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Results for “Hypopigmentation”

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At least 19 recordsLinked to original sources

PubMed2004

The treatment of hypopigmentation after skin resurfacing.

BACKGROUND: Hypopigmentation has plagued all methods of skin resurfacing. Whether the physician uses chemical peels, dermabrasion or laser resurfacing hypopigmentation can develop. OBJECTIVE: To examine the pathogenesis and treatment of hypopigmentation after resurfacing. METHODS: Areas of hypopigmentation after skin resurfacing were blended in with laser-assisted chemabrasion (LACA). The process begins with preconditioning of the skin with vitamin A/glycolic skin conditioning lotions. Then the area is resurfaced with the LACA. This resurfacing usually requires three to four freeze-sand cycles to remove the areas of hypopigmentation associated with dermal fibrosis. The resurfaced skin is then occluded with a combination of polyethylene/silicone sheeting during the acute phase of wound healing. Ultraviolet photography and histologic examination were used to demonstrate the improvement in dermal fibrosis and hypopigmentation. RESULTS: The LACA improved areas of hypopigmentation in the 22 cases studied. Under occlusive wound dressings, the melanocytes migrated into the areas of hypopigmentation, and the wounds healed without extensive fibrosis. This produced a blending of skin color. CONCLUSION: It is possible with skin preconditioning, LACA, and occlusive wound healing to provide for a wound healing environment that blends in areas of hypopigmentation that have developed after previous skin resurfacing.

Adult↗

PubMed1987

Hypopigmentation in the Prader-Willi syndrome.

Cutaneous and ocular pigmentation were evaluated in 29 individuals with the Prader-Willi syndrome (PWS). Criteria for hypopigmentation included the presence of type I or II skin, the lightest skin type in the family by history, and iris translucency on globe transillumination. On the basis of these criteria, 48% of the PWS individuals were hypopigmented. The presence of hypopigmentation correlated with a small interstitial deletion on the proximal long arm of chromosome 15; however, this deletion was also found in individuals who did not meet the full criteria for hypopigmentation. Hairbulb tyrosinase activity and glutathione content, as well as urine cysteinyldopa excretion, were low in PWS individuals with and without hypopigmentation and did not separate these two groups. We conclude that hypopigmentation is found in a significant proportion of individuals with PWS and that the hypopigmentation may be associated with a deletion of the long arm of chromosome 15. The mechanism for the hypopigmentation is unknown.

Chromosome Deletion↗

PubMed2003

Imatinib mesylate causes hypopigmentation in the skin.

BACKGROUND: Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors. In clinical trials with imatinib mesylate, common side effects of nausea, emesis, diarrhea, periorbital edema, fluid retention, and myelosuppression have been documented. METHODS: In this case series, the authors describe unique clinical findings of skin hypopigmentation in six patients with CML who were treated with imatinib mesylate. RESULTS: Most patients developed onset of skin hypopigmentation within the first month of treatment and all of the patients experienced additional drug toxicity. Despite patient susceptibility to toxicity, the presence of hypopigmentation did not appear to predict leukemic cell response or clinical outcome. All six patients established a hematologic response but only two patients had a complete cytogenetic response. Imatinib mesylate induced hypopigmentation also appeared to be reversible and potentially dose related. CONCLUSION: Skin hypopigmentation is a benign side effect from imatinib mesylate treatment that appears to be reversible upon discontinuation or dose reduction. Several lines of evidence have previously reported that KIT and its ligand stem cell factor (SCF) have a regulatory role in melanocyte development and survival, suggesting a rational mechanism of action for imatinib mesylate in the pathogenesis of hypopigmentation. The signal transduction mechanism currently is believed to involve SCF ligand binding of KIT and downstream activation of MAP kinase (Erk-2). Microphthalmia (Mi), a basic helix-loop-helix leucine zipper (bHLHZip) transcription factor, is phosphorylated by MAP kinase at a serine residue (S73). Once phosphorylated, Mi transactivates the tyrosine pigmentation gene promoter and affects pigment production.

Adult↗

PubMed2005

Analysis of hyperpigmentation and hypopigmentation after Er:YAG laser skin resurfacing.

