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We would like to thank the authors for their novel vision regarding the clinical interpretation of these lesions which appeared to be steroid acne.1 Naturally, the analysis of some dermatoscopic images would have been of equal interest, as they may have been able to demonstrate the presence or absence of telangiectasias resulting from the use of steroid creams, and whether Demodex tails, or other dermatoscopic signs of Demodex folliculorum, are associated with the lesions.2.

Glucocorticoids may cause inflammatory lesions on the face and trunk, often referred as "steroid acne".1 Clinical presentation -similar to folliculitis- and limited efficacy of common anti-acne treatments have led us to consider the pathogenic responsibility of infectious agents such as Malassezia and/or Demodex.2-4.

Malassezia (Pityrosporum) folliculitis is a relatively common skin infection that affects the hair follicles. The condition is characterized by monomorphic perifollicular skin lesions and itching without comedones. Malassezia folliculitis significantly resembles acne vulgaris and steroid acne but is subtly distinct and managed differently. Oral antifungals are preferred for the treatment and result in a dramatic improvement in the disease condition. Early recognition of the disease is important for satisfactory clinical outcomes. This case reports about a female in the reproductive age group, who took multiple treatments for erythematous papular lesions on her face with a provisional diagnosis of acne vulgaris. After observing no improvement over the last three months, she visited the Dermatology clinic at a tertiary care hospital. A diagnosis of Malassezia folliculitis was considered and confirmed on microscopic examination and oral and topical antifungals were prescribed. She reported significant improvement in her skin lesions after two weeks of treatment.

Acne is a common disease, and its diagnosis is usually easy. In this chapter, not only unusual or special types of acne but also acne-like diseases that are clinically and etiologically different from acne vulgaris are discussed. The former category includes neonatal acne, acne conglobata, acne fulminans, cosmetic acne, acne excoriee, steroid acne, chloracne, hormonal acne including polycystic ovary syndrome, drug-induced acne, SAPHO syndrome, and so on. The other category is represented by rosacea, perioral dermatitis, folliculitis including Malassezia folliculitis and demodicosis, sycosis barbae, eosinophilic folliculitis, acneiform eruption due to anti-EGFR drugs or other anti-cancer drugs, and other non-follicular diseases such as lupus miliaris disseminatus faciei.

SummaryBackground Given the limited number of therapeutic options, severe childhood alopecia areata (AA) poses a clinical challenge. The best and most rapid response rates can be achieved with high-dose systemic corticosteroids, however, relapse following treatment discontinuation is inevitable. Due to systemic side effects, long-term high-dose corticosteroid regimens are not feasible. Following initial pulse therapy, continuation of corticosteroid therapy at a dose below the Cushing threshold might be able to suppress disease activity without causing severe side effects. Patients and methods Thirteen children with severe AA were enrolled in our open observational study. Seven had alopecia totalis or universalis; the remaining six children had multifocal alopecia affecting more than 50 % of the scalp. The treatment regimen consisted of initial pulse therapy with prednisolone 2 mg/kg PO, which was subsequently tapered to a maintenance dose below the individual Cushing threshold within nine weeks. Children were followed-up for one to three years. Results Sixty-two percent of individuals showed complete hair regrowth. The mean time to response was 6.6 weeks. Said response was sustained with maintenance therapy for the entire follow-up period. Noticeable side effects included weight gain (1–3 kg), which was observed in all children, and mild steroid acne in 23 % of cases. Conclusions Sequential high- and low-dose prednisolone therapy is an effective and safe therapeutic option for childhood AA.

