Periorbital venous stasis may be involved with filler induced malar edema-A duplex ultrasound-imaging-based case series.

INTRODUCTION: Filler injections in the periocular region are regarded as a challenging and advanced maneuver in a high-risk area. Adverse events as malar edema due to filler treatment may occur. To evaluate the possible reasons, the ultrasound images, and medical data of patients that were prospectively referred with malar edema were evaluated. MATERIALS AND METHODS: A total of 17 patients (26 eyes) with malar edema after hyaluronic acid filler treatment were included. All cases were assessed with an 18 MHz linear ultrasound device. Exact location of the filler material was noted. Relations with clinical data were analyzed using chi-square tests. RESULTS: Onset of malar edema after treatment showed a wide range from immediate (0 days) to 3 years. Most patients had an early onset N = 13 (76%), a minority showed late onset N = 4 (24%). In 23 eyes, the filler material was found to be located inside the SMAS. In 3 cases filler material was located on the periosteum of the orbital rim. After duplex-ultrasound guided filler removal, restored venous flow could be seen in the superficial and/or deep fatty layer often accompanied by flow piercing through the SMAS. Minutes after treatment, clinical improvement of malar edema was observed. CONCLUSION: Malar edema after by filler treatments in the periocular region may be caused by veno-lymphatic compression by filler deposits.

Principal component analysis of seven skin-ageing features identifies three main types of skin ageing.

BACKGROUND: The underlying phenotypic correlations between wrinkles, pigmented spots (PS), telangiectasia and other related facial-ageing subphenotypes are not well understood. OBJECTIVES: To analyse the underlying phenotypic correlation structure between seven features for facial ageing: global wrinkling, perceived age (PA), Griffiths photodamage grading, PS, telangiectasia, actinic keratosis (AK) and keratinocyte cancer (KC). METHODS: This was a cross-sectional study. Facial photographs and a full-body skin examination were used. We used principal component analysis (PCA) to derive principal components (PCs) of common variation between the features. We performed multivariable linear regressions between age, sex, body mass index, smoking and ultraviolet radiation exposure and the PC scores derived from PCA. We also tested the association between the main PC scores and 140 single-nucleotide polymorphisms (SNPs) previously associated with skin-ageing phenotypes. RESULTS: We analysed data from 1790 individuals with complete data on seven features of skin ageing. Three main PCs explained 73% of the total variance of the ageing phenotypes: a hypertrophic/wrinkling component (PC1: global wrinkling, PA and Griffiths grading), an atrophic/skin colour component (PC2: PS and telangiectasia) and a cancerous component (PC3: AK and KC). The associations between lifestyle and host factors differed per PC. The strength of SNP associations also differed per component with the most SNP associations found with the atrophic component [e.g. the IRF4 SNP (rs12203592); P-value = 1·84 × 10-22 ]. CONCLUSIONS: Using a hypothesis-free approach, we identified three major underlying phenotypes associated with extrinsic ageing. Associations between determinants for skin ageing differed in magnitude and direction per component. What's already known about this topic? Facial ageing is a complex phenotype consisting of different features including wrinkles, pigmented changes, telangiectasia and cancerous-related growths; it is not clear how these phenotypes are related to each other and to other phenotypes. A few studies have described two main clinical phenotypes for photoageing, namely hypertrophic ageing and atrophic ageing, which have been based solely on the clinical assessment of photoageing characteristics. What does this study add? We are the first to use epidemiology data to identify three main components associated with photoageing, namely a hypertrophic component (global wrinkling; perceived age; Griffiths grading) and atrophic component (pigmented spots; telangiectasia) and a cancer component (actinic keratosis; keratinocyte cancer). Association analysis showed different effects and direction of environmental determinants and genetic associations with the three components, with the most significant gene variants associations found for the atrophic component.

[Unilateral blindness following a non-surgical rhinoplasty with filler]. / Eenzijdige blindheid na een neuscorrectie met filler.

BACKGROUND: A rare but known adverse event following a cosmetic filler treatment is unilateral blindness. In the Netherlands, this complication has not been reported in a patient before. CASE DESCRIPTION: A 26-year-old woman developed unilateral blindness after undergoing a cosmetic treatment of the dorsum nasi in which hyaluronic acid was used as filler. The blindness was caused by backflow of the filler via the ophthalmic artery into the carotid internal artery. CONCLUSION: There is no proven effective treatment for this adverse event. Therefore prevention is of great importance. This requires knowledge of the anatomy of the facial blood vessels and a well-developed injection technique.

Immunofluorescence microscopy of healthy skin from patients with systemic lupus erythematosus: more than just the lupus band.

Many papers have been published on the lupus band in systemic lupus erythematosus (SLE), but little information exists on the possible diagnostic value of the lupus band and other microscopic immunofluorescence phenomena found in clinically normal skin of patients with SLE. In a study of 297 subjects (66 patients with SLE, 81 patients with other forms of LE, and 150 patients with other systemic connective tissue disorders) it was found that: (a) granular deposits of IgA, IgG, and IgM in the basal membrane zone and in the deeper blood vessels were more common in patients with SLE than in the other two groups; (b) depending on the clinical differential diagnosis, IgA and IgG deposits at the epidermal basal membrane can be specific for SLE; (c) using logistic regression analysis sets of variables can be selected with a high potential to discriminate between SLE and the other groups; and (d) immunofluorescence variables do not duplicate the information for the diagnosis of SLE given by the American Rheumatism Association (ARA) criteria or other laboratory methods. From these results, it is concluded that immunofluorescence microscopy of clinically normal skin is a valuable diagnostic method which should be reconsidered as a potential criterion for the diagnosis of SLE in the next evaluation of the ARA criteria.

