Background. Acne vulgaris is a very common chronic disease that affects mainly adolescents and has a negative effect on their quality of life. Objective and methods. The aim of this study was to determine the prevalence of acne in adolescents, to characterize this condition and estimate its impact on adolescents’ quality of life. For this purpose, a questionnaire was distributed in 4 schools to teenagers aged 14 to 17 years in 2021. Results. A sample of 237 adolescents was analyzed. The overall prevalence of acne was 71.3%. The median age was 16 years, acne evolution was favorable in 53.3% of cases, 44.4% had permanent lesions and 75.7% experienced flare ups. Comedonal acne lesions were reported by 74.0% of adolescents and inflammatory acne was reported by 69.2%. As for severity, 27.8% had mild lesions and 12.4% had moderate lesions. We found that female gender, topical and systemic treatment, and acne duration had a statistically significant association with acne severity. There was also an association between female gender, relapses, and acne severity in the last 12 months and worse quality of life scores. Discussion. In our study, the prevalence of acne was high, comedonal and inflammatory lesions were the more frequent type of acne, and severe forms were not frequent. Several adolescents reported relapses and the quality of life was undoubtedly affected. These findings were in accordance with recent literature and strengthen the available data. The extensive characterization of this population along with the risk factors that we found to be associated with acne severity, should be taken into account when treating these adolescents.

Fibrolipomatous hamartoma (FLH) is a benign proliferation characterized by the presence in the deep dermis of mature adipose tissue lobules separated by bundles of fibrous tissue. The variant best known to internists, neurologists and radiologists is the perineural FLH, which is localized around nerves, most frequently the median nerve, followed by the ulnar and sciatic (5). The variant best known to dermatologists and pediatricians is the precalcaneal FLH, which is evident from the earliest stages of life with a medial precalcaneal swelling of parenchymatous consistency and of little clinical importance. It tends to regress spontaneously, but even when it does not regress, it does not hinder walking (4). Rarer variants of FLH can affect the respiratory tree, localizing to the nasopharynx (3), the bronchi (1), or the lung (7).
\nAlthough the most frequently affected skin site is the medial precalcaneal one, FLHs localized always in the calcaneal area, but posteriorly, have been described (6). Both in the latter and in the more frequent one located in the classical site, the most accredited pathogenetic hypothesis is a failure to regress of the pericalcaneal, fetal life adipose tissue. However, this hypothesis does not explain the location to the trunk of the current case.
\nFrom a diagnostic point of view, when FLH is localized in the classical site, the diagnosis is clinical and a biopsy is not necessary. In cases located elsewhere, ultrasound is useful, showing hypoechoic lobules of the same echogenicity as the adipose tissue, separated and surrounded by hyperechoic bands that correspond to the dermal connective tissue (2).
\nThe benignity of the lesion, the absence of functional damage, the lack of esthetic damage, and the tendency to spontaneous regression make any therapy useless, once the diagnosis has been ascertained.

Median canaliform dystrophy is a rare form of nail abnormality, first described by Heller in 1928 (5). It usually involves one or both thumbnails as a midline longitudinal split with multiple transverse lines radiating from the center, resembling a fir tree (5). Toenails or other fingernails are rarely affected (4, 5). There are several reports of median canaliform nail dystrophy occurring after isotretinoin treatment of acne vulgaris (1, 3) and one case report after cryotherapy of periungual warts (2). Although minor trauma to the nail matrix has been hypothesized as an etiology, most cases are idiopathic, and patients could not identify any preceding trauma (2). Familial cases have been reported, but the role of genetic factors in these cases is not well established (5). Median canaliform nail dystrophy should be differentiated from habit tic deformity, in which the patient admits manipulation of the periungual area when questioned appropriately (5). Our patient and his parents denied any habitual picking or trauma to toenails. The involvement of both great toenails and the onset in early infancy made habit tic deformity less probable. Median canaliform nail dystrophy occasionally resolves spontaneously within several months to years (3, 5). The patient should avoid any minor trauma to the nail plate and the periungual area. It is recommended to keep nails short and prevent any nail plate catching by covering it with either tape or a nail wrap (5). Topical corticosteroids or tacrolimus 0.1% under occlusion are other treatment options, but their effectiveness must be elucidated (1). In conclusion, the current case has been described for the exceptional involvement of both big toes and for the early age of onset.

