Cases of cutaneous tattoo due to graphite are not described in the literature, probably due to its banality more than to its rarity; however, some cases (1, 2) of graphite tattoo of the oral cavity were reported. In the mouth the differential diagnosis from amalgam tattoo and melanocytic lesions was discussed, leading sometimes to the histological examination (1) and to an autologous connective graft to obtain an esthetically acceptable outcome (2). The graphite tattoo of the oral cavity occurs earlier than the amalgam; the histology finding shows a foreign body granuloma. In the cases here reported the differential diagnosis from a dermal melanocytic proliferation was easy for the small size of the lesions, which were non palpable, their dot-like or linear aspect and absence of initial growth. Although we did not perform a histological examination, based on the analogy with the oral lesions, it is likely that the histological findings of the skin lesion induced by graphite are consistent with a foreign body granuloma arisen around fragments of the pencil lead. The latter essentially consists of non-degradable carbon and of a various amount of clay that is directly related to the hardness of the mine, and then to the possibility of obtaining a more precise tract. As the perfectly done tattoo, the pencil-induced tattoo is characterized by non-biodegradability and therefore by its long persistence in time.
Xanthelasmoid mastocytosis (XM) is not exceptional, although in the literature only fifteen cases are reported; according to some Authors 25% of cases of childhood mastocytosis really present xanthelasmoid lesions (5). XM poses some problems, the first of which is to understand what is responsible for the yellow color: according to many Authors (6, 7) it depends on massive infiltration of the superficial and mid dermis by mast cells; indeed the yellow color is never found in macular mastocytosis; in some cases it may be related to excessive vascularization (4). A second problem is diagnostic; the yellowish color often leads to suspect juvenile xanthogranuloma and sometimes only histology can resolve this doubt; taking into account that we are dealing with two frequent hyperplastic disorders of the early years of life, the two diseases can coexist (2); XM must also be differentiated from other xanthomas and pseudoxanthoma elasticum (4). A final problem is if the xanthelasmoid aspect is a negative prognostic factor, and in particular whether it is associated with a longer persistence of the disease (1); according to other Authors (3) the xanthelasmoid appearance would have no prognostic relevance, especially no relation to systemic involvement.
ALDY was identified in 2003 by Annessi and Paradisi (1). So far less than 60 cases have been described in the world literature, but its incidence would increase if a biopsy was performed in all cases of clinically suspected superficial scleroderma or patch mycosis fungoides, two conditions that have a clinical course similar to ALDY. Initially described in the Mediterranean basin, ALDY was later also reported in America (6), Japan (4) and elsewhere. ALDY shows no sex preference (33 M, 25 F) and the average age at diagnosis is in the peripubertal period, ranging between 2 (4) and 79 (3) years. We do not know the cause even if hepatitis B vaccination (7), Borrelia (8), contact allergy (2) and mycosis fungoides (5) were hypothesized. The lesions almost always affect the lower trunk and are single or few; anyway they can be counted. We are dealing with erythematous lesions, with fairly sharp borders, that enlarge centrifugally; the mature lesions are 5-20 cm in size, with a red, sometimes brownish peripheral rim, while the central inflammation tends to disappear leaving a hypopigmented outcome. After years the single lesion regresses completely without residua, but usually new lesions appear with the same clinical course; so the disease is chronic, being able to last as in our case more than 10 years. Histological examination shows in the epidermis basket hyperkeratosis, normal granular layer, thinner or quadrangular epidermal ridges according to the evolutionary stage, vacuolar degeneration and keratinocyte necrosis exclusively or mainly at the level of the dermal base of the ridges, and, in the superficial dermis, lichenoid, polyclonal band infiltrate (1). (...).
When facing acquired bullous lesions in a child you can think of viral or bacterial infectious causes such as it happened in the present case; when the lesions last for a long time you must also exclude an autoimmune bullous disorder. In the actual case the correct diagnosis arrived late due to the presence of frankly bullous lesions, which are rare in the hypersensitivity to mosquito, and the localization of lesions even in normally covered sites; the child however lived in the country and often played out-doors naked. Physicians should consider hypersensitivity to mosquito when facing bullous lesions only in exposed locations, mostly on the legs, when the bullous lesions occur on pre-existing wheal lesions, in case of short duration of the bullous lesions that recur for a few weeks, especially at the beginning of the hot season, and coexistence of itchy, papular and vesicular lesions on the typical exposed areas of hypersensitivity to mosquito.
After the propranolol revolution of 2008 (7) other beta-blockers have been used as anti-angiogenic factors in an attempt to decrease the side effects of propranolol, both those related to its activity on beta 2 receptors as hypoglycemia, bronchospasm, and those related to the lipophilicity of propranolol and its ability to cross the blood-brain barrier, such as sleep disorders and possible long-term effects on memory and cognitive activity (6). Atenolol is a beta 1 selective beta blocker medication, then in normal doses does not act on the bronchial muscles. A fundamental difference compared to propranolol is its strong hydrophilicity that significantly reduces its penetration into the brain. After oral administration it is absorbed and enters the bloodstream without being metabolized in the liver unlike propranolol, whose hepatic metabolism, significantly different from subject to subject, could affect its plasma concentration. Another difference compared to propranolol is its longer plasma half-life - 5-8 hours - that allows once-daily dosing. So far in the literature (1, 2, 3, 4, 5, 8, 9, 10, 11) were treated 213 cases of infantile hemangioma with atenolol at the average dosage of 1-1,5mg kg / per day as a single daily administration. In all cases in which atenolol and propranolol were compared, atenolol showed equivalent efficacy, better compliance (single dose) and reduced side effects or similar incidence of them as compared to propranolol. The point in favor of atenolol are administration once a day and minor side effects related to low activity on beta 2 receptors and no exceedance of the blood-brain barrier; the points in favor of propranolol are is more frequent use in children and increased vasoconstrictor peripheral activity related to its action on beta 2 receptors.
