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At least 145 records · Page 8Linked to original sources

Minocycline-induced hyperpigmentation.

A 70-year-old man developed hyperpigmentation of his forearms, hands, fingernails, sclerae, ears, and teeth after 9 years of therapy with minocycline for acne rosacea. Minocycline is widely used in the treatment of acne vulgaris and uncommonly produces the side effect of hyperpigmentation. This effect does not appear to be dose-dependent and usually resolves within months to years after discontinuation of therapy. Discoloration of adult teeth, however, is generally permanent.

Aged↗

The significance of eccentric foci of hyperpigmentation ('small dark dots') within melanocytic nevi. Analysis of 59 cases.

BACKGROUND AND DESIGN: Fifty-nine melanocytic nevi with eccentric foci of hyperpigmentation ("small dark dots") that measured primarily 1 to 2 mm in diameter were prospectively examined to determine the histologic correlates of the dark dots. RESULTS: Forty-one (69%) of the dark dots were due to increased melanin in epidermal melanocytes and/or keratinocytes, usually accompanied by melanophages; of these 41, six (15%) were associated with slight or moderate melanocytic nuclear atypia. Fifteen (25%) of the dark dots were due to increased dermal pigment that was either superficial or deep. Three (5%) of the dark dots were due to melanoma arising within a nevus. CONCLUSIONS: A small percentage of "small dark dots" within melanocytic nevi are due to melanoma. Biopsy specimens of nevi with small dark dots should be sectioned to ensure histologic examination of this focus of hyperpigmentation.

Adolescent↗

Bimatoprost-induced periocular skin hyperpigmentation: histopathological study.

OBJECTIVE: To investigate light microscopic and ultrastructural changes in bimatoprost-induced skin hyperpigmentation. METHODS: Eyelid biopsy specimens from bimatoprost-treated patients and matched controls were examined by light microscopy and transmission electron microscopy. Using an image analyzer, melanin granules were counted on Fontana-Masson-stained sections, and melanosomes were counted on electron micrographs. Immunohistochemical analysis was performed with antibodies against S100 and CD3. Positively labeled cells were counted. RESULTS: By light microscopy, a marked increase in the number of melanin granules was noted in the bimatoprost-treated specimens. Electron microscopy demonstrated dermal melanocytes with prominent rough endoplasmic reticulum and abundant normal-sized melanosomes in different stages of maturation as compared with control specimens. Furthermore, the keratinocytes of the bimatoprost-treated specimens showed abundant mature melanosomes when compared with controls. Also of note, atypical melanocytes were absent in both specimens. The S100-positive melanocytes were comparable in bimatoprost-treated and control specimens. Few CD3- and CD68-positive cells in the bimatoprost-treated specimens were noted in both groups. CONCLUSION: Bimatoprost-induced periocular hyperpigmentation is caused by increased melanogenesis. There was no evidence of melanocyte proliferation or prostaglandin-induced inflammation in the specimens that were examined.

Aged↗

Hypertrophy with hyperpigmentation of the retinal pigment epithelium.

Fifty-two patients (one bilateral) exhibiting hypertrophy with hyperpigmentation of the retinal pigment epithelium (RPE) are described. Visual acuity was not affected, and the patients were asymptomatic. There was no correlation with systemic diseases, family history of eye disease, associated fundus lesions, anterior segment abnormalities, or intraocular pressure. Field defects were rarely demonstrated using standard clinical techniques. There were three characteristic locations and four characteristic pigmentary variations that occurred alone or in any combination. The lesions were gray, black, or brown. The clinical characteristics and histopathology suggest that hypertrophy with hyperpigmentation of the RPE and congenital grouped pigmentation are different expressions of a similar condition, with the former being focal and the latter multifocal.

Adolescent↗

Novel autosomal recessive progressive hyperpigmentation syndrome.

We present a family of Iraqui origin with three siblings affected by a novel type of progressive hyperpigmentation syndrome. The generalized initially diffuse, later disseminated hyperpigmentation started in early infancy and increased during childhood. It also affected palms and soles, and the face but spared the cheeks. Additional features were dry, itchy and sunlight sensitive skin, dystrophy of toe nails, hair loss, and myopia, but normal sweat glands. Light and electron microscopy showed signs of pigment incontinence and compound melanosomes as well as fibrillar bodies. The occurrence of this entity in affected siblings from a consanguineous mating suggests autosomal recessive inheritance. Extensive review of the literature showed no previous report with this distinct combination of clinical and microscopic findings.

Adolescent↗

Diagnosis of lung carcinoid with cutaneous hyperpigmentation eight years after bilateral adrenalectomy.

