Home About us Contact | |||
Tissue Pathology (tissue + pathology)
Selected AbstractsBone and Soft Tissue Pathology (1,6)PATHOLOGY INTERNATIONAL, Issue 2007Article first published online: 29 APR 200 No abstract is available for this article. [source] Necrotizing fasciitis: delay in diagnosis results in loss of limbINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2006Rajat Varma MD A 58-year-old man presented to the Emergency Room with a 1-day history of severe pain in the left lower extremity preceded by several days of redness and swelling. He denied any history of trauma. He also denied any systemic symptoms including fever and chills. His past medical history was significant for diabetes, hypertension, deep vein thrombosis, and Evans' syndrome, an autoimmune hemolytic anemia and thrombocytopenia, for which he was taking oral prednisone. Physical examination revealed a warm, tender, weeping, edematous, discolored left lower extremity. From the medial aspect of the ankle up to the calf, there was an indurated, dusky, violaceous plaque with focal areas of ulceration (Fig. 1). Figure 1. Grossly edematous lower extremity with well-demarcated, dusky, violaceous plaque with focal ulceration Laboratory data revealed a white blood cell count of 6.7 × 103/mm3[normal range, (4.5,10.8) × 103/mm3], hemoglobin of 11.5 g/dL (13.5,17.5 g/dL), and platelets of 119 × 103/mm3[(140,440) × 103/mm3]. Serum electrolytes were within normal limits. An ultrasound was negative for a deep vein thrombosis. After the initial evaluation, the Emergency Room physician consulted the orthopedic and dermatology services. Orthopedics did not detect compartment syndrome and did not pursue surgical intervention. Dermatology recommended a biopsy and urgent vascular surgery consultation to rule out embolic or thrombotic phenomena. Despite these recommendations, the patient was diagnosed with "cellulitis" and admitted to the medicine ward for intravenous nafcillin. Over the next 36 h, the "cellulitis" had advanced proximally to his inguinal region. His mental status also declined, and he showed signs of septic shock, including hypotension, tachycardia, and tachypnea. Vascular surgery was immediately consulted, and the patient underwent emergency surgical debridement. The diagnosis of necrotizing fasciitis was then made. Tissue pathology revealed full-thickness necrosis through the epidermis with subepidermal splitting. Dermal edema was also present with a diffuse neutrophilic infiltrate (Fig. 2). This infiltrate extended through the fat into the subcutaneous tissue and fascia. Tissue cultures sent at the time of surgery grew Escherichia coli. Initial blood cultures also came back positive for E. coli. Anaerobic cultures remained negative. Figure 2. Necrotic epidermis with subepidermal splitting. Marked dermal edema with mixed infiltrate and prominent neutrophils. Hematoxylin and eosin: original magnification, ×20 After surviving multiple additional debridements, the patient eventually required an above-the-knee amputation due to severe necrosis. [source] Immune-mediated control of Chlamydia infectionCELLULAR MICROBIOLOGY, Issue 1 2008Nadia R. Roan Summary Infection with the bacterium Chlamydia trachomatis can lead to a variety of diseases, including ectopic pregnancy, infertility and blindness. Exposure of the host to C. trachomatis stimulates multiple innate and adaptive immune effectors that can contribute towards controlling bacterial replication. However, these effectors are often insufficient to resolve the infection and prevent re-infection, and the continued presence of C. trachomatis within the host may induce immune effectors to chronically produce inflammatory cytokines. This may eventually lead to the tissue pathologies associated with the infection. Reducing the incidence and sequelae of infection will ultimately require the development of a C. trachomatis vaccine that can stimulate sterilizing immunity while avoiding immune-mediated pathology. [source] PEX1 mutations in the Zellweger spectrum of the peroxisome biogenesis disorders,HUMAN MUTATION, Issue 3 2005Denis I. Crane Abstract Diseases of the Zellweger spectrum represent a major subgroup of the peroxisome biogenesis disorders, a group of autosomal-recessive diseases that are characterized by widespread tissue pathology, including neurodegeneration. The Zellweger spectrum represents a clinical continuum, with Zellweger syndrome (ZS) having the most severe phenotype, and neonatal adrenoleukodystrophy (NALD) and infantile Refsum disease (IRD) having progressively milder phenotypes. Mutations in the PEX1 gene, which encodes a 143-kDa AAA ATPase protein required for