Subcutaneous panniculitis-like T cell lymphoma (SPTCL) is a rare peripheral T cell lymphoma presenting with tender nodules. We report a case of a 5-year-old boy who presented with tender nodules, lymphadenopathy, hepatosplenomegaly and pancytopenia and was treated with oral corticosteroids and cyclosporine. The report highlights the rarity of this case, associated features and response to corticosteroids and cyclosporine.

Untreated maternal hyperthyroidism during pregnancy can have severe consequences for both the mother and the fetus (5). The most commonly used drugs are synthetic antithyroid drugs such as methimazole (MT), carbimazole (CR), which is metabolized to MT, and propylthiouracil (PR). These drugs are practically equivalent in terms of activity, which consists in inhibiting the synthesis of thyroxine and 2,5,3 triiodothyronine by the thyroid. The choice of one drug over another basically depends on its side effects. Aplasia cutis is an embryogenetic defect that consists in the failure to close the skin and sometimes the underlying planes; it is in most cases an isolated defect but can be associated with other congenital malformations. Among the causal factors, which in most cases are not identifiable, drugs and genetic factors should be considered. Among the drugs benzodiazepines, low molecular weight heparins, leflunomide, and azathioprine were indicated; however, the drugs most frequently involved are CR and its metabolite MT (3). In a 2016 meta-analysis, the Authors (4) identified 61 cases of ACC induced by synthetic antithyroid drugs in the literature, of which 2 caused by PR and 59 by MT / CR administered in the first 10 weeks of pregnancy. This review showed that in 39.6% of cases ACC is associated with other malformations such as dysmorphism, anomalies of the fingers, persistence of urachus, choanal atresia, and encephalocele, giving rise to the concept of synthetic antithyroid drug embryopathy. The incidence of this embryopathy is less than 3% (4), much lower than other teratogens, for example retinoids. The responsibility of MT is supported by a study (2) that reported a higher incidence of ACC in pregnant women with normal functioning thyroid in a Spanish region where farm animals had been treated with MT to increase their body weight. The clear preponderance of cases induced by MT / CR would suggest preferring the PR in the first three months of pregnancy (6, 7), but there are still doubts about the choice of antithyroid drugs. In fact, although ACC and the malformations we have mentioned are more frequent with MT / CR, PR is also responsible for teratogenic effect, albeit of a different spectrum than MT / CR. Moeover, above all PR is sometimes responsible for liver disease so severe that it leads to liver transplantation (1). It is possible that genetic factors contribute to the pathogenesis of MT / CR embryopathy, as shown by the familiarity rate - 10% - (4), while in our series of 144 cases of ACC we found 8 family cases with an incidence of 5.5%, not unlike that of other Authors (3).

