Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperpigmentation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,117 records · Page 62Linked to original sources
PubMed2004

Oral intake of proanthocyanidin-rich extract from grape seeds improves chloasma.

Chloasma (melasma), an acquired hypermelanosis, is often recalcitrant to various treatments and an amenable, as well as safe, pigment-reducing modality is needed. We investigated that the reducing effect of proanthocyanidin, a powerful antioxidant, on chloasma in a one-year open design study. Proanthocyanidin-rich grape seed extract (GSE) was orally administered to 12 Japanese woman candidates with chloasma for 6 months between August 2001 and January 2002 and to 11 of these 12 for 5 months between March and July 2002. Clinical observation, L* value (lightening) and melanin index, and size (length and width) measurements of chloasma were performed throughout the study period. The first 6 months of GSE intake improved or slightly improved chloasma in 10 of the 12 women (83%, p < 0.01) and following 5 months of intake improved or slightly improved chloasma in 6 of the 11 candidates (54%, p < 0.01). L* values also increased after GSE intake (57.8 +/- 2.5 at the start vs 59.3 +/- 2.3 at 6 months and 58.7 +/- 2.5 at the end of study). Melanin-index significantly decreased after 6 months of the intake (0.025 +/- 0.005 at the start vs 0.019 +/- 0.004 at 6 months) (p < 0.01), and also decreased at the end of study (0.021 +/- 0.005) (p < 0.05). GSE is effective in reducing the hyperpigmentation of women with chloasma. The beneficial effects of GSE was maximally achieved after 6 months and these was no further improvement after this period. The latter GSE intake for 5 months may prevent chloasma from becoming worse prior to the summer season. GSE is safe and useful for improving chloasma.

Administration, Oral↗
PubMedDate not supplied

Juvenile hemochromatosis in the southeastern United States: a report of seven cases in two kinships.

We report clinical and genetic characteristics of seven juvenile hemochromatosis (JH) patients (six females, one male) in two unrelated kinships from the southeastern U.S. All had severe iron overload. Mean age at diagnosis was 20 +/- 5 years (range 8-23 years). In six patients, the mean age at onset of signs and symptoms attributable to iron overload was 15 +/- 2 years (12-18 years); an 8-year-old girl had no symptoms. Six of the seven patients had hypogonadotrophic hypogonadism, two had severe cardiomyopathy, seven had hepatomegaly, two had hepatic cirrhosis, and five had hyperpigmentation. Two of four siblings with JH also had Hashimoto thyroiditis. One patient with severe cardiomyopathy improved with therapeutic phlebotomy, medical therapy for congestive heart failure, and a permanent pacemaker; the other died before phlebotomy was initiated. Estimates of average daily iron absorption before phlebotomy-induced iron depletion were 2.3, 3.1, and 1.7 mg in a male and two females, respectively. Both parents of four siblings with JH were heterozygous at two Ch1q loci (D1S1156, D1S2344); each of the four affected siblings was homozygous at both loci. An unaffected sib was heterozygous at D1S1156. One patient was heterozygous for HFE H63D, five others did not have HFE C282Y or H63D, and one was unavailable for testing. We conclude that JH occurs in the southeastern U.S. It is likely that JH allele(s) in at least one of the present kinships occur(s) on Ch1q, and presumably this represents a mutation(s) of the same gene localized to Ch1q in Italian and Greek JH kindreds. The present cases do not have HFE genotypes typical of hemochromatosis diagnosed in adults. Hashimoto thyroiditis, linked to Ch6p in many kinships, did not segregate with JH alleles on Ch1q in the present kinship.

Adolescent↗
PubMed1998

Role of Mitf in differentiation and transdifferentiation of chicken pigmented epithelial cell.

