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At least 217 records · Page 12Linked to original sources
PubMed1987

Inflammatory acquired oral hyperpigmentation: association with melanophages demonstrating phenotypic characteristics of antigen presenting cells and activated monocytes.

A case of a 30-year-old black woman who developed acute, extensive intraoral hyperpigmentation is reported. Its relationship to previously described entities is discussed. The condition was associated with the presence of melanophages both in the submucosa and in the oral epithelium. The melanophages displayed phenotypic markers of a population of intraepidermal melanophages previously described as potent T cell-activating, antigen presenting cells (T6- DR+ OKM5+ OKM1-) and of activated monocytes (Mo3e+), as well as other monocyte-macrophage markers (Mono 1 and My7). The distinct phenotype of these melanophages suggests that they could play an active role in the promotion of inflammatory disease.

Adult↗
PubMed2003

The mechanism of epidermal hyperpigmentation in café-au-lait macules of neurofibromatosis type 1 (von Recklinghausen's disease) may be associated with dermal fibroblast-derived stem cell factor and hepatocyte growth factor.

BACKGROUND: The mechanism of the accentuated melanization in café-au-lait macules (CALMs) in patients with neurofibromatosis type 1 (NF1; von Recklinghausen's disease) has not been elucidated. OBJECTIVES: To clarify the mechanism involved in the hyperpigmentation of CALMs in NF1. METHODS: Using enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of cultured cells, we measured the levels of cytokines produced and secreted by keratinocytes and fibroblasts derived from CALMs (group RC: Recklinghausen CALM) skin, compared with cells derived from the skin of normal individuals (group NN: Normal skin of Normal individuals) and cells derived from non-CALM skin of NF1 patients (group RN: Recklinghausen Non-CALM). RESULTS: ELISA revealed that the secretion of hepatocyte growth factor (HGF) and stem cell factor (SCF) by cultured fibroblasts was significantly elevated in group RC compared with groups RN and NN. In parallel, semiquantitative real-time RT-PCR of HGF and SCF mRNAs demonstrated increased expression of both types of transcripts by cultured fibroblasts in group RC compared with group NN. In contrast, the secretion of endothelin-1 and granulocyte/macrophage colony-stimulating factor by cultured keratinocytes occurred at a similar level among all three groups, RC, RN and NN. CONCLUSIONS: These findings suggest that increased secretion of HGF and SCF by dermal fibroblasts may be associated with the accentuated epidermal melanization observed in CALMs in the skin of NF1 patients.

Adult↗
PubMed1976

Adrenal insufficiency secondary to hypothalamic corticotropin releasing factor (CRF) insufficiency with hyperpigmentation: a case report.

Partial adrenocortical insufficiency as a result of an insufficiency of the hypothalamic corticotropin releasing factor (CRF) was demonstrated in a 53-year-old female patient. Somatotropic, gonadotropic and thyreotropic functions of the pituitary gland were shown to be normal by a simultaneous pituitary stimulation test. This held true especially for the adrenocorticotrophic function: administration of lysine-vasopressin induced a normal rise in immunoreactive plasma-ACTH. Thus, a pituitary defect as a primary cause of the disease could be excluded and evidence was provided that there was a lack in hypothalamic stimulae absence of elevated ACTH levels hyperpigmentation of the skin existed. Possible explanations are discussed.

Adrenal Insufficiency↗
PubMed2000

Oral mucosal hyperpigmentation secondary to antimalarial drug therapy.

A case of oral mucosal hyperpigmentation resulting from antimalarial drug therapy is presented. The patient reported a history of long-term quinacrine therapy and exhibited diffuse blue-gray pigmentation of the nail beds and the skin of the nasal ala. Microscopic examination of the involved mucosa showed macrophages, containing both melanin and ferric iron, scattered within the connective tissue adjacent to the epithelium. The clinical, historical, and microscopic features of antimalarial-induced pigmentation are discussed. Other causes of diffuse or multifocal oral pigmentation are also addressed.

