V.6 Seborrheic Keratosis Including Lichen Planus-like Keratosis

(1)

V.6.1 Definition

Along with melanocytic nevi, seborrheic keratosis is the most common benign cutaneous neoplasm. The pathogenesis is unknown. There is a strikingly familiar predisposition probably with an autosomal–dominant inheritance pattern.

Seborrheic Keratosis Including Lichen Planus-like Keratosis

Robert Johr

V.6

Contents

V.6.1 Definition . . . 313

V.6.2 Clinical Features . . . 313

V.6.3 Dermoscopic Criteria . . . 315

V.6.4 Relevant Clinical Differential Diagnosis . . . 319

V.6.5 Histopathology . . . .322

V.6.6 Management . . . .323

V.6.7 Lichen Planus-like Keratosis . . . .323

V.6.7.1 Definition . . . .323

V.6.7.2 Clinical Features . . . .323

V.6.7.3 Dermoscopy . . . .323

V.6.7.4 Relevant Clinical Differential Diagnosis . . . .325

V.6.7.5 Histopathology . . . .325

V.6.7.6 Management . . . .326

References . . . .327

V.6.2 Clinical Features

“Warty” and “stuck-on” are adjectives used to describe these ubiquitous epidermal skin neoplasms. Characterizations which are not always apparent clinically.

Most people develop at least one seborrheic keratosis in their lifetime, usually forming de novo in adults and the elderly. They can also be found in the teens, twenties, and thirties. The number varies from less than 20 in the average person to hundreds of lesions that slowly in- crease in size and number with age. Usually developing on any skin surface except the palms, soles, mucous membranes, or sun-exposed areas (Fig. V.6.1) seborrheic keratosis can be skin colored, tan and various shades of brown, alarmingly black, or multicolored. They are well-circumscribed round-to-oval macules, papules, and nodules, most often plaques rang- ing in size from a few millimeters to centime- ters. The borders can also be irregular and notched with unusual distributions such as along skin-cleavage lines, around the areola, or in a raindrop distribution [1] on the backs of the elderly.

The surface can be scaly, crusty, smooth, or greasy (Fig. V.6.2). Most people have many vari- ations on the theme of the possible clinical pre- sentations, and individual seborrheic keratosis can have a combination of clinical characteristics. Rough-surfaced lesions can be brittle and crumble into pieces when picked, leaving a raw red moist surface. In intertriginous areas especially under the breasts, they can be moist, red, and without scales. Follicular plugs and tiny white, yellow, or dark horn pearls can be seen embedded in the surface. The correlation with the dermoscopic criteria of comedo-like open-

(2)

V.6

ings and milia-like cysts aids in the clinical diagnosis before dermoscopy is performed.

Stuccokeratosis and dermatosis papulosa nigra are two very common variants of seborrheic keratosis. Located on the ankles and feet, stuccokeratosis are numerous small whitish scaly papules typically found in older adults.

Dermatosis papulosa nigra is seen in adult dark- er-skinned races and consists of multiple hyper- pigmented soft papules that are often peduncu- lated. They can also be found on the neck and upper trunk.

The majority of seborrheic keratosis are asymptomatic, yet they can become sore or pru- ritic either spontaneously, or secondary to trau- ma from patient manipulation, articles of

Fig. V.6.1. This is a typical older patient with multiple seborrheic keratoses that do not develop where there is no sun exposure. Seborrheic keratosis could be sun-in- duced lesions

Fig. V.6.2. Typical scaly, crusty, and seborrheic keratosis that is easily diagnosed clinically

(3)

clothing, or physical activity. Inflammation can be mild, moderate, or severe with edema, ery- thema of the surrounding skin, thick scale, fri- able crust formation, oozing, and bleeding.

When severe, the typical clinical characteristics are obliterated, and the inflamed seborrheic keratosis might be indistinguishable from a pyogenic granuloma and, if dark, from nodular melanoma (Fig. V.6.3). Another manifestation of inflammation is the Meyerson phenomenon with a halo of eczematization surrounding the lesion. Spontaneous regression is not a common occurrence.