A 26-yr-old male was submitted to bilateral adrenalectomy in 1977 for Cushing's syndrome. Some months later he developed intense skin hyperpigmentation together with increased ACTH levels (149 to 4000 ng/l). The sellar region was always normal in X-ray studies. In April 1985, when the patient complained of chest pain, a chest x-ray showed a polycyclic mass in the upper left lobe of the lung. ACTH ranged from 20,000 to 100,000 ng/l, with no response to CRF or cyproheptadine administration. Urinary 5-OH-indolacetic acid was negative. Thoracotomy was performed in July 1985 with resection of two intrapulmonary masses. Histologic study demonstrated a carcinoid tumor, with positive neuron-specific enolase and ACTH immunochemical stain. ACTH concentration in tumoral tissue was 91 pg/g tissue. After surgery ACTH fell dramatically to 37 ng/l, and has remained at this level since then, associated with resolution of the skin hyperpigmentation.

Adrenalectomy↗

Oral hyperpigmentation in HIV-infected patients.

Six cases of oral hyperpigmentation in HIV-infected patients are reported. While in two patients the lesions could be related to systemic clofazimine or ketoconazole therapy, in the other patients the cause remained unknown. Clinically, the pigmentations were characterized by a sudden onset and the appearance of well-defined, brown-black macules in the buccal mucosa, the gingiva, the hard palate, or the lateral borders of the tongue. In one patient, longitudinal hyperpigmented striae were observed on all fingernails and toenails. Histologically, hyperpigmentations associated with systemic medication revealed accumulation of melanin in phagocytes and extracellularly within the connective tissue. In those lesions with unknown cause, melanin was restricted to keratinocytes of the basal cell layer or to extracellular foci in the lamina propria. The clinical and histologic findings, as well as differential diagnosis, are discussed.

Adult↗

Primary disorders of hyperpigmentation.

A classification of primary hyperpigmentation conditions is presented. The emphasis is on clinical aspects and an attempt has been made to show, when possible, a spectrum beginning with localized involvement and progressing to the more extensive involvement. Most primary hyperpigmentation conditions and syndromes are inherited by autosomal dominant genetics; notable exceptions include incontinentia pigmenti, classic dyskeratosis congenita, and xeroderma pigmentosum. Early German case reports provide insight into the spectrum of uncommon pigmentary conditions, such as dermatopathia pigmentosa reticularis. The Japanese observe pigmentary problems frequently, have presented some of the more unusual cases, and have recently provided us with much-needed research into the problem of abnormal pigmentation.

Acanthosis Nigricans↗

Cutaneous hyperpigmentation induced by amiodarone hydrochloride.

Amiodarone (Cordarone) is an iodinated compound widely used in the treatment of cardiac arrhythmias for more than a decade. A patient who developed a persistent blue-gray skin pigmentation of the light-exposed areas following long-term amiodarone hydrochloride administration is reported. The cutaneous signs and the ultrastructural findings are described. This rare iatrogenic hyperpigmentation is peculiarly due to lipofuscin and not melanin deposits. Its pathogenesis may be related to the basic action of the drug on the lysosome and to the extra phototoxic-induced lysosomal damage, which accounts for the specific location of the hyperpigmentation over the light-exposed areas.

Aged↗

Diffuse, progressive hyperpigmentation: an unusual skin manifestation of mycosis fungoides.

Pigmentary changes in mycosis fungoides usually occur in association with poikiloderma atrophicans vasculare or following therapy and regression of lesions. Several cases of hypopigmented mycosis fungoides have also been reported. We present the case report of a patient who developed pruritic, diffuse macular hyperpigmentation of the skin. Biopsy specimens from hyperpigmented skin revealed histologic and ultrastructural features typical of mycosis fungoides. Giant melanin granules were found in the tumor cells, as well as in keratinocytes and Langerhans cells. As far as we know, this is the first report of cutaneous hyperpigmentation as a single presenting sign of mycosis fungoides.

Aged↗

Ultraviolet light and hyperpigmentation in healing wounds.

The concept of permanent hyperpigmentation in wounds following ultraviolet light exposure during the postoperative period has found a place in plastic surgical literature but has not been documented. This study evaluates the effect of ultraviolet light on healing wounds in paraplegics. It failed to confirm permanent alteration in pigmentation response to ultraviolet exposure and suggests that other factors are of greater importance in the development of hyperpigmentation in the healing wound.

Humans↗

Ultrastructural and x-ray microanalytical observations of minocycline-related hyperpigmentation of the skin.