Adult↗
PubMed1989

Hyperpigmentation due to cyclosporin therapy.

A 51 year old diabetic man had a cadaveric renal transplant performed. Cyclosporin immunosuppressive therapy was commenced routinely. He developed hyperpigmentation of the skin during 3 months' therapy which became increasingly marked and resolved after cyclosporin therapy was discontinued.

Cyclosporins↗
PubMed1987

Upper extremity swelling and hyperpigmentation due to onchocerciasis in an American.

An American woman who had lived in Equatorial Guinea was seen in the United States with intermittent swelling, pruritus, hyperpigmentation, and mild cutaneous atrophy of the right arm. Filarial diseases were considered in the differential diagnosis; skin snips subsequently revealed Onchocerca volvulus microfilariae. There was no evidence of ocular involvement. The case illustrates the importance of obtaining a history of international travel, the need to consider "exotic" parasitic diseases in travelers returning from the tropics, and several of the presenting features of onchocerciasis. In the past, onchocerciasis was treated with diethylcarbamazine and suramin, both of which have appreciable toxicity. A major recent advance has been the introduction of ivermectin, which appears to be more effective and less toxic, and is currently undergoing clinical evaluation in the United States and abroad.

Adult↗
PubMed1992

A case of skin hyperpigmentation due to alpha-MSH hypersecretion.

A case is presented of generalized skin hyperpigmentation due to alpha-MSH hypersecretion from the pituitary that was most marked in the light-exposed areas. The patient also had secondary adrenal dysfunction, peripheral lymphadenopathy, streptococcal glomerulonephritis and malabsorption. Analysis of this patient's alpha-MSH using high-pressure liquid chromatography (HPLC) showed a novel acetylation profile compared to normal individuals and to patients with Cushing's disease and Nelson's syndrome. Glucocorticoid replacement therapy resulted in suppression of alpha-MSH hypersecretion and complete resolution of the illness.

Chromatography, High Pressure Liquid↗
PubMed1988

Hyperpigmentation in megaloblastic anemia.

Hyperpigmentation of the hands and feet developed in a 65-year-old Korean woman who had undergone a total gastrectomy and esophagojejunostomy due to early gastric cancer 7 years previously. A diagnosis of megaloblastic anemia due to vitamin B12 deficiency was made. In the areas of pigmentation, there were abnormally large nuclei in the keratinocytes. All of these findings were reversible upon the administration of vitamin B12. Ultrastructurally, there were many intracytoplasmic desmosomes, numerous aggregated bundles of tonofilaments, and highly condensed keratohyalin granules. The pathophysiologic mechanism of vitamin B12 deficiency associated with pigmentary disturbances and change of nuclear size is discussed.

Anemia, Macrocytic↗
PubMed1989

Hyperpigmentation of the clavicular zone: a variant of friction melanosis.

This paper reports on clinical, laboratory, and pathologic findings of 10 cases of an idiopathic form of hyperpigmentation of the clavicular zone, a peculiar entity of circumscribed, glistening, pigmented lesions affecting young Latin women. Pathologic findings consisted of focal to extensive necrosis of the epidermis, focal areas of junctional cleavage, and melanin deposition within the epidermis, dermis, and melanophages, which places this lesion within the group of brown hypermelanoses. The authors feel that friction with clothing or with scrub pads made of sedge (a very common practice amongst mexicans in the bath room) against clavicular protuberances is fundamental in its pathogenesis.

Adolescent↗
PubMed1987

Postsclerotherapy hyperpigmentation: a histologic evaluation.

