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Background: Linear atrophoderma of Moulin (LAM) is a dermatosis that affects children and adolescents characterized by hyperpigmented and atrophic linear lesions following Blaschko lines. So far, less than 50 cases have been published. Therefore, it is a rare entity with unknown etiology and a chronic and self-limited course. Histologically, it is described as hyperpigmentation of the basal layer without the involvement of the dermis and subcutaneous tissue. No specific treatment exists currently. Localized scleroderma is a chronic and progressive autoimmune connective tissue disorder that affects the skin and adjacent tissues, characterized by abnormal collagen deposition and alteration in elastic fibers, blood vessels, and annexes. No reports have been published on the coexistence of localized scleroderma and LAM. Case report: We describe the case of an 11-year-old male with a clinical diagnosis of linear scleroderma since 5 years of age. Four years later, the patient developed atrophic and hyperpigmented lesions following Blaschko lines in the posterior trunk. A biopsy of both dermatoses was performed: the trunk showed epidermis with hyperpigmentation of the basal layer, and within the dermis, no alteration in the collagen bundles; the forearm biopsy corroborated scleroderma. Based on the clinical-pathological correlation, LAM coinciding with localized linear scleroderma was diagnosed. Conclusions: LAM is an infrequent entity by itself. Moreover, its coexistence with sclerodermiform syndrome has not been reported in the indexed literature.

Introduction: Linear atrophoderma of Moulin (LAM) is a rare dermatologic disorder characterized by hyperpigmented atrophic plaques following the Blaschko lines (BL). The trunk and limbs are the usual sites affected. Isolated facial involvement is an exceedingly rare entity. Despite a comprehensive medical literature search, the author could find only two cases of LAM where the lesions are exclusively localized to the face. In this article, the author presents the third case of LAM localized to face only. Case Presentation: A 26-year-old male complained of multiple linear non-pruritic pigmented lesions over the left side of the nose and glabellar area of six months’ duration. There was no history of erythema, thickening/hardening of skin, or violaceous border surrounding the lesions. On clinical examination, there were multiple hyperpigmented brownish lesions, the majority of which were depressed, involving the left ala and bridge of nose laterally and glabellar area in a Blaschkoid pattern. Diagnosis of LAM was established based on suggestive history and clinical examination. Conclusions: LAM is a rare disorder, and the facial localization makes it exceedingly rare. It should be kept in the differential diagnosis when hyperpigmented depressed lesions are present in a Blaschkoid pattern on the face.

Background Spontaneous atrophic scarring is characterised by an idiopathic, non-inflammatory macular atrophy that typically occurs on the face and presents as shallow atrophic scars having sharp margins and may be linear, rectangular or varioliform. Aim To describe the cases of spontaneous atrophic scarring over perioral region of face having specific feline band pattern in a retrospective study. Materials and methods All patients with facial atrophoderma (perioral region) were evaluated clinically and histopathologically in tertiary care centres over 3 years. Patients with facial atrophoderma but no perioral involvement and secondary atrophoderma were excluded from the study. Patients were evaluated for number, sites, size and shape of lesions and were confirmed histopathologically. Results There were 14 patients (10 females) with facial atrophoderma particularly over the perioral region. Three patients had perioral involvement with a few lesions on the cheeks and forehead. All patients developed atrophoderma spontaneously without preceding inflammation. Most of the patients were asymptomatic except for mild pain or burning at the time of development of atrophic lesions; however, none of the patients were symptomatic at the time of presentation. Histopathology in 5 patients showed epidermal and upper dermal atrophy with no/minimal signs of inflammation. Conclusion Idiopathic atrophodermas over the face can be due to spontaneous atrophia maculosa varioliformis cutis or atrophoderma of Moulin.

Key Clinical Message Idiopathic Atrophoderma of Pasini and Pierini should be considered on the differential in a patient presenting with an asymptomatic atrophic plaque on the skin. Differentiation from Linear Atrophoderma of Moulin and morphea remains a challenge; however, features of the presentation and tissue biopsy can help establish the diagnosis.

Linear Atrophoderma of Moulin (LAM) is characterized byacquired unilateral hyperpigmented depressed band like skinlesions following blaschko’s lines. Moulin et al.1first definedthe condition in 1992 and, later, Baumann et al.2reportedsimilar features on a patient and named the condition asLAM.In our 2 case reports, we described first a 26-year-old femalewith asymptomatic hyperpigmented lesions since one year.On physical examination, there was a depressed band-likelesion on the right side of chin along the neck followingblaschko’s lines (Figure 1A).