The sudden development, inflammation, or regression of multiple seborrheic keratoses is a clinical scenario that can be a cutaneous manifestation of internal malignancy. It is called the sign of Leser–Trelat. If it is associated with other paraneoplastic skin findings, such as acanthosis nigricans, acquired icthyosis, or the development of lanugo hair, it is even more worrisome.

The average age of onset is 61 years, and the most common malignancy is adenocarcinoma, especially of the stomach. Other malignancies associated with the sign of Leser–Trelat include lymphoma, mycosis fungoides, Sezary syndrome, leukemia, and cancer of the lung, breast, pancreas, and esophagus. Most patients already

have metastatic disease; however, its recognition can facilitate the early diagnosis of occult malignancy. Often paralleling the course of the un- derlying malignancy, it can improve with suc- cessful surgery or chemotherapy, and it can worsen if the malignancy returns. The sign of Leser–Trelat has also been associated with preg- nancy, heart-transplant recipients, following chemotherapy, in human immunodeficiency virus infection, and following erythrodermic psoriasis or drug eruptions. If a clinician makes this diagnosis, a comprehensive systemic work- up is indicated [2–8].

V.6.3 Dermoscopic Criteria

Most, but not all, seborrheic keratoses can be diagnosed clinically or with dermoscopy. A small percentage require histopathology. Global patterns and local criteria often require a differential diagnosis. The gold standard of histopathology might not be straightforward with collision lesions when seborrheic keratosis is associated with different benign or malignant pathology. Com- munication between the dermoscopist and der- matopathologist is essential when there is asym- metrical presentation of dermoscopic criteria.

Fig. V.6.3. This irritated seborrheic keratosis lacks the clinical and dermoscopic criteria to make the diagnosis.

Histopathological evaluation should be considered

(4)

V.6

The original algorithm used to diagnose seborrheic keratosis included two classic criteria:

milia-like cysts and comedo-like openings. Ad- ditional criteria are now used to help make the diagnosis [9, 10]. Sharp demarcation and abrupt cut-off of pigmentation and dermoscopic criteria are routinely seen. There can be significant

asymmetry of color and structure, plus the mul- ticomponent global pattern with three or more distinct areas of dermoscopic criteria as seen in melanomas. No single criterion by itself is diag- nostic, and as many criteria as possible should be identified and evaluated before the dermoscopic diagnosis is made. There are innumerable

Fig. V.6.4. In this seborrheic keratosis the milia-like cysts light up like “stars in the sky.” There are also several pigmented round and oval comedo-like openings. The dark blotch of color has a differential diagnosis that includes a collision-tumor possible melanoma

Fig. V.6.5. Are the circular whitish structures the milia- like cysts of a seborrheic keratosis or the appendigeal openings of lentigo maligna?

The general dermoscopic principle “if in doubt, cut it out” led to the diagnosis of lentigo maligna that was surrounded by seborrheic keratosis (arrow)

(5)

combinations and appearances of what can be seen including black, various shades of brown, gray, red, white, blue, and yellow colors.

Milia-like cysts (pseudocysts, pseudohorn cysts, “stars in the sky”) are single or multiple variously sized and irregular distributed round white or yellowish structures that histopathologically represent intraepithelial horn cysts.

They can be opaque and dull or appear to light up like “stars in the sky” (Fig. V.6.4). Usually small, they can be large and irregular in shape.

It is most important to differentiate milia-like cysts from the appendigeal openings of the pseudonetwork seen on the head and neck so that lentigo maligna is not misdiagnosed as a seborrheic keratosis (Fig. V.6.5). Even experi- enced dermoscopists cannot always make the distinction. Multiple or large milia-like cysts favor the diagnosis of a seborrheic keratosis.

When a few in number, they can also be seen in benign melanocytic nevi and occasionally in melanomas.