Mitf encodes a basic helix-loop-helix-leucine-zipper (bHLHzip) protein that is known to function in the development of melanocytes, pigmented epithelial cells (PECs), osteoclasts, and mast cells. In this paper, we report on the isolation, expression, and overexpression of the chicken Mitf and discuss the role of its protein product in the differentiation and transdifferentiation of PECs. Northern blotting showed that chicken Mitf is predominantly expressed in embryonic retinal pigmented epithelium (PE), but is expressed at low levels in other tissues. A 5' RACE analysis revealed differences in the 5' region Mitf nRNA in PE and other tissues. Immunological analysis revealed that Mitf, the protein encoded by Mitf, is first detected in the nuclei of the optic vesicle cells at embryonic stage 13 in a restricted region covered with mesenchymal cells. From stage 14 to 24, the specific staining is observable in the PE and precursor of the PE, the outer layer of the optic cup. In embryos at stages later than stage 29 the signals for Mitf in the future iris, ciliary body, and posterior retinal regions become faint. These results show that expression of Mitf starts at the optic vesicle stage at which no other marker genes for PECs such as mmp115 and tyrosinase are expressed. Dedifferentiation of cultured retinal PECs (rPECs) was induced by phenylthiourea and testicular hyaluronidase, bFGF, or TGF-beta. Mitf expression was inhibited by these factors and reactivated during redifferentiation of the dedifferentiated cells into rPECs, showing the correlation between Mitf expression and rPEC differentiation. Retrovirus-mediated overexpression of Mtif inhibited bFGF-induced dedifferentiation and transdifferentiation of rPECs to both lens and neural cells. These findings showed that downregulation of Mitf expression is essential for the transdifferentiation of rPEC. Mitf overexpression caused hyperpigmentation in cultured rPECs and suppressed the changes in gene expression induced by bFGF. Mitf overexpression promoted expression of mmp115 and tyrosinase in bFGF-treated rPECs suggesting a critical role for Mitf in rPEC differentiation. Mitf overexpression, however, did not promote expression of another rPEC-specific gene, pP344, in bFGF-treated rPECs. This result suggests the presence of other regulatory genes promoting rPEC differentiation. The expression patterns of pax6 and Mitf are complementary both in vivo in vitro. Overexpression of Mitf inhibited expression of pax6 in cultured rPECs. These observations suggest that Mitf regulates pax6 expression negatively.

Amino Acid Sequence↗
PubMed2002

Arsenic, drinking water, and health: a position paper of the American Council on Science and Health.

The purpose of this American Council on Science and Health report is to review issues and sources of uncertainty affecting assessment of potential health risks related to drinking water in the United States. Some background is included on how these issues arose, as is a review of the 1999 National Research Council report (with references to an updated version), to formulate a position based on the current science concerning how much of a risk of adverse health effects actually exists from arsenic in drinking water in the United States. ACSH concludes that there is clear evidence that chronic exposure to inorganic arsenic at concentrations of at least several hundred micrograms per liter may cause: (1) cancer of skin, bladder, lung (and possibly several other internal organs, including kidney, liver, and prostate), and (2) noncancer effects, including classic cutaneous manifestations that are distinctive and characteristic of chronic arsenic poisoning (diffuse or spotted hyperpigmentation and palmar-plantar hyperkeratoses). Noncancer effects may be multisystemic, with some evidence of peripheral vascular, cardiovascular, and cerebrovascular disease, diabetes, and adverse reproductive outcomes. Further study is needed to know if beneficial effects of arsenic in animal studies apply to humans. ACSH concludes that there is little, if any, evidence of a detrimental health effect in humans from inorganic arsenic in drinking water at the current maximum contaminant level (MCL) of 50 microg/L or below, either in the United States or elsewhere. As noted in the 1999 NRC report, "No human studies of sufficient statistical power or scope have examined whether consumption of arsenic in drinking water at the current MCL results in an increased incidence of cancer or noncancer effects" (NRC, 1999, p. 7). Based on our review, described in this article, ACSH finds that the limitations of the epidemiological data available and the state-of-the-science on the mode-of-action of arsenic toxicity, including can cer, are inadequate to support the conclusion that there are adverse health effects in the United States from arsenic in drinking water at or below the limit of 50 microg/L.

Arsenic↗
PubMed2000

DMPS-arsenic challenge test. II. Modulation of arsenic species, including monomethylarsonous acid (MMA(III)), excreted in human urine.

