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Kaz Jaskiewicz

Publications and source records attributed to Kaz Jaskiewicz.

3 recordsLinked to original sources

Microscopic colitis in routine colonoscopies.

Lymphocytic colitis (LC) and collagenous colitis (CC), both known as microscopic colitis (MC), are uncommon entities with increasing incidence as more clinicians take biopsies from macroscopically normal colons and as pathologists use more rigorous diagnostic criteria to be confident of the diagnosis. Information on the incidence of this type of colitis is limited and based on reported cases. The purpose of this work is to estimate the incidence of LC and CC in reviewed routine colonoscopies. We reviewed 2815 colonoscopies performed at a tertiary referral center with an open-access service using restricted histological criteria in order to establish the frequency rate of LC and CC in routine colonoscopic biopsy material. Cases suspicious for MC were stained with Masson's trichrome or Congo red stain and immunohistochemically for lymphocytes, where appropriate. Review of routine colonoscopic biopsies showed that MC is underreported in our colonoscopic material. Incidence rates of LC and CC (0.9 and 0.4, respectively) were based on morphological assessment of colonoscopic biopsies using stringent criteria together with clinical data and after differentiation with other lesions which can mimic MC. The 10.2% rate of this type of colitis in patients with chronic watery diarrhea indicates the necessity to consider these lesions in older individuals with diarrhea and normal endoscopical colonic mucosa.

Adult↗

Pregranulomatous phase of sarcoidosis: immunohistochemical diagnosis.

Histopathological confirmation of clinical suspicion of sarcoidosis is based on the finding of non-caseating granulomas in biopsy material, usually in prescalene lymph nodes or in transbronchial lung biopsies. Lymph node reactive sinus histiocytosis (RSH) seen in relation to various inflammatory and non-inflammatory diseases can mimic the pregranulomatous phase of sarcoidosis (PSH). Differentiation of sinus histiocytosis based on histopathological features alone is limited. The purpose of this study is immunohistochemical determination of lymph node cellular response in granulomatous sarcoidosis, the PSH and RSH using a immunohistochemistry employing a panel of antibodies. Patient groups under study each contained 25 patients and included: those with clinical picture of sarcoidosis and non-caseating granulomatous lymphadenitis; those with confirmed sarcoidosis and with sinus histiocytosis without granuloma formation in lymph nodes; and finally, those without sarcoidosis and with "reactive" sinus histiocytosis in lymph nodes. Lymph node biopsy tissue was fixed in buffered formaldehyde, routinely processed to paraffin wax blocks, cut into 4-microm-thick sections, stained with hematoxylin and eosin and immunohistochemically labelled using a triple-layer APAAP protocol with purified polyclonal antibodies directed against SP 70 and SP90 from Mycobacterium tuberculosis and monoclonal antibodies against CD22, CD4, CD8, CD56, and CD68. Intensity of immunolabelling was assessed semiquantitatively by two independent observers. An increased CD4:CD8 ratio, moderate increase of immunolabelling for CD68 and slight decrease in immunolabelling for CD20, CD56, and SP90 was indicative of PSH when compared with RSH. The most notable difference between the studied groups was a difference in immunoreactivity to SP70 and CD4 antibodies. Lymph nodes with pregranulomatous sinus histiocytosis labelled with both antibodies. This profile of immunolabelling can be used in the differentiation of this condition from reactive sinusoidal lesions.

Adolescent↗

Immunocytes and activated stellate cells in pancreatic fibrogenesis.

INTRODUCTION AND AIMS: Chronic pancreatitis is a progressive chronic inflammatory disease characterized by irreversible destruction of exocrine pancreatic tissue and extensive fibrosis. Excessive alcohol consumption has been identified as the main etiologic factor of this disease in the Western world. Idiopathic pancreatitis accounts for approximately 30% of cases. An autoimmune mechanism may be involved in some patients, but this concept has not been generally accepted as a new clinical entity. The purpose of this work was to investigate the pathogenesis of pancreatic fibrosis and to establish the role of immunocytes and activated stellate cells in chronic pancreatitis, which was categorized into three groups: chronic alcoholic pancreatitis (AP), chronic idiopathic pancreatitis (IP), and chronic pancreatitis in the presence of pancreatic cancer (CA). METHODOLOGY: Fifty-one pancreatic tissue samples were studied histopathologically and immunohistochemically (AP, 16 samples; IP, 12; CA, 12; and samples of tissue with apparently normal pancreatic histology, 11). The following immunohistochemical stains were used: alpha-smooth muscle antibody, desmin, and synaptophysin, as markers of activated stellate cells; and laminin, fibronectin, and collagen IV, as markers of extracellular matrix (ECM) proteins. Immunocytes were stained with antibody to LCA, CD68 antibody (macrophages), and CD8 antibody (natural killer T cell subset), and mast cells were examined using the Giemsa method. Positively stained macrophages, lymphocytes, and mast cells were counted in three high-power fields of a light microscope. The immunoreactivity of activated stellate cells and ECM proteins was assessed by a semiquantitative method (0, lack of positive staining; 5, numerous cells with strong positive immunostaining). Results were assessed statistically. RESULTS: We found no statistical differences between cases of AP, IP, and CA in terms of total lymphocyte count (mean numbers: 416, 418, and 407 per three high-power fields, respectively). The percentage of CD8+ T cells in IP was statistically higher than that in AP. The macrophage count was significantly higher in the IP group than in the AP and CA groups. The mast cell count was markedly higher in the IP group than in the other groups. The stellate cell markers alpha-smooth muscle antibody and desmin showed slightly higher immunoreactivity in IP. The immunopositivity for synaptophysin was also higher in the IP group. There was a positive correlation between alpha-smooth muscle antibody, desmin, and synaptophysin expression and the degree of fibrosis. ECM protein markers showed no statistically significant differences between the three groups. CONCLUSION: Results of this work show that a significant number of IP cases might have an autoimmune etiology. There was a positive correlation between activated stellate cell marker expression and the degree of fibrosis.

Cell Count↗