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Case 2.7
Published in Monica Fawzy, Plastic Surgery Vivas for the FRCS(Plast), 2023
How would you manage this scenario?This photograph shows a baby with what appears to be a medium-sized congenital melanocytic naevus (CMN) on her anterior scalp, the management of which is widely debated.I will first ensure there are no other pigmented naevi, or neurological signs or symptoms, before concentrating on the management of the naevus itself and then counselling the parents.The associated lifetime risk of melanoma is much lower than initially reported and is dependent on the size of the lesion and, more importantly, on any evidence of neurocutaneous melanosis.
Phakomatoses (Neurocutaneous Syndromes)
Published in Swati Goyal, Neuroradiology, 2020
Neurocutaneous melanosis Hairy or deeply pigmented neviMelanosis of the leptomeninges (intensely enhancing)
Malignant tumors
Published in Archana Singal, Shekhar Neema, Piyush Kumar, Nail Disorders, 2019
Arsenical keratoses are mainly seen in regions with a high content of arsenic in the drinking water [India (West bengal), Bangladesh] or after professional exposure.9,10 This may be associated with arsenical melanosis. The therapeutic administration of arsenical compounds such as Fowler’s solution or Asiatic pills was declared obsolete many decades ago, although there are countries in which they are still used to treat psoriasis and lichen planus. With the advent of Ayurvedic medicine, a new source of chronic arsenicism has appeared.11 Patients with arsenical keratoses have a very high risk to develop various cutaneous as well as internal cancers. The diagnosis must therefore prompt a general check-up of the patient. Arsenical keratoses appear as small, hard keratotic papules that develop anywhere on the skin, but particularly on the palms and soles. They are said to exhibit a higher autofluorescence with ultraviolet light than the surrounding epidermis of the palms and soles.10 Around and under the nails, keratotic papules and plaques develop that may eventually degenerate to Bowen’s disease and/or SCC.12 Nail dystrophy is an unspecific sign. Actinic keratosis, Bowen’s disease, SCC, and basal cell carcinoma (BCC) are the most important differential diagnoses.
Association of Candida esophagitis with acute esophageal necrosis
Published in Baylor University Medical Center Proceedings, 2022
Muhammad Sheharyar Warraich, Bashar Attar, Shazaq Khalid, Muhammad Ali Khaqan
AEN is exceedingly rare, with an incidence of 0.01% to 0.28%.3 It was first described in 1914 by Brekke et al but did not get its current name until 1990.2,4 Some commonly described risk factors associated with this condition include renal insufficiency, diabetes mellitus, hypertension, atherosclerotic vascular disease, sepsis, and hypothermia.5 Mucosal barrier dysfunction seems to be the common endpoint of the different theories that have attempted to explain the pathogenesis of AEN. AEN typically occurs in critically ill patients who have multiple chronic conditions. It usually presents with upper gastrointestinal bleeding, but patients may display other symptoms like nausea, vomiting, dysphagia, and abdominal pain. Diagnosis is made on direct visualization during esophagogastroduodenoscopy. Biopsy is associated with a small risk of perforation and is supportive but not required for the diagnosis. It can help rule out infections and some other similar-appearing conditions like melanosis, melanoma, and acanthosis nigricans. Treatment is mostly supportive and includes aggressive hydration, proton pump inhibitors, and antimicrobials for cases that have a histologically confirmed infection. Total parenteral nutrition is a consideration for such patients due to the risk of perforation associated with the use of enteral tubes. Surgical management is necessary for the subset of patients whose disease is complicated by perforation or mediastinal disease. AEN is known to have a high mortality rate, with one study suggesting a rate up to 28%.6
Blue nevi of the palpebral conjunctiva: report of 2 cases and review of literature
Published in Orbit, 2022
Armida L. Suller, Jiawei Zhao, Nickisa M. Hodgson, Gulsun Erdag, Raja R. Seethala, Aparna Ramasubramanian, Roxana Fu
Clinically, blue nevi can simulate other pigmented lesions of the conjunctiva, such as common nevus, racial melanosis, PAM, melanoma, and pigmented squamous cell carcinoma. Common nevus is a benign melanocytic tumor, which typically presents as a variably pigmented, circumscribed, slightly elevated lesion with intralesional cysts in the bulbar conjunctiva.25 Although common nevus is the most frequently encountered pigmented tumor on the ocular surface, it rarely presents in the tarsal conjunctiva.25 Racial melanosis is a bilateral condition typically found in darkly pigmented individuals and appears as flat conjunctival pigmentation.31 PAM presents as a diffuse, flat, patchy brown pigmentation of the bulbar conjunctiva, but it can involve the palpebral conjunctiva as well.31 Malignant melanoma appears as a brown to tan, elevated mass in the bulbar conjunctiva with surrounding PAM and prominent feeder vessels.30,31 Involvement of the palpebral conjunctiva or eyelid margin is unusual in melanoma, but it is associated with higher risk of recurrence, orbital exenteration, metastasis, and death.30 Given the rarity of benign lesions, such as blue nevi in the palpebral conjunctiva, any pigmented lesion in this location should raise suspicion of melanoma.30 Squamous cell carcinoma can be pigmented in rare cases and has been documented in the bulbar and palpebral conjunctiva in both Whites and non-Whites.32,33
A prospective, split-face study comparing 1,064-nm picosecond Nd:YAG laser toning with 1,064-nm Q-switched Nd:YAG laser toning in the treatment of melasma
Published in Journal of Dermatological Treatment, 2022
Jun Ki Hong, Sun Hye Shin, Su Jung Park, Seong Jun Seo, Kui Young Park
Melasma is an acquired skin melanosis and one of the most common facial pigmentation disorders. Three types of melasma exist based on the location of the pigmentation: epidermal, dermal, and mixed. Genetic background, chronic exposure to ultraviolet (UV) radiation, and hormonal factors have been proposed as the main causes of melasma, as they stimulate the abnormal activation of melanogenesis (1,2). A complex pathogenesis with multiple factors makes the treatment of melasma more challenging. Topical agents, such as hydroquinone, retinoic acid, alpha-arbutin, and glycolic acid, have been widely used to exert anti-melanogenic effects (3). However, the outcomes are marginal; local irritation, unwanted hyperpigmentation, and high relapse rates are common. Laser- and light-based devices have been considered as adjuvant treatment options for patients with moderate-to-severe melasma in combination with other modalities, including photoprotection, topical bleaching agents, chemical peels, and systemic therapies; however, they only result in partial improvement, and high rates of recurrence and complications have been reported. In particular, non-ablative fractional laser shows a high likelihood of postinflammatory hyperpigmentation in Asian patients (Fitzpatrick skin type III–IV) (3–5).