Linear atrophoderma of Moulin (LAM) is a rare dermatosis characterized by a hyperpigmented atrophoderma that follows Blaschko's lines, with onset usually occurring during childhood and adolescence. LAM is an etiologically unknown form of dermal atrophy. It is generally characterized by oval or round atrophic, nonsclerotic, hyperpigmented patches following Blaschko's lines. These patches are usually located on the trunk and the upper and lower extremities. This case study discusses a patient that had the nonclassical form of LAM with the initial lesions presenting as papules.

Latin America refers to territories in America where the Spanish or Portuguese languages prevail: Mexico, most of Central and South America, and in the Caribbean, Cuba, the Dominican Republic, and Puerto Rico – in summary, Hispanic America and Brazil [1]. By this definition, Latin America is coterminous with Iberoamerica („Iberian America”) [1]. Latin America has an area of approximately 21,069,500 km2, almost 3.9% of the Earth’s surface or 14.1% of its land surface area. As of 2010, its population was estimated at more than 590 million [1]. Many medical conditions derive their names from either Greek or Latin. In this manuscript, we are reviewing, some selected examples of eponyms, in dermatology literature, linked to the Latin America (Tabl. I) [2-14]. We want also to point out that many scientists in other parts of the world and particularly in USA, for whom medical diseases were eponymously named, were originated from latin America. Just an example is, Bannayan–Riley–Ruvalcaba syndrome (BRRS), which is a dominant autosomal disorder characterized by cutaneous lipomas, macrocephaly, intestinal polyps, and developmental delay [15]. It is named after American physicians. One of them, Rogelio H. Ruvalcaba (born in 1934) received his MD degree from the Universidad de Guadalajara, in Mexico and immigrated to USA. Finally, one can find part of the eponym is originated from Latin America for example, idiopathic atrophoderma of Pasini and Pierini (IAPP), is named after an italian dermatologist Agostino Pasini (1875-1944) and dermatologist from Argentina, Luis Enrique Pierini (1899-1987) (Fig. 8). In 1923, Pasini described the condition under the name progressive idiopathic atrophoderma. In 1936, Pierini and Vivoli extensively studied and defined the condition and its possible link to morphea. Canizares et al, in 1958 renamed it as idiopathic atrophoderma of Pasini and Pierini (IAPP) [16]. There are many clinical and histologic similarities between, atrophoderma of Pasini and Pierini and Linear atrophoderma of Moulin (LAM). LAM was first described by Moulin in 1992 as an acquired unilateral hyperpigmented atrophic band along Blaschko’s lines. EPONYMS IN THE DERMATOLOGY LITERATURE LINKED TO LATIN AMERICA

Linear atrophoderma of Moulin (LAM) is a rare dermatosis in childhood and early adolescence. The exact etiology of LAM is still obscure. Several treatment modalities were reported but none was consistently successful. We report a case of LAM in which a favorable outcome was obtained with topical calcipotriol. The relevant literature is also reviewed.

Linear atrophoderma of Moulin (LAM) is a rare dermatologic disorder characterized by a hyperpigmented atrophoderma that consistently follows the lines of Blaschko. There are many clinical and histologic similarities between LAM, atrophoderma of Pasini and Pierini (APP), and morphea, and whether LAM represents part of a disease spectrum or its own distinct entity is debated. This case of a 16-year-old boy with LAM supports the hypothesis that LAM, APP, and morphea are a spectrum of disorders rather than unique entities. Although the patient's overall clinical picture supports a diagnosis of LAM with hyperpigmented, depressed lesions following the lines of Blaschko and perivascular lymphocytic infiltrate on biopsy, the bilateral presentation typical of APP, collagen entrapment of eccrine ducts typical of morphea, and changes in dermal collagen illustrate features spanning all three disorders, suggesting a relationship between these conditions that represents a spectrum of disease. Furthermore, a review of all reported cases of LAM in the literature suggests an evolving definition beyond what Moulin and colleagues originally described, including features related to those of APP and morphea.

We describe a 28-year-old man with linear atrophoderma of Moulin (LAM), whose serum immunological markers were abnormal (including antinuclear antibody, ribonucleoprotein, immunoglobulin M and anti-SM antibody). In addition, however, a histological analysis identified unexpected connective tissue disease changes in this patient. We speculate that the pathogenesis of LAM is associated with immunity or that LAM itself is a kind of connective tissue disease.

