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Home , Crust (dermatology), Granuloma, Seborrheic keratosis

Chapter V6 Seborrheic Including -like Keratosis V.6 Robert Johr

Contents V.6.2 Clinical Features

V.6.1 Definition ...... 313 “Warty” and “stuck-on” are adjectives used to V.6.2 Clinical Features ...... 313 describe these ubiquitous epidermal skin neo- V.6.3 Dermoscopic Criteria...... 315 plasms. Characterizations which are not always apparent clinically. V.6.4 Relevant Clinical Differential Most people develop at least one seborrheic Diagnosis...... 319 keratosis in their lifetime, usually forming V.6.5 Histopathology...... 322 de novo in adults and the elderly. They can also be found in the teens, twenties, and thirties. The V.6.6 Management...... 323 number varies from less than 20 in the average V.6.7 Lichen Planus-like Keratosis...... 323 person to hundreds of that slowly in- V.6.7.1 Definition ...... 323 crease in size and number with age. Usually de- V.6.7.2 Clinical Features ...... 323 veloping on any skin surface except the palms, V.6.7.3 Dermoscopy ...... 323 soles, mucous membranes, or sun-exposed ar- V.6.7.4 Relevant Clinical Differential eas (Fig. V.6.1) can be skin Diagnosis...... 325 colored, tan and various shades of brown, V.6.7.5 Histopathology...... 325 alarmingly black, or multicolored. They are V.6.7.6 Management ...... 326 well-circumscribed round-to-oval macules, , and nodules, most often plaques rang- References...... 327 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 characteris- V.6.1 Definition tics. Rough-surfaced lesions can be brittle and crumble into pieces when picked, leaving a raw Along with melanocytic nevi, seborrheic kera- red moist surface. In intertriginous areas espe- tosis is the most common benign cutaneous cially under the breasts, they can be moist, red, . The pathogenesis is unknown. There and without scales. Follicular plugs and tiny is a strikingly familiar predisposition probably white, yellow, or dark horn pearls can be seen with an autosomal–dominant inheritance pat- embedded in the surface. The correlation with tern. the dermoscopic criteria of comedo-like open- 314 R. Johr

ings and milia-like cysts aids in the clinical di- agnosis before dermoscopy is performed. Stuccokeratosis and dermatosis papulosa nigra are two very common variants of sebor- rheic 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 as- Fig. V.6.1. This is a typical older patient with multiple ymptomatic, yet they can become sore or pru- seborrheic keratoses that do not develop where there is ritic either spontaneously, or secondary to trau- no sun exposure. Seborrheic keratosis could be sun-in- ma from patient manipulation, articles of duced lesions

Fig. V.6.2. Typical scaly, crusty, and seborrheic keratosis that is easily diagnosed clinically V.6 Seborrheic Keratosis Chapter V.6 315

Fig. V.6.3. This irritated seborrheic keratosis lacks the clinical and dermoscopic criteria to make the diagnosis. Histopathological evaluation should be considered

clothing, or physical activity. can have metastatic disease; however, its recognition be mild, moderate, or severe with , ery- can facilitate the early diagnosis of occult ma- thema of the surrounding skin, thick scale, fri- lignancy. Often paralleling the course of the un- able crust formation, oozing, and bleeding. derlying malignancy, it can improve with suc- When severe, the typical clinical characteristics cessful surgery or chemotherapy, and it can are obliterated, and the inflamed seborrheic worsen if the malignancy returns. The sign of keratosis might be indistinguishable from a Leser–Trelat has also been associated with preg- pyogenic and, if dark, from nodular nancy, heart-transplant recipients, following (Fig. V.6.3). Another manifestation chemotherapy, in human immunodeficiency vi- of inflammation is the Meyerson phenomenon rus infection, and following erythrodermic pso- with a halo of eczematization surrounding the riasis or drug eruptions. If a clinician makes . Spontaneous regression is not a common this diagnosis, a comprehensive systemic work- occurrence. up is indicated [2–8]. The sudden development, inflammation, or regression of multiple seborrheic keratoses is a clinical scenario that can be a cutaneous mani- V.6.3 Dermoscopic Criteria festation of internal malignancy. It is called the sign of Leser–Trelat. If it is associated with other Most, but not all, seborrheic keratoses can be di- paraneoplastic skin findings, such as acanthosis agnosed clinically or with dermoscopy. A small nigricans, acquired icthyosis, or the develop- percentage require histopathology. Global pat- ment of lanugo hair, it is even more worrisome. terns and local criteria often require a differential The average age of onset is 61 years, and the diagnosis. The gold standard of histopathology most common malignancy is , might not be straightforward with collision le- especially of the stomach. Other malignancies sions when seborrheic keratosis is associated with associated with the sign of Leser–Trelat include different benign or malignant . Com- lymphoma, , Sezary syn- munication between the dermoscopist and der- drome, leukemia, and of the lung, breast, matopathologist is essential when there is asym- pancreas, and esophagus. Most patients already metrical presentation of dermoscopic criteria. 316 R. Johr

