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B. Disorders of sebaceous glands

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It most frequently occurs on the face of adolescent men and women. Comedones, folliculitis, papules and pus-tules are produced.

Agents and factors such as Propionibacterium acnes, the Demodex folliculorum mite, endocrine secretion and stress are associated with the occurrence.

Lifestyle guidance and administration of sulfa drugs and antibiotics are effective.

Multiple follicular inflammatory papules occur, most com-monly on the seborrheic areas of the face, precordial region, and back of men and women from the ages of about 10 to 40 (Fig.

19.5). The papules worsen at puberty. The initial eruption, called a comedo, is classified as an open comedo (the follicles are open, also called “blackheads”) or a closed comedo (small yellowish-white nodules in the skin: “yellowish-white heads”). Closed comedos often progress to erythematous papules or pustules. Subjective symp-toms such as itching are not usually present; however, the come-dos become painful as they develop further. Acne vulgaris is characterized by intermingled eruptions of different stages.

The main pathogenesis involves hormonal imbalance, abnor-mal keratinization and bacterial infection (Fig. 19.6). Along with

Pathogenesis Clinical features ● ● ● Outline

1. Acne vulgaris

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DHT receptors inflammation comedo dirt keratinization increase of free fat mechanical stimuli P. acnes increase of sebum

androgen increase, especially in adolescents endogenous factors

Fig. 19.6 Mechanism of acne vulgaris.

B. Disorders of sebaceous glands

Clinical images are available in hardcopy only. Clinical images are available in hardcopy only.

Clinical images are available in hardcopy only.

Fig. 19.5 Acne vulgaris.

Multiple, follicular, inflammatory papules occur on oily areas of the face, such as the cheeks and forehead. The hair follicles are obstructed and appear as yellowish-white nodules (closed come-dos).

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these main factors, hereditary factors, the patient’s age, diet, stress and extrinsic factors such as cosmetics are complicatedly associated with the onset. Acne caused by Demodex folliculorum is called acne demodecica, and it occurs most frequently in women after puberty.

Hormonal imbalance: Androgen in the blood increases

accord-ing to pubertal endocrine changes, and the function of the seba-ceous glands is enhanced by adrenogenic dihydrotestosterone (DHT). Accordingly, sebum retention and bacterial proliferation readily occur.

Follicular hyperkeratinization: The infundibulum is obstructed

by keratin as a result of poor hygiene or hereditary factors. When sebum components are decomposed by bacteria, free fatty acid is produced; stimulated by this phenomenon, the infundibulum induces keratinization. Sebum retention is accelerated by these causative factors to produce an initial comedo.

Bacterial infection: Propionibacterium acnes resident in the

infundibulum break down triglycerides in the sebum, producing free fatty acids that destroy the hair follicles and lead to inflam-mation. The bacteria themselves also cause destruction of folli-cles and inflammation, especially when there is infestation by the Demodex folliculorum mite.

Acne vulgaris is characterized by enlargement of the seba-ceous glands and follicular keratinization. Cystic dilation occurs in follicles, and destruction of the follicular walls causes inflam-matory reaction.

Acne vulgaris must be differentiated from steroid acne, a side effect of oral or topical steroid use, and from lupus miliaris dis-seminatus faciei, and verruca plana. Acne-like eruptions are caused by immunosuppressants in the same mechanism as that in steroid acne; these eruptions must also be differentiated from acne vulgaris. Thorough history-taking is important.

Lifestyle guidance is primary. Observance of a regular sched-ule of sleeping and eating, and avoidance of cosmetics (oily creams and foundation, in particular) are helpful. Washing the face and maintaining regular bowel movements are important. Topical application of retinoids (tretinoin or adapalene cream), sulfa drugs, and antibiotic ointments and oral antibiotics such as tetracyclines and roxithromycin are effective. Chemical peeling or extraction of comedos may be useful in some cases. Unless treated appropriately, acne vulgaris heals with scarring, leaving a cosmetic problem.

