknown; autoimmune complex deposition has been postulated to induce vascular changes that lead to collagen degeneration. Altered collagen and microangiopathy are noted on histology [19].

Therapeutic options are many but none has uniform success. Topical and intralesional steroids are often implemented as rst line treatment. Topical calcineurin inhibitors, topical retinoids, laser therapy, immunomodulators, biologics, and antimalarials have all been reported to improve this condition. Some cases spontaneously involute (Fig.12.8).

Fig. 12.7 Inverted champagne bottle appearance of lipoderma tosclerosis

Fig. 12.8 Necrobiosis lipoidica manifests as shiny, atrophic plaques

12.9 Perforating Folliculitis

Perforating folliculitis is classied as a reactive perforating collagenosis which also includes elastosis perforans serpiginosa and Kyrle disease [20]. Perforating disorders are characterized histologically by the presence of collagen and

12.11 Pretibial Myxedema

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elastin bers that penetrate into the follicular spaces of hair follicles. Many cases are linked to systemic diseases such as chronic renal failure, diabetes, and human immunodeciency virus. Other associations include vitamin A deciency and growth factor receptor inhibitors.

Perforating folliculitis presents with scattered, rm follicular papules distributed on the extremities and buttocks. Papules have varying degrees of erythema and contain central keratotic plugs. Some cases may respond to topical tretinoin or oral therapy with isotretinoin (Fig.12.9) [21].

Fig. 12.9 Perforating folliculitis presenting with multiple follicular papules

12.10 Porokeratosis

Porokeratosis results from an abnormal clonal focal expansion of keratinocytes [22]. Porokeratosis of Mibelli is a variant that most commonly occurs on the lower legs and manifests as an erythematous patch or plaque with an atrophic center. The lesion is surrounded by a keratotic wall termed a coronoid lamella. Males predominate and the condition may arise at any age. Lesions are slow growing and remain asymptomatic. Some cases appear transmitted in autosomal dominant manner, whereas others may be triggered by extrinsic factors such as ultraviolet light exposure, trauma, and certain medications [23].

Basal and squamous cell carcinomas may uncommonly develop within porokeratosis. Various treatment modalities have been utilized with inconsistent results including imiquimod, topical vitamin D analogues, retinoids, and cryosurgery (Fig.12.10) [24].

12.11 Pretibial Myxedema

Pretibial myxedema is a reactive process most commonly associated with thyroid disease. The condition results from deposition of hyaluronic acid and other mucopolysaccharides within the dermis and is believed to be a consequence

Fig. 12.10 (a) Porokeratosis is a disorder of keratinization marked histologically by a coronoid lamella. (b) Eruptive porokeratosis is a rare vari- ant presenting with multiple lesions

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Fig. 12.11 Pretibial myxedema results from accumulation of glycosaminoglycans

12 Skin Signs ofSystemic Disease andReactive Disorders oftheLower Extremity

of an aberrant immune response [25]. Several subtypes have been identied including nonpitting edema, plaque, nodular, and elephantiasic variants [26]. The condition most commonly manifests in the pretibial areas but may also occur elsewhere including on the dorsal surface of the feet.

Pretibial myxedema is asymptomatic but may be of cosmetic concern. The clinical course is variable and some cases improve over time. Both topical steroids and compression may be of value in hastening resolution (Fig.12.11).

References

1. Morgan AJ, Schwartz RA.Diabetic dermopathy: a subtle sign with grave implications. J Am Acad Dermatol. 2008;58(3):447–51.

https://doi.org/10.1016/j.jaad.2007.11.013.

2. Mendes AL, Miot HA, Haddad V Jr. Diabetes mellitus and the skin. An Bras Dermatol. 2017;92(1):8–20. https://doi.org/10.1590/

abd1806- 4841.20175514.

3. Trayes KP, Love G, Studdiford JS.Erythema multiforme: recognition and management. Am Fam Physician. 2019;100(2):82–8.

4. Hafsi W, Badri T.Erythema multiforme. [2021 Aug 7] In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2021.

5. Hafsi W, Haseer Koya H. Erythema, Nodosum. StatPearls Publishing. Updated 12 December 2017. Available at: https://www.

ncbi.nlm.nih.gov/books/NBK470369.

6. Wilk M, Zelger BG, Hayani K, Zelger B. Erythema nodosum, early stage-a subcutaneous variant of leukocytoclastic vasculitis? Clinicopathological correlation in a series of 13 patients. Am J Dermatopathol. 2020;42(5):329–36.