Linear or macular pigmentation occurs in 10-30% of patients following sclerotherapy of vessels between 0.1 and 5 mm in diameter. Its occurrence is related to solution strength, vessel fragility, injection pressure, and the type of solution used. This adverse sequela of treatment has been assumed, by some, to represent post-inflammatory hyperpigmentation (incontinence of melanin pigment), and has been said to occur in individuals with this tendency. Histologic data presented in this paper suggest that this phenomenon does not represent melanocytic alteration, but is secondary to extravasation of red blood cells into the dermis following rupture of fragile vessels with resulting deposition of hemosiderin. Therapy has included bleaching agents (hydroquinones), trichloroacetic acid, and phenolic peeling agents with variable success. Eighty percent of patients who experience this adverse sequela will clear spontaneously within 6-24 months. The remaining patients will have persistence of pigmentation for up to 5 years, with a small number of patients having pigmentation persisting 5 years after therapy.

Biopsy↗
PubMed1981

Hyperpigmentation and hypopigmentation of the skin after long term PUVA therapy. Light and electron microscopic observations on three patients.

An electron microscopic study was performed to demonstrate the pathological changes induced by long term PUVA treatment in recalcitrant psoriasis. Three patients developed mottling (hyperpigmentation and hypopigmentation) during two to three years of treatment. Three different types of morphological changes were found: disarrangement of keratinocytes, clustering and stimulation of melanocytes and homogenization of papillary dermis. Furthermore, the superficial blood vessels were loaded with the same type of amorphous granular substance. These changes might be specific to PUVA treatment or they might occur only in patients with previous treatment with, e.g., arsenic, methotrexate, anthralin + UVB or a combination of these.

Adult↗
PubMed1989

Ultrastructural findings in oral hyperpigmentation of HIV-infected patients.

Oral hyperpigmentation has been observed in six HIV-infected patients, in two of whom systemic medication (ketokonazole, clofazimine) was supposed to be etiologically involved. Histologically, pigment was found in epithelial basal cells and particularly in subepithelial connective tissue. Ultrastructurally, the presence of premature melanosomes in subepithelial keratinocytes was of interest. Stimulation of melanocytes during HIV infection may occur in association with immunopathologic changes in the oral mucosa.

Adult↗
PubMed1983

Syndrome of polyneuropathy, skin hyperpigmentation, oedema and hepatosplenomegaly.

Four middle-aged male Chinese with polyneuropathy, skin hyperpigmentation, oedema, hepatosplenomegaly, ascites, gynaecomastia and white nails are described. In Japan and United States this syndrome has been associated with plasma cell dyscrasia. However, neither M-protein nor skeletal lesions were demonstrated in these four patients.

Adult↗
PubMed1989

Generalized cutaneous hyperpigmentation in hairless mice induced by topical dimethylbenzanthracene.

The skin of hairless (Ng/Bln) mice topically treated with dimethylbenzanthracene (DMBA) was investigated by light microscopy, histochemistry, electron microscopy and autoradiography in order to gain some insight into the mechanisms by which the DMBA-induced cutaneous hyperpigmentation is mediated. The results of the present study indicate that this phenomenon is due to the DMBA-induced stimulation of both the tyrosinase system and the mitotic activity of dopa-inactive dormant melanocytes.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Serpentine supravenous hyperpigmentation induced by the nitrosourea fotemustine.

Two cases of serpentine supravenous hyperpigmentation developing in the area of fotemustine infusions are reported. Histological features showed an increased melanin synthesis and the presence of melanophages without focal degeneration of basal cells or dermal inflammatory infiltrate. Perls' strain was negative. Hypotheses concerning the mechanisms of increased melanin synthesis over the veins are discussed.

Adult↗
PubMed1990

Hyperpigmentation induced by UVB at the application site of estradiol.

We report a case of a 48-year-old woman who presented with chronic essential pruritus and was successfully treated with the transdermal estradiol system because of menopausal discomfort. Suberythemogenic UVB phototherapy was proposed to the patient in order to control her pruritus. She developed hyperpigmentation at the application site of estradiol. To the best of our knowledge, this is the first report suggesting a direct relationship between estrogen and melanin synthesis in humans.

Administration, Cutaneous↗