Treatment

Differential diagnosis Pathology

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Clinical images are available in hardcopy only.

Clinical images are available in hardcopy only.

Clinical images are available in hardcopy only.

Fig. 19.7 Rosacea erythematosa on the tip of the nose.

a: A male patient in his 20’s. b: A female patient in her 30s. c. A male patient in his 30s. Telang-iectasia is remarkable. a a b c d e f h a g i j k l m n o p q r a bbb c d e f g h i j k l m n o p q r a b ccc d e f g h i j k l m n o p q r

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Rosacea is a chronic inflammatory disease that causes diffuse reddening and vascular dilation on the face of middle-aged and older men and women. Acne-like papules and pustules may be produced.

Rosacea is classified by severity into three stages. The first stage (rosacea erythematosa) and second stage (acne rosacea) occur frequently in middle-aged and older women. Progression to the third stage (rhinophyma) is more common in men. In addition to the cutaneous symptoms listed below, eye symptoms (e.g., ketatitis and conjunctivitis) may occur.

① First stage (rosacea erythematosa): Transient reddening appears on the tip of the nose and on the cheeks, glabella and chin. It progresses gradually to become persistent and accompanied by telangiectasia and seborrhea (Fig. 19.7). Cold and warm weather, sunlight and alcohol consumption aggravate it. Subjective symp-toms such as itching, hot flashes and irritability are present. ② Second stage (acne rosacea): In addition to the symptoms of the first stage, follicular papules and pustules occur. Seborrhea is intense (Fig. 19.8). The lesions spread to cover the face.

③ Third stage (rhinophyma): The papules aggregate and coa-lesce to become tumorous. The surface of the nose becomes rough and reddish purple. The skin appears orange-peel-like with open follicles (Fig. 19.9). Rosacea keratitis, conjunctivitis, and blepharitis occur as complications.

Involvement of sunlight, mental stress, intake of alcohol or spicy food, liver dysfunction, and infection by Demodex follicu-lorum is suspected; however, the pathogenesis is unknown.

Rosacea progresses gradually and tends to be intractable. Spicy foods, excessive sun exposure, and stress should be avoid-ed. Laser irradiation is performed on the telangiectasia. The treat-ments for acne rosacea are the same as those for acne vulgaris. Topical metrohidazole, imidazoles and tretinoin may bring improvement. Steroid should never be used. Laser therapy, cryother-apy and surgical treatment are conducted for rhinophyma.

Synonym: Steroid-induced dermatitis

Prolonged application of steroids to the faces induces ● Outline

3. Rosacea-like dermatitis

Treatment, Prognosis Pathogenesis Clinical features Definition, Pathogenesis

2. Rosacea

19

Clinical images are available in hardcopy only.

Fig. 19.8 Acne rosacea in a male patient in his 50s.

A red skin lesion is present on the nose and cheeks.

Clinical images are available in hardcopy only.

Fig. 19.9 Rhinophyma in a male patient in his 60s.

The skin lesion becomes tumor-like and the hair follicles dilate. The skin takes on the appearance of orange peel.

Clinical images are available in hardcopy only.

Fig. 19.10-1 Rosacea-like dermatitis. Eruptions occurred after continuous application of topical steroid for 1 month. Diffuse flushing, exfoliation, itching and burning sensation occurred.

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rosacea-like erythematous papules, diffuse flushing, and acne.

Perioral dermatitis is also known to be caused by topical steroid therapy.

After discontinuation of steroids, the treatments for acne vulgaris are given.

Erythema, telangiectasia, papules, pustules, diffuse flushing, and scaling occur on sites where steroids have been applied. These symptoms are accompanied by itching and burning sensa-tion (Figs. 19.10-1 and 19.10-2). Localized rosacea-like dermati-tis around the mouth is called perioral dermatidermati-tis.

Rosacea-like dermatitis most commonly occurs in middle-aged women. Rosacea-like dermatitis is a typical side effect of topical steroids.

