Venous lakes (VL) are acquired venous ectasies of the superficial dermal venules, usually observed in older people. Thirty-two adult patients with VL in several localizations were treated by carbon dioxide laser vaporization. Two passes were performed to each lesion within the same session. A continuous and defocused mode, with a power density of 5 W/cm2, was used in the first pass, and a continuous focused mode with the same power density was in the second pass. Photographic controls were performed before and after treatment. VLs were removed, and the smooth surface of the treated area was re-established by a single laser session. Only one case recurred after the treatment. No significant secondary effects were observed. Carbon dioxide laser is a good and safe method for treatment of skin VL. With adequate cautions, excellent cosmetic results can be obtained with a single session of treatment.
Palmoplantar tylosis is a focal nonepidermolytic palmoplantar hyperkeratosis, which is inherited as an autosomal dominant condition. Two types have been described: an early onset type B tylosis, which occurs in the first year of life and is usually benign, and type A tylosis, which occurs between the ages of 5 and 15 years. Type A tylosis has been associated with a high incidence of oesophageal carcinoma in three families in England, Germany and the USA. This study describes an additional family from Spain with tylosis A, without any known relation to those described before.
A 43‐year‐old man with a history of recurrent herpes simplex, and without a history of atopy, presented with a sudden appearance of an exanthem 10 days before presenting to the clinic. The exanthem affected the face, flexural areas, hands, and feet. No local symptomatology and no systemic involvement were observed. The exploration revealed a polymorphous exanthem formed by maculopapular lesions, umbilicated vesicles, crusts, and purpuric and necrotic elements, with a pattern of acute pityriasis lichenoides ( Figs 1 and 2). 1 Papular and necrotic lesions localized on the flexion surface of the arm 2 Papular and purpuric elements on the dorsum of the hand The histopathologic examination of a skin biopsy specimen showed a dense lymphohistiocytic infiltrate, with a linear disposition over the entire thickness of the papillary dermis and in the upper part of the reticular dermis. At the dermoepidermal junction, vacuolar alteration of the basal layer was observed, with the presence of mononuclear exocytosis, edema extending to the papillary dermis, and extravasated red cells. Spongiosis, keratinocytic focal necrosis, and parakeratosis were observed in the epidermis ( Fig. 3). 3 Spongiosis, keratinocytic focal necrosis, and parakeratosis are observed in the epidermis. The dermoepidermal junction shows vacuolar alteration of the basal layer and mononuclear exocytosis. In the papillary dermis, a dense lymphohistiocytic infiltrate is present with edema and extravasated red cells Analytical explorations revealed lymphocytosis and slight elevation of transaminases. Serologies to hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, human immunodeficiency virus (HIV) 1 and 2, syphilis, and human parvovirus B19 were negative. The CD4 and CD8 lymphocyte counts were normal. The serology to Epstein–Barr virus (EBV) ( Table 1) was consistent with a primary infection by EBV. Oral acyclovir treatment, 1 g daily for 7 days, was started and the exanthem disappeared in 7 days. Serologic evolution of EBV infection in our patient January 1998 February 1998 April 1998 IgM VCA++–IgG VCA+ (2,63)+ (1,97)+ (2,01)EBNA––+ EBNA, Epstein–Barr nuclear antigen; IgG, immunoglobulin G; IgM, immunoglobulin M; VCA, viral capside antigen.
A 74-year-old woman with chronic auricular fibrillation, arterial hypertension, hypercholesterolemia, ischemic cardiopathy, and peripheral arteriopathy presented with purpuric lesions on the lower limbs (Fig. 1) and, to a lesser extent, on the anterior area of the chest. The mucous membranes were not affected. In 1989, she was diagnosed with anemia that evolved until 1998, when a bone marrow biopsy revealed a myelodysplastic syndrome unclassified in French-American-British Group (FAB). The patient has required periodic transfusions since February 1999. A skin biopsy of the purpuric lesions revealed a leukocytoclastic vasculitis; the lesions cleared with topical corticosteroid treatment. In May 1999, the patient presented with inflammatory and painful lesions localized on the vulva (Fig. 2), which had evolved over several days, without fever. No lesions were observed in other locations. A cutaneous biopsy showed an intense dermal edema and a diffuse and polymorphous dermal infiltrate involving the follicular structures. Exocytosis, spongiosis, and mucin deposits, demonstrated by Alcian blue stain, were observed in the follicular epithelium. Mature neutrophils were predominant in the dermal infiltrate, but a small number of eosinophils and immature cells were also present (Fig. 3). The myelogenous origin of the immature lining cells was further confirmed by positive staining of intracytoplasmic granules with naphthol-ASD chloroacetate sterase (Leder's stain). Vasculitis was not observed. Routine laboratory tests revealed 3030 leukocytes/mm(3) (60% neutrophils), a hemoglobin level of 8.4 g/dL, and 92,000 platelets/mm(3). Treatment with 30 mg/day of prednisone was started, and the lesions cleared slowly within 4 weeks. A new bone marrow biopsy in September 1999 showed a similar appearance to that taken in 1998. The patient died in January 2000 as a result of pneumonia with cardiac and respiratory failure. A 66-year-old man presented with a febrile syndrome that had evolved over 5 days, and painful and pruritic cutaneous lesions on the face and posterior neck (Fig. 4). Three months before, the patient was diagnosed with chronic myelogenous leukemia in acceleration phase. Examination revealed an edematous and erythematous face with pustular lesions on the surface, also involving the neck and the upper part of the back. The histopathologic examination revealed an intense edema and abscesses in the dermis. The infiltrate of these lesions was composed of mature neutrophils with the presence of abundant immature cells with a myelogenous aspect (Fig. 5). Analytical studies revealed 26,130 leukocytes/mm(3) (42% blasts). No specific treatment for Sweet's syndrome was administered and the lesions showed an improvement within 5 days. Eight days after admission, the patient died as a result of acute hemorrhage, before treatment for leukemia was initiated.
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