Textiloma: a case of foreign body mimicking a spinal mass

Items such as cotton or gauze pads can be mistakenly left behind during operations. Such foreign materials (called textilomas or gossypibomas) cause foreign body reaction in the surrounding tissue. The complications caused by these foreign bodies are well known, but cases are rarely published because of medico-legal implications. Some textilomas cause infection or abscess formation in the early stage, whereas others remain clinically silent for many years. Here, we describe a case of textiloma in which the patient presented with low-back pain 4 years after lumbar discectomy. Imaging revealed an abcess-like mass in the lumbar epidural space

SHANK proteins limit integrin activation by directly interacting with Rap1 and R-Ras

SHANK3, a synaptic scaffold protein and actin regulator, is widely expressed outside of the central nervous system with predominantly unknown function. Solving the structure of the SHANK3 N-terminal region revealed that the SPN domain is an unexpected Ras-association domain with high affinity for GTP-bound Ras and Rap G-proteins. The role of Rap1 in integrin activation is well established but the mechanisms to antagonize it remain largely unknown. Here, we show that SHANK1 and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 and R-Ras via the SPN domain and thus limiting their bioavailability at the plasma membrane. Consistently, SHANK3 silencing triggers increased plasma membrane Rap1 activity, cell spreading, migration and invasion. Autism-related mutations within the SHANK3 SPN domain (R12C and L68P) disrupt G-protein interaction and fail to counteract integrin activation along the Rap1-RIAM-talin axis in cancer cells and neurons. Altogether, we establish SHANKs as critical regulators of G-protein signalling and integrin-dependent processes

Ulcerative IgA vasculitis in the setting of warfarin therapy

Henoch-Schönlein purpura (HSP) is a small vessel vasculitis characterized by the presence of vascular immunoglobulin A deposition that usually presents as non-thrombocytopenic palpable purpura. It primarily affects children and is less common in adults. The incidence of hemorrhagic necrotic skin lesions increases with age, similarly to renal involvement. Warfarin is a widely used oral anticoagulant drug that has rarely been associated with leukocytoclastic vasculitis and allergic interstitial nephritis. We report a patient with HSP who presented with cutaneous ulcerative plaques and proteinuria in the setting of warfarin therapy. We would like to raise the awareness of this potential adverse effect of warfarin for prompt diagnosis

Ulcerative IgA vasculitis in the setting of warfarin therapy

Henoch-Schönlein purpura (HSP) is a small vessel vasculitis characterized by the presence of vascular immunoglobulin A deposition that usually presents as non-thrombocytopenic palpable purpura. It primarily affects children and is less common in adults. The incidence of hemorrhagic necrotic skin lesions increases with age, similarly to renal involvement. Warfarin is a widely used oral anticoagulant drug that has rarely been associated with leukocytoclastic vasculitis and allergic interstitial nephritis. We report a patient with HSP who presented with cutaneous ulcerative plaques and proteinuria in the setting of warfarin therapy. We would like to raise the awareness of this potential adverse effect of warfarin for prompt diagnosis

Indolent Acremonium strictum infection in an immunocompetent patient

WOS: 000171586500008PubMed ID: 11679001A 35-year-old housewife presented with an 11-year history of a painless lesion on the right cheek, which had enlarged over the last 2 years. She had no history of travel or trauma. Various topical and systemic antimicrobial and antifungal agents, such as fluconazole, ketoconazole, sulbactam/ampicillin, and mupirocin, had been prescribed, with a probable diagnosis of pyoderma. and blastomycosis, without significant benefit. Her medical history was otherwise unremarkable. Dermatologic examination revealed a well-circumscribed, erythematous, infiltrative, 8 X 10 cm plaque covering the right cheek and a 2 X 3.5 cm vegetative, ulcerated lesion on the chin (Fig. 1). There were no sinus tracts or grains. The following laboratory test results were within the normal limits: complete blood count, blood biochemistry, urinalysis, immunoglobulins and complement levels, T lymphocyte, CD4 and CD8 cell counts, and response to mitogens. X-Rays of the chest and maxillar and mandibular bones were normal. Routine bacterial cultures were negative. Skin biopsies and fungal and mycobacterial cultures were taken with a preliminary diagnosis of deep fungal or mycobacterial infection. Dermatopathologic examination revealed irregular epidermal hyperplasia with follicular plugging. A dense nodular lymphohistiocytic infiltrate was observed within the reticular dermis, with many multinucleated giant cells and plasma cells. In higher magnification, even in hematoxylin and eosin sections, large septate hyphae and spores were noticeable. Periodic acid-Schiff stain revealed abundant fungal structures within the giant cells and extracellularly throughout the inflammatory infiltrate (Fig. 2). Lymphocytes were rather sparse in comparison to the large amount of microorganisms within the tissue. Fungal cultures were performed on Sabouraud's dextrose agar and, within 1 week of incubation, white fungal colonies were observed. On multiple passages at 26 degreesC, white tufted colonies with a salmon-colored base had formed (Fig. 3). Native preparations from the cultured colonies revealed septate hyphae, and 90 degrees angled branches, together with phialides decorated with ellipsoidal conidia with rounded edges (Fig. 4). These findings were consistent with Acremonium strictum, a saprophytic fungus. Further laboratory examinations revealed no systemic involvement. Following the diagnosis of Acremonium infection, amphotericin B therapy and surgical excision of the tumoral lesion were planned, but the patient refused further treatment and failed to respond to our follow-up attempts

The prevalence of Behcet's disease above the age of 10 years - The results of a pilot study conducted at the Park Primary Health Care Center in Ankara, Turkey

PURPOSE The aim of this study was to determine the prevalence of Behcet's disease above the age of 10 years by means of a population-based study

Soluble tumour necrosis factor receptors sTNFR1 and sTNFR2 are produced at sites of inflammation and are markers of arthritis activity in Behçet's disease

OBJECTIVE: We analysed the production of soluble tumour necrosis factor receptors sTNFR1 and sTNFR2 at sites of inflammation and measured their plasma concentrations to evaluate them as biological markers of disease activity. METHODS: Plasma samples of 35 patients with Behçet's disease (BD) were collected prospectively at monthly intervals and grouped for inactive disease, active BD without arthritis, and active BD with arthritis. sTNFR1 and sTNFR2 concentrations were measured using immunoassays and compared with other biological disease activity parameters. Plasma sTNFR levels were compared to synovial fluid (SF) levels in seven patients. Sixteen tissue samples of mucocutaneous lesions were stained for TNFR2 expression by immunohistochemistry. RESULTS: sTNFR1 and sTNFR2 were found at increased plasma concentrations in active BD, with the highest concentration in active BD with arthritis (p<0.001). Concentrations of both sTNFRs were at least three times higher in SF of arthritic joints than in the corresponding plasma samples (p = 0.025). A change of more than 1 ng/mL of sTNFR2 plasma concentrations correlated with a concordant change in arthritic activity (96% confidence interval). Sensitivity to change was superior to that of sTNFR1, and other biological disease activity parameters such as erythrocyte sedimentation rate (ESR), immunoglobulin (Ig)G, IgA, and interleukin (IL)-10 plasma concentrations. A strong staining for TNFR2 was found in mucocutaneous lesions, where mast cells were identified as the major source for this receptor. CONCLUSIONS: This longitudinal study demonstrates that sTNFR2 plasma concentrations are closely linked with active BD, and especially with arthritis. Taken together with the expression of TNFR molecules in mast cells of mucocutaneous lesions, our results indicate a fundamental role for the TNF/TNFR pathway in BD