Linear atrophoderma of Moulin (LAM) is an acquired skin condition that manifests in early childhood and adolescence. It likely represents a form of cutaneous mosaicism that presents with linear, hyperpigmented and atrophic lesions appearing on the trunk and limbs. Its clinical appearance varies and may closely resemble that of atrophoderma of Pasini and Pierini (APP) and linear scleroderma. LAM usually follows a benign course and no effective treatment options exist. We present a case of a young and healthy patient that developed such lesions on her upper and lower extremities over 5 years. The initial clinical impression of linear scleroderma was reviewed in favor of LAM following histological examination of the lesions which revealed no significant inflammatory changes. LAM remains a rare and possibly under recognized entity with reports confined only to the dermatologic literature. This case highlights the importance of recognizing LAM and distinguishing it from linear scleroderma given the significant differences in management and prognosis.

Linear atrophoderma of Moulin is an acquired rare and self-limited skin condition. It is characterized by atrophic bandlike skin lesions that often show hyperpigmentation and always follow the lines of Blaschko. Usually it begins in childhood or adolescence and there is no evidence of any long term progression. We describe a case of a 21-year-old woman with clinical and histological features of linear atrophoderma of Moulin. The patient was successfully treated with methotrexate 20 mg/week during 6 months with an improvement of skin pigmentation and atrophy. Approximately, 30 cases of linear atrophoderma of Moulin were described in the literature. There is not a proven effective treatment of this dermatosis. High dose penicillin, topical corticosteroids, heparin, and oral potassium aminobenzoate have been used but found to be uneffective. To our knowledge, this is the first case of extensive linear atrophoderma of Moulin treated with methotrexate.

We present a 40-year-old woman with asymptomatic, linear, hyperpigmented atrophic plaques in a Blaschkoid distribution on the right back and right upper extremity that is consistent with a diagnosis of linear atrophoderma of Moulin. Clinical lesions developed with a biphasic pattern in late adolescence and in adulthood. The pathogenesis of this acquired, progressive Blaschkolinear dermatosis may hold insight into the pathogenesis of this rare dermatologic condition, as well as other dermotoses, which include those resulting from post-zygotic genetic mosaicism.

childhood. Ambulatory Child Health. 2000;6:59-66. 4. Kalman CM, Laskin OL. Herpes zoster and zosteriform herpes simplex virus infections in immunocompetent adults. Am J Medic. 1986;81:775-8. 5. Nikkels AF, Nikkels-Tassoudji N, Pierard GE. Revisiting childhood herpes zoster. pediatr dermatol. 2004; 21:18-23. 6. Kakourou T, Theodoridou M, Mostrou G, Syriopoulou V, Papadogeorgaki H, Constantopoulus A. Herpes zoster in children. J Am Acad Dermatol. 1998;39:207-10. 7. Requena L. Diagnostico y diagnostico diferencial del herpes zoster. Actas Dermosifiliogr. 2006;97 Supl 3:17-24. 8. Goldman BD. Herpes Serology for Dermatologists. Arch Dermatol. 2000;136:1158-61. 9. Prober CG, Arvin AM. Herpes simplex virus. Varicella-zoster virus. In: Long S, Pickering LK, Prober CG, editors. Principles and Practices of Pediatric Infectious Diseases. 2nd ed. Philadelphia: Churchill-Livingston; 2003. p. 103250. 10. Rabalais GP, Adams G, Yusk JW, Wilkerson SA. Zosteriform denuded skin caused by intrauterine herpes simplex virus infection. Pediatr Infect Dis J. 1991;10:79-80. 11. Brown ZA, Wald A, Morrow RA, Selke S, Zeh J, Corey L. Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant. JAMA. 2003;289:203-9. 12. Kurlan JG, Connelly BL, Lucky AW. Herpes zoster in the first year of life following postnatal exposure to varicella-zoster virus. Arch Dermatol. 2004;140:1268-72. Letters to the editor

Linear atrophoderma of Moulin is a rare, acquired, linear dermatosis. We present a 17-year-old girl with multiple asymptomatic brownish atrophic plaques in a zosteriform distribution on the left side of the trunk. Clinical presentation and dermatopathology was compatible with the diagnosis of linear atrophoderma. Twenty years after its initial description by Moulin, there are yet a limited number of case reports and unanswered questions regarding this entity.

