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PubMedDate not supplied

Azelaic acid and glycolic acid combination therapy for facial hyperpigmentation in darker-skinned patients: a clinical comparison with hydroquinone.

This multicenter, randomized, double-masked, parallel-group, 24-week clinical study compared the efficacy of the combination of azelaic acid 20% cream and glycolic acid 15% or 20% lotion with hydroquinone 4% in the treatment of facial hyperpigmentation in darker-skinned patients. At week 24, overall improvement and reduction in lesion area, pigmentary intensity, and disease severity were comparable in the two treatment groups. At some visits, patients treated with an azelaic/glycolic acid combination had slightly greater levels of peeling, burning, stinging, or dryness than did patients treated with hydroquinone, although scores for cutaneous signs and symptoms were always low. The present study demonstrated that the combination of azelaic acid 20% cream and glycolic acid 15% or 20% lotion was as effective as hydroquinone 4% cream in the treatment of hyperpigmentation in darker-skinned patients, with only a slightly higher rate of mild local irritation. These findings suggest that the addition of glycolic acid to azelaic acid treatment for hyperpigmentation is an appropriate alternative in selected darker-skinned patients.

Dermatologic Agents↗
PubMed2000

Disorders of hyperpigmentation.

Hyperpigmentation is a common disorder of the skin, particularly in brown-skinned patients. Melasma is a common cause of facial hyperpigmentation and can be resistant to treatment. A combination of topical creams and gels, chemical peels, and sunscreens may be necessary for significant improvement. Erythema dyschromicum perstans is a dermal pigmentation seen on the trunk and proximal extremities, most commonly presenting in dark-skinned Hispanics. Drug-induced and postinflammatory hyperpigmentation may last for many months after the offending drug or dermatitis has been eliminated. These disorders, including their management, is reviewed in this article.

Erythema↗
PubMed2003

Hyperpigmentation during interferon-alpha therapy for chronic hepatitis C virus infection.

Many types of skin disorders concomitantly occur with hepatitis C virus infection. These skin lesions may be induced or worsened during antiviral therapy with interferon-alpha (IFN). To our knowledge, hyperpigmentation of the skin--and especially of the tongue--has not been reported so far. We describe two dark-skinned patients who developed hyperpigmented skin and tongue lesions during combination therapy with IFN and ribavirin. Immunohistochemical analysis of tongue biopsies confirmed the suspicion of melanin deposits in these areas of hyperpigmentation. We hypothesize that during interferon therapy, melanocytes may produce more melanin pigment in the presence of alpha-melanocyte stimulating hormone and sufficient amounts of tyrosine, leading to melanin deposits and clinical hyperpigmentation.

Antiviral Agents↗
PubMed1999

Hyperpigmentation caused by hyperthyroidism: differences from the pigmentation of Addison's disease.

Two cases of hyperthyroidism with hyperpigmentation are presented. In both cases, hyperpigmentation was seen on the lower extremities, most strikingly on the shins, backs of the feet and the nail bed. Histology of the pigmented skin showed basal melanosis and heavy deposition of haemosiderin around dermal capillaries and sweat glands. Treatment with mercazol in both cases resulted in no significant waning of pigmentation. Distribution of hyperpigmentation, haemosiderin deposition and poor response to the treatment may be characteristic features of the pigmentation caused by hyperthyroidism, and may represent differences from the pigmentation seen in Addison's disease.

Addison Disease↗
PubMed2003

Microabrasion versus microabrasion followed by 15% trichloroacetic acid for treatment of cutaneous hyperpigmentations in adult females.

BACKGROUND: Cutaneous hyperpigmentations are common skin disorders that are often refractory to currently available treatments. OBJECTIVE: To evaluate the efficacy of microabrasion alone or microabrasion with 15% trichloroacetic acid (TCA) for treatment of cutaneous hyperpigmentations. METHODS: Twenty female patients were treated with microabrasion alone every 2 weeks (group 1), and 20 female patients were treated with microabrasion and application of 15% TCA every 3 weeks (group 2). All patients underwent up to eight treatments. The overall duration of treatment ranged from 2 to 4 months. RESULTS: In group 1, a complete remission was observed in 8 of 20 cases (40%), partial remission in 10 of 20 cases (50%), and no remission in 2 of 20 cases (10%). In group 2, a complete remission was observed in 10 of 20 cases (50%), a partial remission in 8 of 20 cases (40%), and no remission in 2 of 20 cases (10%). No unexpected or serious side effects were observed in either group. CONCLUSIONS: Microabrasion alone or microabrasion with 15% TCA is an effective, well-tolerated treatment for cutaneous hyperpigmentations.

