A 35-year-old man presents with several nodules on the dorsal aspect of his left hand. These lesions have been present for several weeks. On questioning, the patient states that his brother has similar nodules on his fingers. He remembers injuring his hand at work a few days before he noticed the lesions. On examination, a grouping of flesh-colored, rough, scaly nodules is noticed on the patient’s left hand. Each nodule is characterized by several punctate black dots. The lesions do not cause the patient pain or interfere with his daily activities; however, he finds them unsightly.
A 56-year-old woman presents with a translucent nodule on her right index finger. The patient first noticed the lesion a month ago and states that it has gradually increased in size since that time. She denies pain or decreased range of motion, but she states that the lesion is tender to the touch. The patient’s medical history includes hypertension, dyslipidemia, and osteoarthritis. On examination, there is a solitary, 5-mm translucent nodule located between the proximal nail fold and the distal interphalangeal joint on her right index finger. The nail bed distal to the lesion is also slightly atrophic.
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Case #1: Verruca vulgaris
Verruca vulgaris, or common warts, are caused by infection of epidermal or mucosal cells with human papillomavirus (HPV), most commonly HPV type 2.1 The virus induces proliferation of infected cells and results in circumscribed, rough, irregular lesions. Common warts are typically asymptomatic but may result in functional impairment and are often a cosmetic concern for the patient. This skin manifestation is relatively common, with an estimated prevalence of 7% to 12%.2,3 Children and adolescents are the most commonly affected populations, with risk of disease declining after the second decade of life.1,2 The infection can be transmitted by direct or indirect contact with a cutaneous wart. Accordingly, sites of trauma result in an increased risk of inoculation.2 Other risk factors for acquisition of disease include immunosuppression; close contact with infected individuals; nail biting; and the handling of meat, poultry, and fish.2,4
The diagnosis of verruca vulgaris is most often made clinically through the identification of the characteristic lesions. These lesions can present as a solitary, well-circumscribed, rough nodule with an irregular, scaly surface or as grouped lesions. The lesions most commonly occur on the hands, fingers, and knees.1 Paring or filing of the wart often reveals punctate black dots indicative of thrombosed capillaries that can aid in the diagnosis.1,2 If a biopsy is obtained, histopathology reveals papillomatosis, hyperkeratosis, acanthosis, and parakeratosis.2 Arborization, or inward bowing of rete ridges, is also typically seen. Of the common characteristics of verruca vulgaris, there are 3 features in particular that can help to distinguish this diagnosis from other papillomas: koilocytes, columns of parakeratosis, and clumped keratohyaline granules.1
The differential diagnosis for verruca vulgaris can be fairly broad, including syringoma, molluscum, lichen planus and nitidus, actinic keratosis, and seborrheic keratosis, among others.2 A syringoma is a benign tumor of eccrine cells that appears as a small, smooth bump under the skin surface. Infection with molluscum contagiosum, a pox virus, typically results in multiple round, umbilicated, waxy papules. Lichen nitidus produces many flat, flesh-colored micropapules while lichen planus produces violaceous, flat, purple papules. Seborrheic keratoses are noncancerous papules with a warty surface and a “stuck-on” appearance. Although there are multiple pathologies to consider in the differential diagnosis, verruca vulgaris can be morphologically and histopathologically distinguished from these other diseases by the defining characteristics discussed above. As stated previously, most cases of verruca vulgaris are diagnosed clinically upon visual inspection of the lesion; however, on the occasion that a diagnosis is uncertain, shave biopsy followed by histopathologic evaluation may be performed to make a definitive diagnosis.
Once the diagnosis of verruca vulgaris is made, an appropriate treatment plan can be devised. Fortunately, most warts resolve spontaneously, particularly in immunocompetent individuals.5 In two-thirds of children, spontaneous remission occurs within 2 years; however, adult lesions often take several years to resolve.6 Indications for treatment include functional impairment, patient concern, persistence, and immunosuppression.2 First-line treatment for verruca vulgaris is salicylic acid. This treatment option is commonly employed due to its efficacy, ease of use, and minimal side-effect profile. Salicylic acid is an organic acid that works primarily by helping to soften the hyperkeratosis and to exfoliate the HPV-infected epidermal cells; additionally, it activates the local immune response.2,3 Proper use of this treatment requires daily, direct application onto a dry wart. Additionally, hyperkeratotic debris may be removed periodically by soaking and paring of the wart prior to application of salicylic acid to increase the effectiveness of the treatment.
