Keratosis Pilaris Food List
INTRODUCTION Inverted follicular keratosis is a benign skin lesion that is common on the face and less frequently on the eyelids. It occurs in older individuals from the fifth decade on, and is considerably more common in males. It is frequently mistaken for a malignant tumor. These lesions arise from the infundibular epithelium of the hair follicle and therefore are related to epidermoid cysts. Inverted follicular keratosis may be an irritated form of seborrheic keratosis or verruca vulgaris. CLINICAL PRESENTATION Inverted follicular keratosis presents as a small, solitary, well-demarcated, hyper-keratotic or wart-like keratotic mass most commonly on the upper eyelid and cheek, Rarely, it may be pigmented simulating a melanocytic tumor. This lesion may show scaling and exophytic projections presenting as a cutaneous horn. The lesion typically appears weeks to months before presentation, but sometimes may be present for many decades. Inverted follicular keratosis shows a growth...
INTRODUCTION Also known as solar or senile keratoses, these neoplasms are a common form of premalignant skin lesion seen on the face. Actinic keratoses are related to ultraviolet radiation damage of epidermal cells on sun-exposed areas of the face, hands, scalp, and eyelids. They occur more commonly in fair-skinned middle-aged or older individuals. The risk of malignant transformation is low, about 0.25 per year, but the ultimate development of squamous cell carcinoma in untreated lesions is as high as 20 . Up to 60 of squamous cell carcinomas are said to begin as actinic keratosis. Although some individual actinic keratoses will spontaneously resolve when sun-exposure is reduced, new lesions tend to develop. Squamous cell carcinomas arising from actinic keratoses are believed to be less aggressive than those developing de novo. Actinic keratosis may lie on a continuum toward squamous carcinoma, and recent chromosome aberration and gene mutation studies indicate an association between...
INTRODUCTION Seborrheic keratosis is the most common eyelid tumor and the incidence increases with age. CLINICAL PRESENTATION Seborrheic keratoses initially present as painless, movable, sharply defined slightly elevated macules with a variable degree of pigmentation that varies from tan to brown. They sometimes appear in large numbers. As they grow they typically develop a greasy papil-lomatous or verrucous, stuck-on appearance. They are usually sessile, but can sometimes be pedunculated. Older lesions tend to be more verrucous and folded, with multiple keratin plugs creating a pitted surface. Irritation can cause inflammation, swelling, and sometimes bleeding, and crusting. In the variant called dermatosis papulosa nigra a large number of darkly pigmented lesions occurs on the cheeks of black patients. A rapid increase in size and number may represent the sign of Leser-Trelat (multiple eruptive seborrheic keratosis), which may occur in patients with an occult malignancy. squamoid...
From several recent large series looking at the frequency of eyelid lesions benign processes account for approximately 70 to 75 of all lesions, and malignant neoplasms for 25 to 30 (1-5). Among the benign lesions the most frequent diagnoses are squamous papilloma (26 ), nevus (22 ), cysts (20 ), seborrheic keratosis (13 ), vascular lesions (9 ), and neural lesions ( 1 ). The most common malignant tumor on the eyelid is the basal cell carcinoma followed in rapidly descending order by squamous cell carcinoma, sebaceous cell carcinoma, and malignant melanoma. Other rare tumors such as Kaposi's sarcoma, adnexal carcinomas, and Merkel cell tumor are occasionally seen, as are metastatic cancers. One large series of nearly 1100 malignant eyelid tumors from China showed the frequencies of basal cell and sebaceous cell carcinomas to be nearly equal at 38 and 32 , respectively, quite different from the usually quoted values from the Western literature. However, most other studies give the...
Of the benign lesions derived from the epidermis many can look rather similar clinically. Some may remain epidermal in location, but many extend into the underlying dermis. Epidermal lesions include the papilloma, actinic keratosis, seborrheic keratosis, inverted follicular keratosis, ichthyosis, keratoacanthoma, lentigo, milia, molluscum contagiosum, and acquired melanosis. When epidermal cells become buried beneath the surface, keratin can accumulate to form an epidermoid cyst.