The administration of sodium 2,3-dimercapto-1-propane sulfonate (DMPS) to humans chronically exposed to inorganic arsenic in their drinking water resulted in the increased urinary excretion of arsenic, the appearance and identification of monomethylarsonous acid (MMA(III)) in their urine, and a large decrease in the concentration and percentage of urinary dimethylarsinic acid (DMA). This is the first time that MMA(III) has been detected in the urine. In vitro biochemical experiments were then designed and performed to understand the urinary appearance of MMA(III) and decrease of DMA. The DMPS-MMA(III) complex was not active as a substrate for the MMA(III) methyltransferase. The experimental results support the hypothesis that DMPS competes with endogenous ligands for MMA(III), forming a DMPS-MMA complex that is readily excreted in the urine and points out the need for studying the biochemical toxicology of MMA(III). It should be emphasized that MMA(III) was excreted in the urine only after DMPS administration. The results of these studies raise many questions about the potential central role of MMA(III) in the toxicity of inorganic arsenic and to the potential involvement of MMA(III) in the little-understood etiology of hyperkeratosis, hyperpigmentation, and cancer that can result from chronic inorganic arsenic exposure.

Adult↗
PubMed2001

Differential effects of trivalent and pentavalent arsenicals on cell proliferation and cytokine secretion in normal human epidermal keratinocytes.

There is strong evidence from epidemiologic studies of an association between chronic exposure to inorganic arsenic (iAs) and hyperpigmentation, hyperkeratosis, and neoplasia in the skin. Although it is generally accepted that methylation is a mechanism of arsenic detoxification, recent studies have suggested that methylated arsenicals also have deleterious biological effects. In these studies we compare the effects of inorganic arsenicals (arsenite (iAs(III)) and arsenate (iAs(V))) and trivalent and pentavalent methylated arsenicals (methylarsine oxide (MAs(III)O), complex of dimethylarsinous acid with glutathione (DMAs(III)GS), methylarsonic acid (MAs(V)), and dimethylarsinic acid (DMAs(V))) in human keratinocyte cultures. Viability testing showed that the relative toxicities of the arsenicals were as follows: iAs(III) > MAs(III)O > DMAs(III)GS > DMAs(V) > MAs(V) > iAs(V). Trivalent arsenicals induced an increase in cell proliferation at concentrations in the 0.001 to 0.01 microM range, while at high concentrations (>0.5 microM) cell proliferation was inhibited. Pentavalent arsenicals did not stimulate cell proliferation. As seen in the viability studies, the methylated forms of As(V) were more cytotoxic than iAs(V). Exposure to low doses of trivalent arsenicals stimulated secretion of the growth-promoting cytokines, granulocyte macrophage colony stimulating factor and tumor necrosis factor-alpha. DMAs(V) reduced cytokine secretion at concentrations at which proliferation and viability were not affected. These data suggest that methylated arsenicals, products of the metabolic conversion of inorganic arsenic, can significantly affect viability and proliferation of human keratinocytes and modify their secretion of inflammatory and growth-promoting cytokines.

Adult↗
PubMed1994

Epidemiology, clinical spectrum and prognosis of hemochromatosis.

EPIDEMIOLOGY: Eleven prospective epidemiological studies from various countries have as yet evaluated the gene prevalence of HLA-linked hemochromatosis. The estimated frequency ranged from 0.027-0.107, the frequency of homozygotes from 0.00074-0.0116, and the frequency of heterozygotes from 0.052-0.191. In a meta-analysis of the eleven surveys the frequency is 0.0016 (106/64758 subjects) for homozygotes which corresponds to a gene frequency of 0.041 and a frequency of heterozygotes of 0.078. Further analyses showed that some of these studies have probably underestimated the prevalence which in reality is probably two- to threefold higher than estimated by the meta-analysis. CLINICAL SPECTRUM: In the total group of 251 patients diagnosed with hemochromatosis in the University of Düsseldorf from 1959-1992, abnormality in liver function tests (75%), weakness and lethargy (74%), skin hyperpigmentation (70%), diabetes mellitus (48%), arthralgia (44%), impotence (45% in males), and ECG abnormalities (31%) were the most frequent findings and symptoms at diagnosis. In recent years about 50% of patients were detected without having liver cirrhosis and 20% of patients did not have any symptoms and pathology except iron overload. PROGNOSIS: Survival analysis in the 251 patients showed that in the absence of cirrhosis and diabetes iron removal by phlebotomy therapy prevents further tissue damage and guarantees a normal life expectancy. Sex and presence of arthropathy did not predict prognosis. However, patients with massive and long-lasting iron overload had a worse prognosis than patients with less severe iron excess. Iron removal in general ameliorated liver disease, weakness and cardiac abnormalities, and also prevented the progression of endocrine alterations. Therapy, however, did not influence arthropathy which even got worse in several patients. Iron removal also failed to reverse insulin-dependent diabetes. During a mean followup of 13.4 years 69 deaths occurred in the 251 patients. In 19 patients death was due to liver cancer, in 14 due to liver cirrhosis, in 5 due to cardiomyopathy, and in 3 due to diabetes mellitus (all causes significantly more frequent than expected for the general population). The other causes of death were as frequent as expected including extrahepatic malignancies. All liver cancers were seen in cirrhotic livers, but often occurred many years or even decades after complete iron removal. Further strategies have to evaluate the design of screening programs in order to diagnose more patients in the precirrhotic and asymptomatic stage.