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

The original algorithm used to diagnose seb- asymmetry of color and structure, plus the mul- orrheic keratosis included two classic criteria: ticomponent global pattern with three or more milia-like cysts and comedo-like openings. Ad- distinct areas of dermoscopic criteria as seen in ditional criteria are now used to help make the . No single criterion by itself is diag- diagnosis [9, 10]. Sharp demarcation and abrupt nostic, and as many criteria as possible should V.6 cut-off of pigmentation and dermoscopic crite- be identified and evaluated before the dermo- ria are routinely seen. There can be significant scopic diagnosis is made. There are innumerable Seborrheic Keratosis Chapter V.6 317

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

combinations and appearances of what can be ance (Fig. V.6.6). Histopathologically, they rep- seen including black, various shades of brown, resent filled dilated follicular openings gray, red, white, blue, and yellow colors. in the , black-head like structures. Milia-like cysts (pseudocysts, pseudohorn They can be indistinguishable from the dots cysts, “stars in the sky”) are single or multiple and globules used to diagnose melanocytic le- variously sized and irregular distributed round sions (Fig. V.6.7). Clonal seborrheic keratosis white or yellowish structures that histopatho- lacking the stereotypical dermoscopic criteria logically represent intraepithelial horn cysts. can have small dark-brown or black globular- They can be opaque and dull or appear to light like structures similar to those seen in benign up like “stars in the sky” (Fig. V.6.4). Usually melanocytic lesions and melanoma, or larger small, they can be large and irregular in shape. ovoid nests that are often seen in basal cell car- It is most important to differentiate milia-like cinomas [11, 12]. Pressure and side-to-side cysts from the appendigeal openings of the movement with instrumentation will only pseudonetwork seen on the head and neck so change the shape of comedo-like openings. that lentigo maligna is not misdiagnosed as a Multiple comedo-like openings favor the diag- seborrheic keratosis (Fig. V.6.5). Even experi- nosis of seborrheic keratosis; however, they can enced dermoscopists cannot always make the also be seen in melanocytic nevi and occasion- distinction. Multiple or large milia-like cysts fa- ally in melanoma. A recent history of change vor the diagnosis of a seborrheic keratosis. might be the only reason to excise a lesion that When a few in number, they can also be seen in clinically looks like a seborrheic keratosis and benign melanocytic nevi and occasionally in has multiple comedo-like openings typically melanomas. seen in seborrheic keratosis but with subtle der- Comedo-like openings (pseudofollicular moscopic criteria that diagnoses a melanoma openings, follicular openings, irregular crypts, (melanoma incognito) [13]. keratin plugs) present as variously sized, Fissures and ridges (brain-like pattern) are a roundish, oval, or irregularly shaped sharply global pattern commonly found in seborrheic circumscribed single or multiple yellowish, keratosis. They are formed by dark-brown or brown, or black crater-like openings that can black linear and branching depressions creating have a targetoid or three-dimensional appear- a network or cerebriform pattern resembling 318 R. Johr

Fig. V.6.7. It is not possible to determine if this lesion has the dots and globules of a melanocytic lesion or the pig- mented comedo-like open- ings of a seborrheic keratosis. This seborrheic keratosis looks like a melanoma both clinically and dermoscopi- cally.

