Anna Maria Peluso

Drug-induced hair loss and hair growth : incidence, management and avoidance

SummaryA large number of drugs may interfere with the hair cycle and produce hair loss. Drugs may affect anagen follicles through 2 main different modalities: (i) by inducing an abrupt cessation of mitotic activity in rapidly dividing hair matrix cells (anagen effluvium) or (ii) by precipitating the follicles into premature rest (telogen effluvium). In anagen effluvium, hair loss usually occurs within days to weeks of drug administration, whereas in telogen effluvium, hair loss becomes evident 2 to 4 months after starting treatment.Anagen effluvium is a prominent adverse effect of antineoplastic agents, which cause acute damage of rapidly dividing hair matrix cells. Telogen effluvium may be a consequence of a large number of drugs including anticoagulants, retinol (vitamin A) and its derivatives, interferons and antihyperlipidaemic drugs. Drug-induced hair loss is usually reversible after interruption of treatment. The prevalence and severity of alopecia depend on the drug as well as on individual predisposition. Some drugs produce hair loss in most patients receiving appropriate dosages while other drugs are only occasionally responsible for hair abnormalities.Both hirsutism and hypertrichosis may be associated with drug administration. Drugs most commonly responsible for the development of hirsutism include testosterone, danazol, corticotrophin (ACTH), metyrapone, anabolic steroids and glucocorticoids. Hypertrichosis is a common adverse effect of cyclosporin, minoxidil and diazoxide.

Prevalence of nail abnormalities in children with alopecia areata

Abstract: We assessed the prevalence of nail abnormalities in 272 children with alopecia areata who were seen in our department during an eight‐year period. Of these, 126(46%; 50 girls, 76 boys) had nail abnormalities that were related to alopecia areata. Nail pitting was detected in 92 patients, Including 37 with alopecia totalis or alopecia universalis. Three patients experienced an onychomadesis of all 20 nails during the acute onset of alopecia areata universalis. Thirty‐two (11.7%) had nail thinning and severe nail plate surface abnormalities that were consistent with a diagnosis of trachyonychia.

Nail lichen planus: clinical and pathologic study of twenty-four patients.

BACKGROUND We studied a large series of patients with lichen planus (LP) limited to the nails. OBJECTIVE Our purpose was to review the clinical and histopathologic features of 24 patients with LP limited to the nails and to discuss treatment and long-term prognosis. METHODS The records of 24 patients with biopsy-confirmed nail LP were analyzed. Clinical and follow-up data were obtained. RESULTS Nail LP usually appears during the fifth or sixth decade of life. Neither gender-associated susceptibility nor seasonal influences were detected. In most cases, nail LP is self-limiting or promptly regresses with treatment. Recurrences of nail lesions as well as development of LP in other regions of the body are possible. The development of severe and early destruction of the nail matrix characterizes a small subset of patients with nail LP. CONCLUSION Approximately 25% of patients with nail LP have LP in other sites before or after the onset of nail lesions. Long-term observation indicates that permanent damage to the nail is rare even in patients with diffuse involvement of the matrix.

Nail lichen striatus: Clinical features and long-term follow-up of five patients

BACKGROUND Nail involvement in lichen striatus (LS) is uncommon and has always been reported in association with typical skin lesions. OBJECTIVE We attempted to characterize the clinical and pathologic features and the long-term prognosis of nail LS. METHODS Five cases of LS of the nail including three cases with exclusive nail involvement were evaluated and the literature reviewed. RESULTS Biopsy specimens showed a moderately dense bandlike lymphohistiocytic infiltrate affecting the proximal nailfold, the nail bed, and the nail matrix dermis. Exocytosis with slight spongiosis, focal hypergranulosis, and dyskeratotic cells were detectable in the nail matrix epithelium. Spontaneous regression of the onychodystrophy occurred after 4 to 12 months from the time of diagnosis (mean, 8.4 months). CONCLUSION Nail LS is not necessarily associated with skin lesions but can also be an isolated finding. The diagnosis of nail LS should be strongly suspected when a child or a young patient presents with lichen planus-like nail abnormalities localized to the lateral or medial portion of a single nail.

Prevalence and sources of occupational contact sensitization to acrylates in Italy.

Acrytaie‐based products are widely utilised in the indusiriali/cd world and in the domestic environment. The aim of this study was to evaluate the prevalence and sources of occupational contact scnsitization lo aerylales in a selected population. Between January 1987 and April 1992, 82 patients suspected of occupational acrylic sensitization were patch tested with the GIRDCA standard series and an extensive acrylate series. Over this 5‐year period, we detected sensid/ation to acrylates in 13.4% of cases. Dental materials and anaerobic sealants were ihe most important sources of acrylate sensitLzalion. Among acrylic monomers, ethylene glycol ditnethacrylate was the most frequent contact sensitix.er in our study. Acrytate additives were also important sources of contact dermatitis in our patients. Although [he clinical picture of airborne contact dermatitis due to acrykites has rarely been reported in the literature, it was commonly observed in our patients.