Background: Systemic corticosteroids are often used in dermatology. The anti-inflammatory and immunosuppressive properties of corticosteroids make this agent as the first-line option in many disorders such as autoimmune and bullous diseases. However, there are also potential side effects and dermatologists who prescribe corticosteroids have to be aware of them. Case Summary: We report a 16-year-old girl with a history of taking oral methylprednisolone in the past 8 months who came with a acne-like eruption on the face, chest, and extremities as well as lines on the skin. Physical examination revealed monomorphic papules on the facial, thorax, and superior and inferior extremities region. Comedones were absent. Striae were found in the bilateral femur, abdomen, and mammary region. The patient was diagnosed with acneiform eruption and striae distensae rubra. Treatment using a combination of topical clindamycin and tretinoin showed clinical improvement of the acneiform eruption after three months of therapy. However, striae did not show improvement despite topical application of tretinoin and Centella asiatica extract. Conclusion: This case demonstrates the importance of understanding the cutaneous side effects that may result from chronic systemic corticosteroids administration as well as the evidence-based management.

Miliaria is a skin disorder due to blockage/interruption of the eccrine sweat glands that often caused by increased heat, humidity, and resident skin organism. Types of miliaria are miliariacrystalline, miliariarubra, and miliariaprofunda. Miliariapustulosa isarare variant of miliariarubra in which vesicles develop into pustules. Miliariapustulosa is often misdiagnosed because it has a similar appearance like other skin disorder with pustules as their main lesion. A 16-year-old female was consulted from Neurosurgeon Department H. Adam Malik General Hospital with reddish papules and pustules accompanied with pain and itchy at the back and chest since 12 days of hospitalization. They firstly rose in the back region then spread to chest, neck and became pustules. Dermatology status showed in interscapular, thoracic and collie region, miliary pustules and erythematous papules were found. Differential diagnoses were miliariapustulosa, steroid acne and drug allergic eruption with miliariapustulosa as working diagnosis. Lotiofaberi combined with gentamycin sulfate cream 0.1%, and cetirizine 10 mg tablet once daily were given as treatments. The patientwas advised to wear lightweight clothing and avoid exposure to conditions of high heat and humidity. After seven days of treatment, the patient showed good clinical improvement.

Summary Only few data are available on skin disorders in pediatric organ transplant recipients. In order to describe the whole range of dermatological diseases in a population of pediatric organ transplant recipients, we studied a group of 217 consecutive organ transplant recipients (168 kidney, 29 heart, 19 liver, one lung) aged

The Department of Dermatology at Nippon Medical School reported many adverse drug reactions (ADRs) to the Japanese Ministry of Health and Welfare (MHW)'s “Adverse Drug Reaction Monitoring” system. We have assessed causalities of these ADRs (1, 167 cases of 1, 531 ADRs over 10 years), and the suspect drugs. Using theseanalyses, we investigated whether the items on the MHW's report form are sufficient to assess causalities.We investigated 4 aspects of causalities: 1) whether ADRs reappeared after drug reintroduction, 2) whether ADRs are well known, 3) whether ADRs occurred after drug administration and 4) whether ADRs abated after curtailing drug use.As for the first aspect, in 45 cases tested by reintroduction of a drug (po 43, iv 2), the results were positive. In cases where skin tests such as patch tests, scratch-patch tests and other tests were done instead of reintroduction tests, 313, 324 and 22 tests were positive, respectively. We assessed the total 704 ADRs (46%) as “definite”. In most of the patients with rash (74%), contact dermatitis (84%), shock (73%) and photosensitivity reaction (88%), skin tests etc verified the causality.In the second aspect in cases where ADRs are well known, skin tests were not done, because ADRs such as rosacea-like dermatitis and steroid acne occur only after long term use of steroids and because candidiasis, mycosis and futoraful dermatitis were frequent. We assessed these 581 ADRs (38%) as “definite”.Among the rest of the 246 ADRs, 183 occurred after drug administration (aspect 3) in which dechallenge was positive in 128 (8%). We assessed causality of these ADRs as “probable”. Dechallenge was not positive in 55 (4%, including 7 recoveries in which it is unknown whether they came before or after drug curtailment). We assessed causalities of these ADRs as “possible”. In 63 ADRs (4%), it was unclear whether ADR occurred before or after drug administration. We assessed these causalities as “doubtful”.Analysis of MHW's ADR report form revealed cases where the date of onset of administration or the date of ADR occurrence was unknown, and thus whether or not “ADR occurred after drug administration” could not be assessed. The same situation was found in cases in which ADRs abated but the dates of recovery or dates of drug curtailment were unknown, and consequently whether or not “event abated after curtail ment of drug” could not be assessed. The USA's FDA MEDWatch form has a check box for event abated after curtailment of use. MHW's report form has a check box for event recurrence after reintroduction but does not have a check box for whether skin tests were positive or drug concentrations were monitored. These analyses suggest that the MHW's report form needs to be improved.Checking a box indicating that the event occurred after drug administration ranks the causality assessment from “doubtful” up to “possible” or “probable”. Checking a box for event abated after curtailment of drug use changes the causality assessment from “ossible” to “probable”. To improve the assessment of causality, we propose that the MHW form include 4 check boxes for probability of causality: whether the event recurred after reintroduction or not, whether skin tests were positive or negative, whether the event occurred after drug administration or not, and whether the event abated after curtailment of use or not.