Fig. V.6.8. Fissures and ridges characterize this sebor- Fig. V.6.9. The novice dermoscopist might confuse this rheic keratosis with an almost unbelievable resemblance variation of the fissure and ridge pattern of a seborrheic to a sagittal section of the brain. It is truly cerebriform keratosis with the cobblestone pattern of a melanocytic . The clinical characteristics help in making the cor- rect diagnosis

the sulci and gyri of the brain, or one could Flat seborrheic keratosis can be diagnosed by imagine the peaks and valleys of a mountain observing a network-like pattern of thin brown range (Figs. V.6.7, V.6.8). Histopathologically, parallel lines reminiscent of fingerprints (Fig. they represent wedge-shaped invaginations of V.6.9). Fingerprinting is not uncommon and can the epidermis that are filled with keratin. The be found alone or in combination with other pat- novice dermoscopist might confuse the fissure terns. It should not be mistaken for the pigment and ridge pattern with a thickened pigment net- network of melanocytic lesions that form a hon- V.6 work or the cobblestone pattern of melanocytic eycomb-like network. Fingerprinting can also be nevi. found in solar lentigines (Fig. V.6.10). Seborrheic Keratosis Chapter V.6 319

Fig. V.6.10. Fingerprinting on the right and a variation Fig. V.6.11. This seborrheic keratosis demonstrates typi- of the fissure and ridge pattern on the left characterize cal hairpin-shaped blood vessels this seborrheic keratosis

Another network-like pattern with foci of difficult criterion to identify and least impor- thicker-branched and dark-brown or black-line tant in diagnosing seborrheic keratosis using segments often with an abrupt cut-off at the pe- dermoscopy. riphery can be seen. Histopathologically, it rep- resents melanin in or along the dermo-epidermal junction. At times, V.6.4 Relevant Clinical Differential the differentiation of all of these forms of net- Diagnosis work will not be possible. One must formulate a dermoscopic differential diagnosis and search In most cases the clinical diagnosis of sebor- for more criteria to make a diagnosis. rheic keratosis, stuccokeratosis, and dermatosis Hairpin-shaped fine telangiectatic blood ves- papulosa nigra poses no problems; however, sels are commonly seen in seborrheic keratosis clinically atypical lesions can be challenging. If (Fig. V.6.11). At times they can have a white halo in doubt, never hesitate to cut one out, because surrounding them, indicating the keratinizing melanomas are not uncommonly misdiagnosed nature of the tumor. They are also seen in mela- as seborrheic keratosis. Clinical and dermo- nocytic nevi, , basal cell car- scopic features of both can be found in a single cinomas, and when thick and irregular, in mela- lesion. nomas. The less pressure applied to the skin In a retrospective study of 9204 cases submit- with instrumentation, the easier it will be to see ted for histopathological examination with the these fine vessels. Skill and minimal pressure is clinical diagnosis of seborrheic keratosis, or a needed to capture good images of hairpin ves- differential diagnosis including seborrheic ker- sels with digital photography. atosis, a significant number of cases turned out Flat seborrheic keratosis can also have irreg- to be melanomas. Verrucous melanomas might ular borders with small or large concave inden- be especially difficult to differentiate clinically tations that have been compared to moth-eaten from seborrheic keratosis (Figs. V.6.12–V.6.14) garments. “Moth-eaten” borders are a widely [14]. accepted criterion that can also be seen in solar Clinically, they can also be confused with ac- lentigines. tinic keratosis, melanocytic nevi (Fig. V.6.15), Finally, if one looks carefully, the pigment on verruca vulgaris, condyloma acuminatum, solar the surface of the skin in flat seborrheic kerato- lentigines, in-situ and invasive squamous cell sis can appear to be like “jelly spread over the , acrochordon, eccrine poromas, and skin.” The jelly sign would be one of the most epidermal nevi. The patient’s personal and fam- 320 R. Johr

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 clini- copathological 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

ily history, plus the history of the lesion, should sign. If one observes a seborrheic keratosis-like be taken into consideration. For example, a seb- lesion in the genital area, most probably it is a orrheic keratosis-like lesion in a 7-year-old most condyloma acuminatum. probably is an epidermal nevus. Actinic kerato- Seborrheic keratosis is generally regarded as sis tend to be more erythematous with poorly a ; however, melanocytic, non- V.6 defined borders. Melanocytic nevi are soft, melanocytic, benign, and malignant patholo- compressible, non-scaly with a positive wobble gies have been associated with them (Fig. V.6.16). Seborrheic Keratosis Chapter V.6 321

Fig. V.6.14. Another general dermoscopy principle is Fig. V.6.16. A collision lesion consisting of a melano- to eliminate scale to get a better picture. After the scale cytic nevus and a seborrheic keratosis 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 diag- nosis includes a vs seborrheic keratosis. In this case it was a sebor- rheic keratosis.