Comedo-like openings (pseudofollicular openings, follicular openings, irregular crypts, keratin plugs) present as variously sized, roundish, oval, or irregularly shaped sharply circumscribed single or multiple yellowish, brown, or black crater-like openings that can have a targetoid or three-dimensional appear-

ance (Fig. V.6.6). Histopathologically, they represent keratin filled dilated follicular openings in the epidermis, black-head like structures.

They can be indistinguishable from the dots and globules used to diagnose melanocytic lesions (Fig. V.6.7). Clonal seborrheic keratosis lacking the stereotypical dermoscopic criteria can have small dark-brown or black globular- like structures similar to those seen in benign melanocytic lesions and melanoma, or larger ovoid nests that are often seen in basal cell car- cinomas [11, 12]. Pressure and side-to-side movement with instrumentation will only change the shape of comedo-like openings.

Multiple comedo-like openings favor the diagnosis of seborrheic keratosis; however, they can also be seen in melanocytic nevi and occasionally in melanoma. A recent history of change might be the only reason to excise a lesion that clinically looks like a seborrheic keratosis and has multiple comedo-like openings typically seen in seborrheic keratosis but with subtle dermoscopic criteria that diagnoses a melanoma (melanoma incognito) [13].

Fissures and ridges (brain-like pattern) are a global pattern commonly found in seborrheic keratosis. They are formed by dark-brown or black linear and branching depressions creating a network or cerebriform pattern resembling

Fig. V.6.6. This well-demarcated lesion has multiple, irregularly shaped comedo-like openings plus a few subtle whitish milia-like cysts. Im- portant dermoscopic criteria are not always easy to find

(6)

V.6

the sulci and gyri of the brain, or one could imagine the peaks and valleys of a mountain range (Figs. V.6.7, V.6.8). Histopathologically, they represent wedge-shaped invaginations of the epidermis that are filled with keratin. The novice dermoscopist might confuse the fissure and ridge pattern with a thickened pigment network or the cobblestone pattern of melanocytic nevi.

Flat seborrheic keratosis can be diagnosed by observing a network-like pattern of thin brown parallel lines reminiscent of fingerprints (Fig.

V.6.9). Fingerprinting is not uncommon and can be found alone or in combination with other patterns. It should not be mistaken for the pigment network of melanocytic lesions that form a hon- eycomb-like network. Fingerprinting can also be found in solar lentigines (Fig. V.6.10).

Fig. V.6.7. It is not possible to determine if this lesion has the dots and globules of a melanocytic lesion or the pigmented comedo-like openings of a seborrheic keratosis.

This seborrheic keratosis looks like a melanoma both clinically and dermoscopically.

Fig. V.6.9. The novice dermoscopist might confuse this variation of the fissure and ridge pattern of a seborrheic keratosis with the cobblestone pattern of a melanocytic nevus. The clinical characteristics help in making the cor- rect diagnosis

Fig. V.6.8. Fissures and ridges characterize this seborrheic keratosis with an almost unbelievable resemblance to a sagittal section of the brain. It is truly cerebriform

(7)

Another network-like pattern with foci of thicker-branched and dark-brown or black-line segments often with an abrupt cut-off at the pe- riphery can be seen. Histopathologically, it rep- resents melanin in keratinocytes or melanocytes along the dermo-epidermal junction. At times, the differentiation of all of these forms of network will not be possible. One must formulate a dermoscopic differential diagnosis and search for more criteria to make a diagnosis.

Hairpin-shaped fine telangiectatic blood vessels are commonly seen in seborrheic keratosis (Fig. V.6.11). At times they can have a white halo surrounding them, indicating the keratinizing nature of the tumor. They are also seen in melanocytic nevi, keratoacanthomas, basal cell car- cinomas, and when thick and irregular, in melanomas. The less pressure applied to the skin with instrumentation, the easier it will be to see these fine vessels. Skill and minimal pressure is needed to capture good images of hairpin vessels with digital photography.

Flat seborrheic keratosis can also have irregular borders with small or large concave inden- tations that have been compared to moth-eaten garments. “Moth-eaten” borders are a widely accepted criterion that can also be seen in solar lentigines.