7. Schwartz RA, Nervi SJ.Erythema nodosum: a sign of systemic disease. Am Fam Physician. 2007;75(5):695–700.

8. Barbieri JS, Rodriguez O, Rosenbach M, Margolis D. Incidence and prevalence of granuloma annulare in the United States. JAMA Dermatol. 2021;157(7):824–30. https://doi.org/10.1001/

jamadermatol.2021.1847.

9. Piette EW, Rosenbach M.Granuloma annulare: clinical and histologic variants, epidemiology, and genetics. J Am Acad Dermatol. 2016;75(3):457–65. https://doi.org/10.1016/j.jaad.2015.03.054.

10. Wang J, Khachemoune A.Granuloma annulare: a focused review of therapeutic options. Am J Clin Dermatol. 2018;19(3):333–44.

https://doi.org/10.1007/s40257- 017- 0334- 5.

11. Brown F, Crane JS. Idiopathic Guttate hypomelanosis. [Updated 2021 Sep 20]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Available from: https://www.ncbi.nlm.

nih.gov/books/NBK482182/.

12. Takatu CM, Heringer APR, Aoki V, etal. Clinicopathologic correlation of 282 leukocytoclastic vasculitis cases in a tertiary hospital: a focus on direct immunouorescence ndings at the blood vessel wall. Immunol Res. 2017;65(1):395–401. https://doi.org/10.1007/

s12026- 016- 8850- 6.

13. Baigrie D, Bansal P, Goyal A, etal. Leukocytoclastic vasculitis. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2021. Available from: https://www.ncbi.

nlm.nih.gov/books/NBK482159/.

14. Fraticelli P, Benfaremo D, Gabrielli A.Diagnosis and management of leukocytoclastic vasculitis. Intern Emerg Med. 2021;16(4):831–

41. https://doi.org/10.1007/s11739- 021- 02688- x.

15. Kirsner RS, Pardes JB, Eaglstein WH, Falanga V. The clinical spectrum of lipodermatosclerosis. J Am Acad Dermatol. 1993;28(4):623–7. https://doi.org/10.1016/0190- 9622(93)70085- 8.

16. Bruce AJ, Bennett DD, Lohse CM, Rooke TW, Davis MD. Lipodermatosclerosis: review of cases evaluated at Mayo Clinic. J Am Acad Dermatol. 2002;46(2):187–92. https://doi.

org/10.1067/mjd.2002.119101.

17. Campbell LB, Miller OF 3rd. Intralesional triamcinolone in the management of lipodermatosclerosis. J Am Acad Dermatol. 2006;55:166–8. https://doi.org/10.1016/j.jaad.2005.09.043.

18. Lepe K, Riley CA, Salazar FJ. Necrobiosis lipoidica. [Updated 2021 Aug 26]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022. Available from: https://www.ncbi.nlm.

nih.gov/books/NBK459318/.

19. https://emedicine.medscape.com/article/1103467- workup#c7.

20. Mullins TB, Sickinger M, Zito PM.Reactive perforating collagenosis. [Updated 2021 Nov 15]. In: StatPearls [Internet]. Treasure Island, FL): StatPearls Publishing; 2022. Available from: https://

www.ncbi.nlm.nih.gov/books/NBK459214/.

21. https://emedicine.medscape.com/article/1071033- treatment.

22. Vargas-Mora P, Morgado-Carrasco D, Fustà-Novell X.Porokeratosis: a review of its pathophysiology, clinical manifestations, diagnosis, and treatment. Actas Dermosiliogr (Engl Ed). 2020;111(7):545–60. English, Spanish. https://doi.org/10.1016/j.

ad.2020.03.005.

23. Ferreira FR, Santos LD, Tagliarini FA, Lira ML. Porokeratosis of Mibelli--literature review and a case report. An Bras Dermatol. 2013;88(6 Suppl 1):179–82. https://doi.org/10.1590/

abd1806- 4841.20132721.

24. Weidner T, Illing T, Miguel D, Elsner P.Treatment of porokeratosis: a systematic review. Am J Clin Dermatol. 2017;18(4):435–49.

https://doi.org/10.1007/s40257- 017- 0271- 3.

25. Georgala S, Katoulis AC, Georgala C, etal. Pretibial myxedema as the initial manifestation of Graves’ disease. J Eur Acad Dermatol Venereol. 2002;16(4):380–3.

26. Schwartz KM, Fatourechi V, Ahmed DD, Pond GR.Dermopathy of Graves’ disease (pretibial myxedema): long-term outcome. J Clin Endocrinol Metab. 2002;87(2):438–46.

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