Answer: C

Psoriasis is an immune-mediated chronic disorder affecting the skin and joints. Psoriasis likely was described first in Corpus Hippocraticum by Hippocrates, who used the terms psora and lepra to describe a condition later recognized as psoriasis.8-10 In the first century AD, Celsus described 40 dermatoses, one of which was a form of impetigo later interpreted by Willan to be a type of psoriasis.10 In 1809, Willan defined 2 psoriasiform diseases, lepra Graecorum and psora leprosa; in 1841, von Hebra determined these were the same disease.10

Psoriasis affects 2% of the population in North America and Europe and is less prevalent among individuals of Japanese descent.8,11 Patients may develop psoriasis at any age and the prevalence increases steadily between early childhood and adulthood (0.12% at 1 year of age to 1% to 2% at 18 years).8,11 Age at presentation has 2 peaks; at 15 to 20 years and 55 to 60 years.11 Psoriasis is more likely to be severe in men than in women.

Factors hypothesized to impact psoriasis prevalence include ethnicity, sun exposure, and climate.8 Two genes have been associated with psoriasis: HLA-Cw6, which is linked to guttate psoriasis, and CARD14; both mutations may result in improved response to tumor necrosis factor (TNF) inhibitors.12,13 Psoriasis can arise in predisposed individuals after exposure to a trigger such as trauma (Koebner phenomenon), certain medications, or infections.15


Continue Reading

Streptococcal infections have been identified as a risk factor for guttate psoriasis, which classically presents on the trunk of children and adolescents after an infection and is self-limited, resolving in 3 to 4 months.16 Infections with Staphylococcus aureus, Helicobacter pylori, Candida, Malassezia, papillomaviruses, and retroviruses are potential risk factors. HIV can exacerbate existing cases or cause new-onset disease; as immune function declines, HIV is associated with more severe psoriasis.12 Psoriasis can arise as an adverse effect of lithium. TNF inhibitor therapy, paradoxically, can trigger psoriasis.12

Obesity, diabetes mellitus, dyslipidemia, hypertension, and stress have been documented as intrinsic risk factors for psoriasis.14 Patients with psoriasis are at a greater risk for metabolic syndrome, psoriatic arthritis, anxiety, depression, cardiovascular disorders, Crohn disease, lymphoma, and nonalcoholic fatty liver disease.8

Generally, psoriasis is considered to be a disorder of the immune system. Crosstalk between the adaptive and innate immune systems and relationships between dendritic cells, macrophages, cytokines, and T cells result in psoriatic pathology.8,15 When activated, these immune cells will produce inflammatory mediators such as interleukin 12 (IL-12), IL-17, IL-23, and TNF-α.15 TNF-α, in turn, induces production of adhesion molecules and secondary mediators, leading to joint and skin disease in patients with psoriasis.8,15

The most common form of psoriasis is psoriasis vulgaris, also known as plaque psoriasis. It is characterized by red or salmon-pink plaques with overlying silver or white scale.15,16 If psoriatic plaques are scratched, they may reveal tiny bleeding spots (Auspitz sign).15 These lesions can be thin or thick, small or large, and they tend to be most active at the edges. Psoriatic plaques usually are symmetrical and appear most frequently on extensor surfaces of the knees and elbows, scalp, umbilicus, and lumbosacral region.16

Psoriasis also may present as inverse psoriasis, in which patients experience well-demarcated, erythematous areas without scaling in the flexural folds.17 Pustular psoriasis exists in both generalized and localized forms, with the acute generalized form being especially severe, resulting in fever, sterile pustules, and potentially life-threatening systemic toxicity. Localized pustular psoriasis, which presents on the hands and feet, can be associated with plaque psoriasis.

Erythrodermic psoriasis is relatively rare, comprising less than 2% of psoriasis cases. This type of psoriasis can affect the entire surface of the skin and may be accompanied by chills, hypothermia, dehydration, and even sepsis.17 Psoriatic arthritis, characterized by joint pain, stiffness, and swelling, is present in approximately 25% to 30% of patients with psoriasis.15

Histopathology of psoriasis is characterized by 3 main features: hyperplasia of the epidermis, prominent dermal blood vessels, and dermal inflammatory leukocytic infiltrate.16 Epidermal changes include parakeratosis, loss of the granular cell layer, regular elongation of the rete ridges, micropustules of Kagoj, and Munro microabscesses.16

Although laboratory abnormalities in psoriasis generally are nonspecific and not required for diagnosis, serum uric acid, C-reactive protein, sedimentation rate, and serum immunoglobulin A all may be increased.10 Diagnosis usually is made based on characteristic clinical features.10

Potential conditions to consider in the differential diagnosis of psoriasis include eczema, mycosis fungoides, lichen planus, pityriasis rosea, tinea infections, seborrheic dermatitis, syphilis, pityriasis lichenoides et varioliformis, candidiasis, Paget disease, and squamous cell carcinoma in situ.10,11,17 Psoriasis generally can be differentiated from other disorders based on clinical findings and patient history, but biopsy may be needed to confirm the diagnosis.10 In addition, the specific type of psoriasis must be distinguished from other types.17