Bloodletting↗
PubMed1999

Melasma.

Melasma is a common disorder of macular hyperpigmentation which involves mostly in sun exposed areas of the face and neck. Those most affected are women. Multiple factors have been postulated to involve in the etiology and pathogenesis of melasma including pregnancy, oral contraceptives, genetics, sun exposure, cosmetics and race. We have conducted a clinical trial utilizing all trans-retinoic acid (tretinoin, Retin-A) cream 0.1% q pm and hydroquinone lotion 3% (Melanex) applied every morning in Korean women with melasma. Our study patients demonstrated all three clinical patterns common to melasma: centrofacial, malar and mandibular. Wood's light examination was performed on all patients and identified two of the four types of melasma described. Most patients showed epidermal melasma and a few manifested a mixed type. No patients exhibited solely dermal or inapparent type in melasma. With open studies of tretinoin cream and hydroquinone lotion followed by sun screen, we have found significant improvement within 5 months with a few side effects. Histopathologic examination of melasma in the pre-trial biopsies revealed increased pigmentation of the epidermis, dermis or both. In addition, significant alterations of the dermis with solar damage was noted in all melasma patients sampled. Biopsies taken after five months of treatment revealed significant decreases in epidermal pigmentation and improvement of solar damage in the dermis. We reconfirmed that a synergistic mechanism between tretinoin and hydroquinone is responsible for the improvement seen in the female Korean melasma patients from our study.

Adult↗
PubMed1988

Pattern dystrophy of the retinal pigment epithelium with vitelliform macular lesion: evolution in ten years.

We report an unusual case of primary dystrophy of the retinal pigment epithelium (RPE) in which a vitelliform macular appearance was associated with reticular hyperpigmentation resembling the pattern dystrophies of the RPE. The entire evolution of the disease was observed and documented step-by-step during a 10-year follow-up. During the progressive change of the lesions morphologic characteristics of butterfly, reticular and macroreticular dystrophy as well as Best's macular dystrophy could be seen. Pathogenetic relationships between all of these dystrophies of the RPE can be supposed.

Adult↗
PubMed1984

Metastatic small cell carcinoma of the lung presenting as pituitary apoplexy and Cushing's syndrome.

We describe a woman with metastatic small cell carcinoma of the lung who presented with pituitary apoplexy and hyperprolactinemia. Within seventeen months she developed florid Cushing's syndrome with anasarca, hyperpigmentation, hypertension with marked hypercortisolemia (not suppressible with 8 mg dexamethasone), elevated serum ACTH, hypokalemic metabolic alkalosis, and multiple hepatic metastases. This picture suggested the presence of ectopic ACTH syndrome. She died 26 months after the episode of pituitary apoplexy. Primary small cell carcinoma of the lung was diagnosed post-mortem. Metastases were present in the left lung, regional lymph nodes, heart, liver, bone marrow, sphenoid bone, anterior pituitary and pituitary capsule. Posterior pituitary was normal. There was no evidence of pituitary hyperplasia, of adenoma or of primary pituitary carcinoma. The results suggest the presence of a primary ACTH-producing small cell carcinoma of the lung that metastasized to the parasellar sphenoid bone and then extended to the anterior pituitary and dura to mimic a primary intrasellar cause of pituitary apoplexy and Cushing's syndrome. The case demonstrates how difficult it may be to diagnose the etiology of Cushing's syndrome and it emphasizes a unique variation in the presentation of small cell carcinoma of the lung.

Adrenocorticotropic Hormone↗
PubMed1990

A phase I and pharmacokinetic study of trimetrexate using a 24-hour continuous-injection schedule.