In order to elucidate the nature and distribution of the pigment responsible for the circumscribed blue-black cutaneous hyperpigmentation occurring after administration of minocycline hydrochloride, transmission electron microscopy and energy-dispersive electron x-ray microanalysis were performed on lesional skin. Ultrastructural observations demonstrated electron-dense iron-containing particles either incorporated into a variety of siderosomes, within dermal histiocytes, free within the cytoplasm, or, rarely, scattered among dermal collagen fibers. Electron x-ray microanalysis confirmed iron content present within these particles. Although siderosomal inclusions contained occasional melanosome complexes, the degree of deposition of electron-dense iron-containing particles in dermal histiocytes seemed to be primarily responsible for the blue-black discoloration of the skin. The present study is an investigation of the structure and composition of the pigment responsible for minocycline-related cutaneous hyperpigmentation.

Adolescent↗

Postsclerotherapy hyperpigmentation. Treatment with a flashlamp-excited pulsed dye laser.

Seventeen patients with 22 areas of postsclerotherapy hyperpigmentation lasting from 1 to 7 years were treated with a flashlamp-excited pulsed dye laser at 510 nm with a pulse duration of 300 nanoseconds between 2 to 3 J/cm2. Depth of hemosiderin pigmentation ranged from 0.2 to 2.8 mm. Forty-five percent of lesions lightened after treatment with significant lightening occurring in 27% of lesions. Four lesions in two patients developed postinflammatory hyperpigmentation after treatment. There was no significant difference in treatment response to pigment location or laser energy.

Humans↗

Minocycline-related cutaneous hyperpigmentation as demonstrated by light microscopy, electron microscopy and X-ray energy spectroscopy.

A 70-year-old patient with a chronic cutaneous ulcer treated by minocycline hydrochloride developed hyperpigmentation of the forearms. Biopsy material was studied by light microscopy, electron microscopy and X-ray energy spectroscopy. Granular gold-brown pigment was found in dermal histiocytes and eccrine myoepithelial cells, which gave positive reaction with Prussian blue and Fontana-Masson stains. Electron microscopy revealed intracytoplasmic granules of dark, homogeneous material and small fine particles. X-ray energy spectroscopy showed iron and other elements in smaller amounts. The different types of minocycline-related hyperpigmentation and the possible pathomechanism are discussed with special regard to the importance of the diagnostic methods.

Aged↗

[Familial Wilson's disease: copper induced hemolysis, hypersplenism and hyperpigmentation as the main symptoms].

Wilson's disease was diagnosed in a 16-year-old adolescent who presented with signs of hypersplenism due to cirrhosis, with marked hyperpigmentation of both lower legs and neurological disturbances. In view of progressive thrombocytopenia and leukocytopenia, splenectomy was performed during therapy with penicillamine later in the course, and the result was good. The patient's 12-year-old sister was found to have a hepatic form of Wilson's disease with typical biochemical findings. During the initial hospitalization a severe, spontaneous copper-induced hemolysis was noted. Another sister probably has a presymptomatic form of the disease. The parents are healthy but heterozygote carriers with regard to biochemical findings. The importance is stressed of hypersplenism, hyperpigmentation of the legs and especially of acute hemolysis in infancy as pointers in the diagnosis of Wilson's disease. Further diagnostic and therapeutic aspects are discussed.

Adolescent↗

Tegafur-induced acral hyperpigmentation.

Four patients with colorectal cancer treated with tegafur (a fluoropyrimidine structurally similar to 5-fluorouracil) noted a macular, spotted hyperpigmentation limited to the palms, soles, nails, and glans penis. Histopathologic examination disclosed epidermal basal hyperpigmentation with a lentiginous pattern. Mucocutaneous lesions resolved spontaneously two months after treatment was discontinued. This peculiar phenomenon seems to represent a previously unreported side effect of this cytotoxic drug.

Aged↗

An animal model for the study of azidothymidine-induced hyperpigmentation.

Mice fed azidothymidine demonstrated dramatic hyperpigmentation of their tails. Histologic examination demonstrated large quantities of melanin pigment throughout the entire epidermal layer. Control mice had scant melanin pigment localized to the basal layer. Our findings demonstrate that the mouse is a useful model for the investigation of drug-induced hyperpigmentation.

Animals↗

Observations and proposed mechanism of N,N',N''-triethylenethiophosphoramide (thiotepa)-induced hyperpigmentation.

After receiving N,N',N''-triethylenethiophosphoramide (thiotepa) and cyclophosphamide intravenously, five women with metastatic adenocarcinoma of the breast developed a patterned hyperpigmentation confined to skin occluded by adhesive-containing materials. Determinations of thiotepa concentrations in occluded and nonoccluded skin, plasma, bandage with adhesive, and gauze containing sweat were performed. The results suggest that this alkylating agent is excreted onto the skin surface in sweat, accumulates beneath adhesive-containing bandages and electrocardiogram pads, and exerts a local toxic effect resulting in hyperpigmentation.

Adult↗