The association might be by chance, or sebor- ma, melanocytic and dysplastic nevi, actinic ker- rheic keratosis could be a precursor lesion since atosis, actinic lentigo, and eccrine porocarcinoma it contains all of the cells found in the normal have been reported to be associated with sebor- skin. rheic keratosis. Some researchers believe that the Basal cell carcinoma, in-situ and invasive reticulated sub-type of seborrheic keratosis arises , keratoacanthomas, from solar lentigines. The frequency of these as- lentigo maligna, superficial spreading melano- sociations varies from study to study [15–17]. 322 R. Johr

Fig. V.6.17. On the left is a collision tumor consisting of noma with a seborrheic keratosis. Did the malignancies a basal cell carcinoma and a seborrheic keratosis. On the arise from the seborrheic keratosis, a benign proliferation right is another collision tumor, a squamous cell carci- of basaloid and squamous cells?

V.6.5 Histopathology illomatosis and a greatly thickened epidermis. The hyperkeratotic variant is the histological Seborrheic keratosis are true and reverse of the acanthotic type with prominent not a hyperplasia of the epidermis that have , and while the re- a variable proliferation of basaloid and squa- ticulated or adenoid type demonstrates delicate mous cells with pseudohorn cyst formation strands of branching from the epi- (Fig. V.6.17). Acanthotic, hyperkeratotic, reticu- . Intraepithelial nesting gives rise to the lated, irritated, and clonal are the most common Borst–Jadassohn appearance of the clonal sebor- histological subtypes, and many show a mixture rheic keratosis and intradermal or inverted pro- of patterns. There are varying amounts of hy- liferation characterizes the inverted follicular perkeratosis, acanthosis, papillomatosis, pig- keratosis. Stuccokeratosis has histopathological mentation, and inflammation. Cytological features of hyperkeratotic seborrheic keratosis, atypia and perivascular, diffuse, or lichenoid usually without pseudohorn cyst formation, chronic inflammatory infiltrates can be seen whereas dermatosis papulosa nigra has features with irritated lesions. The acanthotic subtype is of the acanthotic variant with pseudohorn cysts most common with little hyperkeratosis or pap- [18]. V.6 Seborrheic Keratosis Chapter V.6 323