In vivo antinuclear antibody of the skin: diagnostic significance and association with selective antinuclear antibodies.

Immunofluorescence microscopy of the skin has disclosed antibodies bound to epidermal cell nuclei in several connective tissue disorders. To establish the diagnostic potential of this phenomenon the results of immunofluorescence microscopy of biopsy specimens from 1651 subjects with various diseases and from 315 patients with systemic connective tissue disorders and related diseases were reviewed. It was found that the predictive value of the phenomenon for the presence of a systemic connective tissue disorder was, in general, 88%. Except for the homogeneous and thready patterns, which seldom appear, but are specific for SLE, in vivo antinuclear antibody (ANA) does not discriminate better between the various disorders than do serum antibodies. The presence of in vivo ANA in the skin was related to serum antibodies against non-histone nucleoproteins, but not to anti-dsDNA antibodies. Combined with the finding that antibodies against non-histone nucleoproteins can bind on the surface of human keratinocytes, this suggests that ANA of the skin occurs in vivo.

Binding of antibodies to nonhistone nucleoproteins on keratinocytes in suspensions.

Antibody binding on the cell surface of epidermal cells, recently established on cultured neonatal foreskin cells, is supposed to play a role in the pathogenesis of in vivo antinuclear antibodies (ANA) of the skin. To study this phenomenon in suspensions of adult human keratinocytes, a cell system more closely related to the in vivo situation, we investigated the binding capacity of nine sera with various antibody profiles against nuclear components, as well as a murine monoclonal Sm-antibody. It was found that sera containing antibodies against nonhistone nucleoproteins bound to the cell surface of keratinocytes, whereas monospecific anti-dsDNA sera and the murine anti-Sm serum did not. This binding was found in both basal and suprabasal keratinocytes. The percentage of cells showing antibody binding was not significantly enhanced by preirradiation with ultraviolet light, as was found in a previously study. The cell surface binding is probably an antigen-antibody binding and not the result of cross-reactivity. Such cell surface binding may be important for the formation of in vivo ANA in the skin.

Immunohistopathology of light-induced skin lesions in lupus erythematosus.

Recently we have been able to induce pathological skin reactions with UVB, UVA and visible light in patients with lupus erythematosus (LE). The pathological skin reactions had the appearance of spontaneously developed LE lesions. In the present study, using patients with polymorphic light eruption as controls, we subsequently investigated what types of immunohistochemical abnormalities were found in these lesions. It was shown that in the induced skin lesions, phenotypically similar inflammatory cells were found as in spontaneously evolved lesions. Granular deposits of immunoreactants, as found in most spontaneously evolved LE lesions, occurred in 12 out of 16 LE patients 7-10 days after onset of the artificial irradiation. The dermal infiltrates in light-induced LE lesions differed mainly from those in polymorphic light eruption, by the amounts of CD1+ cells (Langerhans' cells). In polymorphic light eruption, the relatively large amount of these cells suggests an active migration of antigen-presenting cells, a mechanism apparently not operative in LE. Our results underline the importance of the pathogenic action of light in LE.

Light-induced skin lesions in lupus erythematosus: photobiological studies.

To investigate the light sensitivity to various wavelength regions in lupus erythematosus (LE), phototests were performed in 24 LE patients with clinical photosensitivity (7 had systemic LE, 9 discoid LE, and 8 subacute cutaneous LE). Skin areas (measuring 40-60 cm2) were irradiated daily, maximally six times. With all three light sources used (emitting UVB, UVA, and visible light respectively) abnormal papular or papulosquamous reactions could be induced. In four of the 20 patients reacting abnormally, lesions occurred 10 or more days after cessation of the phototests; this indicates that the problem of photosensitivity in LE may be greater than appreciated so far.

A prospective immunofluorescence study of immune deposits in the skin of primary Sjögren's syndrome.

There are conflicting opinions concerning the epidermal immunofluorescence pattern in primary Sjögren's syndrome. In a prospective study of 12 patients we found a characteristic pattern of epidermal nuclear/cytoplasmic IgG deposits in 8 (67%). This pattern was associated with the presence of antibodies against SSA/Ro and SSB/La in the serum and was also found in 2 out of 5 LE patients with monospecific antibodies against SSA/Ro. There is a resemblance to the pattern of dust-like particles described in the diseased skin of patients with subacute cutaneous LE. In one patient with primary Sjögren's syndrome, IgG deposits were confined to epidermal cell nuclei (in vivo ANA). Instead of antibodies against SSA/Ro or SSB/La, this particular patient had nRNP-antibodies. From this study, we conclude that the epidermal IgG deposits in primary Sjögren's syndrome may represent antibody binding to the sites within epidermal cells where the respective antigens are located.

Is there a linear IgM dermatosis? Significance of linear IgM junctional staining in cutaneous immunopathology.

A linear IgM staining of the basal membrane zone (BMZ) is difficult to classify as denoting any known dermatological disorder. In a group of 2,771 persons biopsied for routine immunofluorescence microscopy, 25 cases (0.9%) with this phenomenon were found, whereas the incidences of bullous pemphigoid and linear IgA dermatosis in this group were resp. 1.2% and 0.01%. The IF patterns, serological data and clinical pictures of the linear IgM group were reviewed for a common denominator. One patient had bullous pemphigoid. The others showed a variety of symptoms and diagnoses. In the majority of cases the linear IgM deposits were monoclonal, a feature not understood. Immunoelectronmicroscopy performed in one patient proved IgM deposits below the basal lamina. It is concluded that there is no such entity as a linear IgM dermatosis and furthermore, that linear IgM staining at the BMZ has to be distinguished from related patterns such as the granular BMZ deposits ('lupus band') in SLE.