peroxisome biogenesis, are the most common cause of the Zellweger spectrum diseases. The PEX1 mutations identified to date comprise insertions, deletions, nonsense, missense, and splice site mutations. Mutations that produce premature truncation codons (PTCs) are distributed throughout the PEX1 gene, whereas the majority of missense mutations segregate with the two essential AAA domains of the PEX1 protein. Severity at the two ends of the Zellweger spectrum correlates broadly with mutation type and impact (i.e., the severe ZS correlates with PTCs on both alleles, and the milder phenotypes correlate with missense mutations), but exceptions to these general correlations exist. This article provides an overview of the currently known PEX1 mutations, and includes, when necessary, revised mutation nomenclature and genotype,phenotype correlations that may be useful for clinical diagnosis. Hum Mutat 26(3), 167,175, 2005. © 2005 Wiley-Liss, Inc. [source] Eosinophilic fasciitis: demographics, disease pattern and response to treatment: report of 12 cases and review of the literatureINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2008Lindsay Bischoff Senior Medical Student Background, Eosinophilic fasciitis is a rare scleroderma-like illness. The clinical spectrum of the disease has evolved since its initial description. Methods, We identified all patients diagnosed with eosinophilic fasciitis over the past 10 years at our scleroderma clinic. Demographics, disease pattern, serologies, tissue pathology and reponse to treatment were all recorded. Results, Twelve patients with eosinophilic fasciitis were identified in our clinic over the past 10 years. The mean age at diagnosis was 49.8 ± 9.8 years, with nine female and three male patients. The first symptoms were noticed at an average of 8.8 ± 6.1 months before diagnosis. The mean initial absolute peripheral blood eosinophil count was 1188 ± 1059 cells/L. Two patients had a monoclonal gammopathy, and two had positive ANA titers. All patients received corticosteroids, 10 of whom received the equivalent dose of > 20 mg/day of prednisone for more than a month. Five patients received hydroxychloroquine, two received methotrexate, one received cyclosporine, one received topical tacrolimus, and one received sulfasalazine. At a mean follow up of 17.6 months (range 2,94 months), 8 patients had a good response to treatment, 2 patients had no effect, and 2 patients had a poor response to treatment. Conclusion, High dose corticosteroid treatment lasting longer than a month with or without an immunosuppressive agent helped most patients with eosinophilic fasciitis, best results seen in those patients who were initiated treatment early on after their first symptoms. [source] An evaluation of current diagnostic tests for the detection of infectious salmon anaemia virus (ISAV) following experimental water-borne infection of Atlantic salmon, Salmo salar L.JOURNAL OF FISH DISEASES, Issue 3 2003M Snow Abstract Four commonly used diagnostic tests [reverse transcription polymerase chain reaction (RT-PCR), indirect fluorescent antibody test (IFAT), virus culture and light microscopy] were evaluated for their ability to detect infectious salmon anaemia virus (ISAV) or tissue pathology following experimental infection of Atlantic salmon. Fish were infected with ISAV by water-borne exposure which mimics the route of natural infection. Forty-five per cent of pre-clinical fish tested yielded positive results by RT-PCR for at least one of the organs tested (kidney, heart, gill, liver, blood). No significant difference was detected between organs in the number or time of first occurrence of positive result. Virus culture identified a total of 14% of pre-clinical fish as ISAV-infected. The presence of ISAV in heart tissue was particularly notable (13% of fish sampled) as was the inability to culture virus from spleen tissue. In the case of IFAT, 15% of fish sampled were positive, although tissue other than kidney proved unsuitable for use in this method. Only limited ISAV-specific pathology was detectable by histological examination of fish prior to the onset of clinical disease. These findings reveal important information regarding the optimal choice of both tissue sample and diagnostic test for the routine diagnosis of ISAV. [source] In vivo detection of microglial activation in frontotemporal dementiaANNALS OF NEUROLOGY, Issue 6 2004Annachiara Cagnin MD Using positron emission tomography and [11C](R)-PK11195, a marker of "peripheral benzodiazepine sites" that is upregulated on activated microglia during progressive tissue pathology, we show increased binding of [11C](R)-PK11195 in