V.6.6 Management dence, they are typically found on the upper trunk, distal upper extremities, and uncom- Seborrheic keratosis comes to clinical attention monly, on the head and neck. A small percent- for cosmetic reason if they become symptomatic age of people can have two or three of these le- or appear to break into pieces for no apparent sions. reason. They account for a large number of There is a correlation of the clinical appear- ­office visits and significant health care costs. ance with their chronicity and histopathologi- Seborrheic keratosis that have undergone cal findings. Acute, rapidly developing lichen recent change, are symptomatic, or look suspi- planus-like lesions of less than 3 months tend to cious clinically should be considered for der­ be erythematous or pinkish. Subacute lesions of moscopic and histopathological evaluation. Sig- 3 months to 1 year have a dusky-red or viola- nificant pathology, such as melanoma or basal ceous color, and if present for more than 1 year, cell carcinoma, could be surrounded by numer- they are regularly or irregularly pigmented with ous seborrheic keratosis, or individual sebor- shades of brown or gray. The diagnosis can be rheic keratosis could have malignant changes suspected even before dermoscopy is used by themselves. Careful physical examination is es- seeing a small lesion with a combination of sential. Complete excision, rather than a shave brown and gray colors. The surface can be scaly, or curettage, will be more helpful to the pathol- verrucous, or smooth and pearly. They range in ogist to evaluate for malignancy. size from a few millimeters to a centimeter or Treatment is most often for cosmetic reasons, more, and can be asymptomatic, slightly pru- so the least destructive method should be used. ritic, or have a mildly stinging sensation. Malig- Cryotherapy, with and without curettage, is the nant degeneration of lichen planus-like kerato- treatment of choice. Shave excision, electrodes- sis has never been reported. iccation, and CO2 laser vaporization are other methods of treatment that have increased risks of scarring. V.6.7.3 Dermoscopy Erythematous or pinkish lichen planus-like V.6.7 Lichen Planus-like Keratosis keratosis are featureless or feature poor with remnants of pigment network, subtle blotches V.6.7.1 Definition of brown color, plus dotted, irregular linear, and other-shaped telangiectatic blood vessels Lichen planus-like keratosis (synonyms: benign (Fig. V.6.18). They cannot be distinguished clin- lichenoid keratosis; solitary lichen planus; invo- ically or dermoscopically from melanocytic, luting lichenoid plaque) is a common benign non-melanocytic benign, malignant, or inflam- tumor of adulthood. matory lesions that have the same characteris- tics including amelanotic melanoma. With the pigmented variant, the dermoscop- V.6.7.2 Clinical Features ic picture depends on the age of the lesion. Early lesions can have the dermoscopic features of a The pathogenesis of lichen planus-like keratosis solar lentigo or flat seborrheic keratosis with is thought to be an immunologically mediated “moth-eaten” borders, fingerprinting, milia- regression of an existing lesion. This theory like cysts, comedo-like openings plus small foci does not account for the lesions that develop of melanophages. Also referred to as peppering de novo. Ninety percent of these lesions are soli- or granular dust, melanophages have a distinc- tary macules or papules, occasionally nodules tive dermoscopic appearance with fine irregular or plaques that develop between the third to dots that can be black, shades of brown, gray, seventh decade in Caucasians and which are oc- or blue. Typically they are smaller than the casionally seen in Hispanics, Asians, or Afri- dots and globules seen in melanocytic lesions can-Americans. With a 2:1 female to male inci- (Fig. V.6.19). 324 R. Johr

Fig. V.6.18. Pinkish macules and papules can be mela- nocytic, non-melanocytic, benign, malignant, or inflam- matory. This worrisome was discovered hidden on the chest of a very hairy patient. It is feature poor with dotted and linear ir- regular-shaped blood vessels. It turned out to be a lichen planus-like keratosis and not amelanotic melanoma

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

As time passes increasingly more melano- ential diagnosis could include regressive mela- phages are seen, and they might be the only noma. The clinical, dermoscopic, and histo- dermoscopic criteria found in older lesions pathological differentiation might not be (Fig. V.6.20). One can also see larger clumps of possible. Special staining, such as S-100 and a pigment plus foci of whitish color. In the later good clinicopathological correlation, is ad- V.6 stages of development, the dermoscopic differ- vised. Seborrheic Keratosis Chapter V.6 325

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 pic- ture. With experience one will not excise many lesions with this dermoscopic appearance

V.6.7.4 Relevant Clinical Differential be normal, acanthotic, or atrophic with hyper- Diagnosis keratosis, focal , and hypergranu- losis. Civatte colloid body formation represent- In most, but not all, cases the diagnosis of lichen ing necrotic keratinocytes is frequently found. planus-like keratosis is made after a . There are variable amounts of vacuolar degen- The clinical impression does not usually corre- eration of the basal cell layer plus a band-like late with the histopathology. Past experience lymphocytic infiltrate that can obscure the der- and a high index of suspicion are helpful. mo-epidermal junction. The differential diagnosis includes basal cell Melanin incontinence with melanophages, carcinoma, especially when the surface is dermal scarring, plus variable numbers of eo- smooth and pearly, in-situ and invasive squa- sinophils, plasma cells, , and neutro- mous cell carcinoma, actinic or seborrheic kera- phils can also be found. Features of solar lentigo tosis, pigmented , and solar or seborrheic keratosis are often seen at the pe- lentigines. Older pigmented variants, especially riphery of the lesion. if there is a history of change, should be differ- In a study of 1040 lichen planus-like kerato- entiated from banal and dyspastic nevi or mela- sis, five histopathological subtypes were identi- noma. An erythematous or pinkish macule or fied [19]: the classic and early interface types, papule cannot be differentiated clinically from plus bullous lesions with intra- and subepider- amelanotic banal and dyspastic nevi, amelanot- mal vesiculation. There was an atypical variant ic melanoma, and even solitary inflammatory with at least five atypical and an lesions such as or granuloma annu- absence of criteria to diagnose mycosis fun- lare. giodes. In another retrospective study, 15 cases of mycosis-fungoides-pattern, lichen planus- like keratoses were presented that had Pautrier V.6.7.5 Histopathology micro-, epidermotropism, and lym- phocytes with hyperconvoluted nuclei [20]. In general, lichen planus-like keratosis are char- Atrophic late lesions were the last subtype iden- acterized by epidermal and dermal changes that tified. reflect the age of the lesion. The epidermis can 326 R. Johr