A macrophage containing phagocytized melanin is referred to as a melanophage. Melanin granules are dark brown and non-refractile in sections stained with hematoxylin and eosin. Melanophages are seen in the dermis in inflammatory conditions affecting the epidermis, as well as in neoplasms such as seborrheic keratosis, blue nevus, and melanomas. Papillomatosis is characterized histologically by abnormally elongated epidermis and papillary dermis resulting in irregular undulation of the epidermal surface. Papillomatosis is seen most commonly in seborrheic keratosis and verruca vulgaris (shown). Parakeratosis is an increased thickness of the horny layer (stratum corneum) by nucleated cells. Parakeratosis represents a defect in cellular differentiation and is usually associated with a thinned or absent granular layer. An example of parakeratosis in a specimen with actinic keratosis is shown here.
Figure 10 Lichen planus-like keratosis. The histologic presentation can be identical to lichen planus (A). Differentiating features may include focal parakeratosis (B), and residual solar lentigo at the edge of the lesion (C). Figure 10 Lichen planus-like keratosis. The histologic presentation can be identical to lichen planus (A). Differentiating features may include focal parakeratosis (B), and residual solar lentigo at the edge of the lesion (C).
Depression heat, humidity, stress, sunlight, and UVB rays exacerbate the condition lesions on palms, including punctate keratosis, palmar pits, and hemorrhagic macules verrucous papules present on the backs of the hands nail changes, including white and red longitudinal bands, longitudinal nail ridges, and splits
Elastosis perforans serpiginosum elastosis intrapapillare elastoma intrapapillare perforans elastoma intrapapillare perforans verruciformis elastosis perforans elastoma verruciform perforans keratosis follicu-laris et parafollicularis serpiginosa keratosis follicularis serpiginosa reactive perforating elastosis
A 44-year-old man requests evaluation of an irritated brown lesion on his left shoulder. Evaluation reveals a typical 5-mm stuck on seborrheic keratosis. He also has multiple lentigines of various sizes in a solar distribution over his upper back, shoulders, and upper chest. An asymmetric multicolored 4 x 8 mm lesion is present on his left anterior shoulder. It has a notched margin and stands out from the other lesions.
Squamous cell carcinoma in situ (SCCIS) is a histologic term with many diverse clinical presentations. The biologic importance is also variable from a benign course in bowe-noid papulosis to possible invasive growth potential in Bowen's disease. It is extremely important to make a clinico-pathologic correlation (CPC) when a histologic diagnosis of SCCIS is made. For example, bowenoid papulosis has the histologic features of SCCIS, which is considered to be a benign, virally induced condition. Lack of CPC can lead to unnecessary surgery. Similarly, SCCIS seen in the context of actinic keratosis should be managed as actinic keratosis and a wide excision is unnecessary just because it shows areas of SCCIS. The clinical and pathologic features of several variants of SCCIS are listed in Table 1.
Actinic keratosis Basal cell carcinoma Contact dermatitis Dermatomyositis Herpes simplex Impetigo Perioral dermatitis Rosacea Sarcoidosis Sebaceous hyperplasia Seborrheic dermatitis Seborrheic keratosis Squamous cell carcinoma Varicella-zoster infection Vitiligo Keratosis pilaris Pyoderma gangrenosum Seborrheic keratosis Stasis dermatitis Ulcer Vasculitis Seborrheic dermatitis Seborrheic keratosis Skin tag Tinea cruris
Figure 17 Inverted follicular keratosis. Downward growing lobule with more squamous eddies and less of a clear cell appearance than trichilemmoma. Figure 17 Inverted follicular keratosis. Downward growing lobule with more squamous eddies and less of a clear cell appearance than trichilemmoma.
When intra-epidermal or juxtaepidermal, poroma may closely simulate the configuration of a seborrheic keratosis. Recognizing areas of ductular differentiation and associated highly vascularized stroma are helpful in making the distinction. Hidradenoma is always in the differential diagnosis of poroma and differs in that the epithelial cells that comprise
Terminology Oral white plaques share many histological features, and idiopathic forms are often not distinguishable histologically from those with defined causes such as frictional keratosis, but may show dysplasia microscopically. Features of oral white lesions include the following in varying combinations Microscopy Hyper(ortho)keratosis a superficial eosinophilic layer Dysplasia (sec pp. 93-94) may be associated with keratosis but there is no consistent relationship. Frictional keratosis This shows non-spccific keratosis microscopically (Fig. 162) and is distinguishable only by clinical evidence of mechanical trauma and resolution with removal of the irritant. Smoker's keratosis Pathology The keratosis is non-specific but there is Microscopy Features of epithelial keratosis arc not specific but Rg. 162 Frictional keratosis. Rg. 162 Frictional keratosis. Rg. 163 Smoker's keratosis swollen palatal salivary tissue.