BACKGROUND AND OBJECTIVES: Pigmentary disorders--such as hyperpigmentation and hypopigmentation, are devastating complications of erbium:yttrium-aluminum-garnet (Er:YAG) laser resurfacing. This study was undertaken to assess the clinical and histopathologic features of hyperpigmentation and hypopigmentation following Er:YAG laser resurfacing, especially in darker skin. STUDY DESIGN/MATERIALS AND METHODS: One hundred and ninety patients (skin phototypes III and above), treated with Er:YAG lasers--short-pulsed and modulated (variable-pulsed and dual-mode) Er:YAG lasers--for skin resurfacing were recruited. The clinical features of hyperpigmentation and hypopigmentation were evaluated retrospectively using medical charts and serial photographs. For histopathologic examinations, skin biopsies were performed in three patients at hyperpigmentation sites and in four patients at hypopigmentation sites. RESULTS: Hyperpigmentation was observed in 38.4% of the patients. Mean onset and duration were 3.5 and 7.2 weeks, and then it has faded away within 16 weeks in 93.2% of cases. Hypopigmentation was observed in 13.7% of the patients; its mean onset was 2 months after treatment, and it faded within 1 year in 85% of cases. The incidences and mean durations of these side effects were more intense and longer in patients treated with short-pulsed, variable-pulsed, and dual-mode Er:YAG lasers, in increasing order. In terms of histopathologic examinations, melanin amounts in the epidermal basal layer were observed to vary. CONCLUSIONS: Hyperpigmentation and hypopigmentation are frequent complications of Er:YAG laser resurfacing. Long pulse duration-induced thermal damage seems to be the most important factor in terms of the induction of pigmentary disorders.

Adult↗

PubMed2004

Lack of difference in the rates of hypopigmentation with 90-microsecond pulsed and longer dwell time carbon-dioxide laser resurfacing.

BACKGROUND: Hypopigmentation is an adverse outcome associated with carbon-dioxide (CO(2)) laser resurfacing. A 90-microsecond pulse produces a more favorable postoperative course of healing, erythema, and pain compared with a 900-microsecond dwell time. The rate of hypopigmentation after 90-microsecond pulsed CO(2) resurfacing may also be reduced. To date, there have been no comprehensive reports on the effect of varying pulse duration on the occurrence of hypopigmentation. OBJECTIVE: We sought to investigate the relationship between pulse duration and the occurrence of hypopigmentation after CO(2) laser resurfacing. METHODS: We conducted a retrospective review of 447 consecutive patients who were treated with a 90-microsecond pulsed CO(2) laser (n = 229) or a continuous wave CO(2) laser with a modifiable dwell time (100-950 microseconds, n = 218). Follow-up ranged from 8 to 61 months (median: 27). RESULTS: A series of 4 threshold dwell times (range: 90-950 microseconds) were used to divide patients into 2 treatment groups (above and below) at each threshold. The rates of hypopigmentation between groups were similar (range: 6.37%-9.09%) and serial chi-square testing revealed no statistical differences between groups for each dwell time tested (P < 1.0). CONCLUSION: No significant relationship between pulse duration and the occurrence of hypopigmentation was observed.

Acne Vulgaris↗

PubMed2001

Laser resurfacing-induced hypopigmentation: histologic alterations and repigmentation with topical photochemotherapy.

BACKGROUND: Hypopigmentation is a relatively common side effect of CO2 laser resurfacing. Little is known regarding the histologic features of the areas of pigmentation loss. To date, hypopigmentation is considered a permanent complication of this procedure. OBJECTIVE: To assess the histologic features of hypopigmentation caused by laser resurfacing and to evaluate the efficacy and safety of topical psoralen photochemotherapy. METHODS: Ten patients were included in this pilot study. Four had baseline biopsies performed. Histologic parameters assessed included epidermal melanin, dermal melanophages, perivascular inflammation, Mel-5 immunostaining for melanocytes, and dermal fibrosis. Seven patients were treated twice a week with topical photochemotherapy utilizing 0.001% 8-methoxypsoralen. RESULTS: All of the biopsy specimens demonstrated varying quantities of epidermal melanin and residual epidermal melanocytes. Mild perivascular inflammation was evident in two specimens. Superficial dermal fibrosis was noted in all biopsy specimens. Topical photochemotherapy induced moderate to excellent repigmentation in 71% of the treated patients. Adverse effects were minimal. CONCLUSION: The results of this investigation suggest that hypopigmentation induced by laser resurfacing may result from a suppression of melanogenesis rather than destruction of area melanocytes. The preliminary data further suggest that hypopigmentation caused by laser resurfacing can be effectively treated by topical photochemotherapy.