Background Steroid acne is a folliculitis that can result from systemic or topical administration of steroid, and has been described as showing a similar clinical picture to Pityrosporum folliculitis, but there have been few reports about the incidence of Pityrosporum ovale and the effect of antimycotic drugs in steroid acne and other acneiform eruptions. Our purpose was to describe the association between steroid acne and P. ovale, and to confirm the superior efficacy of oral antifungal drugs over anti-acne drugs in the treatment of steroid acne. Methods The history, clinical features direct microscopy, histopathologic analysis, and therapeutic results of 125 cases with steroid acne or other acneiform eruptions were described and compared. Results Over 80% of patients with acneiform eruption receiving systemic steroid revealed significant numbers of P. ovale in the lesional follicle. Furthermore, oral antifungal drug (itraconazole) showed significantly better clinical and mycologic effects than any other group of medications used in this study. Conclusions Steroid acne and other acneiform eruptions showing discrete follicular papules and/or pustules localized to the upper trunk and acneiform facial skin lesions associated with multiple acneiform lesions on the body in the summer period should be suspected as Pityrosporum folliculitis. In addition, oral antifungal drugs recommended for Pityrosporum folliculitis; however, it will require a larger case-control study to confirm the superiority of antifungal therapy over anti-acne treatment.

Acne occurs more frequently in newborns and infants than one would gather from written accounts. Acne neonatorum tends to be overlooked because it is usually minor and transient. In contrast, acne infantum, which generally does not make its appearance until after 3 months of life, is more serious. Even acne conglobata may develop in infants. There are many other types of acne in childhood reflecting different pathogenetic mechanisms; included in this group are acne venenata infantum, steroid acne, hormonal disturbances, and toxic reactions.

A combination of oral Prednisolon and ventilation tube insertion was tried in 5 patients (6 ears) with the primary middle ear cholesterol granuloma manifesting blue eardrums. The patients, aged 6 to 19 years, were given 0.5-4mg/kg of body weight of oral prednisolon tapered over 10 to 14 days, and a ventilation tube was inserted during or immediately after the course of prednisolon. All 6 middle ears have been dry and well ventilated with the ventilation tubes in position with good hearing for 4 to 31 months, and CTs have revealed good aeration of the mastoids. Three courses of this therapy were required to obtain a dry middle ear in 1 of the 6 ears, but only 1 course was necessary in the remaining 5 ears. No serious side effects of this therapy were observed except for transient steroid acne in 1 patient. This combination therapy was considered to be worth trying in the treatment of the middle ear cholesterol granuloma.

Pityriasis versicolor and malassezia folliculitis were studied clinically and mycologically. The main results were as follows: 1) The average age of pityriasis versicolor patients has gradually become higher. 2) Negative rates of Malassezia furfur after treatment were very high by direct examination but relatively low by culture. 3) Patients who were negative by culture on completion of treatment seldom recurred within 2 months. 4) We can evaluate the effectiveness of antifungal application by using Malassezia furfur as normal skin flora on the volunteer's back. 5) Malassezia furfur (orbiculare or ovale type) is detected in follicular contents of steroid acne and acne vulgaris, which makes it necessary to establish criteria for diagnosis of malassezia folliculitis.