Trimetrexate (TMTX) is an analog of methotrexate and a potent inhibitor of the enzyme dihydrofolate reductase. In this phase I study, TMTX was given intravenously to 32 patients as a constant infusion over 24 hours every 28 days. The maximum-tolerated dose of TMTX was 200 mg/m2, with myelosuppression as the dose-limiting toxicity. Other toxicities included nausea and vomiting, stomatitis, erythema and phlebitis at the site of infusion, rash and skin hyperpigmentation, and elevated serum hepatic enzymes. Two drug-related deaths occurred secondary to leukopenia and sepsis. Twenty-six patients were evaluable for antitumor response. Twenty-one patients had progressive disease, while three patients had disease stabilization. There were two partial responses observed--one in a patient with breast cancer and a second in a patient with nasopharyngeal carcinoma. TMTX pharmacokinetics were studied in 15 patients. The drug had a mean terminal half-life of 13 hours. Steady-state was not achieved during the 24-hour infusions. Only 6% of the parent compound was excreted unchanged in the urine, and CSF levels averaged less than 2% of simultaneously measured plasma levels. A dose of 150 mg/m2 is recommended for phase II trials of TMTX using this 24-hour infusion schedule.

Adult↗
PubMed1986

Autosomal dominant juvenile vitreoretinal degeneration and retinal detachment.

To study the inheritance and clinical picture of a new form of vitreoretinal dystrophy I examined 18 family members of a family with six generations. Seven patients, three male and four female, in three consecutive generations were observed to be affected indicating autosomal dominant inheritance. The disease was characterized by juvenile degeneration of the vitreous with detachment of the vitreous body and some floating vitreous opacities, cystoid degeneration of the peripheral retina with whitish glistening stippled areas of superficial retinal degeneration, spotty hyperpigmentation, patches of retinal atrophy with pigmentations, occasional atrophic retinal holes, and in four family members at the age of 4 to 12 years, unilateral or bilateral retinal detachment with breaks in the peripheral retina. Most patients had hyperopia with or without astigmatism. In eyes without detached retina, the disease did not show any marked progression, the lens was clear, the posterior fundus and the retinal and choroidal vessels were normal, and the visual acuity, visual fields, dark adaptation, colour vision, electroretinograms, and visually evoked response findings were normal.

Adult↗
PubMed1985

A phase II study of sequential methotrexate and fluorouracil in advanced colorectal cancer.

Twenty-nine patients with advanced colorectal cancer were treated with methotrexate (MTX) 200 mg/m2 followed 1 h later by fluorouracil (FU) (1000 mg/m2) and 24 h later by oral leucovorin 20 mg every 6 h for six doses. The cycle was repeated every 2 weeks. Among the 25 evaluable patients there were 2 complete responses (confirmed by liver scan) and 5 partial responses. Although hematological toxicity was mild, there were four episodes of nonfatal sepsis. The majority of patients developed an erythematous scaly rash on the palms and soles plus eye irritation after six courses of chemotherapy. In addition, the sequential MTX-FU had to be discontinued in 6 of the 7 responders because of (a) severe chills, (b) severe hyperpigmentation, or (c) neurologic complications (ataxic gait or disorientation). These results indicate that this sequential MTX-FU has modest activity in colorectal cancer but is associated with moderately severe toxicity. Only randomized trials of FU alone versus sequential MTX-FU can determine whether sequential MTX-FU has a therapeutic advantage over FU alone in the treatment of advanced colorectal cancer.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1985

A new syndrome in the group of euhidrotic ectodermal dysplasia. Pilodental dysplasia with refractive errors.

A new form of ectodermal dysplasia was observed in two siblings, offspring of healthy non-consanguineous parents. The main findings in both children are: hypodontia, abnormally shaped teeth, scalp hypotrichosis, pili annulati, follicular hyperkeratosis on the trunk and limbs, intensified delineation and reticular hyperpigmentation of the nape, and hyperopia; one of the siblings also has astigmatism. As both patients have normal nails and are euhidrotic, this is an ectodermal dysplasia of the pilodental subgroup. The cause is probably genetic and autosomal-recessive inheritance is most likely.

Child↗
PubMed1991

Inhibitory effect of azelaic acid on neutrophil functions: a possible cause for its efficacy in treating pathogenetically unrelated diseases.

