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At least 19 recordsLinked to original sources
PubMed1987

Reticulate hyperpigmentation distributed in a zosteriform fashion: a new clinical type of hyperpigmentation.

We have recently seen two cases of hyperpigmentation in children, which was reticulate and distributed in a zosteriform fashion. As another two cases of hyperpigmentation of this kind in children have been reported previously, described as reticulate hyperpigmentation distributed in a zosteriform fashion, this gives a total of four cases of hyperpigmentation of this kind reported recently from Japan. These four cases differed from progressive cribriform and zosteriform hyperpigmentation, the condition which these cases resembled most closely, with respect to the age of onset of the hyperpigmentation, which in the four Japanese cases was not confined to a dermatome. Like a variant of incontinentia pigmenti (IP), all four cases showed eosinophilia. But they differed from IP in that there was no inflammatory stage, no pigmentary incontinence detectable on histology, and no evidence that the condition was hereditary. These four cases do not conform completely to any described entities and we suggest that they represent a new clinical entity.

Child, Preschool↗
PubMed1992

Selective cutaneous hyperpigmentation in mice following zidovudine administration.

BACKGROUND AND DESIGN: C57BL/6N mice fed zidovudine in their drinking water develop selective hyperpigmentation of the tails and footpads. Zidovudine-fed and identical control mice were observed and sequential biopsy specimens were obtained. Routine light microscopy, electron microscopy, and image analysis of unstained biopsy specimens were used to evaluate the extent, nature, and amount of cutaneous hyperpigmentation. RESULTS: Beginning at day 14 selective hyperpigmentation of the tails and footpads of the mice was noted. Histologic evaluation revealed a gradual increase in melanin, beginning in the lower levels of the epidermis, with eventual pigmentation of the stratum corneum. Electron microscopy demonstrated a sixfold increase in melanosomes in the tail skin of the zidovudine-fed mice. Using image cytometry, melanin was quantitatively shown to increase, paralleling the clinically apparent hyperpigmentation. The hyperpigmentation was reversible on discontinuation of zidovudine. CONCLUSIONS: This animal model parallels the human in developing reversible and selective hyperpigmentation on administration of zidovudine. In this model the increased pigmentation is due to increased numbers of melanosomes within epidermal keratinocytes. Image cytometry may be useful in semiquantitatively studying the pathogenesis of various disorders of hyperpigmentation.

Animals↗
PubMed1997

Fluorescence photography in the evaluation of hyperpigmentation in photodamaged skin.

BACKGROUND: Treatment-related changes in hyperpigmentation are difficult to quantify with visible light photography, especially when the changes are subtle. OBJECTIVE: Our purpose was to determine the utility and reliability of fluorescence photography to measure changes in mottled and diffuse hyperpigmentation. METHODS: Thirty-two subjects, with mildly to moderately photodamaged skin, completed a 36-week, double-blind, vehicle-controlled study of tretinoin cream 0.025%. Clinical evaluation of hyperpigmentation as well as standard flash photographs and fluorescence photographs were obtained at baseline and week 36. RESULTS: The fluorescence photographs were evaluated blindly and yielded macule counts that decreased significantly from baseline in tretinoin-treated subjects compared with vehicle-treated subjects (31% vs 11% decrease; p = 0.02). Diffuse hyperpigmentation, as evaluated from the fluorescence photographs, decreased 16% from baseline for tretinoin-treated subjects and increased 5% for vehicle-treated subjects (p < 0.01). No significant differences in mottled or diffuse hyperpigmentation were observed between groups through clinical evaluation. CONCLUSION: Fluorescence photography is a noninvasive method that is sensitive in the evaluation and quantification of distribution and changes of mottled and diffuse hyperpigmentation.

Adult↗
PubMed1993

Postsclerotherapy hyperpigmentations. Chromated glycerin as a screen for patients at risk (a retrospective study).