Adolescent↗
PubMed2002

Cutaneous hyperpigmentation induced by doxycycline: histochemical and ultrastructural examination, laser microprobe mass analysis, and cathodoluminescence.

Skin hyperpigmentation induced by minocycline is a well-recognized side effect of minocycline but has rarely been reported for other tetracyclines. Based on a previously reported unusual case of chronic doxycycline abuse in a psychotic patient, we have investigated the nature of the observed pigment changes in the same patient. Histopathologic investigation of lesional skin by light microscopy disclosed hyperpigmentation of the basal keratinocytes and pigment-laden histiocytes in the dermis and subcutaneous fat. Only the pigment in the histiocytes of the upper dermis was reactive for Fontana Masson stain and could be bleached by hydrogen peroxide. The other histiocytes contained iron and calcium deposits as shown by von Kossa and Perls staining as well as by laser microprobe mass analysis. Ultrastructurally, these histiocytes contained amorphous material within the cytoplasm and stored in lysosomal structures. Comparative cathodoluminescence disclosed the presence of doxycycline in affected skin by means of overlapping emission spectra between the patient's skin and pure doxycycline. Taken together, the histomorphologic and ultrastructural changes induced by doxycycline shared several features with cutaneous hyperpigmentation caused by minocycline. Our biophysical findings further suggest a direct deposition of doxycycline, probably chelated with iron and/or calcium, within the lesional skin. Based on the presented unique case and the reviewed literature, only suprapharmacologic doses of doxycycline may be sufficient to cause such pigment changes.

Adult↗
PubMed2000

Experience with a strong bleaching treatment for skin hyperpigmentation in Orientals.

Although a variety of topical treatments have been used for skin hyperpigmentation, the effectiveness of each varies after prolonged treatment. In this study, 136 Oriental patients who were followed up for more than 12 weeks were analyzed. The treatment protocol was composed of two steps: bleaching (2 to 6 weeks) and healing (2 to 6 weeks); 0.1% to 0.4% all-trans retinoic acid aqueous gel was originally prepared and applied concomitantly with hydroquinone-lactic acid ointment for bleaching. After obtaining sufficient improvement of the hyperpigmentation, a corticosteroid was applied topically with hydroquinone and ascorbic acid for healing. Improvement was evaluated with a narrow-band reflectance spectrophotometer. The results were successful in more than 80 percent of cases of senile lentigines and postinflammatory hyperpigmentations, especially on the face. Sixty percent of cases of nevus spilus were also successfully treated. Although the transient adverse effects of this treatment may be more severe than conventional treatment, this strong bleaching protocol improves a variety of hyperpigmented lesions, including nevus spilus, with a higher success rate and a shorter treatment period than conventional protocols.

Administration, Topical↗
PubMed1994

Minocycline hydrochloride hyperpigmentation complicating treatment of pyoderma gangrenosum.

Minocycline-associated hyperpigmentation is an uncommon side effect. We report the case of a patient with pyoderma gangrenosum successfully treated with oral minocycline but complicated by marked hyperpigmentation in his pyoderma gangrenosum and acne scars. One of the clinical forms of minocycline hyperpigmentation includes dark-blue or black macules in depressed acne scars or other sites of skin inflammation; this pattern seems to be independent of the total cumulative dose and the skin process.

Adult↗
PubMed1994

Progressive hyperpigmentation: case report with a clinical, histological, and ultrastructural investigation.

A clinical, histological and ultrastructural study of a 38-year-old woman with generalized progressive hyperpigmentation is reported. Hyperpigmentation started in early infancy, progressed during childhood and has increased to a dark bronze-brown color with 'mottling' in the last 8 years. Histology and electron microscopy revealed epidermal hypermelanosis and 'negroid' distribution of melanosomes in keratinocytes. In our family, autosomal dominant phenotype transmission with 'variable expression' is suggested. The literature on the entity has been reviewed. This case is another rare example of familial progressive hyperpigmentation.

Adult↗
PubMed2004

Optimal management of recalcitrant disorders of hyperpigmentation in dark-skinned patients.