If salicylic acid is not effective in treating the affected area, then second-line treatment with a combination of cryotherapy with liquid nitrogen followed by daily salicylic acid application may be considered.2,3 It is important to note that cryotherapy is typically avoided in young children due to the pain associated with this treatment in comparison to the benign nature of the wart. The use of this combination therapy is particularly beneficial for hand warts; however, the provider must use caution when treating periungual warts in order to avoid nail matrix damage and nail dystrophy.7,8 Recommendations for cryotherapy include application every 2 to 3 weeks until resolution is achieved. Transition to another treatment should be considered if the wart persists after 3 months or 6 treatments.5,9 Treatment-refractory warts may require novel therapies such as topical immunotherapy, imiquimod, intralesional bleomycin, or topical 5-fluorouracil; surgical removal may also be considered.2
Our case patient was diagnosed with verruca vulgaris. This patient was advised to apply salicylic acid to his warts daily with occlusion until resolved. He was also instructed to soak and file his warts several times a week to remove excess debris. Following this regimen, the patient’s warts resolved within 1 month.
Case #2: Digital mucoid cyst
A digital mucoid cyst (DMC), otherwise known as a myxoid cyst or digital mucus pseudocyst, is a benign translucent cyst typically located between the dorsal surface of the distal interphalangeal joint and the proximal nail fold.10,11 Contrary to its name, a DMC is technically a pseudocyst because of its lack of an epithelial lining. How these lesions arise remains unclear; however, 2 mechanisms have been proposed.12,13 The first way in which a DMC can arise is by the extravasation of fluid as it leaks from the neighboring joint through a communicating canal. The second method by which a DMC can arise is from the excess production of hyaluronic acid by fibroblasts. When DMCs develop by this method, they are independent of the joint and typically involve the proximal nail fold.
Second to cutaneous warts, DMCs are the next most common ungual tumor.10 Osteoarthritis is the greatest risk factor for the development of a DMC, with 64% to 93% of patients with osteoarthritis having coexisting DMCs.12,14,15 The population most commonly affected by DMCs are adults aged 40 to 70 years, likely because osteoarthritis is more common in this age group.10 Additionally, women are twice as likely as men to develop a DMC.12,16
DMCs most commonly present lateral to midline on the middle or index finger of the dominant hand and can occasionally, yet uncommonly, present on the toes.10,13 This type of cyst is typically a slow-growing, localized, solitary lesion that ranges in size from 3 mm to 10 mm. A DMC typically contains clear viscous fluid that often stains positive for hyaluronic acid.17 These cysts are often asymptomatic but may cause pain, tenderness, decreased range of motion, nail deformities, and fluid drainage in some patients. Additionally, a lesion located distal to the proximal nail fold may result in a longitudinal depression in the nail bed, commonly referred to as a “groove sign.”10
The diagnosis of a DMC can be obtained through a variety of techniques; however, the diagnosis for uncomplicated DMCs is classically made clinically. For cases more difficult to diagnose, transillumination, fine needle aspiration of clear gelatinous fluid, methylene blue infusion, and histopathologic examination may be necessary to confirm the diagnosis.10 If a biopsy is performed, microscopic examination of a DMC will show fibroblast metaplasia within the dermis and excess hyaluronic acid production. Because these lesions are pseudocysts, an epithelial lining will be noticeably absent and a lining consisting of fibroblasts and compressed connective tissue will be present instead. DMCs are filled with collagen, basophilic mucin, and acid mucopolysaccharides.10,18
The differential for a DMC includes ganglion cyst, rheumatoid nodule, heberden node, epidermoid cyst, and many other similarly appearing lesions. Although sometimes difficult to distinguish, these diagnoses all have defining characteristics that can be used to differentiate one from another. A ganglion cyst is typically larger and deeper than a DMC, and ganglion cysts are associated with larger joints. A rheumatoid nodule is a cutaneous manifestation of rheumatoid arthritis that presents as a firm localized swelling typically found on finger joints, elbows, forearms, knees, and heels whereas heberden nodes are hard, bony swellings at the distal interphalangeal joint. An epidermoid cyst can be differentiated from a DMC by the fact that an epidermoid cyst is a true cyst with a squamous epithelial lining containing keratin and lipid. These lesions, unlike DMCs, are more common in men. Despite the varied differential, the presentations described above can help elucidate the correct diagnosis. In most cases, a clinical diagnosis is sufficient, but as described previously, for complex cases imaging and or histopathology can provide a definitive answer.
