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Results for “Pigmentation Disorders”

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At least 55 records · Page 3Linked to original sources
PubMed1995

[Treatment of vascular malformations and pigment disorders of the face and neck by pulsed dye laser, Photoderm VL and Q-switched ruby laser].

BACKGROUND: Two new types of lasers, the pulsed dye laser and the Q-switched ruby laser, have shown good to excellent results in the treatment of vascular malformations and benign pigmented lesions of the skin. A new and very effective alternative to pulsed dye laser is the recently introduced Photoderm VL. This device is based on the use of a wide-band non-coherent intense pulsed light source which emits a continuous spectrum in the range of 515 nm to 1200 nm. PATIENTS AND METHODS: More than a 1000 patients with a variety of lesions of the skin were treated by these new laser systems and the Photoderm VL. The Q-switched ruby laser (wavelength 694 nm, pulse duration 25 ns) is suitable for the treatment of benign lentigines, café-au-lait macules, seborrhoic ceratosis, tattoos, and traumatic tattoos. The pulsed dye laser (585 nm, 0,3-0,45 ms) treats nevi flammei, capillary hemangiomas, telangiectasias, xanthelasma, hypertrophic scarring, and adenoma sebaceum. In addition we present the facilities of the new Photoderm VL (515 nm-1200 nm, 0,5-20 ms) for the treatment of nevi flammei, benign hemangiomatous malformations, telangiectasias, erythrosis interfollicularis colli, hypertrophic scarring, and hypertrichosis. RESULTS AND CONCLUSIONS: the Q-switched ruby laser, the pulsed dye laser, and the Photoderm VL show excellent results in the treatment of lesions of the skin, which otherwise would have been difficult to treat of untreatable. The efficiency of the laser types presented is based on the theory of selective photothermolysis. Scarring is almost never seen and hypo- or hyperpigmentation is in most cases transient.

Adolescent↗
PubMed2004

Spotlight on spotted mice: a review of white spotting mouse mutants and associated human pigmentation disorders.

Mutation of genes that regulate neural crest-derived melanoblast development and survival can result in reduction and/or loss of mature melanocytes. The reduction in melanocyte number in the skin and hair follicles manifests itself as areas of hypopigmentation, commonly described as white spotting in mice. To date ten genes have been identified which are associated with white-spotting phenotypes in mouse. Seven of these genes are associated with neural crest and melanocyte disorders in humans. This review summarizes the phenotypes associated with mutation of these genes in both mouse and man. We describe our current understanding of how these genes function in development, and explore their complex roles regulating the various stages of melanocyte development.

Animals↗
PubMed1983

Segmental pigmentation disorder.

Pigmentary changes with a dermatomal distribution are described in 30 children. The disorder, up to now unrecognized as an entity, is apparently caused by an embryological determination. It is more obvious in children with darker skin, and seems to fade very slowly over the years. In our experience the incidence is 0.35%. No relation to other anomalies could be established.

Adolescent↗
PubMed1985

Spastic paraparesis, mental retardation, and cutaneous pigmentation disorder. A new syndrome.

Four siblings in a family with a highly consanguineous background presented with an unusual combination of spastic paraparesis, muscle wasting, microcephaly, mental retardation, skeletal deformities, and cutaneous manifestations, ie, hypopigmented and hyperpigmented lesions and graying of the hair. An extensive workup including electromyography, muscle biopsy, and chromosomal analysis was unrewarding. An autosomal recessive inheritance is probable. A similar entity was recently reported from israel. The possibility that this previously unrecognized condition represents a new syndrome is suggested.

Adolescent↗
PubMed2004

Progressive hyperpigmentation and generalized lentiginosis without associated systemic symptoms: a rare hereditary pigmentation disorder in south-east Germany.

Familial progressive hyperpigmentation is rarely described in the literature. We report on five patients from three different families presenting with a peculiar progressive pigmentary disorder. The patients show a progressive diffuse, partly blotchy, hyperpigmentation, intermixed with scattered small hypopigmented macules, a few large hypopigmented areas, occasional café-au-lait spots and, most remarkably, a generalized lentiginosis. Histology revealed different degrees of basal layer hyperpigmentation and pigment incontinence, also in the spots appearing hypopigmented. Ultrastructural analysis showed a normal mode of Caucasian-like melanogenesis with varying content of regular melanosome complexes within the keratinocytes. All families are clustered in a small area around the town of Teublitz in south-east Germany with about 20,000 inhabitants, suggesting a genetic founder effect. Pedigree analysis is compatible with an autosomal dominant mode of inheritance with variable penetrance. Only a few similar, but not identical, cases have been reported in the past. This cluster of cases may therefore represent a rare and perhaps novel variant of a familial progressive disorder of hyperpigmentation.

Adolescent↗
PubMed2006

Guidelines for clinical trials in melasma. Pigmentation Disorders Academy.

There have been very few well-conducted trials in melasma and this makes the process of comparing treatment outcome between trials difficult. The Pigmentary Disorders Academy has examined the issues relating to clinical trials on melasma, and has proposed recommendations on how they should be conducted. This covers all aspects including correct diagnosis of the condition, evaluation of efficacy and safety outcome, and overall clinical trial design. It is anticipated that the establishment of accepted guidelines on the conduct of clinical trials in melasma will greatly assist the dermatological community.

Clinical Trials as Topic↗