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Reticular Pattern (reticular + pattern)

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Medical Sciences	100%

Selected Abstracts

Regression of Atypical Nevus: An Anecdotal Dermoscopic Observation

DERMATOLOGIC SURGERY, Issue 10 2006
MARIA A PIZZICHETTA MD
BACKGROUND Clark nevi (atypical melanocytic nevi) can be considered as risk markers and potential precursors of melanoma. The authors report on the morphologic changes of an atypical nevus by dermoscopic follow-up examination over a 7-year period. CASE REPORT A 43-year-old man had a brown macule on his back, sized 5 mm, with an irregular shape, clinically and dermoscopically diagnosed as an equivocal melanocytic lesion. Dermoscopically during the initial examination, a predominant reticular pattern with peripheral eccentric hyperpigmentation in the lower portion of the lesion could be seen. After 7 months, the area of peripheral eccentric hyperpigmentation had regressed, and after 4.5 years the atypical pigment network had almost disappeared. After 7 years of follow-up, a diffuse area of hypopigmentation and a residual light brown pigmentation were detectable. The histopathologic diagnosis was consistent with an atypical junctional nevus with regression with features of a Clark nevus. CONCLUSION Based on our observation, even a dermoscopically atypical nevus may undergo regression as documented by long-term dermoscopic follow-up. [source]

Lichenoid photodermatitis associated with nimesulide

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 12 2001
Umit Tursen MD
An 81-year-old-female patient presented with a 2 week history of erythematous to violaceous lichenoid papules and plaques exhibiting a reticulated pattern on the ,,V'' area of the chest and dorsal hands. Fine, whitish reticulated networks were present over the surface of many well developed papules. The lesions were sharply demarcated and moderately pruritic (Fig. 1). Figure 1. ,Violaceous lichenoid papules with reticular pattern located on the ,,V'' area of the chest The result of routine complete blood cell count, urinalysis, erythrocyte sedimentation rate, liver and kidney function tests were within normal limits. Antinuclear and anti-DNA antibodies were negative, and total C3 and C4 complement levels were normal. Hepatitis B surface antigen, anti-Hepatitis B surface antigen, anti-Hepatitis B core IgM antibody were negative, while anti-Hepatitis C virus antibody was positive. A skin biopsy specimen obtained from the neck of our patient revealed an interface lichenoid dermatitis accompanied by individual necrotic epidermal keratinocytes, parakeratosis and eosinophils in the infiltrate (Fig. 2). Figure 2. ,Interface lichenoid dermatitis accompanied by individual necrotic epidermal keratinocytes and parakeratosis (Hematoxylin and eosin; original magnification, × 200) Nimesulide therapy was stopped and the patient was treated with topical corticosteroids and systemic antihistamines. The eruption resolved within 5 days. The rash returned following nimesulide rechallenge. [source]

Nailfold capillary abnormalities are prevalent in sclerodermoid graft-versus-host disease and readily detected with dermatoscopy

BRITISH JOURNAL OF DERMATOLOGY, Issue 5 2010
B.N. Akay
Summary Background, Well-recognized videocapillaroscopic patterns have been described in systemic sclerosis (SS). However, no studies have described the capillary abnormalities of sclerodermoid chronic graft-versus-host disease (Scl GVHD) developed after allogeneic haematopoietic stem cell transplantation (allo-HSCT). Objectives, The aims of this study were to find the characteristics of nailfold capillary changes in Scl GVHD after allo-HSCT. Patients and methods, Eighteen patients affected by Scl GVHD and a control group of 15 patients with lichenoid GVHD were evaluated. Duration and type of sclerodermoid GVHD, Raynaud phenomenon (RP), dysphagia, joint contractures, antinuclear antibodies (ANA), anti-Scl-70 and anticentromere (ACA) antibodies were investigated parameters. A nailfold capillary examination using a standard dermatoscope was performed on all fingers of each subject. Results, Twelve patients were male and six were female with a mean age of 37 ± 11·6 years. Joint retractions and dysphagia developed in 27·8% and 38·9% of the patients, respectively. Three (16·7%) patients had RP. Autoimmune markers like anti-Scl-70 and ACA were negative in all. Capillaroscopy was abnormal in 15 patients with Scl GVHD. A regular disposition of the capillary loops along with avascular whitish linear areas at the level of the last row, neovascularization with reticular pattern, capillary disorganization, haemorrhages, enlarged capillaries and avascular areas were the main features. No capillary abnormalities were observed in patients with lichenoid GVHD. There was no statistically significant correlation between ANA positivity, RP, joint retractions, dysphagia, extensiveness of Scl GVHD, duration of sclerodermoid lesions and nailfold capillaroscopy analysis. Conclusions, This study shows the identification of distinct nailfold capillaroscopy patterns in patients with Scl GVHD but it does not confer special risk for any other specific clinical symptoms of the disease. [source]