Side Effects GI N&V, diarrhea, peptic ulcer activation, abdominal pain. Dermatologic Flushing, warm feeling, skin rash, pruritus, dry skin, itching and tingling feeling, keratosis nigricans. Other Hypotension, headache, macular cystoid edema, amblyopia. NOTE Megadoses are accompanied by serious toxicity including the symptoms listed in the preceding as well as liver damage, hyperglycemia, hyperuricemia, arrhythmias, tachycardia, and dermatoses.
Actinic keratosis (erythematous) Part V Atypical nevi Part V Common benign nevi (pigmented) Part V Ephelides Part V Erysipelas (erythematous) Part III Erythema multiforme (erythematous) Part III Erythrasma Part III Fixed drug eruption Part III Halo nevi Part V Impetigo (deep red) Part VI Lentigines Part V Malignant melanoma Part V Nodules Scabies (papulovesicle at end of burrow) Part II Seborrheic dermatitis (red-brown, follicular) Part II Seborrheic keratosis Part V SLE (sharply defined, may coalesce) Part IV Squamous cell carcinoma (indurated) Part V Striae distensae (yellow papules as secondary lesions) Part IV Tinea (follicular) Part III Verruca vulgaris Part II Patches Actinic keratosis (erythematous) Part V Asteatosis Part IV Atopic dermatitis Part IV Erythrasma Part III Malignant melanoma Part V Rosacea (erythematous) Part VI Seborrheic keratosis Part V Senile purpura (purple) Part IV Striae distensae (linear) Part IV Tinea Part III Actinic keratosis (thin) Part V Malignant...
CLINICAL PRESENTATION The most common site of eyelid involvement is the lower lid. Initial changes can look like a chronic eczema-like lesion. The tumor often originates in an actinic keratosis, but tends to be thicker, larger and have a more heaped-up keratinization. These lesions have a DIFFERENTIAL DIAGNOSIS The differential diagnosis includes basal cell carcinoma, sebaceous cell carcinoma, Bowen's disease, actinic keratosis, keratoacanthoma, inverted follicular keratosis, papilloma, pseudoepitheliomatous hyperplasia, seborrheic keratosis, trichilemomma, fungal infection, and verruca vulgaris.
Benign tumors Cherry angiomas, chondrodermatitis nodularis helicis, seborrheic keratosis, skin tags Eczemas Asteatotic dry skin, contact, seborrheic Infections Candidiasis, herpes zoster, onychomycosis, scabies Photodamage Actinic elastosis, colloid milium, Favre-Racouchot syndrome, freckling, photoaging (wrinkling, solar lentigo), poikiloderma of Civatte Premalignant Actinic keratosis, Bowen disease Malignancies BCC, lentigo maligna melanoma, MF, SCC Ulcerations leg, pressure decubitus Other Cutaneous horn, pruritus
Carcinoma, and actinic keratosis has been observed (13). Atypical manifestations of cutaneous B-CLL have included chronic paronychia (14), subungual erythematous nodules involving several fingers (15), dystrophy of toenails resembling onychomycosis (16), finger clubbing with periosteal bone destruction of the distal digits (17), and papulovesicular eruption of the face (18). The prognosis varies, depending upon clinical stage the presence of specific skin lesions in patients with B-CLL does not seem to be an independent poor prognostic sign (8).
Nakamura H, Hirota S, Adachi S, et al. Clonal nature of seborrheic keratosis demonstrated by using the polymorphism of the human androgen receptor locus as a marker. J Invest Dermatol 2001 116 506. 2. Kossard S, Berman A, Winkelmann R. Seborrheic keratosis and trichostasis spinosa. J Cutan Pathol 1979 6 492. SEBORRHEIC KERATOSIS, COMMON HISTOLOGIC VARIANTS
INTRODUCTION The term cutaneous horn, also known as cornu cutaneum, is a descriptive designation for a protuberant projection of packed keratin that resembles an animal horn. It is more common in elderly individuals, but can be seen in young adults as well. It is associated with a large variety of benign, premalignant, and malignant lesions at the base, thus masking the true diagnosis. About 60 to 75 of such inciting lesions are benign and 8 to 10 malignant. Malignant diagnoses tend to occur more commonly in males and in patients 8 to 10 years older than those with benign diagnoses. The most common inciting diagnoses are seborrheic keratosis, actinic kerato-sis, and squamous cell carcinoma. HISTOPATHOLOGY Cutaneous horn is a clinical diagnosis that corresponds histologically to a protuberant mass of keratin. To be designated a horn , the height should exceed at least one-half of the greatest diameter of the lesion from which it arises. Cutaneous horns are most commonly associated with...
