Cause Of Pigmentation Research Articles

Perioral pigmentation

Perioral pigmentation is a commonly encountered condition in the skin Out Patient Department (OPD), occurring due to a variety of primary as well as secondary causes. The affection of the perioral skin being readily visible negatively impacts the patient’s quality of life. As the etiology of perioral pigmentation is multifactorial, treatment modalities vary according to the cause. The perioral skin, because of its location close to the mouth, is exposed to various allergens associated with food, saliva, toothpaste, cosmetics, etc., which can all lead to allergic manifestations resolving with pigmentation. Certain other dermatoses like melasma can first present with pigmentation over the perioral region. Infections like chikungunya and dengue and infestation with Demodex mite can also lead to pigmentation at this site. Perioral pigmentation can also be a marker of underlying systemic disease. Localized lentigines-like pigmentation can be associated with various cancer predisposition syndromes like Peutz-Jeghers syndrome. Diffuse pigmentation can occur due to Addison disease, vitamin deficiencies, or can be drug-induced. All these causes of pigmentation are seen more commonly in type IV and V skin. Currently, very little literature is available elucidating the cause of perioral pigmentation and the diagnostic approach. This article reviews the causes of perioral pigmentation and highlights their important features.

Oral and nail pigmentations: a useful parallelism for the clinician.

Oral (OP) and nail (NP) pigmentations may occur simultaneously in physiological or pathological conditions, and may be a sign of underlying syndromic conditions that necessitate further investigation and treatment. Interestingly, the nail unit and oral cavity show a clinical parallelism that may help the clinician to conduct a correct examination and reach a prompt diagnosis. Both OP and NP can manifest clinically with focal or diffuse involvement and are due to external factors (exogenous pigmentation, drug-induced pigmentation) or endogenous factors (racial pigmentation, post-inflammatory pigmentation, nevi, genetic conditions and other disorders). The most concerning differential diagnosis is melanoma. Here we report the pathogenetic basis of OP and NP, together with the description of similar clinical features. To the best of our knowledge this is the first paper to summarize and describe the causes of pigmentation of both the oral cavity and the nail unit.

Dermoscopy and confocal microscopy patterns of mucosal melanosis

Melanosis is the most common cause of pigmentation of the mucosal areas. Mucosal melanoma is rare; however, at early stages, the differential diagnosis with benign melanosis can be challenging. Here, we provide a brief review of dermoscopy and reflectance confocal microscopy features of melanosis of the genital and oral mucosa.

Optic nerve gray crescent can confound neuroretinal rim interpretation: review of the literature

The optic nerve gray crescent can be of clinical significance if unrecognized during assessment for glaucoma. It has a characteristic appearance of a slate gray area of pigmentation within the disc margins and commonly appears along the inferotemporal or temporal neuroretinal rim areas. This type of disc rim pigmentation can create the impression of neuroretinal rim thinning, and thus lead to the misdiagnosis of glaucoma or “glaucoma suspect” with attendant implications for overtreatment or unnecessary close monitoring of such patients. The gray crescent is more common in African Americans than whites (prevalence rate 27% vs 7%) and is bilateral in at least 58% of cases. It has been reported in association with Kjer optic atrophy type 1. Suggested causes of the gray crescent include an accumulation of melanocytes, or retinal pigment epithelium cells partially located in the optic nerve head region if Bruch’s membrane extends internal to the peripapillary scleral ring. Other causes of pigmentation that may resemble gray crescent are conus pigmentosus and variations of peripapillary atrophy. When a gray crescent is present, clinicians should endeavour to identify the true anatomical disc margins via the scleral lip and, if necessary, evaluate the patient further with imaging and visual field studies.

Review of Topical Lightening Agents

Hyperpigmentation occurs when there is an increase in melanin content in the skin. It can be localised i.e. limited to a certain area or it can be diffuse i.e. occurring all over the body. Localised form of hyperpigmentation can happen as a result of injury or inflammation from conditions such as Acne, contact dermatitis, lupus etc known as post inflammatory hyperpigmentation or Melasma. Diffuse generally results from a systemic disease, drug or neoplasm. Localised hyperpigmentation like PIH and melasma can lead to a lot of psychological distress with skin type IV and above being particularly susceptible. It is not only important to find the cause of pigmentation in order to arrest further progression but it is also important to treat the pigmented lesions. Further prevention should advocate the use of daily sun protection with sunscreen agents and other sun avoidance measures.

