Pink-to-red scaly raised lesions - Clinical Advisor

Pink-to-red scaly raised lesions


  • Case #2

    June 2015 Dermatology Look-Alikes

    Case #2

  • Case #1

    June 2015 Dermatology Look-Alikes

    Case #1

Case #1

A man, aged 60 years, presents with a 1-year history of a red scaly lesion on his hand. The lesion feels rubbery and soft. It sometimes bleeds and is occasionally painful when he scratches or with any friction. He has no personal or family history of skin cancer. The lesion has grown in size slightly and is occasionally pruritic. He denies any trauma to the area. He has not tried any topical therapies.

Case #2

A 43-year-old woman presents with a new rash that developed 1 week ago. She has a family history of heart disease and her grandmother had psoriasis. The rash is very itchy and consists of raised, pink-to-red, scaly papules. She has tried over-the-counter hydrocortisone, which has provided some, but incomplete, relief. She had a sore throat a few weeks ago with a slight fever. She denies any joint pain and has no nail changes. Her Streptococcus antibody screen is positive.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Round, confluent patches on infant’s face and Small, erythematous papules on the face, scalp, and neck. Then take the post-test here.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Round, confluent patches on infant's face and Small, erythematous papules on the face, scalp, and neck. Then take the post-test here.Case #1Poroma is a benign adnexal...

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This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Round, confluent patches on infant’s face and Small, erythematous papules on the face, scalp, and neck. Then take the post-test here.

Case #1

Poroma is a benign adnexal neoplasm of the intraepidermal portion of the sweat gland duct, called the acrosyringium.1 First described in 1956, poroma was originally identified as a tumor originating from the eccrine sweat gland.2 With time, it became evident that poromas of an eccrine lineage also exist, but the historic view of poromas as neoplasms of eccrine lineage has persisted such that many poromas are assumed to be eccrine poromas.3

Poromas are often grouped within the greater classification of acrospiroma, which includes dermal duct tumors, hidroacanthoma simplex, and nodular, clear-cell, and poroid hidradenomas.1

The cause of poroma is unknown. The condition most commonly presents in middle-aged and elderly patients, and it is not known to have any racial, sex, or ethnic predilection. The prevalence of poroma is not clearly defined, but it is regarded as a relatively rare tumor.

A poroma manifests clinically as a solitary, dome-shaped papule, plaque, or nodule that extrudes from a shallow depression and measures from a few millimeters to a few centimeters in diameter.4 It tends to present on the acral surfaces (hands and feet), but it can also appear on the face, scalp, trunk, and extremities.1,4 The poroma’s color can be the same as that of the skin or pink, red, white, or in rare cases, blue; its surface can range from smooth to verrucous.1 Lesions are normally slow-growing and asymptomatic, but they occasionally cause pruritus and/or pain.

Rapid enlargement, ulceration, spontaneous bleeding, and pain are signs that the lesion may be developing into its malignant counterpart, porocarcinoma.4 Data regarding the likelihood of malignant transformation are divergent, with studies reporting the frequency of transformation as low as 18% and as high as 100%.5,6 Poromatosis, or the emergence of multiple poromas in an acral or a widespread distribution, is also rare and occurs more commonly in patients with a history of immunosuppression from either chemotherapy or radiation.7

Most diagnoses of poromas are made by histological examination. Histologically, a poroma is a well-circumscribed tumor that arises in the lower epidermis and extends into the dermis. Cells consist of small, cuboidal, epithelial (poroid) cells that appear paler than normal keratinocytes.8 A highly vascularized stroma, dispersed duct-like structures, and sharp demarcation between poroid cells and surrounding keratinocytes is seen.4,8

Although the histological features of apocrine and eccrine poromas are nearly identical, the presence of homogenous eosinophilic intraluminal secretion, lining cells with intensely eosinophilic cytoplasm, and small clusters of sebaceous cells surrounded by poroid cells is suggestive of apocrine lineage.3

Because the clinical and histopathologic features of poromas are similar to several other skin conditions, biopsy, dermoscopy, and immunohistochemical staining to identify the presence of eccrine or apocrine ducts can aid diagnosis.1