Occupational skin hazards from synthetic plastics.

Epoxy and acrylic resins have numerous industrial applications but are also widely used in the household environment. These compounds are presently one of the most important sources of occupational contact dermatitis. Contact sensitization to epoxy resins is usually caused by the resin itself but hardeners or other additives, such as reactive diluents, plasticizers, fillers and pigments, can occasionally be responsible. Since completely cured epoxy resins are not sensitizers, epoxy resin sensitization is always due to the presence, in the final polymer, of uncured allergenic low molecular weight oligomers. Acrylates are now considered the fourth most common cause of contact sensitization due to resins. Unpolymerized monomers of acrylic compounds are known to be responsible for the contact allergy. Accelerators, inhibitors and catalysts, which are usually added to the acrylates to promote the polymerization process, can also sensitize. Both allergic and irritant contact dermatitis may be caused by exposure to epoxy or acrylic resins and their additives. Contact urticaria, allergic or irritant airborne contact dermatitis caused by volatile compounds, onychia and paronychia can also occur. From January of 1984 to May of 1992 we detected 39 cases of occupational allergic contact dermatitis to epoxy resin system substances and 11 cases of occupational contact sensitization to acrylic compounds. In our experience, the electronics industry as well as paint and glue related activities were the most important sources of epoxy sensitization. Dental materials and anaerobic sealants were found to be the most frequent acrylate sensitizers.

Diffuse hypertrichosis during treatment with 5% topical minoxidil

Five women affected by androgenetic alopecia developed severe hypertrichosis of the face and limbs after 2‐3 months of treatment with 5% topical minoxidil. Minoxidil was discontinued and in all patients the hypertrichosis disappeared from the face and arms after 1‐3 months, and from legs after 4‐5 months. Systemic absorption of minoxidil, and a high sensitivity to minoxidil of the follicular apparatus in these areas, is hypothesized.

Clinical Features and Long-Term Follow-Up of 20 Cases of Parakeratosis Pustulosa

Abstract: We report the clinical features and long‐term follow‐up of 20 pediatric patients with parakeratosis pustulosa (PKP). In eight children PKP was considered as a clinical manifestation of psoriasis. Of these, three children had skin psoriasis at the time of our observation, two developed nail psoriasis, and three developed psoriatic pitting during follow‐up. Parakeratosis pustulosa was considered a symptom of allergic contact dermatitis in four patients, whereas atopic dermatitis was possibly responsible for PKP in two patients. A complete recovery from disease was observed in 11 patients. The results of our study suggest that PKP is not a single entity but rather represents a nail symptom that can be produced by several inflammatory diseases, including nail psoriasis, atopic dermatitis, and contact dermatitis.

Contact and irritant stomatitis.

Contact stomatitis is rather uncommon because of the relative resistance of the oral mucosa to irritant agents and allergens. The clinical manifestations of contact stomatitis are extremely variable and include erythema, erosions, ulcerations, leukoplakia-like lesions, and lichenoid reactions. Clinical signs are frequently less pronounced than subjective symptoms, and patients commonly experience severe functional problems despite only mild mucosal alterations. Allergic stomatitis is rare and almost always attributable to metallic mercury and gold salts. A careful history and an accurate examination of the oral cavity, teeth, and dental restorations are essential for a correct diagnosis. Patch testing is indicated in all lesions that are not clearly related to trauma or physical injuries. Patch testing is not useful in the burning mouth syndrome. Evaluation of clinical relevance of patch test results is always very difficult and requires an interdisciplinary approach to the patient. Successful treatment requires the identification and elimination of the causative factor, when possible. It is important to bear in mind that replacement of dental restorations and prostheses may be very expensive and stressful for the patient and thus should not be recommended when their causative role is doubtful.

Reflex sympathetic dystrophy with prominent involvement of the nail apparatus

After closed hand trauma, a 17-year-old boy had acute inflammatory changes that resembled bacterial whitlows of the third and fourth right fingers. Clearing of the inflammatory changes was followed by the development of cyanosis, hyperhidrosis, and roentgenographic evidence of patchy osteoporosis in the involved extremity. Findings of a biopsy specimen revealed that the inflammatory lesions in the proximal nail folds were caused by proliferation of capillary vessels embedded in edematous loose connective tissue. This is the first report of cutaneous histopathologic findings in the first stage of reflex sympathetic dystrophy, although similar features have been described in synovial and bone biopsy specimens of patients with reflex sympathetic dystrophy.