Atopic dermatitis (AD) is a common eczematous skin condition; as many as 10-17 percent of all children are affected, and 35-60 percent of affected patients manifest symptoms manifest during the first year of life. Treatment principles for AD in young children involve conservative measures such as avoidance of hot water and environmental irritants, combined with liberal use of emollients after bathing. Low potency topical corticosteroids (TCS) are the current standard of therapy for AD in young children, reserving mid- and high-potency TCS for severe disease. However, complications of long-term use of TCS include skin atrophy, stria formation, telangiectasia, hypopigmentation, secondary infections, steroid acne, allergic contact dermatitis, and miliaria. The pediatric population is also at increased risk for systemic absorption because of their high ratio of skin surface to body mass. Systemic absorption may result in hypothalamic-pituitary-adrenal axis suppression and ultimately growth retardation. Although most topical and systemic corticosteroids are not approved by the Food and Drug Administration for use in children less than 2 years of age, conservative treatment often fails in this age group and frequently patients are treated with TCS, antibiotics, and antihistamines.

QUESTION: A 50-year-old woman is seen for evaluation of a facial eruption that has been present intermittently for at least 5 years. The process is located on her mid and lower face. She has used the topical corticosteroid creams diflorasone diacetate 0.05% and hydrocortisone valerate 0.2% for a prolonged period. Indeed, she presents crimped empty tubes to us in hopes of refills (figure 1). These preparations provide temporary relief, but the eruption always returns. Figure 1 Nearly empty tubes of medium- and high-potency topical steroids presented by patient Examination shows that she has a light complexion and marked erythema and scaling of the lower face, extending up to the cheeks. The lower lids show minor involvement (figure 2). The eruption spares the vermilion border of the lips and the lips themselves. Figure 2 Marked erythema and scaling of the patient's lower face What are the diagnosis, differential diagnosis, and treatment of this condition? What role do prescription topical steroids play in this eruption? ANSWER: This patient has steroid-induced perioral dermatitis, a condition marked by perioral or periorbital erythema and scaling with or without papules that characteristically shows a rim of sparing around the vermilion border of the lips. The process usually starts in a perioral distribution with later involvement of the chin, nasolabial folds, and occasionally the eyelids. It occurs mostly in women. The differential diagnosis includes classic perioral dermatitis, rosacea, and acne. Perioral dermatitis can begin by itself and is seen mostly in women aged 15 to 50 years,1 although it also may rarely affect prepubertal children of both sexes.2 Perioral dermatitis can become steroid-induced perioral dermatitis after prolonged use of topical corticosteroids on the face. Steroid-induced perioral dermatitis is differentiated from common perioral dermatitis by history and clinical behavior. Patients with rosacea and acne can also develop steroid rosacea, steroid acne, or the red-face syndrome after corticosteroid abuse.3 Steroid-induced facial dermatoses tend to have more erythema, inflammation, and scaling than their noniatrogenic counterparts. Mid- or high-potency topical corticosteroids are known to exacerbate perioral dermatitis, acne, and rosacea. They often initiate a cycle of temporary relief and increasingly severe flare-ups on attempt to stop the medicine. This has been described as an “addiction” of the skin to the steroid, requiring increasingly larger and more frequent applications of steroid creams to bring relief.4 Although temporarily reducing the inflammatory reaction, the steroid may increase the overgrowth of the bacteria through local immunosuppression. We have observed that patients with steroid-induced perioral dermatitis often present with vigorously squeezed tubes of corticosteroids that they have used for many months to years. These patients have tried to extract as much of the precious cream as possible to counter the latest flare of the dermatitis. Thus, we term this presentation the “tortured tube” sign. Treatment involves cessation of the topical steroid. Often this regimen initially results in moderate to severe flare-ups of the eruption. The administration of tetracycline, 500 mg by mouth twice a day, and cold tap water compresses will help to alleviate the inflammation. The lesions typically resolve after a few weeks, but occasionally may last as long as 6 months. To ensure therapeutic success, the physician must educate the patient about the course of the disease and the need to discontinue the use of topical corticosteroids. Prevention is more important than cure. Physicians should never prescribe mid- to high-potency topical corticosteroids for facial use without clear oral and written instructions that limit the time of application to no more than 1 to 2 weeks. Even weaker corticosteroid creams have been implicated in initiating facial disorders. Refills of these medicaments should not be given over the phone. A 15-gram tube of a steroid cream may last a patient 6 to 12 months when used only on the face and is sufficient to cause cutaneous addiction with the development of uncomfortable and unsightly dermatoses. In this case, on follow-up several months later, the patient's rash had resolved (figure 3). Figure 3 Resolution of the patient's rash several months after abstaining from steroid use

