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Disorders of Pigmentation
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Michael Joseph Lavery, Charles Cathcart, Hasan Aksoy
Differential diagnosis: Piebaldism is a rare autosomal dominant disorder due to mutation in the KIT-proto-oncogene. It is characterized by a white forelock and depigmented patches, which are commonly located on the forehead. The presence of a white forelock, a depigmented patch, sensorineural deafness, and iris heterochromia are consistent with Waardenburg’s syndrome. The differential diagnosis of localized hypopigmentation is summarized in Table 25.2.
Disorders of pigmentation
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
In many countries, the fear of leprosy makes the differential diagnosis of a ‘white patch’ an urgent and vitally important issue. The causes of hypopigmentation are summarized in Table 22.1. Examination in long-wave UVR enhances loss of epidermal pigment (as in vitiligo) and helps identify areas of developing depigmentation. It may also detect a yellow–green fluorescence in some cases of pityriasis versicolor.
Skin disorders causing post-inflammatory hypopigmentation
Published in Electra Nicolaidou, Clio Dessinioti, Andreas D. Katsambas, Hypopigmentation, 2019
Polytimi Sidiropoulou, Dimitrios Sgouros, Dimitris Rigopoulos
It has been suggested that hypopigmentation is usually associated with a decrease, but not absence, of pigment.2,4 As tumor necrosis factor (TNF)-α and IL-17 are known to synergistically suppress pigmentation-related signaling and melanin production, it is possible to represent a potential mechanism by which inflammatory dermatoses such as psoriasis are complicated by hypopigmentation.7 However, when there is severe local inflammation, loss or even death of functional melanocytes occurs, resulting in permanent pigmentary changes.2,4
Neuropsychological and Social Characteristics of a 7 Year Old Child with Hypomelanosis of Ito Followed for 11 Years
Published in Developmental Neuropsychology, 2022
George P. Prigatano, Alexandra Novak, Vinodh Narayanan
Hypomelanosis of Ito (HI) “is a neurocutaneous disorder with hypopigmented lesions following the lines of Blaschko” (Ream, 2015, p. 281). The single genetic etiology of this condition has not been defined, but there has been an association with chromosomal mosaicism. “Mosaicism occurs when there are two different populations of cells during embryologic development, often due to mutation or chromosomal nondisjunction in one cell line” (Ream, 2015, p. 286). While skin hypopigmentation is the most prominent feature of HI, this clinical condition is often associated with a variety of musculoskeletal and central nervous system abnormalities. While the neuropsychological and neurobehavioral symptoms of these children can be variable (e.g., attentional disturbances, autism, Asperger’s syndrome, developmental delays, and poorly defined learning disorders (Kumar, Radhakrishnan, Chowdhary, & Giampietro, 2001; Pavone, Praticò, Ruggieri, & Falsaperla, 2015)), delays in speech production and reduced intellectual ability are commonly reported (Ruggieri & Pavone, 2000). Esquivel, Pitt, and Boyd (1991) have also reported that many children with HI have seizures during early childhood without a common pattern of abnormal rhythmic EEG findings.
Postinflammatory hypopigmentation: a comprehensive review of treatments
Published in Journal of Dermatological Treatment, 2022
Pamela N. Madu, Nicole Syder, Nada Elbuluk
Postinflammatory hypopigmentation occurs secondary to an intrinsic or external insult to the skin. A thorough clinical history is essential to diagnosing this condition and identifying the underlying cause. The pathogenesis of PIH has not been fully elucidated. Proposed mechanisms include decreased melanin production, blocked transfer of melanosomes to keratinocytes, and melanocyte loss (14). Histopathological studies suggest that suppression of melanogenesis serves a primary role in postinflammatory hypopigmentation as opposed to melanocyte loss (1,14). In a theory known as ‘individual chromatic tendency’, Ruiz et al. proposed a genetic predisposition toward hyperpigmentation or hypopigmentation through the inheritance of ‘strong’ and ‘weak’ melanocytes, respectively (15). They purport that ‘weak’ melanocytes are easily damaged in response to inflammation leading to hypopigmentation, and ‘strong’ melanocytes are more likely to respond with hyperpigmentation (15). Since the emergence of this theory, there have been no countering theories or additional studies to evaluate this hypothesis further.
Intense pulsed light treatment for Becker’s nevus
Published in Journal of Dermatological Treatment, 2021
Pin-Ru Wu, Lan-Jun Liu, Yi-Xin Zhang, Ying Liu, Xiao-Xi Lin, Gang Ma
The long-pulse lasers had been used for the treatment of hypertrichosis in BN. Long-pulsed alexandrite 755-nm laser without cryogen spray cooling was found to be reasonably efficacious minimizing both hyperpigmentation and hypertrichosis in a study of 11 patients who received 2–12 treatments (10). The 694-nm long-pulsed ruby laser effectively reduced hair density and pigmentation by 90% in a single case (11). While hypopigmentation and skin texture change were observed in some patients. The long-pulsed 808/810-nm diode lasers with low-fluence high-repetition-rate were used for hair removal of hypertrichosis in 15 BN patients, there was significant hair clearance at 6 months (score 3.9) and 12 months (3.5) without reduction of pigmentation (12). A case report of combination long-pulsed 1064nm Nd:YAG and 755-nm alexandrite lasers with skin cooling obtained a significant reduction in both hyperpigmentation and hypertrichosis (13).