Finally, if one looks carefully, the pigment on the surface of the skin in flat seborrheic keratosis can appear to be like “jelly spread over the skin.” The jelly sign would be one of the most

difficult criterion to identify and least important in diagnosing seborrheic keratosis using dermoscopy.

V.6.4 Relevant Clinical Differential Diagnosis

In most cases the clinical diagnosis of seborrheic keratosis, stuccokeratosis, and dermatosis papulosa nigra poses no problems; however, clinically atypical lesions can be challenging. If in doubt, never hesitate to cut one out, because melanomas are not uncommonly misdiagnosed as seborrheic keratosis. Clinical and dermoscopic features of both can be found in a single lesion.

In a retrospective study of 9204 cases submit- ted for histopathological examination with the clinical diagnosis of seborrheic keratosis, or a differential diagnosis including seborrheic keratosis, a significant number of cases turned out to be melanomas. Verrucous melanomas might be especially difficult to differentiate clinically from seborrheic keratosis (Figs. V.6.12–V.6.14) [14].

Clinically, they can also be confused with actinic keratosis, melanocytic nevi (Fig. V.6.15), verruca vulgaris, condyloma acuminatum, solar lentigines, in-situ and invasive squamous cell carcinoma, acrochordon, eccrine poromas, and epidermal nevi. The patient’s personal and fam-

Fig. V.6.11. This seborrheic keratosis demonstrates typical hairpin-shaped blood vessels

Fig. V.6.10. Fingerprinting on the right and a variation of the fissure and ridge pattern on the left characterize this seborrheic keratosis

(8)

V.6

ily history, plus the history of the lesion, should be taken into consideration. For example, a seborrheic keratosis-like lesion in a 7-year-old most probably is an epidermal nevus. Actinic keratosis tend to be more erythematous with poorly defined borders. Melanocytic nevi are soft, compressible, non-scaly with a positive wobble

sign. If one observes a seborrheic keratosis-like lesion in the genital area, most probably it is a condyloma acuminatum.

Seborrheic keratosis is generally regarded as a benign tumor; however, melanocytic, non- melanocytic, benign, and malignant patholo- gies have been associated with them (Fig. V.6.16).

Fig. V.6.12. At times it is very difficult to differentiate melanoma from a seborrheic keratosis. In this case it was a seborrheic keratosis. If one does not have a good clinicopathological correlation, another biopsy or another pathologist’s opinion can be considered

Fig. V.6.13. This large, well-demarcated scaly and greasy-appearing lesion was present for years without a history of any changes. With dermoscopy multiple milia- like cysts were thought to be seen reinforcing the diagnosis of a seborrheic keratosis

(9)

The association might be by chance, or seborrheic keratosis could be a precursor lesion since it contains all of the cells found in the normal skin.

Basal cell carcinoma, in-situ and invasive squamous cell carcinoma, keratoacanthomas, lentigo maligna, superficial spreading melano-

ma, melanocytic and dysplastic nevi, actinic keratosis, actinic lentigo, and eccrine porocarcinoma have been reported to be associated with seborrheic keratosis. Some researchers believe that the reticulated sub-type of seborrheic keratosis arises from solar lentigines. The frequency of these as- sociations varies from study to study [15–17].

Fig. V.6.14. Another general dermoscopy principle is to eliminate scale to get a better picture. After the scale was removed with a swipe of an alcohol prep, a different picture emerged. This nodular melanoma demonstrated asymmetry of color and structure, irregular pigment network, globules and blotches, plus a diffuse blue-white structure

Fig. V.6.15. The clinical and dermoscopic differential diagnosis includes a melanocytic nevus vs seborrheic keratosis.

In this case it was a seborrheic keratosis.