BACKGROUND: Chromated glycerin reportedly causes less post-sclerotherapy hyperpigmentations than polidocanol. OBJECTIVE: To investigate whether replacing polidocanol with chromated glycerin lowers the incidence of postsclerotherapy hyperpigmentation. METHODS: Retrospective study of 134 records of patients treated for leg telangiectasia. At the first session only chromated glycerin was injected. From the second session on treatment was continued--according to the response--either with chromated glycerin or with the stronger polidocanol. RESULTS: Chromated glycerin caused strong sclero-inflammatory reaction in 27% of patients, who were therefore treated with chromated glycerin only; in the remaining 73%, chromated glycerin was replaced with polidocanol, because of mild (or absent) reaction. Postsclerotherapy hyperpigmentation developed in three patients, all treated with chromated glycerin, while no postsclerotherapy hyperpigmentation developed in the patients treated with polidocanol. CONCLUSIONS: Single "trial" session with chromated glycerin permits to select patients at risk of developing postsclerotherapy hyperpigmentation, and treat these with a milder sclerosant. This approach also reduced the incidence of early postsclerotherapy hyperpigmentation compared with similar series treated with polidocanol alone.

Adolescent↗
PubMed1993

[Hyperpigmentation in primary adrenal cortex insufficiency: Addison disease].

Diffuse hyperpigmentation of the skin may develop without preceding inflammatory skin disease or be associated with various inflammatory disorders. The differential diagnosis of the diffuse hyperpigmentation is complex and difficult. We present a 36-year-old woman with diffuse hyperpigmentation caused by adrenal insufficiency, with special reference to the diagnosis and differential diagnosis of hyperpigmentation associated with endocrine disorders. In addition, metabolic, toxic, nutritional and internal factors and the skin-associated diseases leading to hyperpigmentation are categorized. A classification of diffuse hyperpigmentation is presented.

Addison Disease↗
PubMed1996

Localized cisplatin hyperpigmentation induced by pressure. A case report.

BACKGROUND: The spectrum of side effects induced by chemotherapy includes skin hyperpigmentation. This is prone to occur following treatment with alkylating agents and doxorubicin. More recently, hyperpigmentation was discovered in patients treated exclusively with intra-arterial cisplatin and was likely to develop over the dorsal surfaces of the hands and feet, elbows and knees, and operative incisions (trauma). METHODS: We followed the clinical course of a patient with osteosarcoma treated with intravenous (i.v.) cisplatin, doxorubicin, and high-dose methotrexate. RESULTS: Following two courses of chemotherapy, hyperpigmentation developed along the sides of the thorax juxtaposed to the rubber shoulder pads of the patient's crutches. It appeared that the pigmentary change was due to localized pressure in the skin of the patient exposed to i.v. cisplatin. CONCLUSIONS: Factors associated with skin hyperpigmentation as a complication of chemotherapy are discussed. We believe that cisplatin was the major contributing factor. The mechanism for cisplatin-induced hyperpigmentation is undetermined. However, it has occurred in patients treated exclusively with intra-arterial cisplatin and can possibly be attributed to an effect on the melanocytes. / This is supported by experiences in which cisplatin extravasated into the tissues and resulted in a similar phenomenon. Reasons for excluding doxorubicin and methotrexate as causative agents are presented.

Adolescent↗
PubMed1995

Cutaneous necrosis, telangiectatic matting, and hyperpigmentation following sclerotherapy. Etiology, prevention, and treatment.

BACKGROUND: Telangiectatic matting and hyperpigmentation are some of the most commonly observed side effects of sclerotherapy. Cutaneous necrosis is relatively rare and often of limited sequelae but most commonly related to extravasation of sclerosant. Physicians treating varicosities and telangiectasia by sclerotherapy must be familiar with causes and means for minimization of all three side effects. OBJECTIVE: This review article discusses the proposed etiology, risk factors, approach for minimizing, and suggested treatment for the three side effects of cutaneous necrosis, telangiectatic matting, and hyperpigmentation. RESULTS: Cutaneous necrosis may occur with the injection of any sclerosing agent even under ideal circumstances and does not necessarily represent physician error. When sclerosant extravasation occurs, dilution must occur immediately. Telangiectatic matting is a recognized complication occurring in approximately 15-20% of patients treated by sclerotherapy. Although the exact mechanism of the phenomena remains unknown, reactive inflammatory and/or angiogenic mechanisms are felt to play a role. Patients are advised that telangiectatic matting is usually not permanent and usually resolves spontaneously in 3-12 months. Postsclerosis pigmentation is defined as the appearance of persistent, increased pigmentation running the course of an ectatic blood vessel treated by sclerotherapy. The general incidence of hyperpigmentation ranges from 10 to 30%. Although hyperpigmentation may persist for months, its presence rarely deters patients from continuing treatment. Spontaneous resolution occurs in 70% at 6 months with 99% resolution occurring within 1 year. CONCLUSIONS: With understanding the etiology, risk factors, and ways to minimize these side effects our goal is to reduce their incidence. Attempting prevention may ultimately be the most effective means of treatment. Dermatol Surg 1995;21:19-29. LEARNING OBJECTIVES: After studying the following article, participant should be able to: 1. Understand the definition and potential causes of cutaneous necrosis, telangiectatic matting, and hyperpigmentation following sclerotherapy. 2. Advise patients prior to treatment on the common risks involved in sclerotherapy and to advise them on the relative incidence. 3. Understand the concept of minimal sclerosant concentration and how it can help the physician to choose sclerosing solution concentrations to minimize risks.

