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Linear eruptions of the nose in childhood: a form of lichen striatus?

We report four children with linear eruptions on the nose, with overlapping features of lichen striatus and linear cutaneous lupus erythematosus. However, linear lupus erythematosus has rarely been reported, and lichen striatus, although classically linear, rarely affects the face. The linear distribution of lesions from the glabella to the ala nasi may represent distribution following Blaschko's lines.

Adolescent↗

Red facial pseudochromhidrosis.

We describe a 9-year-old girl with pseudochromhidrosis simulating apocrine chromhidrosis. Treatment with topical and systemic erythromycin resulted in complete clearance of the reddish discoloration of the face. No relapse or recurrence was observed over a 3-month period.

Anti-Bacterial Agents↗

Effective treatment of frontal hyperhidrosis with botulinum toxin A.

BACKGROUND: Focal hyperhidrosis is a common condition mostly confined to the axillae, palms and soles. In some individuals, predominantly men, increased sweating of the forehead may be the major complaint and may interfere with the person's quality of life. Botulinum toxin A has been shown to be a very effective treatment for focal hyperhidrosis of the axillae and palms. OBJECTIVES: To assess the response in 10 men suffering from frontal hyperhidrosis treated with botulinum toxin A. METHODS: Botulinum toxin A Botox was injected at multiple sites evenly distributed over the forehead (mean dose 86 mouse units). RESULTS: The mean +/- SEM amount of sweat was significantly reduced, 4 weeks after treatment, from 173.8 +/- 38.6 mg min(-1) to 53.7 +/- 17.6 mg min(-1). The effect lasted at least 5 months in nine of the 10 patients. All patients subjectively judged the treatment as very effective. Minor side-effects included painful injections and a transient weakness of forehead muscles without ptosis. CONCLUSIONS: In this study, we provide evidence that botulinum toxin A is an effective and safe treatment for frontal hyperhidrosis.

Adult↗

Rosacea-like demodicidosis associated with acquired immunodeficiency syndrome.

We present a 35-year-old patient with acquired immunodeficiency syndrome who had demodicidosis on his face, characterized by multiple papules and papulopustules, associated pruritus, numerous mites on skin-surface biopsy and in biopsy specimens, and rapid response to topical treatment with permethrin. It seems likely that Demodex infestation does not manifest unless local or systemic immune function is altered, leading to the proliferation of the organism and subsequent disease.

AIDS-Related Opportunistic Infections↗

Lymphocytic infiltration of the skin is a photosensitive variant of lupus erythematosus: evidence by phototesting.

BACKGROUND: Lymphocytic infiltration of the skin (LIS) is a disorder in which photosensitivity has been suspected but never proven. OBJECTIVES: To carry out a systematic photobiological investigation in patients with LIS and to compare the photobiological features of LIS with those of other photosensitive disorders. METHODS: We performed provocative phototesting with ultraviolet (UV) A and UVB in 10 patients with active LIS. RESULTS: In all patients, UVA and/or UVB elicited abnormal papular phototest reactions resembling lesions of LIS both clinically and histologically. Lesions typically developed 3--6 days (mean +/- SD 100.8 +/- 20.9 h) after the first UV exposure. CONCLUSIONS: This characteristic latency interval together with certain clinical features, i.e. onset in summer, predilection for the face and persistence of the lesions, indicate that LIS is a photosensitive disorder distinct from polymorphic light eruption but indistinct from lupus erythematosus (LE). Both our photobiological findings and the effective treatment with hydroxychloroquine in half of our patients strengthen the proposal that the two entities LIS and LE tumidus are identical. As diagnosis cannot be made by histological, immunofluorescence or laboratory criteria, provocative phototesting may be a diagnostic aid in this disorder.

Adult↗

Homozygous variegate porphyria: a compound heterozygote with novel mutations in the protoporphyrinogen oxidase gene.

Homozygous variegate porphyria results from mutations in both alleles of the protoporphyrinogen oxidase (PPOX) gene. Our patient, a 36-year-old woman, has severe cutaneous manifestations. Her clinical and biochemical features are similar to the few other reported cases, including onset before 18 months of age, photosensitivity, absence of acute porphyric attacks, and elevated erythrocyte protoporphyrin. Mutation analysis of the PPOX gene revealed an in-frame 12 bp insert (c. 657-658 ins AAGGCCAGCGCC) encoding lysine-alanine-serine-alanine (KASA), and a G to A transition at the splice donor site of exon 11 (IVS 11-1 G-->A). Neither of these mutations has been reported previously. Our patient's mother has the splice site mutation and has had acute porphyric episodes. A maternal first cousin has the same mutation but no clinical manifestations. The medical and family history of our patient's father is uncertain.

Adult↗