Fig. V.6.16. A collision lesion consisting of a melanocytic nevus and a seborrheic keratosis

(10)

V.6

V.6.5 Histopathology

Seborrheic keratosis are true neoplasms and not a hyperplasia of the epidermis that have a variable proliferation of basaloid and squamous cells with pseudohorn cyst formation (Fig. V.6.17). Acanthotic, hyperkeratotic, reticulated, irritated, and clonal are the most common histological subtypes, and many show a mixture of patterns. There are varying amounts of hyperkeratosis, acanthosis, papillomatosis, pigmentation, and inflammation. Cytological atypia and perivascular, diffuse, or lichenoid chronic inflammatory infiltrates can be seen with irritated lesions. The acanthotic subtype is most common with little hyperkeratosis or pap-

illomatosis and a greatly thickened epidermis.

The hyperkeratotic variant is the histological reverse of the acanthotic type with prominent hyperkeratosis, and papillomatosis while the reticulated or adenoid type demonstrates delicate strands of epithelium branching from the epidermis. Intraepithelial nesting gives rise to the Borst–Jadassohn appearance of the clonal seborrheic keratosis and intradermal or inverted proliferation characterizes the inverted follicular keratosis. Stuccokeratosis has histopathological features of hyperkeratotic seborrheic keratosis, usually without pseudohorn cyst formation, whereas dermatosis papulosa nigra has features of the acanthotic variant with pseudohorn cysts [18].

Fig. V.6.17. On the left is a collision tumor consisting of a basal cell carcinoma and a seborrheic keratosis. On the right is another collision tumor, a squamous cell carci-

noma with a seborrheic keratosis. Did the malignancies arise from the seborrheic keratosis, a benign proliferation of basaloid and squamous cells?

(11)

V.6.6 Management

Seborrheic keratosis comes to clinical attention for cosmetic reason if they become symptomatic or appear to break into pieces for no apparent reason. They account for a large number of office visits and significant health care costs.

Seborrheic keratosis that have undergone recent change, are symptomatic, or look suspicious clinically should be considered for dermoscopic and histopathological evaluation. Sig- nificant pathology, such as melanoma or basal cell carcinoma, could be surrounded by numerous seborrheic keratosis, or individual seborrheic keratosis could have malignant changes themselves. Careful physical examination is essential. Complete excision, rather than a shave or curettage, will be more helpful to the pathologist to evaluate for malignancy.

Treatment is most often for cosmetic reasons, so the least destructive method should be used.

Cryotherapy, with and without curettage, is the treatment of choice. Shave excision, electrodes- iccation, and CO2 laser vaporization are other methods of treatment that have increased risks of scarring.

V.6.7 Lichen Planus-like Keratosis V.6.7.1 Definition

Lichen planus-like keratosis (synonyms: benign lichenoid keratosis; solitary lichen planus; invo- luting lichenoid plaque) is a common benign tumor of adulthood.

V.6.7.2 Clinical Features

The pathogenesis of lichen planus-like keratosis is thought to be an immunologically mediated regression of an existing lesion. This theory does not account for the lesions that develop de novo. Ninety percent of these lesions are solitary macules or papules, occasionally nodules or plaques that develop between the third to seventh decade in Caucasians and which are occasionally seen in Hispanics, Asians, or Afri- can-Americans. With a 2:1 female to male inci-

dence, they are typically found on the upper trunk, distal upper extremities, and uncommonly, on the head and neck. A small percentage of people can have two or three of these lesions.

There is a correlation of the clinical appearance with their chronicity and histopathological findings. Acute, rapidly developing lichen planus-like lesions of less than 3 months tend to be erythematous or pinkish. Subacute lesions of 3 months to 1 year have a dusky-red or violaceous color, and if present for more than 1 year, they are regularly or irregularly pigmented with shades of brown or gray. The diagnosis can be suspected even before dermoscopy is used by seeing a small lesion with a combination of brown and gray colors. The surface can be scaly, verrucous, or smooth and pearly. They range in size from a few millimeters to a centimeter or more, and can be asymptomatic, slightly pru- ritic, or have a mildly stinging sensation. Malig- nant degeneration of lichen planus-like keratosis has never been reported.