Dermatology↗
PubMed1988

Periungual hyperpigmentation mimicking Hutchinson's sign associated with minocycline administration.

An assessment of the occurrence rate of periungual hyperpigmentation with subungual melanoma (Hutchinson's sign) and periungual hyperpigmentation with other subungual lesions has not been published, although periungual hyperpigmentation with a pigmented streak or other pigmented lesion of the nail has been considered pathognomonic for subungual melanoma for a century. We report a case of minocycline hyperpigmentation presenting as a longitudinal pigmented streak of the nail associated with periungual hyperpigmentation. These pigmentary changes could be mistaken for Hutchinson's sign.

Adult↗
PubMed1999

Imipramine-induced hyperpigmentation: four cases and a review of the literature.

BACKGROUND: Hyperpigmentation is a side effect of several medications, including amiodarone, bleomycin, chlorpromazine, and minocycline. OBJECTIVE: The purpose of this study is to describe the clinical and light microscopic findings in 4 patients with imipramine-induced hyperpigmentation and to better understand its origin. METHODS: All 4 patients underwent a skin biopsy for light microscopy. In 1 patient, a biopsy specimen was obtained for electron microscopy. Tissue from patient 1 was analyzed with a mass spectrophotometer, and energy-dispersive x-ray analysis was performed on tissue from patients 1 and 2. RESULTS: All 4 women had been taking imipramine for at least 2 years. Hyperpigmentation occurred in a photodistribution on the face, arms, and backs of the hands. Light microscopy in all cases demonstrated golden-brown granules in the superficial dermis, which were strongly positive for Fontana-Masson stain. Electron microscopy demonstrated areas of electron-dense inclusion bodies within macrophages, which were distinct from melanosomes. Mass spectrophotometric and energy-dispersive x-ray analysis of the electron-dense bodies showed the presence of sulfur atoms, and no peak corresponding to that expected for imipramine was found. A peak closely corresponding to phaeomelanin, a sulfur-containing compound, was found. CONCLUSION: Hyperpigmentation is a side effect of long-term imipramine use. It may result from the deposition of melanin in an unusual form. The melanin pigment is possibly complexed with a metabolite of imipramine, and does not represent the deposition of imipramine in its native form.

Aged↗
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↗
PubMed1999

Effect of pretreatment on the incidence of hyperpigmentation following cutaneous CO2 laser resurfacing.

BACKGROUND: Transient hyperpigmentation is the most common complication seen following cutaneous carbon dioxide (CO2) laser resurfacing. OBJECTIVE: The purpose of this study was to determine whether the use of a topical skin lightening regimen prior to cutaneous laser resurfacing reduces the incidence of post-laser resurfacing hyperpigmentation. METHODS: One hundred consecutive CO2 laser resurfacing patients (skin types I-III) were randomized to receive preoperative treatment with 10% glycolic acid cream twice daily (n=25), hydroquinone 4% cream qHS and tretinoin 0.025% cream twice daily (n=25) or no pretreatment (n=50, control) for at least 2 weeks. Clinical and photographic assessments were performed prior to laser resurfacing and at 4 and 12 weeks following treatment. RESULTS: There was no significant difference in the incidence of post-CO2 laser resurfacing hyperpigmentation between subjects who received pretreatment with either topical glycolic acid cream or combination tretinoin/hydroquinone creams and those who received no pretreatment regimen. CONCLUSION: It is postulated that reepithelialization after cutaneous laser resurfacing includes follicular melanocytes that have not been affected by topical pretreatment. When instituted as a component of the skin care regimen postoperatively, topical hydroquinone, tretinoin and/or glycolic acid preparations may be helpful in reducing post-laser resurfacing hyperpigmentation.