The classic, atypical, and bullous patterns V.6.7.6 Management were associated with erythematous or pinkish lesions. Interface subtypes were erythematous In most cases lichen planus-like keratosis is to brown macules, whereas the late atrophic le- found by physicians that perform careful skin sions tended to be grayish, violaceous, or irreg- examinations. Baseline gross and digital der- ularly pigmented. moscopic images can be taken of minimally The histopathological differential diagnosis suspicious lesions to follow over time. Side-by- is extensive and includes other conditions with side comparisons of the baseline and follow-up a band-like infiltrate such as lichen planus, li- images can be checked for significant changes. chenoid erythematosus, and lichenoid When a more suspicious lesion is found, a com- drug reactions. Inflamed actinic and seborrheic plete excision, rather than an incisional biopsy, keratosis, porokeratosis, melanocytic lesions, is recommended. Since melanoma is in the dif- including melanoma, are also in the differential ferential diagnosis of pigmented and pinkish le- diagnosis. Melanomas simulating lichen pla- sions, the pathologist will need the entire speci- nus-like keratosis have increased numbers of men for a complete evaluation. Although the atypical melanocytes that can be partially ob- technique is controversial, skilled clinicians can scured by a dense lymphocytic infiltrate. Pa- accomplish this easily with a deep-shave exci- thologists considering the diagnosis of mycosis sion. fungoides should search for criteria that might Skin biopsies are not always needed, espe- indicate that the lesion is a lichen planus-like cially if the lesion is examined with dermoscopy keratosis. Clinicopathological correlation plus and no high-risk criteria are identified. Once dermoscopic examination will help the clini- the diagnosis is confirmed histopathologically, cian make the differentiation. 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.

V.6 Seborrheic Keratosis Chapter V.6 327

C Core Messages

■ Seborrheic keratosis are ubiquitous If the diagnosis is made, a comprehen- benign epidermal neoplasms that, in sive systemic work-up is indicated. most but not all cases, can be diag- ■ Treatment is most often for cosmetic nosed clinically and with dermoscopy; reasons and the least destructive and some will need a histopathological scarring method should be used. diagnosis. ■ Lichen planus-like keratosis are usually ■ It is important to be aware of the diagnosed histopathologically. Exci- clinical differential diagnosis of sional, rather than incisional, tech- atypical lesions. niques are recommended. ■ Melanomas can be misdiagnosed as ■ The more skilled clinician can make seborrheic keratosis, especially the the diagnosis by putting the clinical verrucous variant. Any lesion that and dermoscopic findings together, looks suspicious clinically or with thus avoiding surgery. dermoscopy to be symptomatic or ■ There is an extensive clinical and changing should be considered for histopathological differential diagnosis histopathological evaluation. which includes melanoma, non- ■ Seborrheic keratoses can be associated melanoma , and mycosis with melanocytic, non-melanocytic fungoides. A good clinicopathological benign, or malignant pathology. correlation is essential. ■ Cutaneous malignancies can be ■ Solitary erythematous or pinkish surrounded and camouflaged by macules and papules could be melano- multiple seborrheic keratoses, or an cytic, non-melanocytic, benign, individual seborrheic keratosis could malignant, or inflammatory. Dermos- undergo malignant change. Careful copy is usually not helpful with these physical examination is essential. lesions. ■ The sudden appearance, irritation of ■ Once the diagnosis of a lichen planus- pre-existing lesions, or regression of like lesion is made, aggressive therapy seborrheic keratosis is called the sign of is not indicated. Reassurance to the Leser–Trelat and can be a cutaneous patient of the benign nature of this manifestation of an internal malignancy pathology will be appreciated.