Dermoscopic examination of poroma reveals polymorphous vessels consisting of glomerular vessels, hairpin vessels, and linear irregular vessels, all surrounded by a white-pink halo and multiple structureless pink-white areas.9

The differential diagnosis for poroma includes pyogenic granuloma, verruca vulgaris, hidradenoma, seborrheic keratosis, melanocytic nevi, and guttate psoriasis. Poromas that have a thickened collar of epidermis may resemble pyogenic granuloma, but poromas grow much slower and are more common than pyogenic granuloma in children.10 Poromas can be unambiguously distinguished from pyogenic granuloma by histologic examination, as poromas contain compact cuboidal cells and highly vascularized stroma, whereas pyogenic granulomas contain numerous capillaries embedded in an edematous stroma.4 Verruca vulgaris may be confused with poroma because both can manifest as small, rough, slightly elevated lesions on the hands and feet.4 However, verruca vulgaris commonly presents during childhood as one or more hyperkeratotic, rough, flesh-colored papule(s), whereas poroma tends to present later in life as a solitary papule, plaque, or nodule and can be pigmented and/or smooth. Hidradenomas can be distinguished histologically from poromas, as they are composed of larger epithelial cells and have ample pale or clear cytoplasm. On histology, poromas are composed of compact cuboidal cells with scant cytoplasm.10 Histologic examination can also distinguish between poromas and seborrheic keratosis. Areas of ductular differentiation and a highly vascularized stroma are prominent in poromas but absent in seborrheic keratosis.10 Pigmented poromas may be confused with melanoma, but the two can usually be distinguished clinically. Poromas tend to be slightly elevated, surrounded by a shallow depression, and skin-colored or pink, whereas melanomas are typically flat and brown or black in color. Lesions of guttate psoriasis may resemble poromas, as both can be small, raised, red or pink papules or plaques. However, guttate psoriasis tends to present as multiple pruritic, scaly lesions after a Streptococcal infection in contrast to poroma, which tends to present as an asymptomatic, solitary spot that is not associated with Streptococcal infection.

Due to the risk of malignant transformation of poromas, surgical excision with narrow margins of normal tissue is recommended.4 The recurrence rate of poromas is low after removal.

For the patient in our case, a diagnosis of eccrine poroma was confirmed for the first patient via shave excisional biopsy. He was educated on the diagnosis and reassured regarding the prognosis. The lesion has not recurred and, the patient is doing well since the procedure. 

Case #2

Psoriasis is a chronic, inflammatory, noninfectious autoimmune skin disorder, characterized by raised, pink-to-red, scaly patches, papules, and plaques that are often accompanied by dryness and itching. The lesions of psoriasis are well-circumscribed and distributed symmetrically on the scalp, elbows, knees, lumbosacral area, and body folds.11

Psoriasis affects approximately 2% to 4% of the world’s population and is estimated to affect 6.7 million adult Americans.12 Higher prevalence rates among nonHispanic whites and persons with arthritis and cardiovascular disease have been reported.12 The age of onset of psoriasis has a bimodal distribution, with peak onset between age 15 years and 20 years and between age 55 years and 60 years.13

There are five types of psoriasis: plaque (also called psoriasis vulgaris), guttate, inverse, pustular, and erythrodermic. Plaque psoriasis is the most common type and appears as erythematous plaques covered with a silvery-white, dry scale. The plaques are often extensive and can cover more than 10% of the body surface area. 

