In the literature are reported zosteriform herpes simplex virus (HSV) infections, both primary and post-primary (1, 3, 5, 6). In this case we are not able to say if the first episode, particularly extensive, was a primary or postprimary infection because when we had to make a diagnosis had been too long from the first episode to search for specific IgM. However, in our opinion the first was a primary infection, due to its significant extension, much larger than the next two episodes. Numerous experimental data show that zosteriform VHS infection is related to the path that the virus runs from the sensory nerve ganglia to the skin; even in case of primary infection, VHS after entering the organism arrives first to the residential nervous ganglion and then from this site goes to the skin giving the zosteriformi manifestations. It was also shown that the coming and going of the VHS from the skin to the nervous ganglion and vice versa occur along the Schwann cells of the perineural sheath (2, 4). The zosteriform HSV infection testifies the neurotropism of HSV that is also confirmed by the concomitant painful paresthesias and the well-known encephalitis that can complicate the HSV infection. This case also shows that it is not always easy to differentiate the clinical manifestations of herpes zoster from those of herpes simplex; you have to think about the possibility that a zosteriform eruption is linked to HSV when as in this case, the child has not had contact with the wild and vaccine VVZ and this history is confirmed by the absence of anti-VVZ antibodies.
We could not find in the literature cases similar to what we describe here, characterized by circumscribed lymphangiomas (customary name that we prefer even aware that these are small lymphatic microcystic malformations), randomly distributed throughout the skin and probably present since birth even if they were noted for the first time at 2 years of age due to their poor visibility. Although their distribution is reminiscent of the familial glomus tumors and cutaneous hemangiomatosis, the transitory color changes from white to bluish-red of the individual elements and the microcystic dermoscopy finding testify on behalf of their lymphatic nature. The term lymphangioma should be reserved for acquired progressive lymphangioma or benign lymphangioendothelioma (4), due to a proliferation of lymphatic endothelial cells, which is clinically manifested by a reddish plaque on the abdominal wall or lower limbs; we do not use the term diffuse lymphangiomatosis (5), although it would be justified by the distribution of the lesions similar to that of hemangiomatosis, because this term is used in the literature for severe, progressive malformations, infiltrating the chest and abdominal cavities (2). Circumscribed lymphangiomas are really lymphangiectases, whether they are acquired and secondary to tumors (1), radiotherapy (3) or otherwise obstruction of the normal lymph circulation, whether they are congenital and separated from normal lymph circulation. It should not be considered strange that congenital circumscribed lymphangiomas should undergo transient changes in color from white to bluish-red due to spontaneous or traumatic intralesional hemorrhage, because the lymphatic and venous malformations often coexist and even ultrasound can demonstrate the presence of malformed blood vessels into the interstitial tissue between the lymphatic cavities of macrocystic lymphangiomas.
The lesions distributed according to the lines of Blaschko assume a condition of mosaicism, i.e. the existence of an already present at birth cell clone, different from other skin cells. This diversity of the cutaneous clone can be already evident from the earliest ages of life and manifest the features of a hereditary disease, for example incontinentia pigmenti, or of a nevus malformation, for example epidermal verrucous nevus. When as in this case the lesions are acquired, are located on only one segment of skin and are eczematous in type, it is reasonable to think that the different cell clone is originated by a de novo post-zygotic mutation of one of the genes responsible for atopic dermatitis as occurring in mosaicism type 1. Three similar cases have been already described in the relevant literature (1, 2, 3).
The discovery of the pediatric dermatology school of Bordeaux regarding the efficacy of propranolol, a nonselective beta-blocker, on infantile hemangioma (IH) was revolutionary because it has changed the problematic IH therapy, has significantly improved the efficacy / side effect relationship in this disorder thus allowing to extend the treatment to IH responsible for esthetic and psychosocial damage, and has stimulated research on antiangiogenic drugs also in other fields such as retinopathy of prematurity and carcinogenesis. (...).
Despite the significant clinical evolutionary differences between the common infantile hemangioma (IH) and congenital hemangioma (CH), the latter was identified only 20 years ago. It is important to differentiate CH from IH because their clinical course and their therapy are significantly different.
Melanocytic nevi are due to a benign, thus self-limiting, proliferation of melanocytes. The proliferation can give raise to a flat (Fig. 1091) or raised lesion. The pathological findings of the former consist of groups or nests of melanocytes level with the dermal-epidermal junction (Fig. 1092). This is why it is named junctional nevus. On the other hand, intradermal nevus is clinically raised and characterized, from a pathological point of view, by the presence in the dermis of melanocytes and nevus cells (Fig. 1094). However, intradermal nevus is often preceded by a junctional nevus, as supported by a junctional halo at its periphery in many cases (...).
The diagnosis of these disorders is initially done by neonatologists, pediatricans and pediatric dermatologists, who should be therefore aware of the problem. Although rare, these disorders, included progressive osseous heteroplasia (POH), are not exceptional. In fact, in our opinion many patients with POH are misdiagnosed. Moreover, some patients with osteomata cutis barely evident from a clinical point of view are never seen by expert physicians. (...)
Before talking about defect epidermal nevi, we would like to emphasize that their pathogenetic mechanisms are more complex than those ones of excess nevi, because mutations and monoclonal cell proliferations are not responsible for these defect nevi. The concept of defect nevus was underlined with regard to hypopigmented nevus, which is the counterpart of hyperpigmented nevus. Hypopigmented nevus has been already discussed (Eur. J. Pediat. Dermatol. 10, 145-54, 2000). (...).
In the 60’s sunscreens did not yet exist. The protection against the side effects of sun radiations mainly relied on the clothes, rational exposure and fear of burning. There were only tanning lotions and oils after sun bathing, which were produced by the cosmetic industry, whereas the drug industry was apparently not interested in this market. Only dermatologists knew that squamous cell and basal cell carcinomas were due to the side effects of sun radiations. However, they did not believed that melanoma was clearly related to sun exposure. Common people did not know anything about the relationship between sun and skin malignancy and the panic of nevi did not exist. A widely diffuse prejudice talked about “nevi should not be touched”. Also due to this prejudice, at that time nevi were not easily removed. (...).