Administration, Cutaneous↗
PubMed1995

Hyperpigmentation due to calcipotriol (MC 903) plus heliotherapy in psoriatic patients. Three case reports.

Calcipotriol is a synthetic analogue of vitamin D, used in the treatment of psoriasis. Until now no specific sid-effects have been described after combined therapy with calcipotriol and UV. We describe 3 patients, who in the summer of 1993, after a combined treatment of calcipotriol and heliotherapy, developed hyperpigmentation in the site where the ointment had been applied. Hyperpigmentation healed spontaneously in less than 7 months. To the best of our knowledge there are no other reports of this side-effect due to calcipotriol. In our opinion the fact that the 3 patients presented the hyperpigmentation only on the treated lesions and that, in the past, they had not presented similar lesions after exposure to sunlight confirms the relationship between the hyperpigmentation and the combined treatment used.

Adult↗
PubMed1990

Nail and mucocutaneous hyperpigmentation with azidothymidine therapy.

Hyperpigmentation developed in six patients while they were receiving azidothymidine. All demonstrated hyperpigmentation of the nails; hyperpigmentation of the skin (two patients) and oral mucosa (two patients) also developed. The degree of nail pigmentation was related to the intrinsic skin color of the patient. Mucosal hyperpigmentation developed only in dark-skinned blacks. The pigmentation was due to increased melanin in the epidermis and dermis.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Reactive lentiginous hyperpigmentation after cryosurgery for lentigo maligna.

BACKGROUND: Twenty patients treated for lentigo maligna of the face with cryosurgery developed benign lentiginous hyperpigmentation mimicking a recurrence. OBJECTIVE: When cryosurgery is used in the treatment of lentigo maligna, it is important to know whether repigmentation of the scar represents true recurrence or a benign process. METHODS: Twenty patients were treated with cryosurgery for lentigo maligna of the face. Within a follow-up period of 7 to 80 months, frequent clinical observations were made. RESULTS: Lentiginous hyperpigmentation developed within the treatment area in eight patients. Histologic investigation revealed recurrence of lentigo maligna in three and benign hyperpigmentation in five. CONCLUSION: Genetic factors and UV exposure after cryosurgery may favor the development of benign lentiginous hyperpigmentation. Because recurrence of lentigo maligna must be considered, histologic evaluation of repigmentation is mandatory.

Aged↗
PubMed1989

Mechanisms for hyperpigmentation in postinflammatory pigmentation, urticaria pigmentosa and sunburn.

Our in vitro studies demonstrate that normal human epidermal melanocytes become swollen and more dendritic with an increase in amount of immunoreactive tyrosinase when they are cultured for several days with arachidonic acid metabolites, vitamin D3 or histamine. From these data we propose the following possible mechanisms for hyperpigmentations noted at postinflammatory sites and suntanned areas as well as at skin lesions of urticaria pigmentosa. Arachidonic acid metabolites and histamine, which are found in increased amounts in inflammatory skin, are thought to play a key role in the induction of postinflammatory hyperpigmentation. In sunburnt skin the increased proinflammatory mediators, particularly arachidonic acid metabolites, are also thought to stimulate melanocytes in the production of hyperpigmentation. Thus tanning after sun exposure may be induced not only by the effect of vitamin D3 and direct UV irradiation on the melanocytes but also by the effect of various arachidonic acid metabolites which are increased in sunburnt skin. Mast cells massively proliferate in the skin lesions of urticaria pigmentosa. Thus hyperpigmentation in the skin lesions of urticaria pigmentosa is quite likely to be induced by the chemical mediators, including histamine and leukotrienes, that are released from these cells.

Arachidonic Acids↗
PubMed1998

[Minocycline-induced hyperpigmentation].

A common adverse effect of minocycline therapy is cutaneous pigmentation. We describe two patients who presented with hyperpigmentation caused by minocycline. One patient, aged 54 years, had taken minocycline due to lung silicosis for 3 years before black pigmentation of the face occurred. The other 49 year-old patient developed grey-black hyperpigmentation on both lower legs after a 6-month therapy with minocycline for folliculitis. This patient was treated with the Q-switched ruby laser and the pigmentation resolved in the treated area. The different clinical and histological forms of minocycline-induced hyperpigmentation are discussed.

Administration, Oral↗