Guttate psoriasis is the second most common type of psoriasis, and in contrast to plaque psoriasis, guttate psoriasis is characterized by the acute onset of multiple (from 5 to more than 100), small (2 mm to 10 mm in diameter), monomorphic lesions that are not as thick as those of plaque psoriasis and are covered in a scale that is finer than that of plaque psoriasis.11 The word guttate appropriately derives from the Greek word gutta, which means droplet, as the lesions resemble erythematous-to-salmon-pink drops on the skin.11 The lesions are typically spread in a centripetal fashion, but they can involve the head and limbs.11

Eruption of guttate psoriasis is triggered by infection, stress, or injury to the skin. The most common trigger is infection of the pharynx or tonsils by group A beta-hemolytic Streptococci.11 Guttate psoriasis is usually seen in patients aged less than 30 years and is generally a self-limited process, with full resolution occurring within a few weeks to months without treatment. However, episodes of guttate psoriasis can recur, and some individuals may progress to chronic plaque psoriasis. Even patients that recover fully from guttate psoriasis are at a higher risk of developing chronic plaque psoriasis. One small study showed that approximately one-third of children who experienced a single episode of acute guttate psoriasis will develop chronic, plaque-type psoriasis within 10 years.14

Pruritus and pain tend to accompany guttate psoriasis. When the lesions are scratched, scales often flake off and pinpoint spots of blood may appear (Auspitz’s sign).11

In addition to physical symptoms, psoriasis can cause substantial psychological, emotional, and social difficulties. Individuals with psoriasis have more frequent mental distress, depression, anxiety, self-consciousness, and impaired social functioning.12 They also tend to have decreased work productivity or greater rates of unemployment, higher body mass indices, more frequent smoking habits, and greater alcohol consumption than individuals without psoriasis.12

Patient history and clinical examination are usually sufficient to make the diagnosis of guttate psoriasis. However, if the diagnosis is uncertain, a skin biopsy can confirm the diagnosis. Microscopic features of guttate psoriasis include discrete mounds of parakeratosis with associated collections of neutrophils overlying the epidermis, along with dilated papillary dermal blood vessels.15 In guttate psoriasis, the epidermis does not display pronounced acanthosis, due to the rapid onset of guttate psoriasis.15 This is unlike the epidermis in plaque psoriasis. 

Topical agents are typically used to treat guttate psoriasis, and these include emollients, corticosteroids, vitamin D3 analogues, topical calcineurin inhibitors (off-label), anthralin, and coal-tar preparations.16 However, because of the numerous lesions in guttate psoriasis, application of a topical agent is often arduous and time-consuming. Therefore, phototherapy may be used to treat guttate lesions. The most common phototherapies for guttate psoriasis are narrow-band ultraviolet (UV)-B and psoralen-UVA (PUVA).16 It is recommended that narrow-band UVB be combined with topical therapies.16

Anti-streptococcal antibiotics are often administered to treat patients with guttate psoriasis, but there is no evidence of any definite benefit.17,18

The differential diagnosis for guttate psoriasis includes pityriasis rosea, pityriasis lichenoides, small-plaque parapsoriasis, poroma, and secondary syphilis. Pityriasis rosea differs from guttate psoriasis in that lesions of pityriasis rosea tend to initiate as solitary, large, oval-to-round, scaly, skin-to-salmon-pink-colored patch or plaque (“herald patch”), which develops a collarette scaling.19 Over time, new lesions appear that are angled to form a “Christmas-tree” pattern along skin-cleavage lines on the trunk.19 Additional differences between pityriasis rosea and guttate psoriasis can be seen on histology, on which a diagnosis of guttate psoriasis is supported by discrete mounds of parakeratosis with collections of neutrophils.15 Pityriasis lichenoides can be distinguished from guttate psoriasis, as the eruptions of pityriasis lichenoides are more often polymorphic instead of monomorphic, and the papules of pityriasis lichenoides are generally smaller. Small-plaque parapsoriasis may mimic guttate psoriasis but can be differentiated from it, as lesions of small-plaque parapsoriasis tend to be flatter and present as elongated, finger-like patches, producing a digitate pattern. Lesions of guttate psoriasis may resemble poromas, as both can be small, raised, red or pink papules or plaques. However, guttate psoriasis tends to present as multiple pruritic, scaly lesions after a streptococcal infection in contrast to poroma, which tends to present as an asymptomatic, solitary spot that is not associated with streptococcal infection. Secondary syphilis can be differentiated from guttate psoriasis in that syphilis produces more systemic complaints, is transmitted sexually, and often involves the palms, soles, and face—locations that are uncommonly affected in guttate psoriasis. 