Goldenhar syndrome (GS) or oculo-auriculo-vertebral dysplasia (4) is a diverse and poorly understood disorder that is usually apparent at birth. The incidence of Goldenhar syndrome has been reported to be varying from 1:3500 to 1:5600 live births and it is present in 1:1000 children with congenital deafness with a male to female ratio of 3:2 (9). Its origin is due to the abnormal development of vascularization in 4th week of pregnancy when it comes to the development of the 1st and 2nd pharyngeal arches responsible for growth of craniofacial structures (2). There is not enough information to identify its etiologic factors. Some cases appear to be genetic, while others occurring in a sporadic manner (2) are probably due to environmental factors. Abnormalities of chromosomes have been identified (10). The ingestion of some drugs such as cocaine, thalidomide, retinoic acid, and tamoxifen by the mother during pregnancy were also related to the development of the disease (6), so as maternal diabetes (1). It was not possible to determine the etiology in our case since the mother and other close relatives were not available for interrogation. The spectrum of GS abnormalities ranges from mild forms to severe ones and include patients with barely noticeable facial asymmetry to very pronounced facial defects with more or less severe abnormalities of internal organs and/or skeleton. GS can involve ocular anomalies, including microphthalmia, anophthalmia, epibulbar dermoid (or lipodermoid) tumors, eyelid colobomas, and hypertelorism, aural defects, such as preauricular tags, anotia, microtia, and hearing loss, and vertebral abnormalities, such as scoliosis, hemivertebrae, and missing ribs (8). The patient can exhibit also dentofacial abnormalities with unilateral facial hypoplasia, due to hypoplasia of the zygomatic, maxillary and mandibular area, and prominent forehead. There may be an association with other major organ system anomalies including cardiac structural defects, renal agenesis, pulmonary agenesis, and vascular anomalies. Despite the reported frequency of cardiovascular alterations (tetralogy of Fallot and transposition of the great vessels) ranging from 5 to 58% (7), in our patient no cardiovascular alterations were found. Renal problems commonly associated to malformations of the ears were not diagnosed. Central nervous system anomalies such as hydrocephalus, meningoencephalocoele and mental retardation (5) have been associated with the syndrome; however, our patient did not exhibit any of those defects. However, as far as we know, this is the first case described presenting breast hypertrophy with retraction of the nipple. With all these anomalies, no agreeable clinical diagnostic criteria have been reported in the literature. There are no specific genetic tests. The presence of auricular abnormalities, mandibular hypoplasia, and spinal abnormalities can be put together to consider it as a case of OAV spectrum. Feingold and Baum offered for the delineation of Goldenhar syndrome working criteria that included a lipodermoid or lipoma of the conjuctiva, an epibulbar dermoid or an upper lid coloboma and two of the following three criteria: small size or abnormal shape of the ears or preauricular skin tags or both, unilateral aplasia or hypoplasia of the ramus of the mandible and vertebral anomalies (3). In our case, the diagnosis was established according to these criteria. Treatment of patients with GS is complex and should be divided into stages, according to patient’s age, as well as the extent and severity of observed abnormalities. In some mild cases, no treatment is needed. In uncomplicated cases, cosmetic damage is a basic concern. Otherwise, correction of all malformations requires long-lasting, multistage and complex treatment plan. Cleft repair, corrections of colobomas, ear anomalies at the age of 6 to 8 years and removal of dermoids and preauricular tags at the age of 5 are principal reconstructions. The complex treatment is focused not only on physical care, but also on the prevention and treatment of the psychosocial aspects of the malformation.

The common embryonic origin of neuroid and melanocytic cells justifies the simultaneous presence of the two cell types in the same neoformation (3). Neurofibroma (NF) can be solitary, diffuse when it has a large extension, and plexiform when it appears as a collection of multiple nodules and cordoniform structures. 10% of diffuse NFs and almost all plexiform NFs are associated with neurofibromatosis (1, 2). Then there is the so-called pigmented or melanotic NF, in which a part of the cells making up the neoplasm is loaded with melanin; this finding is present exclusively in syndromic NF, ie associated with neurofibromatosis. Thus, screening for neurofibromatosis is warranted in the case of plexiform, diffuse, multi-element and melanotic NF (4). In 28% of syndromic NFs and in 4.6% of sporadic NFs there is also a proliferation of epidermal melanocytes, most often in the form of lentiginous melanocytic hyperplasia, but exceptionally in the form of junctional nevus (4). Before assuming that melanocytic hyperplasia is related to NF, it must be considered that melanocytic hyperplasia is also found in café au lait spots and therefore we could face a café au lait spot superimposed on the NF; this hypothesis should be discarded since lentiginous hyperplasia is also found in sporadic NF and because in any case the histological finding does not always correspond to a clinically evident hyperpigmentation. A casual collision between two different pathologies could also be hypothesized, but this hypothesis is discarded because the limits of melanocytic hyperplasia coincide perfectly with those of the underlying NF (4).