Alterations in skin pigmentation may often have a dramatic expression in individuals with a dark skin complexion and can be a source of significant emotional distress in these individuals. Hyperpigmented disorders such as melanosis (melasma), post-inflammatory hyperpigmentation, drug-induced hyperpigmentation, and erythema dyschromicum perstans tend to have a prolonged course and, in many cases, are refractory to treatment, further contributing to the psychological impairment of the affected patients. Melanosis, is a common form of facial pigmentation attributable to sunlight and hormonal factors. A range of treatment modalities, such as depigmenting agents, topical retinoids, and chemical peels in conjunction with rigorous sun protection, can improve the melanosis but the condition usually recurs. Combination regimens, including frequent applications of superficial- and medium-depth chemical peels, appear to be particularly effective and well tolerated in dark-skinned patients with melanosis. Post-inflammatory hyperpigmentation is the result of excess pigment deposition following an inflammatory skin disorder. Topical tretinoin, hydroquinone, azelaic acid, kojic acid, and glycolic acid peels have been employed with variable degrees of success. Drug-induced pigmentation is a frequent cause of acquired hypermelanosis, its clinical expression depending on the triggering molecule and the underlying pathogenetic mechanism. Identifying and discontinuing the offending agent is the main approach in this condition, although, recent reports have demonstrated the efficacy of Q-switched lasers in accelerating the pigment removal. Erythema dischromicum perstans is a characteristic dermal pigmentation occurring mainly in dark-skinned individuals. Immunomodulating agents, such as clofazimine and dapsone have been shown to lighten this disorder, although, the exact mode of action is not clear.

Humans↗
PubMedDate not supplied

[Cutaneous T-cell lymphoma, cutaneous hyperpigmentation and paraneoplastic pemphigus].

BACKGROUND: Paraneoplastic pemphigus is an autoimmune mucocutaneous disease usually associated with neoplasia as lymphoid proliferations. We report the original case of a patient who had developed a mycosis fongoide preceded by a paraneoplastic pemphigus. To our knowledge, this association has never been reported before. Cutaneous manifestations of mycosis fongoide as pigmentary change are known. This mycosis fongoide was particular in its progressive cutaneous hyperpigmentation. CASE REPORT: A 70-year-old male patient developed a mycosis fongoide with CD30 positive cells in the dermis several months after the diagnosis of a paraneoplastic pemphigus. Simultaneously, a cutaneous hyperpigmentation was predominantly noticed on photo-exposed areas, which improved after chemotherapy. DISCUSSION: Paraneoplastic pemphigus may precede the cancer, as is shown by our present case. This paraneoplastic pemphigus is singular because of the lack of oral erosions, patient's prolonged survival and its association with a mycosis fongoide. The diagnosis of mycosis fongoide with CD30 + cells was finally established together with its relationship to the cutaneous hyperpigmentation. Indeed, a few cases of pigmentary changes in mycosis fongoide have already been reported. The pathogenesis is still unknown, but the role of mast cell and stem cell factor in hyperpigmented mycosis fongoide has been proposed.

Aged↗
PubMed2002

Capecitabine induced cutaneous hyperpigmentation: report of a case.

We report an unusual case of cutaneous and mucosal hyperpigmentation in a thirty-six year old African American woman who was receiving capecitabine chemotherapy for Stage IV breast carcinoma. Possible etiologies for the hyperpigmentation are discussed. To our knowledge, this is the first reported case of capecitabine associated cutaneous hyperpigmentation.

Adult↗
PubMed2004

Amlodipine associated hyperpigmentation.

Amlodipine is a potent peripheral and coronary vasodilator with high selectivity for vascular smooth muscle, and is widely used in mild to moderate hypertension, chronic stable angina and vasospastic angina. Its most prevalent side effects are peripheral edema, flushing and headache. Cutaneous adverse reactions associated with amlodipine have been rarely reported. Herein, a male patient is described to develop oral mucosal and cutaneous hyperpigmentation one year after starting amlodipine, which became more noticeable with time. Although cutaneous hyperpigmentation was most prominent on the photoexposed areas, there was no history of previous photosensitivity, pruritus or flushing. To our knowledge, no case of oral and cutaneous hyperpigmentation associated with amlodipine has been formally reported up to date.

Amlodipine↗
PubMedDate not supplied

Topical agents used in the management of hyperpigmentation.

Disorders of hyperpigmentation are difficult to treat, particularly in dark-skinned individuals. The goal is to reduce the hyperpigmentation without causing undesirable hypopigmentation or irritation in the surrounding normally pigmented skin. The psychosocial impact caused by these disorders must be considered. Although there are many effective therapeutic modalities available, there are potentially significant side-effects associated with treatment. The most commonly used treatment is topical hydroquinone. There are other phenolic agents, such as N-acetyl-4-cystaminylphenol (NCAP), that are currently being studied and developed. The non-phenolic agents, which include tretinoin, adapalene, topical corticosteroids, azelaic acid, arbutin, kojic acid, and licorice extract, are also used for hyperpigmentation disorders.