Acne Vulgaris↗

PubMed1992

Perifollicular hypopigmentation. A cause of variegate pigmentation and irregular border in melanocytic nevi.

BACKGROUND AND DESIGN: Clinical and histologic features of perifollicular hypopigmentation within melanocytic nevi are described. RESULTS: Perifollicular hypopigmentation was observed in congenital and acquired melanocytic nevi. When the area of hypopigmentation was found within the nevus, it was circular. When the hypopigmentation was located at the edge of the nevus, however, it formed a half circle that resulted in a notch in the outline of the lesion. The phenomenon occurred in nevi with terminal hairs as well as nevi with vellus hairs. In biopsy specimens from 15 melanocytic nevi, one or more of the following findings were observed around hair follicles when compared with the remainder of the nevus: decrease in the number of junctional melanocytes as nests and solitary units (n = 12), decrease in pigment within keratinocytes (n = 14), decrease in the number of melanocytes in the papillary dermis (n = 6), and decrease in the number of melanophages (n = 6). CONCLUSIONS: Perifollicular hypopigmentation is a cause of variegate pigmentation and irregular border in melanocytic nevi.

Adult↗

PubMed1997

Hypopigmentation in the Prader-Willi syndrome correlates with P gene deletion but not with haplotype of the hemizygous P allele.

The Prader-Willi syndrome (PWS) usually results from a paternal deletion of 15q11-q13 or maternal disomy for chromosome 15. Reduced pigmentation of skin, hair, and eyes is common in PWS and was suggested previously to be associated with the 15q11-q13 deletion. The P gene, located in this same region, is associated with OCA2, an autosomal recessive disorder that is the most frequent form of tyrosinase-positive oculocutaneous albinism. We studied 28 individuals with PWS and found that hemizygosity for the P gene was significantly correlated with the occurrence of hypopigmentation among PWS patients. However, we found little or no relationship between the occurrence of hypopigmentation and the polymorphism haplotype of the intact P allele. Thus, our results indicate that hypopigmentation is likely the result of deletion of the P gene in the context of PWS but do not support the linked hypothesis that hypopigmentation results from hemizygosity for variant P alleles with reduced function.

Alleles↗

PubMed2004

Cutaneous hypopigmentation following a posterior sub-tenon triamcinolone injection.

PURPOSE: To report a case of cutaneous skin hypopigmentation following a posterior sub-Tenon triamcinolone acetonide injection for uveitis. DESIGN: Observational case report. METHODS: A 28-year-old African American female with Adamantiades-Behcet disease and panuveitis was administered a posterior sub-Tenon injection of triamcinolone acetonide and developed cutaneous hypopigmentation. RESULTS: The patient developed skin hypopigmentation of the upper eyelid adjacent to the site of the sub-Tenon injection. CONCLUSION: Injection of corticosteroids into the sub-Tenon space can cause hypopigmentation of the adjacent tissues, especially in heavily pigmented individuals.

Adult↗

PubMed2006

Pilot trial of 1% pimecrolimus cream in the treatment of seborrheic dermatitis in African American adults with associated hypopigmentation.

BACKGROUND: African Americans with seborrheic dermatitis may manifest associated hypopigmenation. Corticosteroids and antifungals are often used for treatment, yet chronic use of corticosteroids may be associated with skin atrophy, increased intraocular pressure, or further hypopigmenation. Pimecrolimus has been used successfully in a few patients with seborrheic dermatitis. OBJECTIVES: This open-label, pilot trial assessed the efficacy and tolerability of pimecrolimus in the treatment of seborrheic dermatitis in African Americans with hypopigmentation. METHODS: Five African American adults with seborrheic dermatitis used a thin layer of pimecrolimus on the involved areas twice per day for 16 weeks. Clinical measures of improvement included erythema, scaling, and pruritus. Hypopigmentation was measured objectively using a mexameter. RESULTS: All participants noted a marked decrease in the severity of their condition. An improvement in hypopigmentation was also noted. For all indicators, the magnitude of improvement was most marked during the initial 2 weeks of treatment. LIMITATIONS: This was an open-label pilot trial limited to just 6 participants, only 5 of whom completed the study. CONCLUSIONS: Topical pimecrolimus cream may be an excellent alternative therapeutic modality for treating seborrheic dermatitis in African Americans, particularly in those with associated hypopigmentation.

Adult↗

PubMed1997

Postinflammatory hypopigmentation and hyperpigmentation.