V.6.7.3 Dermoscopy

Erythematous or pinkish lichen planus-like keratosis are featureless or feature poor with remnants of pigment network, subtle blotches of brown color, plus dotted, irregular linear, and other-shaped telangiectatic blood vessels (Fig. V.6.18). They cannot be distinguished clinically or dermoscopically from melanocytic, non-melanocytic benign, malignant, or inflammatory lesions that have the same characteristics including amelanotic melanoma.

With the pigmented variant, the dermoscopic picture depends on the age of the lesion. Early lesions can have the dermoscopic features of a solar lentigo or flat seborrheic keratosis with

“moth-eaten” borders, fingerprinting, milia- like cysts, comedo-like openings plus small foci of melanophages. Also referred to as peppering or granular dust, melanophages have a distinctive dermoscopic appearance with fine irregular dots that can be black, shades of brown, gray, or blue. Typically they are smaller than the dots and globules seen in melanocytic lesions (Fig. V.6.19).

(12)

V.6

As time passes increasingly more melanophages are seen, and they might be the only dermoscopic criteria found in older lesions (Fig. V.6.20). One can also see larger clumps of pigment plus foci of whitish color. In the later stages of development, the dermoscopic differ-

ential diagnosis could include regressive melanoma. The clinical, dermoscopic, and histopathological differentiation might not be possible. Special staining, such as S-100 and a good clinicopathological correlation, is ad- vised.

Fig. V.6.19. Fingerprinting of a flat seborrheic keratosis can be seen on the right side of this lesion. The grayish- colored fine dots representing melanophages on the left side are the most important clues in diagnosing this lichen planus-like keratosis Fig. V.6.18. Pinkish macules and papules can be melanocytic, non-melanocytic, benign, malignant, or inflammatory. This worrisome papule was discovered hidden on the chest of a very hairy patient. It is feature poor with dotted and linear irregular-shaped blood vessels.

It turned out to be a lichen planus-like keratosis and not amelanotic melanoma

(13)

V.6.7.4 Relevant Clinical Differential Diagnosis

In most, but not all, cases the diagnosis of lichen planus-like keratosis is made after a skin biopsy.

The clinical impression does not usually corre- late with the histopathology. Past experience and a high index of suspicion are helpful.

The differential diagnosis includes basal cell carcinoma, especially when the surface is smooth and pearly, in-situ and invasive squa- mous cell carcinoma, actinic or seborrheic kera- tosis, pigmented dermatofibromas, and solar lentigines. Older pigmented variants, especially if there is a history of change, should be differentiated from banal and dyspastic nevi or melanoma. An erythematous or pinkish macule or papule cannot be differentiated clinically from amelanotic banal and dyspastic nevi, amelanotic melanoma, and even solitary inflammatory lesions such as psoriasis or granuloma annu- lare.

V.6.7.5 Histopathology

In general, lichen planus-like keratosis are char- acterized by epidermal and dermal changes that reflect the age of the lesion. The epidermis can

be normal, acanthotic, or atrophic with hyperkeratosis, focal parakeratosis, and hypergranu- losis. Civatte colloid body formation representing necrotic keratinocytes is frequently found.

There are variable amounts of vacuolar degeneration of the basal cell layer plus a band-like lymphocytic infiltrate that can obscure the dermo-epidermal junction.

Melanin incontinence with melanophages, dermal scarring, plus variable numbers of eo- sinophils, plasma cells, histiocytes, and neutro- phils can also be found. Features of solar lentigo or seborrheic keratosis are often seen at the pe- riphery of the lesion.

In a study of 1040 lichen planus-like keratosis, five histopathological subtypes were identified [19]: the classic and early interface types, plus bullous lesions with intra- and subepider- mal vesiculation. There was an atypical variant with at least five atypical lymphocytes and an absence of criteria to diagnose mycosis fun- giodes. In another retrospective study, 15 cases of mycosis-fungoides-pattern, lichen planus- like keratoses were presented that had Pautrier micro-abscesses, epidermotropism, and lymphocytes with hyperconvoluted nuclei [20].

Atrophic late lesions were the last subtype identified.