It has been shown that acne, hyperpigmentation and lentigo malignant are more or less related pathogenetically to reactive oxygen species (ROS). It has recently been reported that azelaic acid is effective in treating these conditions and that it possesses anti-enzymatic and antimitochondrial activity, including cytochrome-P450 reductase and 5 alpha-reductase in microsomal preparations with nicotinamide adenine dinucleotide phosphate (NADPH). We therefore investigated the effects of azelaic acid on human neutrophil functions, such as chemotaxis, phagocytosis and ROS generation. ROS generation in a cell-free system was also assessed. The results revealed that neutrophil chemotaxis and phagocytosis as well as ROS generated in a xanthine-xanthine-oxidase system were not significantly changed in the presence of azelaic acid. However, azelaic acid markedly decreased O2- and OH. generated by neutrophils. It may be concluded that the reported clinical effectiveness of azelaic acid is partly due to its inhibitory action on neutrophil-generated ROS, leading to a reduction both in oxidative tissue injury at sites of inflammation and in melanin formation.

Chemotaxis↗
PubMed1990

A possible mechanism of action for azelaic acid in the human epidermis.

Azelaic acid, and other saturated dicarboxylic acids (C9-C12), are shown to be competitive inhibitors of tyrosinase (KI azelaic acid = 2.73 X 10(-3) M) and of membrane-associated thioredoxin reductase (KI azelaic acid = 1.25 X 10(-5) M). The monomethyl ester of azelaic acid does not inhibit thioredoxin reductase, but it does inhibit tyrosinase, although double the concentration is necessary compared with azelaic acid (KI azelaic acid monomethyl ester = 5.24 X 10(-3) M). Neither azelaic acid nor its monomethyl ester inhibit tyrosinase when catechol is used as a substrate instead of L-tyrosine. Therefore, the weak inhibitory action of azelaic acid on tyrosinase appears to be due to the competition of a single carboxylate group on this inhibitor for the alpha-carboxylate binding site of the L-tyrosine substrate on the enzyme active site. Based on the inhibitor constant on tyrosinase, at least cytotoxic levels of azelaic acid would be required for the direct inhibition of melanin biosynthesis in melanosomes if this mechanism is responsible for depigmentation in the hyperpigmentation disorders lentigo maligna and melasma. Alternatively only 10(-5) M azelaic acid is required to inhibit thioredoxin reductase. This enzyme is shown to regulate tyrosinase through a feedback mechanism involving electron transfer to intracellular thioredoxin, followed by a specific interaction between reduced thioredoxin and tyrosinase. Furthermore, the thioredoxin reductase/thioredoxin system is shown to be a principal electron donor for the ribonucleotide reductases which regulates DNA synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1986

Lymphocyte proliferation and nucleoid sedimentation in a case of premature aging distinct from Werner's syndrome.

Lymphocyte proliferation and nucleoid sedimentation were studied in a patient with premature aging resembling the Werner's syndrome (WS). Onset of patchy brown hyperpigmentations at the age of 9 months permitted distinction from classical WS and suggested a WS-like premature aging disease. By photometric recording of density changes during cell culture, we examined the course of cell proliferation after PHA stimulation over 7 days and compared these results to those obtained in two normal controls. Cultured cells of the patient displayed an aberrant proliferation pattern characterized by continuous growth without an initial reduction phase. The markedly reduced proliferative capacity of purified cells from the patient could in part be corrected by fetal bovine serum. The cells of the patient displayed a characteristic nucleoid sedimentation profile after ultraviolet irradiation indicating retarded DNA replication, which may be a common feature of various premature aging diseases. The absence of thermolability of cell proliferation and the presence of a high number of chromatid aberrations disclosed differences from classical WS.

Cell Division↗
PubMed1979

Ichthyosis nigricans: ultrastructural study of the melanin pigmentary disturbances.

Hyperpigmented skin from a 10-year-old white boy with ichthyosis nigricans has been studied. Histological and ultrastructural studies reveal that the hyperpigmentation is related to both epidermal and dermal hypermelanosis. Melanocytes are hyperactive. The different stages of melanosome synthesis and melanisation appear to be normal. Increased dermal pigmentation probably results from a dischargement of the melanin granules into the dermis secondary to melanocyte alterations. Ichthyosis nigricans is a typical example of melanin pigmentary disturbances of the skin, resulting from disturbances in the normal interactions between melanocytes and keratinocytes.

Child↗