Along Blachko’s lines are distributed diseases with Mendelian inheritance such as incontinentia pigmenti, polygenic hereditary diseases such as psoriasis or atopic dermatitis (3), nevi such as verrucous epidermal nevus (VEN) and its inflammatory variant (1), and acquired diseases such as lichen striatus (LS). All these diseases share a condition of mosaicism, that is, they presuppose the existence of a gene mutation, often post-zygotic, that gives rise to a clone of cells different from all the others. The type of mutated gene is responsible for the different morphology of these diseases, but the distribution on the skin of the mutated clone is always the same; therefore, it does not depend on the gene, but on the time in which the mutation occurred and on the stereotyped movements of the migrations that skin cells undergo during fetal life. If the nevus is very extensive and therefore secondary to an early mutation, other organs may be involved such as the nervous system, the eye, the skeletal system, as happening in epidermal nevus syndrome (4) or even some gonadal cells with the risk that the mutation is transmitted to the zygote of the offspring thus giving rise to a generalized inherited disease (5). VEN is usually present at birth; when it is localized in hidden locations or when it initially manifests with just hyperpigmented lesions it may become evident later. However, it is exceptional that it manifests itself at 8 years as in the present case. Its earliness and its morphology are able in most cases to easily differentiate it from an acquired inflammatory condition such as LS. LS is a self-healing inflammatory skin disease, usually asymptomatic, which affects the first years of age, usually between 5 and 15 years, and is distributed linearly along Blaschko’s lines, suggesting that on the line in which it occurs there is a clone of mutated cells as a result of a post-zygotic mutation: this mutation would give the cells involved a particular susceptibility towards an exogenous agent that, upon its arrival, would cause the transient inflammatory reaction (2). There are various hypotheses on the pathogenetic mechanisms that lead to the inflammatory reaction and its spontaneous regression. The present case has posed problems of differential diagnosis between VEN and LS. The histological findings were not able to eliminate the clinical doubt, indeed they added another possible differential diagnosis, i.e. inflammatory linear verrucous epidermal nevus. The latter diagnosis was discarded due to the lack of itching and obvious clinical signs of inflammation. Only prolonged clinical observation over time resolved the diagnostic doubt thanks to the persistence of the lesions and the greater evidence of papillomatous and warty structures.

Starting from the analysis of a clinical case of infantile mastocytosis followed for 18 years, the role of the history is emphasized both from the diagnostic and clinical monitoring point of view. The history is so significant that in most cases it is not necessary to perform a histological examination and sometimes even to evoke Darier’s sign to be sure of the diagnosis. And to monitor the clinical course of mastocytosis, which in the child is almost always characterized by spontaneous regression, it is sufficient for the mother to record the episodes of flushing, blisters, and wheals: their rarefaction with time attests to the regression of the disease. Systemic mastocytosis in the child is practically non-existent, so the dosage of serum tryptase is of little importance.

LPP is a rare variant of LP that is infrequently encountered in children. In a retrospective analysis of 316 pediatric patients with LP, only nine (2.8%) were diagnosed with LPP (4). Similarly, in a recent retrospective study of 76 pediatric patients with LP in South India, only one (1.3%) was diagnosed with LPP (6). It is commonly seen in middle-aged patients with high skin phototypes. LPP presents as chronic, acquired, violaceous to brownish-gray, oval macules, with poorly-defined borders (7). The lesions appear more frequently in the neck and face, but they can also affect the upper and lower extremities, and torso as well. LPP rarely affects the oral mucosa, scalp, palms, soles, and nails. Flexural involvement is seen in around 20% of cases with a concurrent photo-exposed distribution (5). LPP-inversus is a variant of LPP, limited to intertriginous and flexural areas, and sparing sun-exposed areas (3, 5). A skin biopsy will confirm the diagnosis. The histopathology findings include hyperkeratosis and vacuolar degeneration of the basal layer, dermal band-like or perivascular infiltrate, and melanophages. Superficial pigmentary incontinence can be seen (7). The main differential diagnosis of LPP is erythema dyschromicum perstans (EDP) or ashy dermatosis. EDP presents as non-pruritic, blue-gray macules and patches, with or without raised erythematous borders in photo-exposed areas and trunk. Histopathology reveals lichenoid features within the peripheral active border. A perivascular infiltrate and numerous melanophages can be seen. The clinical features and histopathology of LPP and EDP can overlap, so much so as to suggest that the two conditions can be part of the spectrum of a unique entity. Other differential diagnoses include post-inflammatory hyperpigmentation, pigmented contact dermatitis, fixed drug eruption, and urticaria pigmentosa, among others (2, 7). LPP treatment is difficult, with limited results in most cases. The available topical treatments include medium to high potency corticosteroids, calcineurin inhibitors (mostly tacrolimus 0.1% ointment) and skin lightening creams containing hydroquinone and retinoids in conjunction with an anti-inflammatory treatment (3, 7, 9). Some Authors (3) recommend that in order to prevent steroid atrophy, corticosteroids should be used for a short period (2-4 weeks). Later on they could be followed by a calcineurin inhibitor over a longer period (3-6 months). In recalcitrant or widespread cases, systemic treatments with or without topical therapy can be used. They include oral corticosteroids, dapsone, and isotretinoin (7, 9, 10). The use of narrow band ultraviolet B (NB-UVB) phototherapy in LPP has been recently reported. Complete resolution of lesions was achieved after 20 exposures and no adverse effect was observed (1).