Do Patients With Skin Psoriasis Show Subclinical Axial Inflammation on Magnetic Resonance Imaging of the Sacroiliac Joints and Entire Spine?

OBJECTIVE: To explore potential subclinical involvement of the axial skeleton by magnetic resonance imaging (MRI) of the sacroiliac (SI) joints and the entire spine in patients with skin psoriasis without clinical evidence of peripheral or axial inflammation. METHODS: Twenty patients with skin psoriasis but no clinical evidence of peripheral or axial inflammation and 22 healthy controls underwent standardized dermatologic and rheumatologic clinical examination and unenhanced 1.5T MRI of the SI joint and the entire spine. Two blinded readers globally assessed the presence or absence of SI joint inflammation simultaneously on T1-weighted and short tau inversion recovery MRI sequences with a confidence estimate. Bone marrow edema, fat metaplasia, erosion, and ankylosis of the SI joint, and vertebral corner inflammatory lesions and fat lesions were recorded using standardized modules. The prevalence of each lesion type was calculated in both groups, averaged across 2 readers. The number of subjects with lesions in the SI joint and spine (≥1, 2, 3, 4, or 5 lesions) as concordantly assessed by both readers was recorded. RESULTS: The median duration of skin psoriasis was 23.0 years, the median age of patients was 48.5 years, and 25.0% of patients and 9.1% of healthy controls were concordantly classified by both readers as having SI joint inflammation (P = 0.23). The prevalence of bone marrow edema and structural lesions was comparable across patients and controls, both on SI joint and spine MRI. CONCLUSION: In this controlled study, patients with skin psoriasis but no clinical arthritis or spondylitis showed limited evidence of concomitant subclinical axial involvement by SI joint and spine MRI. These findings do not support routine screening for subclinical axial inflammation in patients with longstanding skin psoriasis.

Endovascular extraction of a migrated large self-expanding laser-cut renal venous stent from the right ventricle.

Endovascular stent placement for decompression of an entrapped left renal vein (LRV) between the aorta and superior mesenteric artery is an alternative to surgical decompression for treating the nutcracker syndrome. However, an interventional approach may be challenging because of the unfavorable configuration of the LRV, leading to insufficient stent anchoring. We provide a case of a life-threatening stent migration from the LRV into the right ventricle 2 days after stent placement and its endovascular retrieval.

Cell counting in human endobronchial biopsies--disagreement of 2D versus 3D morphometry.

QUESTION: Inflammatory cell numbers are important endpoints in clinical studies relying on endobronchial biopsies. Assumption-based bidimensional (2D) counting methods are widely used, although theoretically design-based stereologic three-dimensional (3D) methods alone offer an unbiased quantitative tool. We assessed the method agreement between 2D and 3D counting designs in practice when applied to identical samples in parallel. MATERIALS AND METHODS: Biopsies from segmental bronchi were collected from healthy non-smokers (n = 7) and smokers (n = 7), embedded and sectioned exhaustively. Systematic uniform random samples were immunohistochemically stained for macrophages (CD68) and T-lymphocytes (CD3), respectively. In identical fields of view, cell numbers per volume unit (NV) were assessed using the physical disector (3D), and profiles per area unit (NA) were counted (2D). For CD68+ cells, profiles with and without nucleus were separately recorded. In order to enable a direct comparison of the two methods, the zero-dimensional CD68+/CD3+-ratio was calculated for each approach. Method agreement was tested by Bland-Altmann analysis. RESULTS: In both groups, mean CD68+/CD3+ ratios for NV and NA were significantly different (non-smokers: 0.39 and 0.68, p<0.05; smokers: 0.49 and 1.68, p<0.05). When counting only nucleated CD68+ profiles, mean ratios obtained by 2D and 3D counting were similar, but the regression-based Bland-Altmann analysis indicated a bias of the 2D ratios proportional to their magnitude. This magnitude dependent deviation differed between the two groups. CONCLUSIONS: 2D counts of cell and nuclear profiles introduce a variable size-dependent bias throughout the measurement range. Because the deviation between the 3D and 2D data was different in the two groups, it precludes establishing a 'universal conversion formula'.

Nitrogen dioxide induces apoptosis and proliferation but not emphysema in rat lungs.

BACKGROUND: Apoptosis of alveolar septal cells has been linked to emphysema formation. Nitrogen dioxide, a component of cigarette smoke, has been shown to induce alveolar epithelial cell apoptosis in vitro. It is hypothesised that exposure of rats to nitrogen dioxide may result in increased alveolar septal cell apoptosis in vivo with ensuing emphysema-that is, airspace enlargement and loss of alveolar walls. METHODS: Fischer 344 rats were exposed to 10 ppm nitrogen dioxide for 3, 7, 21 days or 21 days followed by 28 days at room air. Age-matched control rats were exposed to room air for 3, 21 or 49 days. Lungs fixed at 20 cm fluid column, embedded in paraffin wax, glycol methacrylate and araldite, were analysed by design-based stereology. Alveolar septal cell apoptosis (transferase dUTP nick end labelling assay, active caspase 3) and proliferation (Ki-67), airspace enlargement, total alveolar surface area, and absolute alveolar septal volume as well as the ultrastructural composition of the alveolar wall were quantified. RESULTS: Nitrogen dioxide resulted in an eightfold increase in alveolar septal cell apoptosis at day 3 and a 14-fold increase in proliferation compared with age-matched controls. Airspace enlargement, indicated by a 20% increase in mean airspace chord length, was evident by day 7 but was not associated with loss of alveolar walls. By contrast, nitrogen dioxide resulted in an increase in the total surface area and absolute volume of alveolar walls comprising all compartments. The ratio of collagen to elastin, however, was reduced at day 21. Lungs exposed to nitrogen dioxide for 21 days exhibited quantitative structural characteristics as seen in control lungs on day 49. CONCLUSIONS: Nitrogen dioxide exposure of rats results in increased alveolar septal cell turnover leading to accelerated lung growth, which is associated with an imbalance in the relative composition of the extracellular matrix, but fails to induce emphysema.