Treatment of psoriasis is aimed at reducing symptoms and disease control. The majority of patients (70% to 80%) will require only topical medications to control their condition.8,9 For mild disease, the first-line treatment is topical corticosteroids.15 Vitamin D derivatives are another option, often combined with topical corticosteroids.8 Tazarotene and calcineurin inhibitors, such as pimecrolimus and tacrolimus, also have shown success. Widespread psoriasis may warrant ultraviolet (UV) light therapy, and more severe disease may require systemic therapies such as acitretin, apremilast, cyclosporine, or methotrexate.8,15

Biologic agents are a more recent development for treatment of psoriasis and typically are used when patients fail topical treatment, light therapy, and conventional systemic medications, or when these treatments are poorly tolerated or contraindicated. Biologic agents are targeted immunomodulators that block cytokines involved in psoriasis pathogenesis including TNF-α, IL-12, IL-23, and IL-17.8

The patient in this case was diagnosed with psoriasis that was resistant to topical treatments. After the patient was counseled about his treatment options, he was started on biologic treatment for his psoriasis and psoriatic arthritis. The patient is tolerating his treatment well and has experienced near-clearance of his psoriasis and improvement in his joint symptoms.

Dina Zamil, BS, is a medical student at Baylor College of Medicine in Houston, Texas; Tara L. Braun, MD, is a resident in the Department of Dermatology at Baylor College of Medicine in Houston, Texas; Christopher Rizk, MD, is a dermatologist at Elite Dermatology in Houston, Texas.

References

1. Lotti T, Buggiani G, Prignano F. Prurigo nodularis and lichen simplex chronicus. Dermatol Ther. 2008;21(1):42-46. doi:10.1111/j.1529-8019.2008.00168.x

2. Prajapati V, Barankin B. Dermacase. Lichen simplex chronicus. Can Fam Physician. 2008;54(10):1391-1393.

3. Soter N. Chapter 23: Nummular eczema and lichen simplex chronicus/prurigo nodularis. In: Freedberg IM, Eisen AZ, Wolff K, Austen FK, Goldsmith LA, Katz S, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. McGraw-Hill Professional; 2003.

4. Charifa A, Badri T, Harris BW. Lichen simplex chronicus. In: StatPearls. StatPearls Publishing; 2021. Accessed August 17, 2021. http://www.ncbi.nlm.nih.gov/books/NBK499991/

5. Ringel NE, Iglesia C. Common benign chronic vulvar disorders. Am Fam Physician. 2020;102(9):550-557.

6. Liao Y-H, Lin C-C, Tsai P-P, Shen W-C, Sung F-C, Kao C-H. Increased risk of lichen simplex chronicus in people with anxiety disorder: a nationwide population-based retrospective cohort study. Br J Dermatol. 2014;170(4):890-894. doi:10.1111/bjd.12811

7. Lichon V, Khachemoune A. Lichen simplex chronicus. Dermatol Nurs. 2007;19(3):276.

8. Boehncke W-H, Schön MP. Psoriasis. Lancet. 2015;386(9997):983-994. doi:10.1016/S0140-6736(14)61909-7

9. Furue M, Kadono T. Psoriasis: behind the scenes. J Dermatol. 2016;43(1):4-8. doi:10.1111/1346-8138.13186

10. Christophers E, Mrowietz U. Chapter 42: Psoriasis. In: Freedberg IM, Eisen AZ, Wolff K, Austen FK, Goldsmith LA, Katz S, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. McGraw-Hill Professional; 2003.

11. Langley RGB, Krueger GG, Griffiths CEM. Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18-23; discussion ii24-25. doi:10.1136/ard.2004.033217

12. Lee EB, Wu KK, Lee MP, Bhutani T, Wu JJ. Psoriasis risk factors and triggers. Cutis. 2018;102(5S):18-20.

13. Coto-Segura P, González-Fernández D, Batalla A, et al. Common and rare CARD14 gene variants affect the antitumour necrosis factor response among patients with psoriasis. Br J Dermatol. 2016;175(1):134-141. doi:10.1111/bjd.14461

14. Kamiya K, Kishimoto M, Sugai J, Komine M, Ohtsuki M. Risk factors for the development of psoriasis. Int J Mol Sci. 2019;20(18):4347. doi:10.3390/ijms20184347

15. Schleicher SM. Psoriasis: pathogenesis, assessment, and therapeutic update. Clin Podiatr Med Surg. 2016;33(3):355-366. doi:10.1016/j.cpm.2016.02.004

16. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;370(9583):263-271. doi:10.1016/S0140-6736(07)61128-3

17. Oji V, Luger TA. The skin in psoriasis: assessment and challenges. Clin Exp Rheumatol. 2015;33(5 Suppl 93):S14-S19.