Administration, Topical↗
PubMedDate not supplied

Reticulate Hyperpigmentation secondary to 5-fluorouracil and idarubicin.

Although cutaneous reactions from antineoplastic therapy are common, a reticulate pattern of hyperpigmentation has not been frequently reported in the literature. We report 2 cases of reticulate hyperpigmentation associated with cancer chemotherapy with 5-fluorouracil and idarubicin. These 2 cases serve to raise awareness of this particular pattern of hyperpigmentation as a potential side effect of chemotherapeutic regimens.

Antibiotics, Antineoplastic↗
PubMedDate not supplied

Linkage of a locus determining familial progressive hyperpigmentation (FPH) to chromosome 19p13.1-pter in a Chinese family.

Familial progressive hyperpigmentation (FPH) is a rare autosomal dominantly inherited disorder characterized by patches of hyperpigmentation in the skin which are present at birth or in early infancy and increase in size and number with age. Although previous studies showed that FPH is a monogenic trait, the genetic basis for this disease is unknown. Using a genome screening with 182 STR markers from autosomes in a three-generation Chinese family with 17 members, including 6 affected individuals, we identified a locus linked to chromosome 19p13.1-pter responsible for FPH, spanning 45.48 cM between D19S593 and 19pter. Interestingly, this region harbors the LKB1 gene, in which germline mutations were shown to be associated with Peutz-Jeghers Syndrome (PJS). PJS and FPH share the disorder of hyperpigmentation, the fine mapping of the FPH gene is expected to lead to a better understanding of the etiology for both FPH and PJS. The linkage of FPH locus to human chromosome 19p13.1-pter provides a genetic basis for further fine mapping.

China↗
PubMed1996

Analysis of 54 cases of hypopigmentation and hyperpigmentation along the lines of Blaschko.

OBJECTIVE: To define the spectrum of disease in cases of hypopigmentation and hyperpigmentation along the lines of Blaschko more accurately. Pigmentary anomalies along the lines of Blaschko, including hypomelanosis of Ito, linear and whorled nevoid hypermelanosis, and nevus depigmentosus, can be associated with notable abnormal systemic features. We believe that the incidence of associated abnormal features described in previous studies is exaggerated owing to referral and reporting bias. DESIGN: Retrospective review of case series. SETTING: An ambulatory, university hospital, pediatric dermatology practice and a large, city hospital, pediatric dermatology clinic. PATIENTS: Fifty-four children referred consecutively over a 5-year period for evaluation of segmental, linear, or swirled hypopigmentation and/or hyperpigmentation along the lines of Blaschko. MAIN OUTCOME MEASURE: Incidence of associated abnormal systemic features. RESULTS: Extracutaneous abnormal features were present in 16 (30%) of 54 children with aberrant pigmentation along the lines of Blaschko: in 9 (33%) of 27 with hypomelanosis of Ito, in 4 (31%) of 13 with linear and whorled nevoid hypermelanosis, in 1 (11%) of 9 with nevus depigmentosus, and in 2 (40%) of 5 with coexistent hypopigmentation and hyperpigmentation. CONCLUSIONS: Pigmentary anomalies along the lines of Blaschko are associated with abnormal systemic features far less often than has been reported previously. These pigmentary anomalies should not be considered distinct syndromes but rather grouped as a heterogeneous collection of disorders indicative of underlying genetic mosaicism. Such a classification will allow better understanding and evaluation of affected persons.

Adolescent↗
PubMed1997

Cutaneous hyperpigmentation and polyglandular autoimmune syndrome type II.

Primary adrenal insufficiency (Addison's disease) may initially present with cutaneous hyperpigmentation. Addison's disease, when associated with autoimmune thyroid disease and/or insulin-dependent diabetes mellitus, is referred to as polyglandular autoimmune syndrome type II. We present the case of a patient who initially was diagnosed as having Grave's disease and eventually Addison's disease due to persistent cutaneous hyperpigmentation, fatigue, weight loss, hypotension, hyponatremia, peripheral eosinophilia, and positive results of a synthetic corticotropin stimulation test. Addison's disease, polyglandular autoimmune syndrome type II, and cutaneous hyperpigmentation are reviewed.

Anti-Inflammatory Agents↗