frontotemporal lobar degeneration in the typically affected frontotemporal brain regions. This implies the presence of an active glial response reflecting progressive neuronal degeneration. It also suggests that increased [11C](R)-PK11195 binding, previously demonstrated for Alzheimer's disease, may occur independently from increased amyloid plaque formation, given that it is not a characteristic feature of frontotemporal lobar degeneration. Ann Neurol 2004;56:894,897 [source] Synovial tissue heterogeneity in rheumatoid arthritis in relation to disease activity and biomarkers in peripheral blood,ARTHRITIS & RHEUMATISM, Issue 6 2010Lisa G. M. van Baarsen Objective To investigate the clinical relevance of synovial tissue subtypes in rheumatoid arthritis (RA) and to search for peripheral blood (PB) markers that may serve as biomarkers for tissue subtypes. Methods Gene expression analysis using complementary DNA microarrays was applied on paired synovial tissue biopsy and PB samples obtained from 17 RA patients. Molecular tissue subtypes were correlated with histologic parameters (CD3, CD22, CD38, CD68, CD163, tumor necrosis factor ,, intercellular adhesion molecule 1, vascular cell adhesion molecule, and E-selectin), disease characteristics, and PB markers. PANTHER classification was used for pathway analysis. Results Genomic subtyping of high- and low-inflammation rheumatoid synovial tissues based on gene expression profiles exactly matched immunohistochemical classification. The patients with the high-inflammation tissue type had higher Disease Activity Scores in 28 joints, higher C-reactive protein levels, higher erythrocyte sedimentation rates, increased numbers of platelets, and shorter disease durations. Comparative analysis of PB gene expression profiles yielded no statistically significant differences between the 2 tissue groups at the single-gene expression level. PANTHER pathway analysis revealed a significant association of increased protein biosynthesis with high-inflammation tissue. Conclusion High-inflammation tissue is associated with more severe disease and shorter disease duration. While pathway-level analysis revealed that coordinate differential expression of genes involved in protein synthesis in PB is associated with high-inflammation tissue types, differential tissue pathology was not reflected in the PB by differential expression of single genes. [source] Jaccoud's arthropathy in systemic lupus erythematosus: Differentiation of deforming and erosive patterns by magnetic resonance imagingARTHRITIS & RHEUMATISM, Issue 1 2003Benedikt Ostendorf Objective To evaluate alterations of the soft tissues, tendons, and bones as detected by magnetic resonance imaging (MRI) in patients with systemic lupus erythematosus (SLE),associated arthritis of the finger joints. Methods Both hands of 14 patients with SLE of various activities and durations and with arthritis and/or deformities of the finger joints were examined by MRI and conventional radiography. Coronal T1-weighted spin-echo (with and without gadolinium contrast), axial T2-weighted turbo spin-echo, coronal fat-suppressed short tau inversion recovery, and 3-dimensional double-echo steady-state sequences were acquired and analyzed, and the findings were compared with those from conventional radiographs. Results MRI detected periarticular capsular swelling in all 14 patients, joint effusion in 7, edematous tenosynovitis in 6, proliferative tenosynovitis (flexor and/or extensor tendons) in 4, and intraarticular signs of synovial membrane hypertrophy in 10 patients, 9 of whom showed enhancement after administration of contrast medium. Bony erosions were identified in 8 patients by MRI; conventional radiography missed these erosions in 2 of the 8 patients. Four of the 14 patients were designated as Jaccoud's arthropathy index,positive, and all 4 showed severe edematous tenosynovitis and capsular swelling, but no signs of bony erosions despite longstanding disease (mean 21.5 years). Four of the 10 patients with mild deformity exhibited prominent soft tissue pathology, with minimal destruction of bone; the other 6 patients had bony alterations that resembled rheumatoid arthritis. Conclusion In SLE patients with arthritis of the finger joints, MRI detects characteristic signs of soft tissue pathology (e.g., capsular swelling, edematous and proliferative tenosynovitis, synovial hypertrophy) and bony alterations (e.g., erosions, some of which are missed by conventional radiography). MRI thus helps to distinguish different types of lupus arthritis/Jaccoud's arthropathy, which allows more differentiated treatment strategies and monitoring. [source] |