A Japanese case of Kindler syndrome

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2000
Yasushi Suga MD
A 25-year-old Japanese woman presented with contracture of the fingers and toes, and difficulty in opening her mouth. Her grandparents are first cousins, but none of the other members of the family are affected. Bulla formation started at birth on areas of the skin that received pressure, and in infancy and early childhood the lesions were limited only to the acral areas. She also had bilateral, incomplete syndactylies involving all web spaces ( Fig. 1a). The formation of blisters ceased after the age of 15 years, but a generalized progressive poikiloderma then appeared with accompanying cutaneous atrophy of the skin of the neck, trunk, and extremities ( Fig. 1b). The patient experienced mild photosensitivity of the face and neck. At age 18 years, surgical removal of the webbing of all her fingers was performed. Oral examination showed atrophy of the buccal mucosa, and an inability to fully open the mouth. The patient also suffered from poor dentition and easily bleeding gums, but had no symptoms of esophageal dysfunction. Figure 1. Clinical manifestations of the patient with Kindler syndrome. (a) Dorsal surface of the patient's hands. Note the marked cutaneous atrophy with a severely wrinkled appearance on the dorsal surface of the hands, as well as the proximal fusion of the fingers. (b) Lower left leg of the patient. Atrophic thinning of the skin and poikiloderma with reticular pigmentation are evident Histology of separate biopsy specimens, taken from the poikilodermatous pretibial and trunk skin, showed classical features of poikiloderma, namely epidermal atrophy with flattening of the rete ridges, vacuolization of basal keratinocytes, pigmentary incontinence, and mild dermal perivascularization ( Fig. 2a). Interestingly, dyskeratotic cells ( Fig. 2b) and eosinophilic rounded bodies (colloid bodies) ( Fig. 2c) were frequently found at the basal keratinocyte layer and in the upper dermis, respectively. Pigment was also present in the upper epidermis. Figure 2. Hematoxylin and eosin staining of a biopsy specimen taken from pretibial skin. (a) Epidermal atrophy with flattening of the rete ridges. Note the dyskeratotic cells (arrowheads) and vacuolar degeneration of the basal layer in the epidermis. Bar = 50 ,m. (b) Higher magnification of dyskeratotic cells (arrowheads). Bar = 10 ,m. (c) Higher magnification of colloid bodies (arrowheads) in the superficial dermis. Bar = 10 ,m To rule out the possibility of a congenital epidermolysis bullosa, ultrastructural and immunofluorescence studies were performed. Ultrastructural studies demonstrated the reduplication of the basal lamina with branching structures within the upper dermis and cleavage between the lamina densa and the cell membrane of the keratinocytes ( Fig. 3a). The numbers of associated anchoring fibrils did not seem to be reduced, and colloid bodies and dyskeratotic cells were detected. Immunofluorescence studies with the antibody against type VII collagen (LH 7 : 2) were subsequently carried out. The results showed extensive broad bands with intermittently discontinuous and reticular staining at the dermo-epidermal junction (DEJ) ( Fig. 3b), whereas a linear distribution is typically seen in healthy tissue (data not shown). Interestingly, direct immunofluorescence studies revealed intracellular accumulation of immunoglobulin G (IgG), IgM, IgA, and C3 in colloid bodies under the basement membrane ( Fig. 3c). Figure 3. Ultrastructural and immunohistochemical findings of the patient with Kindler syndrome. (a) Ultrastructural study of the dermo-epidermal junction. The branching structures of the lamina densa (arrowheads) were frequently seen. The asterisks show the cleavage in the lamina lucida. Bar = 1 ,m. (b) Immunohistochemical studies with the antibody to type VII collagen (LH 7 : 2). An extensive broad band with reticular patterns is evident. Bar = 50 ,m. E, epidermis; D, dermis. (c) Direct immunofluorescence study. Intracytoplasmic deposition of IgM in the basal keratinocytes is evident (arrowheads). Bar = 50 ,m. E, epidermis; D, dermis [source]