Linear atrophoderma of Moulin is a rare skin condition, fist described in 1992 by Moulin et al. who reported 5 patients affected by unilateral, hyperpigmented, depressed plaques self limited along Blaschko’s lines on the trunk and extremites, without any evidence of long-term progression. The main histologic finging was a basal hyperpigmentation, while other epidermal layers and dermis were normal, including normal-appearing collagen and elastic fibers. Thus, the clinical atrophy was initially linked to an alteration of the subcutaneous tissue, but a deep biopsy on both the affected and controlateral sides was originally not performed. Moulin et al. suggested the term “blaschkose” in opposition to “ blaschkitis” with an inflammatory and acquired significance. Later, this skin desease was named “LAM” by Baumman et al. who classified this disease as belonging to the group of acquired linear dermatoses following BL and thought LAM as a variant of prpogressive atrophoderma of Pasini and Pierini. In the literature, the clinical and histopathological criteria for the diagnosis of LAM heve been expanded in the last years and cases with different clinical and histological features have been classified as LAM

Linear atrophoderma of Moulin is a rare acquired disorder arising most commonly during childhood or adolescence, occurring equally in both sexes and characterized by hyperpigmented atrophoderma in a unilateral bandlike distribution along the lines of Blaschko. Since Moulin et al described the condition in 1992, only a few dozen cases have been reported. It has been postulated that linear atrophoderma of Moulin may be due to mosaicism. A 66-year-old man pre­sen­ted with a 46-year his­to­ry of evol­ving tan soft atro­phic con­fluent plaques in a striking­ly Blasch­koid dis­tri­bu­tion, in­vol­ving the left up­per back, shoulder, up­per arm, chest and flank. Ini­tial on­set, at age 20, con­sis­ted of a single mildly pru­ritic pink patch on the left back that was un­res­pon­sive to topical anti­fun­gals. Each new le­sion arose simi­larly as a pink pru­ritic patch, sub­se­quent­ly be­co­ming de­pressed, hy­per­pig­men­ted, and asym­pto­ma­tic over se­ve­ral years. Le­sions were never scaly, firm, or indu­rated. Punch biopsy speci­mens were obtained. The clinical and histo­patho­lo­gi­cal features con­firmed the diagnosis of linear atrophoderma of moulin. Our present case has the characteristic clinical and histopathological features of linear atrophoderma of Moulin, but is the first reported case with mild pruritus at the onset of each new lesion and progressing slowly over 46 years. The lack of any systemic symptoms or other complications in our patient reaffirms the benign nature of this skin disease.

Background: Linear atrophoderma of Moulin (LAM) is a rare clinical entity which was first described by Moulin et al. in 1992. The diagnosis is clinical, characterized by acquired unilateral hyperpigmented, depressed band-like skin lesions following Blaschko's lines. The disease typically affects children or adolescents and has a good prognosis without evidence of long-term progression. To date, the pathophysiology is unclear. Different authors hypothesize that the disease is secondary to a mosaic manifestation as a result of a post-zygotic mutational event. Observations: Four patients (2 men, 2 women) had a history of unilateral band-like skin lesions located on the lower legs (50%) or the trunk (50%). Physical examination showed atrophic and hyperpigmented skin lesions along Blaschko's lines, which appeared during childhood in 3 cases and at the age of 20 in the last case. Lesions had progressed rapidly but seemed to have stabilized so far except for 1 case who presented spontaneous improvement. Histopathological examination revealed a normal epidermis with a hyperpigmented basal layer and a perivascular lymphocytic infiltrate in the dermis. Conclusion: LAM is a rare disease with 32 reported cases and remains an exclusion diagnosis. Since the problem is mainly esthetic, treatments should not be too aggressive.

Many different congenital and acquired skin diseases are seen along Blaschko's lines. In 1992, Moulin et al. [40] described five patients affected with a new clinical entity characterized by acquired atrophic band-like skin lesions showing hyperpigmentation. We report on a further patient with this skin disease. Characteristic features are hyperpigmented atrophoderma arranged in a pattern following the lines of Blaschko, with no preceding inflammation and no subsequent induration or scleroderma. The lesions usually appear during childhood or adolescence, but sometimes in young adults. For this skin disease we propose the term `linear atrophoderma of Moulin'.

Background: Linear atrophoderma is a rare disease, first described by Moulin in 1992 in 5 patients. It is an acquired unilateral hyperpigmented, depressed band-like areas following the lines of Blaschko. It affects children or adolescents of both genders involving the trunk or the limbs. It is considered to be a rare cutaneous form of mosaicism. Main observation: A 39-year-old woman with a 22 years history of unilateral slightly depressed hyperpigmented lesion on her neck was admitted to us. The skin texture was normal and there were no signs of induration or sclerosis. The histopathological examination revealed a normal epidermis outlined by a hyperpigmented basal layer. In the papillary dermis proliferation of superficial vessels with mild lymphocytic infiltrate and melanin-laden macrophages were present. The collagen fibres and elastic fibres were normal. The clinical and histopathological features confirmed the diagnosis of linear atrophoderma of moulin. We discussed the case according to the other cases reported in the literature. Conclusion: Approximately 28 cases of linear atrophoderma have been reported in literature. The present case has the charecteristic clinical and histopathological features of linear atrophoderma as defined by Moulin, but the localization of the lesion is unusual. ( J Dermatol Case Rep. 2011; 5(3): 47-49)

