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Examples
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Mucocutaneous lesions: trichilemmomas (facial), acral keratoses, papillomatous lesions, and/or mucosal lesions
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Mucocutaneous pigmentation (altered coloring of the skin, gums and other mucus membranes) is rarely present at birth, but develops during early childhood (usually before 5 years of age) as dark blue to dark brown flat spots in the following areas:
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Mucocutaneous leishmaniasis (MCL), or espundia, produces lesions which can lead to extensive and disfiguring destruction of mucous membranes of the nose, mouth and throat cavities.
Chapter 1 2000
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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Mucocutaneous candidiasis is commonly seen in persons with deficient T-cell-mediated immunity, including newborn infants, patients with the acquired immunodeficiency syndrome, and those with genetically defined primary T-cell deficiencies. 1 In their Brief Report about human dectin-1 deficiency and mucocutaneous fungal infections, Ferwerda et al. (Oct. 29 issue) 2 suggest that chronic mucocutaneous candidiasis may also be caused by a genetic defect of the β-glucan receptor dectin-1.
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