Steroids are immediately discontinued. After that discontinua-tion, rebound phenomenon occurs. Reddening and swelling aggravate, and erosion may persist for several weeks to several months. The same treatments as for acne vulgaris are performed. Topical steroids are tapered off only when rebound is severe.

Synonym: Acne agminata

Multiple small papules of 2 mm to 5 mm in diameter the color of normal skin or redder occur on the face, particu-larly the lower eyelids. They are asymptomatic.

The histology is epithelioid cell granuloma with central necrosis.

Tetracyclines are administrated in small doses.

Lupus miliaris disseminatus faciei (LMDF) occurs in both sexes equally, most patients being in their 20s and 30s. Multiple small papules with central necrosis of 2 mm to 5 mm in diameter the color of normal skin or redder occur symmetrically on the face, especially on the lower eyelids, cheeks and sides of the nose, accompanied by pustules (Figs. 19.11-1 and 19.11-2). The disorder is asymptomatic. Small yellowish-white nodules are observed by diascopy. These heal with concave scarring one to several years after onset. The scars become indistinct in about 1 year.

LMDF is first thought to be a form of tuberculid, but an

Pathogenesis Clinical features ● ● ● Outline

4. Lupus miliaris disseminatus faciei (LMDF)

Treatment Pathogenesis Clinical features ● ●

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Clinical images are available in hardcopy only.

Fig. 19.11-1 Lupus miliaris disseminatus faciei (LMDF).

Small multiple papules of normal skin color or red and 2 mm to 5 mm in diameter occur sym-metrically on the face. Some heal with scarring.

Clinical images are available in hardcopy only. Clinical images are available in hardcopy only.

Fig. 19.10-2 Rosacea-like dermatitis as a side effect of topical steroids.

a: Eruption at the early stage. b: Eruption that has progressed.

a

a b c d e f h

a g i j k l m n o p q r

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association with tuberculosis has been excluded. Tuberculin reac-tion test is negative in most cases. The mechanism is predomi-nantly thought to be reaction against the hair follicle tissues or their contents.

A biopsy from a well established lision shows that epithelioid granuloma with central necrosis is present.

Syringoma, milium, rosacea and acne vulgaris should be dif-ferentiated from LMDF.

Tetracyclines are administered in small doses. Topical steroids may be the inductive factor in some cases. After a period of months or up to 2 years, the condition resolves spontaneously.

Dehydration of the horny cell layer and decrease of sebum cutaneum lead to dryness and coarseness of skin, resulting in pityroid scaling. These symptoms tend to aggravate during the winter. Xerosis is often caused by excessive washing and rubbing during bathing. It may be observed as a change in the aging process. It may also be caused by specific climates and environ-ments. It appears as a symptom of nutritional deficiency or atopic dermatitis in some cases. It may progress to pruritus, nummular eczema or asteatotic eczema (Chapter 7).

Round, sharply margined hair loss suddenly occurs. Hair regrows spontaneously in several months in most cases. Cases with multiple alopecia areata may progress to alopecia totalis or alopecia universalis.

Topical steroids and PUVA are applied.

Alopecia areata is quite common, affecting up to 1% of the population. Sharply margined hair loss occurs suddenly without prodromes or subjective symptoms (Figs. 19.12-1 and 19.12-2). Alopecia areata is usually a round or oval, single but sometimes multiple, alopecia of 2 cm to 3 cm in diameter. The alopecia patches may coalesce, progressing to complete scalp hair loss (alopecia

Clinical features ● ● ● Outline

1. Alopecia areata

5. Xerosis, Asteatosis

Treatment Differential diagnosis Pathology

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Clinical images are available in hardcopy only.

Fig. 19.11-2 Lupus miliaris disseminatus faciei.

Clinical images are available in hardcopy only.

Clinical images are available in hardcopy only.

Fig. 19.12-1 Alopecia areata.

Sharply demarcated hair loss occurs. In active alopecia areata, the hairs around the lesion easily come out.

C. Disorders of the hair

References

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