Linear atrophoderma, first described by Moulin, is an acquired unilateral dermatitis localized along the Blaschko lines. It affects children or adolescents of both genders, involving the trunk and the limbs. It is, presumably, a rare cutaneous form of mosaicism. The differential diagnosis of atrophoderma of Moulin involves congenital dermopathies along the Blaschko lines, atrophoderma of Pasini and Pierini, and linear scleroderma. We present here a peculiar case of linear atrophoderma affecting a teenager.

Linear atrophoderma of Moulin (LAM) is a rare and distinct skin condition characterized by unilateral, hyperpigmented and atrophic band-like skin lesions following the lines of Blaschko. Usually the disease begins in childhood or adolescence on the trunk or limbs, with no preceding inflammation or subsequent sclerodermatous changes. Approximately 25 cases have been reported in the English language literature. We describe a case of LAM occurring in a 9-year-old Peruvian boy with exclusive involvement of the neck. To our knowledge, this is the first report of LAM with this unusual localization.

We report an infant with depressed, hypopigmented, linear plaques of congenital onset on the lower extremity. The lesions were asymptomatic and the child was otherwise healthy. Despite the clinically obvious change in skin texture and color, histopathologic changes were subtle: a biopsy specimen showed hypopigmentation and a decrease in elastic fibers in the papillary and upper reticular dermis. Diagnoses considered included various congenital syndromes, idiopathic atrophoderma of Pasini and Pierini, and especially, linear atrophoderma of Moulin. However, because of the significant clinical and histopathologic differences when compared to the aforementioned entities, our patient appears to have a unique presentation of congenital linear atrophoderma.

Linear atrophoderma of Moulin is a distinctive disease pattern characterized by hyperpigmented atrophoderma and described originally in 1992. It follows the lines of Blaschko, and occurs without preceding inflammation, subsequent induration or scleroderma. The lesions usually develop during childhood or adolescence, and the prognosis is good. The differential diagnoses include linear dermatoses, e.g. linear scleroderma, epidermal naevi, inflammatory linear verrucous epidermal naevus, lichen striatus, Blaschkitis acuta, reticulate hyperpigmentation of Iijima and linear lupus erythematosus. Diagnosis is made clinically and histologically. We report a 22-year-old woman with a 17 year history of linear atrophoderma which involved the right arm and trunk.

Hyperpigmented atrophoderma arranged in a pattern following the lines of Blaschko and appearing during childhood or adolescence on the trunk or the limbs is a characteristic feature of linear atrophoderma of Moulin. We review 15 published reports and describe 4 additional cases. Histopathologically, there is no clear sign of atrophy found in specimens examined by light microscopy. It might well be argued that a focal reduction of subcutaneous fatty tissue contributes to the obvious clinical atrophy. The cause and pathogenesis of the disorder remains unknown. It may reflect mosaicism caused by a postzygotic mutation that occurred at an early developmental stage, in analogy to many other diseases distributed along Blaschko's lines. Linear atrophoderma of Moulin may reflect the action of an autosomal lethal gene surviving by mosaicism. There are so far no reports of a familial occurrence that could favor a paradominant transmission of linear atrophoderma of Moulin. However, theoretically, the postzygotic mutation giving rise to an aberrant cell clone could still be nonlethal. In a heterozygous individual, a postzygotic mutational event might lead to loss of the corresponding wild-type allele at the atrophoderma locus. This would give rise to a homozygous cell clone, which becomes manifest along the lines of Blaschko later in life.

Linear atrophoderma of Moulin is a distinctive disease originally described in 1992 and characterized by acquired, mildly atrophic, non-sclerotic, slightly hyperpigmented lesions following the lines of Blaschko. Here, we describe a 15-year-old girl with a 13-year history and a 29-year-old male with a 6-year history of prominent linear telangiectatic erythema and mild atrophoderma following the lines of Blaschko that involved the right leg and hip, and both legs, the trunk and both arms, respectively. As pronounced telangiectatic erythema within lesions of atrophoderma of Moulin has not hitherto been described, we propose that the disease in our patients represents a novel variant of linear atrophoderma of Moulin. Due to considerable overlap, we do not favour the notion that our cases constitute an entity entirely separate from linear atrophoderma of Moulin.