For the patient in this case, a diagnosis of guttate psoriasis was confirmed by biopsy. She was treated with antibiotics and topical steroids with improvement.

Kate Travis, BA, is a medical student and Rana Mays, MD, is a dermatology resident at Baylor College of Medicine in Houston.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Round, confluent patches on infant’s face and Small, erythematous papules on the face, scalp, and neck. Then take the post-test here.


  1. Sawaya JL, Khachemoune A. Poroma: A review of eccrine, apocrine, and malignant forms. Int J Dermatol. 2014;53(9):1053-1061. Available at 

  2. Goldman P, Pinkus H, Rogin JR. Eccrine poroma; tumors exhibiting features of the epidermal sweat duct unit. AMA Arch Derm. 1956;74(5):511-521. 

  3. Kamiya H, Oyama Z, Kitajima Y. “Apocrine” poroma: Review of the literature and case report. J Cutan Pathol. 2001;28(2):101-104. 

  4. Baykal C, Yazganoglu KD. Clinical Atlas of Skin Tumors. Berlin Heidelberg: Springer-Verlag; 2014:149-186.
  5. Robson A, Greene J, Ansari N, et al. Eccrine porocarcinoma (malignant eccrine poroma): A clinicopathologic study of 69 cases. Am J Surg Pathol. 2001;25(6):710-720. 

  6. Shaw M, McKee PH, Lowe D, Black MM. Malignant eccrine poroma: A study of twenty-seven cases. Br J Dermatol. 1982;107(6):675-680. 

  7. Deckelbaum S, Touloei K, Shitabata PK, et al. Eccrine poromatosis: Case report and review of the literature. Int J Dermatol. 2014;53(5):543-548. 

  8. Jain S. Dermatology: Illustrated Study Guide and Comprehensive Board Review. New York: Springer-Verlag; 2012:235. 

  9. Sgouros D, Piana S, Argenziano G, et al. Clinical, dermoscopic, and histopathological features of eccrine poroid neoplasms. Dermatology. 2013;227(2):175-179. Available at 

  10. Grant-Kels JM. Color Atlas of Dermatopathology. London: CRC Press; 2007:238-239. 

  11. Langley RGB, Krueger GG, Griffiths CEM. Psoriasis: Epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(Suppl 2):ii18-ii23. Available at 

  12. Helmick CG, Lee-Han H, Hirsch SC, et al. Prevalence of psoriasis among adults in the U.S.: 2003-2006 and 2009-2010 National Health and Nutrition Examination Surveys. Am J Prev Med. 2014;47(1):37-45. 

  13. Smith AE, Kassab JY, Rowland Payne CM, Beer WE. Bimodality in age of onset of psoriasis, in both patients and their relatives. Dermatology. 1993;186(3):181-186. 

  14. Martin BA, Chalmers RJ, Telfer NR. How great is the risk of further psoriasis following a single episode of acute guttate psoriasis? Arch Dermatol. 1996;132(6):717-718. 

  15. Billings SD, Cotton J. Inflammatory Dermatopathology: A Pathologist’s Survival Guide. New York: Springer; 2010:21-26. 

  16. Fotiadou C, Lazaridou E, Ioannides D. Management of psoriasis in adolescence. Adolesc Health Med Ther. 2014;5:25-34. Available at 

  17. Owen CM, Chalmers RJ, O’Sullivan T, Griffiths CE. Antistreptococcal interventions for guttate and chronic plaque psoriasis. Cochrane Database Syst Rev. 2000;(2):CD001976. 

  18. Krishnamurthy K, Walker A, Gropper CA, Hoffman C. To treat or not to treat? Management of guttate psoriasis and pityriasis rosea in patients with evidence of group A Streptococcal infection. J Drugs Dermatol. 2010;9(3):241-250.

  19. Wood GS, Reizner G. Other papulosquamous disorders. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. Philadelphia, Pa.: Saunders; 2008.

All electronic documents accessed on June 4, 2015.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Round, confluent patches on infant’s face and Small, erythematous papules on the face, scalp, and neck. Then take the post-test here.

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