Postinflammatory hypopigmentation and hyperpigmentation are frequently encountered problems and represent the sequelae of various cutaneous disorders as well as therapeutic interventions. However, the underlying mechanisms and the variability individuals show for developing hypopigmentation or hyperpigmentation are not well understood. The authors propose an inherited individual chromatic tendency that is based on "weak" or "strong" melanocytes and their tendency to respond to trauma or inflammation with either hypopigmentation or hyperpigmentation. Clinical examples and management of both hypopigmentation and hyperpigmentation are discussed.

Dermatitis↗

PubMed2003

Long-lasting hypopigmentation induced by long-pulsed alexandrite laser photo-epilation.

BACKGROUND: Long-lasting hypopigmentation induced by laser hair removal systems has been reported. OBJECTIVE. : To evaluate clinical aspects of a female Caucasian that developed long-lasting hypopigmentation in the arms and forearms after photodepilation with a long-pulsed alexandrite laser. METHOD: A 29-year-old Caucasian female (phototype III) with localized hypertrichosis in the upper limbs was submitted to long-pulsed alexandrite laser-assisted hair removal. One treatment session was done with these laser parameters: a pulse width of 2 ms, a spot of 7 mm, and fluence energy of 18 J/cm2. RESULTS: The patient developed long-lasting hypopigmentation (more than 6 months) in the arms and forearms after a single treatment session of photodepilation. CONCLUSION: Long-pulsed alexandrite laser may induce reversible melanocyte suppression and long-lasting hypopigmentation.

Adult↗

PubMed2006

The zebrafish mutant vps18 as a model for vesicle-traffic related hypopigmentation diseases.

Hypopigmentation is a characteristic of several diseases associated with vesicle traffic defects, like the Hermansky-Pudlak, Chediak-Higashi, and Griscelli syndromes. Hypopigmentation is also a characteristic of the zebrafish mutant vps18(hi2499A), which is affected in the gene vps18, a component of the homotypic fusion and protein sorting complex that is involved in tethering during vesicular traffic. Vps18, as part of this complex, participates in the formation of early endosomes, late endosomes, and lysosomes. Here, we show that Vps18 is also involved in the formation of melanosomes. In the zebrafish mutant vps18(hi2499A) the retroviral insertion located at exon 4 of vps18, leads to the formation of two abnormal splicing variants lacking the coding sequence for the clathrin repeat and the RING finger conserved domains. A deficiency of Vps18 in zebrafish larvae results in hepatomegaly and skin hypopigmentation. We also observed a drastic reduction in the number of melanosomes in the eye's retinal pigmented epithelium along with the accumulation of immature melanosomes. A significant reduction in the vps18(hi2499A) larvae visual system capacity was found using the optokinetic response assay. We propose that the insertional mutant vps18(hi2499A) can be used as a model for studying hypopigmentation diseases in which vesicle traffic problems exist.

Adaptation, Biological↗

PubMed2000

Spatially restricted hypopigmentation associated with an Ednrbs-modifying locus on mouse chromosome 10.

We have used the varied expressivity of white spotting (hypopigmentation) observed in intrasubspecific crosses of Ednrb(s) mice (Mayer Ednrb(s)/Ednrb(s) and C3HeB/FeJ Ednrb(s)/Ednrb(s)) to analyze the effects of modifier loci on the patterning of hypopigmentation. We have confirmed that an Ednrb(s) modifier locus is present on mouse Chromosome 10. This locus is now termed k10, using the nomenclature established by Dunn in 1920. The k10(Mayer) allele is a recessive modifier that accounts for almost all of the genetic variance of dorsal hypopigmentation. Using intercross analyses we identified a second allele of this locus or a closely linked gene termed k10(C3H). The k10(C3H) allele is semidominant and is associated with the penetrance and expressivity of a white forelock phenotype similar to that seen in Waardenburg syndrome. Molecular linkage analysis was used to determine that the k10 critical interval was flanked by D10Mit10 and D10Mit162/D10Mit122 and cosegregates with mast cell growth factor (Mgf). Complementation crosses with a Mgf(Sl) allele (a 3-5-cM deletion) confirm the semidominant white forelock feature of the k10(C3H) allele and the dorsal spotting feature of K10(Mayer) allele. MgF was assessed as a candidate gene for k10(Mayer) and k10(C3H) by sequence and genomic analyses. No molecular differences were observed between the Mayer and C57BL/6J alleles of MgF; however, extensive genomic differences were observed between the C3HeB/FeJ and C57BL/6J alleles. This suggests that alteration of MgF expression in C3H mice may account for the k10(C3H) action on white forelock hypopigmentation. Crosses of Ednrb(s) with Kit(WJ-2) (the receptor for MGF)-deficient mice confirmed the hypothesis that synergistic interaction between the Endothelin and MGF signaling pathways regulates proper neural crest-derived melanocyte development in vivo.