Fig. V.6.20. Surgery can be avoided with this small oval lichen planus-like keratosis filled with melanophages.

There is no suggestion with dermoscopy that this could be a regressive melanoma;

therefore, dermoscopy over rides the atypical clinical picture. With experience one will not excise many lesions with this dermoscopic appearance

(14)

V.6

The classic, atypical, and bullous patterns were associated with erythematous or pinkish lesions. Interface subtypes were erythematous to brown macules, whereas the late atrophic lesions tended to be grayish, violaceous, or irregularly pigmented.

The histopathological differential diagnosis is extensive and includes other conditions with a band-like infiltrate such as lichen planus, lichenoid lupus erythematosus, and lichenoid drug reactions. Inflamed actinic and seborrheic keratosis, porokeratosis, melanocytic lesions, including melanoma, are also in the differential diagnosis. Melanomas simulating lichen planus-like keratosis have increased numbers of atypical melanocytes that can be partially ob- scured by a dense lymphocytic infiltrate. Pa- thologists considering the diagnosis of mycosis fungoides should search for criteria that might indicate that the lesion is a lichen planus-like keratosis. Clinicopathological correlation plus dermoscopic examination will help the clinician make the differentiation.

V.6.7.6 Management

In most cases lichen planus-like keratosis is found by physicians that perform careful skin examinations. Baseline gross and digital dermoscopic images can be taken of minimally suspicious lesions to follow over time. Side-by- side comparisons of the baseline and follow-up images can be checked for significant changes.

When a more suspicious lesion is found, a complete excision, rather than an incisional biopsy, is recommended. Since melanoma is in the differential diagnosis of pigmented and pinkish lesions, the pathologist will need the entire speci- men for a complete evaluation. Although the technique is controversial, skilled clinicians can accomplish this easily with a deep-shave excision.

Skin biopsies are not always needed, especially if the lesion is examined with dermoscopy and no high-risk criteria are identified. Once the diagnosis is confirmed histopathologically, if part of the lesion remains, liquid nitrogen or electrosurgery and curettage can be performed.

Topical steroids can also be used, or they can be left alone.

(15)

References

1. Hefferman MP, Khavari PA. Raindrop seborrheic keratosis: a distinctive pattern on the backs of elderly patients. Arch Dermatol 1998; 134:382–383 2. Hsu C, Abraham S. Campanelli A et al. Sign of Les-

er–Trelat in a heart transplant recipient. Br J Der- matol 2005; 153(4):861–862

3. Patton T, Zirwas M, Nieland-Fisher N, Jukie D.

Inflammation of seborrheic keratoses caused by cytarabine: a pseudo sign of Leser–Trelat. J Drugs Dermatol 2004; 3(5):565–566

4. Pentenero M, Carrozzo M, Pagano M, Gandolfo S.

Oral acanthosis nigricans, tripe palms and sign of Leser–Trelat in a patient with gastric adenocarcinoma. Int J Dermatol 2004; 43(7):530–532

5. Inamadar AC, Palit A. Eruptive seborrheic keratosis in human immunodeficiency virus infection: a coincidence or “the sign of Leser–Trelat?” Br J Der- matol 2003; 149(2):435–436

6. Flugman SL, McClain SA, Clark RA. Transient eruptive seborrheic keratosis associated with erythrodermic psoriasis and erythrodermic drug erup- tion: report of two cases. J Am Acad Dermatol 2001;45(6 Suppl):S212–S214

7. Vielhauer V, Herzinger T, Korting HC. The sign of Leser–Trelat: a paraneoplastic cutaneous syndrome that facilitates early diagnosis of occult cancer. Eur J Med Res 2000; 5(12):512–516

8. McCrary ML, Davis LS. Sign of Leser–Trelat and mycosis fungoides. J Am Acad Dermatol 1998;

38(4):644

C Core Messages

■ Seborrheic keratosis are ubiquitous benign epidermal neoplasms that, in most but not all cases, can be diagnosed clinically and with dermoscopy;

some will need a histopathological diagnosis.

■ It is important to be aware of the clinical differential diagnosis of atypical lesions.