Five patients with melanosis of the nipple and areola clinically mimicking melanoma

Pigmented lesions on the nipple and areola concern patients and physicians as melanoma and pigmented mammary Paget's disease must be considered in the differential diagnoses. There have been only six case reports of melanosis of the nipple and areola in the medical literature yet five cases presented to our department in a 26-month period. Five women aged between 26 and 34years presented with pigmentation of the areola and/or nipple. Two patients were pregnant and one also had vitiligo. All lesions were solitary, eccentrically located with a sharp but irregular contour, and homogeneous pigmentation. Dermoscopy was performed and reassuring features included light to dark brown cobblestone pigmentation with ring-like structures and reticulation. Blue-white veil and irregular centred black dots were not seen. Histology confirmed melanosis of the nipple and areola. Melanosis of the nipple and areola is probably significantly underreported in the medical literature and, based on our experience, is likely to be the most common cause of pigmentation at this site. Considering this, benign condition on clinical and dermoscopic features should lead to biopsy rather than excision to confirm the diagnosis. Further reports of the dermoscopic features will help to define this condition further.

Persistent post‐sclerotherapy pigmentation due to minocycline. Three cases and a review of post‐sclerotherapy pigmentation

Post-sclerotherapy pigmentation, usually overlying the treated veins and independent of any drug ingestion, is common. This pigmentation is brown and represents haemosiderin and sometimes melanin as well. It usually slowly fades over a period of months, only uncommonly persisting for years. Cutaneous pigmentation due to minocycline ingestion is a known but rare adverse effect. It usually appears as a round or irregular shaped patch that is dark blue to black, representing minocycline moieties and iron complexes. Its persistence for years is common. Clinically and histopathologically, these two causes of pigmentation are quite distinct. In the absence of ulceration, minocycline pigmentation koebnerised by sclerotherapy has not previously been reported. To determine the nature of the pigmentation appearing in three patients who had been taking minocycline at the time, or shortly after, they had received sclerotherapy. Clinically, although this pigmentation had the usual distribution observed after sclerotherapy, it was persistent and appeared dark blue to black. The persistent post-sclerotherapy linear pigmentation observed in all three patients had the characteistics of minocycline pigmentation. This is the first report of such minocycline-aggravated post-sclerotherapy pigmentation. Persistent post-sclerotherapy pigmentation caused by minocycline is a risk associated with ingestion of this drug. Patients need to be warned of this risk because, unlike post-sclerotherapy pigmentation that develops in the absence of drug ingestion, minocycline-aggravated post-sclerotherapy pigmentation may persist for years.

Tracheobronchial Melanosis

The term “melanosis” originates from the Greek words: “melas” meaning “black,” and “osis” meaning “condition.” In medical literature, the term merely describes a condition in which there is an abnormal grayish-black or brownish-black pigmentation of an organ or a part. It does not imply that the pigment is “melanin,” although this may be true in most of the cases. Lipofuscin or other black pigment may be the cause of pigmentation. When the pigment is lipofuscin, sometimes the term “lipofuscinosis” is used; however, melanosis is the preferred term to avoid confusion caused by multiple terms. We define “tracheobronchial melanosis” (TBM) as “grayish or brownish-black pigmentation of the tracheobronchial mucosa” and describe a case of TBM with relevant review of the literature.

Apd1+, a gene required for red pigment formation in ade6 mutants of Schizosaccharomyces pombe, encodes an enzyme required for glutathione biosynthesis: a role for glutathione and a glutathione-conjugate pump.

Mutants in the adenine biosynthetic pathway of yeasts (ade1 and ade2 of Saccharomyces cerevisiae, ade6 and ade7 of Schizosaccharomyces pombe) accumulate an intense red pigment in their vacuoles when grown under adenine-limiting conditions. The precise events that determine the formation of the pigment are however, still unknown. We have begun a genetic investigation into the nature and cause of pigmentation of ade6 mutants of S. pombe and have discovered that one of these pigmentation defective mutants, apd1 (adenine pigmentation defective), is a strict glutathione auxotroph. The gene apd1+ was found to encode the first enzyme in glutathione biosynthesis, gamma-glutamylcysteine synthetase, gcs1+. This gene when expressed in the mutant could confer both glutathione prototrophy and the characteristic red pigmentation, and disruption of the gene led to a loss in both phenotypes. Supplementation of glutathione in the medium, however, could only restore growth but not the pigmentation because the cells were unable to achieve sufficient intracellular levels of glutathione. Disruption of the second enzyme in glutathione biosynthesis, glutathione synthetase gsh2+, also led to glutathione auxotrophy, but only a partial defect in pigment formation. A reevaluation of the major amino acids previously reported to be present in the pigment indicated that the pigment is probably a glutathione conjugate. The ability of vanadate to inhibit pigment formation indicated that the conjugate was transported into the vacuole through a glutathione-conjugate pump. This was further confirmed using strains of S. cerevisiae bearing disruptions in the recently identified glutathione-conjugate pump, YCF1, where a significant reduction in pigment formation was observed. The pump of S. pombe is distinct from the previously identified vacuolar pump, hmt1p, for transporting cadystin peptides into vacuoles of S. pombe.