Multicentric reticulohistiocytosis - a case with minimal articular changes.
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Biomedical subjects
Publications and source records attributed to M Bukilica.
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We report a 69-year-old Caucasian female with non-Hodgkin's lymphoma who subsequently developed leg ulcers as a manifestation of the antiphospholipid syndrome. Investigations revealed a mixed cryoglobulinaemia with monoclonal IgM-kappa and antiphospholipid activity with anticardiolipin antibodies, antimitochondrial type M5 antibodies and lupus anticoagulant. Significantly increased concentration of anticardiolipin antibodies was detected in the cryoprecipitate. Our case illustrates a connection between cryoglobulinaemia and lymphoproliferative and autoimmune disorders. Both cryoglobulins and anticardiolipin antibodies could participate in the vascular damage. Cutaneous manifestations in the presence of these disorders associated with non-Hodgkin's lymphoma have not been described previously.
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Sera from Wistar rats subjected to different stress procedures were tested by ELISA for the presence of autoantibodies with specificity for neuron-specific enolase (NSE) and S100 protein that are preferentially localized in neurons and glia, respectively. Autoantibodies were present in sera of animals before exposure to stress, and raised with age. Anti-NSE and anti-S100 autoantibody levels were increased one day after termination of restraint (2 hours daily, 10 days) and electric tail shock (80 shocks daily, 19 days), and in fifth and tenth week of overcrowding stress. Differences between stressed and control animals were not present one month following restraint and electric tail shock and in twentieth week of overcrowding.
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There have been many reports of the immunomodulatory effects of stress, but the influence of stress on anaphylaxis has been given little attention till now. In this study we investigated the influence of tail-shock stress on the course of anaphylactic shock (AS) in the rat. For this purpose, rats were sensitized to ovalbumin and subjected to stress procedure before the induction of AS. In the first series of experiments we used chronic (4 day) stress consisted of 80 inescapable tail shocks delivered at the same time each day. Anaphylactic shock was induced 24 hours later by intraperitoneal injection of 3 mg of ovalbumin. Results showed that stressed rats exhibited lower intensity of three investigated parameters of AS: clinical signs, hematocrit values, and drop of rectal temperature. In order to investigate whether acute stress procedure could also influence course of AS, rats were given various shock doses of ovalbumin immediately after the end of acute (1 day) tail-shock stress. Anti-anaphylactic effect of acute stress was demonstrated to be dose-dependent: the greatest protective effect was in animals that received the highest shocking dose of ovalbumin. Finally, we examined the duration of protective effect of acute inescapable tail shocks on AS, and these results showed that observed anti-AS phenomenon disappears 72 hours after the end of acute stress session.
Numerous experiments have demonstrated that physical stress can alter immunological parameters. However, little attention has been paid to the interrelationship between stress and autoimmune processes. The present study was designed to determine the influence of electric shock and sound stress on the development of experimental allergic encephalomyelitis (EAE). Ten-week-old male DA rats highly susceptible to EAE were used. Rats were subjected to the stress procedure during 19 days either before or after immunization with intradermal injection of 0.1 ml of an emulsion containing guinea pig spinal cord (20 mg/rat) in an equal volume of complete Freund's adjuvant (CFA). In addition, rats received subcutaneous injection of Bordetella pertussis in the dorsum of the same foot. Electric stress procedure consisted of 80 inescapable, unpredictable tail shocks (5 s, 1 mA) delivered at the same time each day. Sound stress procedure consisted of exposure of rats to a 90 dB fire alarm bell which rings 60 times for 5 s during one hour, at the same time of the day. Rats were observed daily for clinical signs of EAE and survived animals were sacrificed on day 20 after immunization. The brain and spinal cord sections were examined histologically for mononuclear cell infiltrates characteristics for EAE. The results clearly indicate that inescapable tail shocks suppressed the appearance and development of EAE when rats were subjected to stress procedure during 19 days after immunization, but not when rats were stressed during 19 day before the induction of EAE. On the other hand, in rats exposed to sound stress there was only delay in the onset of the disease.
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More than 75% of grass pollen-allergic patients produce specific IgE antibodies against group-4 allergens. Purification and characterization of different grass group-4 allergens should help to further understand their allergenicity. In this study, an attempt was made to isolate and characterize Fes p 4 allergen by several biochemical and immunochemical methods. Fes p 4 was purified by a combination of chromatographic techniques (gel permeation and ion exchange chromatography). Isolated protein revealed four main spots at a molecular weight of 60 kDa and a pI ranging from 8.7 to 9.1. Eight sera were selected from patients with positive result of skin prick test to the mixture of grass pollen extracts. ELISA inhibition technique was used to study Fes p 4-specific IgE in the patients' sera. ELISA to Festuca pratensis was inhibited up to 80% by F. pratensis pollen extract and up to 48% by Fes p 4. 2D-PAGE-immunoblot was used to identify allergenic and antigenic components of Fes p 4 with patients' IgE and monoclonal antibodies (MABs). Three components of purified protein expressed IgE binding ability. Two MABs which recognized unrelated regions on Phl p 4, bound three components of Fes p 4. The role of the carbohydrate moiety in allergenicity was examined with individual patient sera by using periodate-treated Fes p 4. Six out of eight patients reduced IgE binding to periodate-treated allergen. Isolated Fes R 4 glycoprotein consisted of four components, three of which were allergenic, and share common epitopes specific for grass group-4 homologs. The results of periodate oxidation of Fes p 4 suggest that the carbohydrate moiety is involved in IgE binding.
Sharp's syndrome is a systemic mixed connective tissue disease that is defined with specific ribonucleoprotein antibody (U1RNP). The key diagnostic criterion is positive antinuclear antibodies in stain form. The disease is primarily localized on joints, muscles and skin; however, there are not widely used diagnostic criteria. There are USA, Mexican and Japanese diagnostic criteria. A 18-year-old male who fulfilled Sharp's diagnostic criteria is presented in the paper. In this patient the disease was manifested in pleura and pericardium. We wish to point out the importance of immunologic approach to the aetiology of pleural and pericardial inflammatory effusions in young patients, as well as the therapeutical dilemmas in the treatment of the disease.
The human mast-cell population is composed of a heterogenous group of cells with respect to structure and function. Mast-cells can no longer be regarded simply as cells that initiate acute allergic reactions through the release of rapidly metabolized mediators, such as histamine and products of arachidonic acid oxidation. The production of a wide range of cytokines by mast-cells in the centre of the allergic inflammation. These cytokines influence migration and activation of other different cells including basophils and eosinophils and also lymphocytes, thus perpetuating allergic inflammation. Mediators release from human basophils are considered to contribute to the late phase of allergic response.
Monitoring of allergic inflammation includes direct examination of biopsy specimens from mucosa and epithelium, and indirect study by sputum, bronchoalveolar and nasal lavage fluid and peripheral blood. Although, some of these detection assays are not applicable to clinical use, it is now possible to measure a number of inflammatory mediators released from cells participating in allergic disease. The release of performed histamine from peripheral blood basophils challenged with specific antigen remains a valuable in vitro correlate of immediate hypersensitivity reactions. However, other mediators such as LTC4 and IL-4 are also generated by basophils upon IgE dependent activation. Tryptase and PGD2 are released from mast cells upon activation. Eosinophils contain in their granules proteins that cause damage to the bronchial epithelium: MBP and ECP. It is possible to measure soluble markers from other cells (T cells, macrophages, platelets, endothelial cells) involved in allergic inflammation. Detection of mediators have produced data that have significantly added to our understanding of the mechanisms and allowed better pharmacological control of allergic inflammation.