What would you have to know about stretch marks ?
Synonyms: Striae distensae, Striae atrophicans, Striae rubra (red), and Striae alba (white).
* Very common especially in adolescent girls (70%) and boys (40%).
* Sites of predilection: Areas in which the skin is exposed to continuous and progressive stretching:
1. Abdomen and breast in pregnant women
2. Adolescents undergoing growth spurts (thighs, buttocks, breasts)
3. Shoulders in body-builders
4. Obese or overweight people
2. Periods of rapid growth
3. Heavy weight lifters and body builders
4. Excessive or prolonged use of corticosteroids (topical, oral, parenteral) and anabolic steroids
5. Excessive endogenous corticosteroids (Cushing’s syndrome)
6. Marfan syndrome.
* Striae caused by corticosteroid use or Cushing’s syndrome are often larger and wider than those caused by other causes.
* Treatment is unsatisfactory in most cases, however, the following options may be tried:
1. Topical retinoids
2. Chemical peels
3. Pulsed dye laser therapy
4. Fractional thermolysis
5. Skin needling
* Striae are usually of no medical significance but may cause considerable cosmetic concern.
Angiolymphoid hyperplasia with eosinophilia (ALHE)
Synonyms: Epithelioid hemangioma and Histiocytoid hemangioma
* A non-malignant, locally proliferating lesion composed of channels of small blood vessels surrounded by lymphocytes and eosinophils, hence the name ALHE.
* Reported from different parts in the world but particularly common in Japan.
* The cause is unknown, but antigenic stimulation following insect bites has been postulated. It sometimes follows an injury (trauma).
* Age: commonly young adults, with mean age in mid-thirties.
* Affects both sex but there is a female preponderance.
* Clustered small, translucent, brown, pink or red, dome-shaped dermal papules and nodules.
* Grouped lesions merge to form plaques or grape-like clusters.
* The lesions may be asymptomatic, itchy or painful.
* The most common site is the scalp especially around the ear (retroauricular area) or the hairline, however, lesions may also involve the inside of the mouth, trunk, extremities or genitals (penis and vulva).
* Kimura’s disease is thought to be a distinct entity from ALHE. For differentiation:
1. The lesions of Kimura’s disease are deeper-seated and larger (massive subcutaneous swelling).
2. Kimura’s disease is associated with allergic conditions such as asthma, rhinitis, and eczema, and it is frequently accompanied by lymphadenopathy, peripheral blood eosinophilia, and elevated IgE level. Peripheral blood eosinophilia is more common in Kimura disease than in ALHE.
3. Skin biopsy:
ALHE: A central thick-walled vessels with hobnail endothelium. A cellular infiltrate composed mainly of lymphocytes and large numbers of eosinophils is seen around the blood vessels.
Kimura’s disease: Prominent germinal centers with eosinophils are present in the subcutaneous tissue.
* There is controversy about spontaneous regression of the lesions of ALHE!
* The response to active treatment is variable and not always successful.
* In ALHE, an underlying AV shunt is present as a result of damage to and repair of an artery or vein. The lesions may recur if this underlying AV shunt is not excised, that is why treatment with surgical excision is successful in 65% of cases. Mohs micrographic surgery, including excision of the abnormal vessels at the base of the lesion, may be more effective. There tends to be a lot of bleeding during surgery.
2. Intralesional corticosteroids.
3. Lasers: Pulsed dye, Nd:YAG, or CO2 lasers.
5. Success in some patients had been reported with: cryotherapy, electrodessication. pentoxifylline, indomethacin, imiquimod, IFN alfa-2b, isotretinoin, vinblastine, and intralesional bleomycin.
Erythema toxicum neonatorum
* Synonyms: Toxic erythema of the newborn, Erythema toxicum.
1. Common condition affects as many as half of all full-term newborn infants.
2. Many differential diagnoses in early infantile life with similar rash.
3. Characteristic histological picture.
* Onset: First few days after birth (usually second or third day of life), although onset can be as late as two weeks of age.
* Aetiology: Unknown.
* Presentation: Combinations of erythematous macules, red patches, papules and pustules. There may be confluent erythema on the face.
The general condition of the infant is usually well (no fever).
Sites: Often begins on the face and spreads to affect the trunk and limbs. Palms and soles are not usually affected.
* Course: Typically waxes and wanes over several days and the eruption
generally disappears by the 10th day.
* Diagnosis: Primarily clinically based. In atypical cases smears of the pustules demonstrating eosinophils are adequate to confirm the diagnosis.
* Histopathology: diffuse infiltrate of eosinophils and neutrophils in the upper dermis. Papules shows an eosinophilic infiltration around the hair follicle.
Pustular lesions show perifollicular subcorneal pustules filled predominantly with eosinophils.
* DDX: The most important are:
1. Infections (folliculitis, impetigo, congenital cutaneous candidiasis, herpes simplex, varicella and CMV).
2. Miliaria (rubra and pustulosa).
3. Eosinophilic pustulosis (infantile Ofuji syndrome).
4.Transient pustular melanosis, and
Treatment: Not required (Benign self-healing condition).
Lichen planus actinicus
Synonyms: Actinic LP and LP subtropicus.
* Common in tropical and subtropical regions including Africa, Middle East and India. It is also common in Iraq.
* Aetiology is presumed to be long exposure to sun light (may be regarded as one of photo-sensitive disorders).
* Shows seasonal variation with the onset in spring and summer and may remit or be quiescent during winter.
* Third decade of life (young adults) is the most common age of occurrence in both sexes. However, it may affect children and elderly.
* Classical presentation of LPA is with annular plaques having hyperpigmented centers and violaceous borders. Other patterns of presentation include:
(1) Ordinary LP-like LPA (Confined to sun-exposed areas).
(2) Lichen nitidus-like LPA (Confined to sun exposed areas with no involvement of genitalia especially the male).
(3) Pigmented LPA: Melasma-like LPA.
* Sites: usually sun-exposed parts like the face, neck, V-shaped area of the chest and the dorsa of the hands. The face is almost always most severely affected.
* Itching is usually absent or mild.
* The diagnosis is primarily clinical, however skin biopsy may be arranged in query cases.
1.Strict avoidance of sun exposure is most important step in management .
2. Use of sunscreens.
3. Topical corticosteroids (intermediate to potent) are the mainstay of treatment.
4. Bleaching agents such as Hydroquinone (+ CS) in pigmented variety of LPA.
Personal experience: Practically, it is very difficult to manage LPA and even success sometimes is gained but it is usually temporary and the rule exacerbation will follow !
A 24-year-old man suffered a painful vesicular rash involving the left side of the chest of 5 days duration. One day before, the rash was preceded by severe left- sided chest pain with burning sensation. On examination, a classical zosteriform vesicular rash on erythematous background involving T3-T4 dermatomes was seen.
A 50-year-0ld woman with long history of atopic dermatitis presented in winter with chilblains-like pruritic, red-purplish, scaly patches and plaques with some fissures and erosions involving chiefly the hands especially the dorsal surface of the fingers and also the feet with few lesions on the trunk of two months duration. A superpotent corticosteroid in ointment base (Clobetasol) twice daily plus antihistaminics greatly improved the rash within 2 weeks.
An 80-year-old woman with Fitzpatrick type 1 skin presented with an irregular ulcer with rolled up border involving the upper medial part of the right cheek extending to the nasolabial fold and upper part of the melolabial fold of about one year duration. A 0.5 cm incisional biopsy was taken and showed an ulcerative BCC on histological examination.
Asymptomatic, multiple, linear, purplish atrophic linear plaques developed after two injections of triamcenolone acetonide.