References 5. Inamadar AC, Palit A. Eruptive seborrheic kerato- sis in human immunodeficiency virus infection: a 1. Hefferman MP, Khavari PA. Raindrop seborrheic coincidence or “the sign of Leser–Trelat?” Br J Der- keratosis: a distinctive pattern on the backs of el- matol 2003; 149(2):435–436 derly patients. Arch Dermatol 1998; 134:382–383 6. Flugman SL, McClain SA, Clark RA. Transient 2. Hsu C, Abraham S. Campanelli A et al. Sign of Les- eruptive seborrheic keratosis associated with eryth- er–Trelat in a heart transplant recipient. Br J Der- rodermic psoriasis and erythrodermic drug erup- matol 2005; 153(4):861–862 tion: report of two cases. J Am Acad Dermatol 3. Patton T, Zirwas M, Nieland-Fisher N, Jukie D. 2001;45(6 Suppl):S212–S214 Inflammation of seborrheic keratoses caused by 7. Vielhauer V, Herzinger T, Korting HC. The sign of cytarabine: a pseudo sign of Leser–Trelat. J Drugs Leser–Trelat: a paraneoplastic cutaneous syndrome Dermatol 2004; 3(5):565–566 that facilitates early diagnosis of occult cancer. Eur 4. Pentenero M, Carrozzo M, Pagano M, Gandolfo S. J Med Res 2000; 5(12):512–516 Oral , tripe palms and sign of 8. McCrary ML, Davis LS. Sign of Leser–Trelat and Leser–Trelat in a patient with gastric adenocarci- mycosis fungoides. J Am Acad Dermatol 1998; noma. Int J Dermatol 2004; 43(7):530–532 38(4):644 328 R. Johr

9. Braun RP, Rabinovitz HS, Krischer J et al. Dermos- 16. Lim C. Seborrheic keratosis with associated lesions: copy of pigmented seborrheic keratosis: a morpho- a restrospective analysis of 85 lesions. Australas J logical study. Arch Dermatol 2002; 138:1556–1560 Dermatol 2006; 47(2):109–113 10. Elgart GW. Seborrheic keratosis, solar lentigines 17. Johr R, Saghari S, Nouri K. Eccrine porocarcinoma and lichenoid keratosis. Dermatoscopic features arising in seborrheic keratosis evaluated with der- and correlation to and clinical signs. Der- moscopy and treated with Moh’s technique. Int J matol Clin 2001; 19(2):347–357 Dermatol 2003; 42:653–657 11. Zalaudek I, Ferrara G, Argenziano G. Clonal sebor- 18. Mckee PH et al. (eds). Tumors of the surface epithe- rheic keratosis: a dermoscopic pitfall. Arch Derma- lium. Pathology of the skin, 3rd edition with clini- tol 2004; 140:1169–1170 cal correlations, 2005; Elsever Mosby, Amsterdam, 12. Hirata SH, Almeida FA, Tomimori-Yamashita J et pp 1158–1163 al. “Globulelike” dermoscopic structures in sebor- 19. Morgan MB, Stevens GL, Switlyk S. Benign lichnoid rheic keratosis. Arch Dermatol 2004; 140:128–129 keratosis. A clinical and pathologic reappraisal of 13. Argenziano G, Rossiello L, Scalvenzi M et al. Mela- 1040 cases. Am J Dermatopathol 2005; 27(5):387– noma simulating seborrheic keratosis: a Dermos- 392 copy pitfall. Arch Dermatol 2003; 139:389–391 20. Higail IA, Crawford RI. Benign lichenoid keratosis 14. Izikson L, Sober AJ, Mihm MC et al. Prevalence of with histologic features of mycosis fungoides: clini- melanoma clinically resembling seborrheic kerato- copathologic description of a clinically significant sis. Arch Dermatol 2002; 138:1562–1566 histologic pattern. J Cutan Pathol 2002; 29:291–294 15. Vun Y, De’ambrosis B, Spelman L, et al. Seborrheic keratosis and malignancy: collision tumour or ma- lignant transformation? Australas J Dermatol 2006; 47(2):106–108

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