Alleles↗

PubMed1994

Vitiligo- and melanoma-associated hypopigmentation: a similar appearance but a different mechanism.

The significance of the association between the appearance of hypopigmentation in patients with melanoma and the prognosis is still not clear. It was postulated that, in melanoma, an immune response is responsible for the destruction of the malignant as well as the normal pigmented cells, and that the eventual development of vitiligo-like patches in melanoma patients improves their prognosis. We studied the level of anti-melanoma antibodies in the sera of patients with melanoma with hypopigmentation and compared it to the titer in patients with melanoma only, to the titer of patients with vitiligo, and to that of healthy subjects. Only IgG-type antibodies were found in the sera of patients with vitiligo, with melanoma, or with melanoma with hypopigmentation. No significant differences in the titer of anti-melanoma antibodies could be found between the patients with melanoma when subgrouped according to the initial stage and the status of the disease at the time when the test was carried out. Statistically significantly (P < 0.001) higher titers of antibodies were detected in the sera of patients with vitiligo in comparison to the lower titers in the other groups. Our results point to a similar immunobiological status, which probably does not give any advantage to patients with melanoma with hypopigmentation compared to patients without it. The appearance of hypopigmentary plaques in melanoma patients should be regarded, in our opinion, as a concomitant immunological phenomenon of the disease.

Adolescent↗

PubMed1987

Prognostic significance of hypopigmentation in malignant melanoma.

It has been suggested that the presence of cutaneous hypopigmentation favorably influences the prognosis of patients with malignant melanoma (MM). To examine this possibility, we have compared the actual with the predicted survival of 46 patients with MM and hypopigmentation who were among 1130 patients with MM entered in a long-term prospective study of MM at the New York University Medical Center. The actual average five-year survival rate of the patients with MM and hypopigmentation (86.3%) was significantly better than predicted (74.8%) on the basis of the risk factors present in each patient at the time of entry into the study. The findings suggest that hypopigmentation is a factor that beneficially influences the prognosis of MM, and that the mechanisms that inhibit or destroy normal melanocytes in patients with MM may also slow the growth of this cancer.

Humans↗

PubMed1998

An unusual hypopigmentation in occupational dermatology: presentation of a case and review of the literature.

Contact dermatitis to cooling lubricants is commonly encountered in occupational dermatology, but it rarely induces pigmentary skin changes. It is sometimes difficult to differentiate between toxic leukoderma and postinflammatory hypopigmentation when examining a depigmentation. A differential diagnosis is described in the case of a 31-year-old metal worker, spending most of his time on a computer-numerically controlled machine, who presented with cumulative irritant hand dermatitis and secondary hypopigmentation. Patch tests gave negative reactions to the European standard series, the disinfection and preservative series, the base preparation and emollient series, the metal series, the mechanical worker series as well as to the cooling lubricant itself. Atopy screening was positive for a variety of pollens. Based on biopsy findings, toxic leukoderma could be diagnosed even though none of the known melanotoxic compounds could be identified in his work environment. The patient was advised to avoid further contact with the regular composed cooling lubricant and the contact eczema improved dramatically, whereas the condition of hypopigmentation got better slowly within weeks under PUVA therapy.

Adult↗

PubMed2003

Hypopigmentation in an African patient treated with imatinib mesylate: a case report.

Imatinib mesylate (STI 571, Gleevec) is a potent bcr-abl tyrosine kinase inhibitor. It also inhibits c-kit tyrosine kinase. Imatinib mesylate is active in the treatment of cronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST). It is considered by some authorities to be the standard of care in newly diagnosed CML as well as patients in chronic phase who do not have a related match. C-kit and its ligand stem-cell factor regulate melanocyte development and survival. Hypopigmentation in patients receiving imatinib mesylate for CML has been reported recently. In this article, we report a black Nigerian male with GIST, who developed hypopigmentation of distal parts of digits, as well as generalized lightening of skin on the body three months after receiving imatinib mesylate. We believe that this is the first case of hypopigmentation reported in a black patient with GIST.

Aged↗