Steroid acne is a common unwanted effect in patients undergoing corticosteroid therapy. Eight women in a series of 1276 adult patients had acne after orthognathic surgery in which short-course parenteral corticosteroid therapy was used to reduce postoperative swelling. Steroid-induced acneiform eruption is different from acne vulgaris in that the former usually resolves on its own, without scar formation, after withdrawal of the drug.

Steroid acne (SA) may occur after the administration of topical or systemic corticosteroids. Because of several consultations of spinal injury patients with a very abrupt onset of a uniform papular eruption (i.e. days) initially misdiagnosed as a drug reaction or sepsis, we followed hospitalized patients who received intravenous corticosteroids (IVC) for the development of acute-onset SA in order to determine its incidence. Fifty-one consecutive subjects receiving IVC were followed for the duration of their hospital stay and examined for the development of acneiform lesions. Acute-onset SA occurred in 1 subject (2%). Acute spinal cord injury may represent a high-risk clinical setting for acute-onset SA.

A case of steroid acne sparing a patch of Hansen's disease on the forehead of an 18 year old girl is presented here for its unique presentation.

A preparation of dexamethasone 0.02% in Eutanol G (n octyldodecanol) was applied once daily for three weeks, to the right side of the forehead of 25 male healthy test subjects. Eutanol G without dexamethasone was applied in the same way to the left side of the forehead. Before and at the end of the treatment period bacteria were removed from the pilo-sebaceous ducts by the method of Holland et al. [8]. Bacteria that grew under anaerobic conditions were evaluated quantitatively. Dexamethasone induced a significant increase in P. acnes, in all Propionibacteria and in the total bacterial count. The importance of these findings is discussed in relation to the development of steroid acne.

Therapy-resistant acne developed about one month after the initiation of oral steroid therapy for Bell's palsy, chiefly on the paralyzed side of the face of a middle-aged woman who had once suffered from acne vulgaris. It was speculated that the lack of normal facial movement contributed to the development of acne.

A lipid-free preparation containing 0.076% dexamethasone-21-sodium-m-sulfobenzoate (corresponding to 0.05% dexamethasone) has been applied to the right side of the back and the same vehicle without the agent to the left side of the back of 16 male subjects without any skin diseases. The applications were made twice daily over a period of 26 days. Two days after the final application the skin surface lipids were analysed quantitatively by means of the direct extraction method and the paper absorption method. Thin layer chromatograpical analyses were also carried out. The sum of skin surface lipids is not altered by dexamethasone-21-sodium-m-sulfobenzoate. This agent does, however, induce a significant increase in the free fatty acids at the expense of the triglycerides. The importance of this result is discussed with reference to the pathogenesis of steroid acne.

An acneforme eruption was regularly induced in human adult male volunteers by topical application of corticosteroid solutions and various commercial creams. Within 7 to 14 days smooth, firm, dome-shaped, reddish papules of rather uniform size appeared followed by comedones several weeks later. Factors promoting the development of steroid acne were (I) high concentrations, (II) continuous occlusion, (III) young adults below age 30, (IV) whites in preference to blacks, (V) history or signs of acne, (VI) applications to acne areas of face and upper back. Increased formation of horny cells was demonstrated by radiolabelling with3H-thymidine,3H-glycine and3H-histidine. Histologically, the first event was a focal degeneration of the follicular epithelium with the formation of a circumscribed intra- and perifollicular abscess.