The histopathology of actinic keratosis is epidermal dysplasia with alterations in cell polarity and mild nuclear atypia. Alternating hyperkeratosis and parakeratosis, irregular acantho-sis and thinning of the granular layer are commonly seen, with buds of atypical keratinocytes extending downward into the papillary dermis. Epithelium of the hair follicles is shielded from actinic damage and maintains normal structure, reaching the epidermis and extending over adjacent atypical cells to produce the characteristic umbrella sign. The dermis reveals solar elastosis and there is often a mild chronic inflammatory infiltrate.
HISTOPATHOLOGY Melanocytic nevi are composed of nevus cells, which are melanocytes that have lost their long dendritic processes. Nevus cells are oval to cuboidal, have clear to pale eosinophilic cytoplasm, and contain a variable amount of melanin. The nevus cells form nests, which often coalesce when they are in the dermis. Melanocytic nevi may have discrete nests of nevus cells at the dermoepidermal junction ( junctional melanocytic nevus ), both at the dermoepidermal junction and within the dermis ( compound melanocytic nevus ), or confined within the dermis ( intradermal melanocytic nevus, shown below). On the eyelid, compound nevi may be papillomatous with a seborrheic keratosis-like appearance to their epidermis. DIFFERENTIAL DIAGNOSIS The differential diagnosis includes lentigo maligna, malignant melanoma, neurofibroma, balloon cell nevus, papilloma, seborrheic keratosis, inverted follicular keratosis, oculodermal melanocytosis, dermatofibroma, pigmented basal cell carcinoma,...
DIFFERENTIAL DIAGNOSIS The differential diagnosis includes malignant melanoma, sebaceous cell carcinoma, squamous cell carcinoma, actinic keratosis, radiation dermatitis, keratoacanthoma, cutaneous horns, dermoid and sebaceous cysts, eccrine and apocrine cysts, papillomatous lesions, seborrheic kertosis, blepharitis, chalazion, eczema, psoriasis, and seborrheic dermatitis.
Epidermal growths such as actinic keratosis, lentigines or thin seborrheic keratoses can all be treated effectively with 25-35 TCA peels. Thicker epidermal growths or growths involving the dermis will be more resistant to treatment such as hypertrophic actinic keratoses and thicker seborrheic keratoses and may even be resistant to a medium-depth peel. Resistant lesions many times are best treated with a combination of a medium-depth chemical peel and other modalities such as manual dermasanding or CO, laser.
This type of keratosis is seen with increased incidence in patients from the fifth decade of life onward. The individual lesions begin insidiously as erythematous patches of vasodilation that are often more apparent after solar exposure. Early lesions are usually otherwise asymptomatic.
DIFFERENTIAL DIAGNOSIS The differential diagnosis includes benign lesions such as seborrheic keratosis, apocrine hidradenoma, nevus sebaceous, sebaceous hyperplasia, and dermoid cyst, as well as malignant tumors such as sebaceous cell carcinoma, and basal cell carcinoma.
HISTOPATHOLOGY Papillomas (acrochordons skin tags) are highly variable histologically. Furrowed papules are most common on the eyelids and are characterized histologically by epidermal hyperplasia with a seborrheic keratosis-like appearance, as illustrated here. The hyperplastic epidermis forms interdigitating cords. Horn cysts may be present, though they are not common. DIFFERENTIAL DIAGNOSIS The differential diagnosis includes seborrheic keratosis, actinic keratosis, verruca vulgaris, intradermal nevus, keratoacanthoma, and sebaceous carcinoma. Occasionally malignant lesions can look like a papilloma, but these more often have telangiectatic vessels or are associated with lash loss or ulceration.
Some poisonings are not accomplished with one large dose, but with multiple smaller doses. Here, the action of the arsenic on the skin causes an initial erythematous flush with subsequent development of melanosis, hyper-keratosis, and desquamation. Months after an acute ingestion of arsenic, transverse white bands (Mees's lines) can be seen on the nails. Arsenic can also cause anemia, leukopenia, thrombocytopenia, and basophilic stippling.
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