While observation of asymptomatic lesions is appropriate, treatment is typically required for elimination of troublesome DMCs as spontaneous regression rarely occurs.10 Even with treatment, recurrence is common. One noninvasive treatment option involves several weeks of daily firm compression. For painful or cosmetically unappealing lesions, surgical removal may be required. This approach boasts the lowest rates of recurrence. Cure rates for surgical removal are high at 90%; however, there is an associated risk of developing septic osteoarthritis following surgery.11 Additional options include repeated needling to induce fibrosis and close the communicating canal, intralesional steroid injection with a triamcinolone solution, percutaneous sclerotherapy with sodium tetradecyl sulfate or polidocanol, and cryotherapy with liquid nitrogen.10,19,20
The case patient was diagnosed with a digital mucoid cyst. She was advised to apply a firm compress to the lesion daily for 2 weeks. The lesion regressed; however, one month after treatment it returned. Annoyed by the cyst, the patient opted for surgical removal and at 1-year follow-up is happy to report no recurrence.
McKenna Boyd is a medical student, Joan Fernandez is a medical student, and Christopher Rizk, MD, is a dermatology resident at the Baylor College of Medicine in Houston.
- Fazel N, Wilczynski S, Lowe L, Su LD. Clinical, histopathologic, and molecular aspects of cutaneous human papillomavirus infections. Dermatol Clin. 1999;17(3):521-536.
- Lynch MD, Cliffe J, Morris-Jones R. Management of cutaneous viral warts. BMJ. 2014;348:3339-3345.
- Ockenfels HM. Therapeutic management of cutaneous and genital warts. J Dtsch Dermatol Ges. 2016;14(9):892-899.
- Kilkenny M, Marks R. The descriptive epidemiology of warts in the community. Australas J Dermatol. 1996;37(2):80-86.
- Pyrhönen S, Johansson E. Regression of warts. An immunological study. Lancet. 1975;1(7907):592-596.
- Sterling JC, Gibbs S, Haque Hussain SS, Mohd Mustapa MF, Handfield-Jones SE. British Association of Dermatologists’ guidelines for the management of cutaneous warts 2014. Br J Dermatol. 2014;171(4):696-712.
- Kwok CS, Gibbs S, Bennett C, Holland R, Abbott R. Topical treatments for cutaneous warts. Cochrane Database Syst Rev. 2012;9:CD001781.
- Bunney MH, Nolan MW, Williams DA. An assessment of methods of treating viral warts by comparative treatment trials based on a standard design. Br J Dermatol. 1976;94:667-679.
- Berth-Jones J, Hutchinson PE. Modern treatment of warts: cure rates at 3 and 6 months. Br J Dermatol. 1992;127:262-265.
- Li K, Barankin B. Digital mucous cysts. J Cutan Med Surg. 2010;14(5):199-206.
- De Berker DAR, Lawrence CM. Treatment of myxoid cysts. Dermatol Surg. 2001;27:296-299.
- Jabbour S, Kechichian E, Haber R, Tomb R, Nasr M. Management of digital mucous cysts: systemic review and treatment algorithm. Int J Dermatol. 2017;56(7):701-708.
- Zuber TJ. Office management of digital mucous cysts. Am Fam Physician. 2001;64:1987-1990
- Kleinert HE, Kutz JE, Fishman JH, McCraw LH. Etiology and treatment of the so-called mucous cyst of the finger. J Bone Joint Surg Am. 1972;54:1455-1458.
- Fritz GR, Stern PJ, Dickey M. Complications following mucous cyst excision. J Hand Surg Br. 1997;22:222-225.
- Sonnex TS. Digital myxoid cysts: a review. Cutis. 1986;37:89-94.
- Nishimura M, Kohda H, Takazono I, Tanaka Y. Chemical components of jelly-like matrix in digital mucous cyst. Clin Exp Dermatol. 1985;10:116-120.
- Abimelec P, Dumontier C. Basic and advanced nail surgery (part 2: indications and complications). In: Scher RK, Daniel RC III, et al (eds). Nails: Diagnosis, Therapy, and Surgery. Philadelphia, PA: Elsevier Saunders; 2005:291.
- Park SE, Park EJ, Kim SS, Kim CW. Treatment of digital mucous cysts with intralesional sodium tetradecyl sulfate injection. Dermatol Surg. 2014;40(11):1249-1254.
- Esson GA, Home SA. Treatment of 63 subjects with digital mucous cysts with percutaneous sclerotherapy using polidocanol. Dermatol Surg. 2016;42(1):59-62.