Disease relevance of Hyperpigmentation

• Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopenia, short stature, radial ray defects, skin hyperpigmentation and a predisposition to cancer [1].
• We studied a six-month-old infant with severe megaloblastic anemia, coma and hyperpigmentation of the extremities [2].
• Familial gastrointestinal stromal tumor with hyperpigmentation: association with a germline mutation of the c-kit gene [3].
• Only one had the triad of hepatomegaly, hyperpigmentation, and diabetes [4].
• Complications of therapy in cancer patients: Case 1. Paronychia and skin hyperpigmentation induced by gefitinib in advanced non-small-cell lung cancer [5].

High impact information on Hyperpigmentation

• Tretinoin for hyperpigmentation in black patients [6].
• We investigated the treatment of this hyperpigmentation with topical tretinoin (0.1 percent retinoic acid cream) [7].
• Letter: Serpentine supravenous fluorouracil hyperpigmentation [8].
• Minocycline-induced oral hyperpigmentation [9].
• Melanocyte-stimulating-hormone levels in doxorubicin-induced hyperpigmentation [10].

Chemical compound and disease context of Hyperpigmentation

• Clinical images: Hydroxychloroquine-associated mucocutaneous hyperpigmentation [11].
• Oxyresveratrol showed potent inhibitory effect with an IC(50) value of 1.2 microm on mushroom tyrosinase activity, which was 32-fold stronger inhibition than kojic acid, a depigmenting agent used as the cosmetic material with skin-whitening effect and the medical agent for hyperpigmentation disorders [12].
• Nail, hair and skin hyperpigmentation associated with indinavir therapy [13].
• LKB1, the human gene encoding a serine threonine kinase, was recently identified as a susceptibility gene for Peutz-Jeghers syndrome (PJS), a disease characterized by the constellation of intestinal hamartomata, oral mucocutaneous hyperpigmentation, and an increased risk for gastrointestinal as well as extraintestinal malignancies [14].
• These patients are usually seen in early childhood with very low cortisol concentrations, normal mineralocorticoids, hyperpigmentation, and increased bodily growth [15].

Biological context of Hyperpigmentation

• These findings suggest that PAN allergy provides a new mechanism of hyperpigmentation in which biological factors such as the GRO-alpha superfamily generated within allergy-induced skin stimulate melanocytes through activation of the PKC-related signal transduction pathway [16].
• The results reveal that ELA may be an effective inhibitor of hyperpigmentation caused by UV irradiation or by pigmented skin disorders through a mechanism involving IL-6-mediated downregulation of Mitf rather than a direct inhibition of tyrosinase activity [17].
• The clinical characteristics best supported type II minocycline hyperpigmentation, but the histology revealed that the pigmentation was solely limited to the subcutaneous adipose tissue, completely sparing the dermis [18].
• The degree of stimulation of SCF, HGF and b-FGF production varied between individual cell lineages, which may reflect the true variation of post-laser hyperpigmentation in clinical practice [19].

Anatomical context of Hyperpigmentation

• Nf1+/- mice also showed a 2-fold increase in the development of pigmented skin patches stimulated by dimethylbenzanthracene; patches were characterized by hair follicles in anagen phase, implicating keratinocytes in the aberrant hyperpigmentation [20].
• Frequently reported side effects of clofazimine are hyperpigmentation of the skin and conjunctiva, and abdominal pain [21].
• The correlation coefficients were generally higher for zone "Beta," characterized by complete chorioretinal atrophy with visible large choroidal vessels and sclera, than for zone "Alpha," which showed irregular hypo- and hyperpigmentation [22].
• Latanoprost and hyperpigmentation of eyelashes [23].
• Two patients are presented with a fixed drug eruption to acetaminophen characterized by recurring erythematous, circular plaques of the skin and oral mucosa along with multiple sites of deep (postinflammatory) hyperpigmentation clinically characteristic of fixed drug eruption [24].

Gene context of Hyperpigmentation

• Expression of PC2 was considered to induce hyperpigmentation by producing alpha MSH [25].
• We previously reported that accentuated expression of the endothelin-1 (ET-1)/endothelin B receptor (ET(B)R) cascade is involved in the mechanism of hyperpigmentation in lentigo senilis (LS) lesions [26].
• These findings suggest that in addition to the stimulated expression of the ET-1/ET(B)R cascade, the accentuated expression of SCF in lesional skin plays an important role in the mechanism involved in the epidermal hyperpigmentation of LS [26].
• Pharmacologic manipulation of Fas and c-kit signaling pathways might be useful for the correction of skin hyperpigmentation as a side-effect of chemotherapy [27].
• Adrenal insufficiency secondary to hypothalamic corticotropin releasing factor (CRF) insufficiency with hyperpigmentation: a case report [28].

Analytical, diagnostic and therapeutic context of Hyperpigmentation

• We define Nelson's syndrome as the presence of an enlarging pituitary tumour associated with elevated fasting plasma ACTH levels and hyperpigmentation in patients with Cushing's disease after bilateral adrenalectomy [29].
• OBSERVATIONS: We report a case of flagellate hyperpigmentation after intralesional injection of 14 U of bleomycin for verrucae plantaris and review the literature associated with this cutaneous complication [30].
• CONCLUSIONS--This animal model parallels the human in developing reversible and selective hyperpigmentation on administration of zidovudine [31].
• No milia or postinflammatory hyperpigmentation was experienced by patients treated with tretinoin when the drug was resumed within 1 week after dermabrasion [32].
• Data from multicentre clinical trials have shown that 0.05% tretinoin emollient cream reduced fine wrinkling, surface roughness and mottled hyperpigmentation caused by photodamage [33].

References