Cockade nevus consists of three concentric lesions as follows: a central common nevus, surrounded by a halo of non pigmented skin and finally by an external nevus ring, which is concentric to the previous other two. The central nevus can be junctional, compound or dermal. The latter can be pigmented (3, 5) or skin colored (6). The two external rings of cockade nevus are less variable. The same individual has a single cockade nevus or two or many, even thirty (4). Histologically, in the non pigmented intermediate ring there is a junctional nevus. The latter lacks pigment and inflammatory infiltrate. However, the immunohistochemical studies show that the epidermal melanocytes of the poorly or not pigmented intermediate ring are DOPA-positive, testifying their capability of synthesizing melanin. These findings confirm that the lack or scarcity of pigmentation in the intermediate ring is only due to a functional block of melanin synthesis (4) and not to a destruction of melanin or melanocytes. The presence of cockade nevi has been related to other problems such as heart malformations (2), juvenile diabetes and mainly spinal dysraphism (1).
The diagnosis, prognosis and therapy of a cutaneous proliferation of melanocytes first observed due to its rapid growth are strongly influenced by the age of the subject (14): in the child it is almost always a nevus, in adults it is very often a melanoma. This dilemma did not exist until 1948: until then any fast-growing melanocytic proliferation was a melanoma regardless of the age. In 1948 Spitz (12) sensed that the melanocytic proliferations in the child had a better prognosis and the following year Allen (1) declassified juvenile melanoma to the role of nevus, which is rightly known today under the name of Spitz nevus (SN). However, the memory of the previous situation is not entirely disappeared and still today dermatologists who do not see many children (13) deal with Spitz nevus as if it was a melanoma; therefore, the natural history of SN is little known because usually SN is removed. The natural history of SN, which is well-known by pediatric dermatologists, shows an initial growth phase lasting 6-12 months, followed by a phase of involution, like so many other childhood proliferations, from infantile hemangioma to juvenile xanthogranuloma and mastocytoma. This natural history is observed both in the non-pigmented, angioma-like variant and in the pigmented SN that in the child have a similar frequency; the pigmented variant of SN is indistinguishable from Reed nevus (11) based on clinical or dermoscopic and sometimes even histological findings, so that some Authors (8) speak of Spitz-Reed nevus. The non-pigmented variant of SN, which is usually palpable in the form of plaque or nodule, in the involution phase may undergo a complete clinical regression with mild atrophy or become a common pigmented melanocytic nevus (4); the pigmented variant, usually junctional or plaque, in the involution phase tends to flatten when palpable or, when junctional, to take on a more regular profile with loss of pseudopods, which are clinically visible in the growth phase, and reduced pigmentation (2, 3, 6, 7, 10, 13). (...)
Congenital melanocytic nevus can mimic all the features of melanoma as size, morphological changes, inflammation, ulceration, regression, recurrence after excision. The clinical features of the here reported congenital nevus simulate a melanoma of the nail matrix, in particular the Hutchinson sign - involvement of the lateral nail fold and hyponychium - and the pseudo-Hutchinson - involvement of the epinychium-. In the nevi of children affecting the nail lamina also the dermoscopy signs can simulate melanoma, mainly the darker pigmentation, the pseudo-Hutchinson sign, the sign of the triangle - larger proximal part of melanonychia - and the presence of points and globules (2). This is why the irregularities of the dermoscopic pattern according to some Authors (1) are not a valid discriminating criterion between nevus and melanoma in children (1).
Annular lichenoid dermatitis of youth (ALDY) is a chronic-recurrent dermatitis of unknown etiology; ALDY is characterized clinically by annular erythema and histologically by vacuolar degeneration and keratinocyte necrosis exclusively or mainly at the level of the dermal base of the ridges, and, in the superficial dermis, by lichenoid, polyclonal band infiltrate. The confusion with superficial localized scleroderma can only be clinical because both often have abdominal annular erythematous lesions.
The cellular proliferations of the skin, especially malignant tumors, are rare in children as compared with adults. However, such proliferations are concentrated in the first months of age (Fig. 790). According to some Authors (25), this is why in the neonatal period whatever tumefaction of doubtful diagnosis should induce to rule out tumors. Characteristically, the proliferations of the first months present a very wide clinical spectrum, ranging from an isolated cutaneous lesion to the generalized involvement of the skin till the multisystem involvement. Their prognosis is also very variable, ranging from the spontaneous regression to the exitus. The tendency to the spontaneous regression is much higher at this age. It does not depend on the cell type affected, being practically detectable in all the neonatal proliferations, both benign and malignant, from hemangioma to mastocytoma, to juvenile xanthogranuloma, myofibromatosis, Langerhans cell histiocytosis and neuroblastoma. (...).