■ Melanomas can be misdiagnosed as seborrheic keratosis, especially the verrucous variant. Any lesion that looks suspicious clinically or with dermoscopy to be symptomatic or changing should be considered for histopathological evaluation.

■ Seborrheic keratoses can be associated with melanocytic, non-melanocytic benign, or malignant pathology.

■ Cutaneous malignancies can be surrounded and camouflaged by multiple seborrheic keratoses, or an individual seborrheic keratosis could undergo malignant change. Careful physical examination is essential.

■ The sudden appearance, irritation of pre-existing lesions, or regression of seborrheic keratosis is called the sign of Leser–Trelat and can be a cutaneous manifestation of an internal malignancy

If the diagnosis is made, a comprehensive systemic work-up is indicated.

■ Treatment is most often for cosmetic reasons and the least destructive and scarring method should be used.

■ Lichen planus-like keratosis are usually diagnosed histopathologically. Exci- sional, rather than incisional, tech- niques are recommended.

■ The more skilled clinician can make the diagnosis by putting the clinical and dermoscopic findings together, thus avoiding surgery.

■ There is an extensive clinical and histopathological differential diagnosis which includes melanoma, non- melanoma skin cancer, and mycosis fungoides. A good clinicopathological correlation is essential.

■ Solitary erythematous or pinkish macules and papules could be melanocytic, non-melanocytic, benign, malignant, or inflammatory. Dermos- copy is usually not helpful with these lesions.

■ Once the diagnosis of a lichen planus- like lesion is made, aggressive therapy is not indicated. Reassurance to the patient of the benign nature of this pathology will be appreciated.

(16)

V.6

9. Braun RP, Rabinovitz HS, Krischer J et al. Dermos- copy of pigmented seborrheic keratosis: a morpho- logical study. Arch Dermatol 2002; 138:1556–1560 10. Elgart GW. Seborrheic keratosis, solar lentigines

and lichenoid keratosis. Dermatoscopic features and correlation to histology and clinical signs. Der- matol Clin 2001; 19(2):347–357

11. Zalaudek I, Ferrara G, Argenziano G. Clonal seborrheic keratosis: a dermoscopic pitfall. Arch Derma- tol 2004; 140:1169–1170

12. Hirata SH, Almeida FA, Tomimori-Yamashita J et al. “Globulelike” dermoscopic structures in seborrheic keratosis. Arch Dermatol 2004; 140:128–129 13. Argenziano G, Rossiello L, Scalvenzi M et al. Mela-

noma simulating seborrheic keratosis: a Dermos- copy pitfall. Arch Dermatol 2003; 139:389–391 14. Izikson L, Sober AJ, Mihm MC et al. Prevalence of

melanoma clinically resembling seborrheic keratosis. Arch Dermatol 2002; 138:1562–1566

15. Vun Y, De’ambrosis B, Spelman L, et al. Seborrheic keratosis and malignancy: collision tumour or malignant transformation? Australas J Dermatol 2006;

47(2):106–108

16. Lim C. Seborrheic keratosis with associated lesions:

a restrospective analysis of 85 lesions. Australas J Dermatol 2006; 47(2):109–113

17. Johr R, Saghari S, Nouri K. Eccrine porocarcinoma arising in seborrheic keratosis evaluated with dermoscopy and treated with Moh’s technique. Int J Dermatol 2003; 42:653–657

18. Mckee PH et al. (eds). Tumors of the surface epithelium. Pathology of the skin, 3rd edition with clinical correlations, 2005; Elsever Mosby, Amsterdam, pp 1158–1163

19. Morgan MB, Stevens GL, Switlyk S. Benign lichnoid keratosis. A clinical and pathologic reappraisal of 1040 cases. Am J Dermatopathol 2005; 27(5):387–

20. Higail IA, Crawford RI. Benign lichenoid keratosis 392 with histologic features of mycosis fungoides: clini- copathologic description of a clinically significant histologic pattern. J Cutan Pathol 2002; 29:291–294