In a previous paper it was postulated that both androgens and corticosteroids or their metabolites are essential for the development of steroid acne and acne vulgaris. The corticosteroids appear to be required for the induction of follicular keratotic plugging (1). If such be the case, it must be assumed that the steroids or their metabolites reach the pilosebaceous apparatus via the systemic circulation. It has already been shown that steroid compounds in addition to cholesterol are present in the skin surface lipids (2). This study was undertaken in order to determine the extent to which systemically administered corticosteroid compounds appear in skin surface lipid.

To the Editor.— A number of adverse side effects have been described after prolonged or excessive use of topical corticosteroids. These include skin atrophy, telangiectasia, purpura, striae atrophicae, delayed healing of ulcers, a florid facies, steroid acne, infection, perioral dermatitis, hypertrichosis, hyperpigmentation, hypopigmentation, skin blanching, granuloma gluteale infantum, allergic contact dermatitis, photosensitivity, stellate pseudoscars, and nodular elastoidosis with cysts and comedones (Favre-Racouchot syndrome). 1,2 We present herein another side effect—milia, which are induced on aged skin by long-term application of topical corticosteroids. Report of Cases.— Nine patients, 63 to 85 years of age, six men and three women, had several to numerous (more than 20) milia, which were whitish, globoid, and firm lesions, 1 to 3 mm in size, on their neck, upper chest, and upper arms where topical corticosteroids had been used. In all the patients, telangiectasia and skin atrophy with fine wrinkles were always seen around the milia

To the Editor.— Both Goodpasture's syndrome and follicular mucinosis are uncommon or even rare conditions, both of obscure cause. We recently had the opportunity to study a patient with both conditions. Report of a Case.— In July 1974, a 12-year-old girl developed hemoptysis and subsequently hematuria. She was hospitalized and thoroughly examined, and the diagnosis of Goodpasture's syndrome was confirmed by characteristic routine and immunofluorescence findings on lung and renal biopsy specimens, as well as by positive circulating antiglomerular basement membrane antibodies. She was treated with high doses of prednisone (60 to 100 mg daily), azathioprine (Imuran) (100 mg daily), as well as methyldopa (Aldomet), hydralazine hydrochloride, furosemide (Lasix), and potassium chloride. She did well, except for seizures due to hypertensive encephalopathy, and her prednisone was gradually tapered. In December, she developed a follicular eruption on her forehead and cheeks, which was believed to be steroid acne. This was treated

To the Editor.— We were recently contacted by telephone to renew a prescription for fluocinolone acetonide ointment. The patient indicated he had been using the medication to treat atopic dermatitis on his face and arms, and that it had been prescribed by another physician. When we learned he had been applying the fluorinated steroid to his face daily for 16 years, we insisted he come down to our office and expected to see a horrendous case of steroid rosacea, steroid acne, perioral dermatitis, telangiectasia, and skin atrophy. When he arrived, we had trouble believing our eyes. He had no side effects whatsoever! The patient was a 31-year-old black man whose facial skin showed even pigmentation and normal texture. His atopic dermatitis was under excellent control. How can one explain the complete absence of side effects in this case? The effects of prolonged use of fluorinated steroids on the face have

High doses of corticosteroids in connection with immunosuppressive therapy precipitate a distinctive eruption, steroid acne. A sudden outcropping of densely aggregated, uniform, follicular, reddish papules is succeeded in wave-like progression by numerous whiteheads (closed comedones) that eventually transform into blackheads (open comedones). Crowds of persistent, mixed comedones characterize the mature disease. Topical application of a 0.05% solution of tretinoin, once to twice daily, was found to be an effective treatment for obliterating the dense aggregates of comedones in 12 patients with steroid acne. Complete clearing can be obtained in most instances within two to three months, despite continued therapy with high doses of steroids.