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PubMed2003

The diagnosis and management of recurrent aphthous stomatitis: a consensus approach.

BACKGROUND: Recurrent aphthous stomatitis, or RAS, is a common oral disorder of uncertain etiopathogenesis for which symptomatic therapy only is available. This article reviews the current data on the etiopathogenesis, diagnosis and management of RAS in a primary care setting. METHODS: The authors reviewed publications on Medline from 1995 through 2000, the period since the last major reviews were published. RESULTS: RAS may have an immunogenetic background owing to cross-reactivity with Streptococcus sanguis or heat shock protein. Predisposing factors seen in a minority include haematinic (iron, folate or vitamin B12) deficiency, stress, food allergies and HIV infection. While topical corticosteroids remain the mainstay for therapy, a number of other immunomodulatory modalities now are available. CONCLUSIONS: There is still no conclusive evidence relevant to the etiopathogenesis of RAS, and therefore therapy can attempt only to suppress symptoms rather than to address the basic issues of susceptibility and prevention. CLINICAL IMPLICATIONS: In the majority of patients, symptomatic relief of RAS can be achieved with topical corticosteroids alone, with other immunomodulatory topical agents or by combination therapy.

Adjuvants, Immunologic↗

PubMed1994

Recent progress in TSH receptor studies with a new concept of "autoimmune TSH receptor disease".

Recent progress in the studies of epitope analysis of the TSH-R against TSH-R Ab was reviewed extensively. Using both site-directed mutagenesis and synthetic TSH-R peptide, binding and/or action sites of TSH-R Ab have been known to be multiple and discontinuous, but the significance of two unique and TSH-R specific regions has been implicated. Further, the possible existence of heterogeneity among stimulatory TSH-R Ab has also been indicated. As for immunogenetic factors related to autoimmune thyroid diseases, studies on HLA analysis, TSH-R specific T lymphocyte analysis and VH analysis of TSH-R Ab were discussed. Of note was the negative association of HLA-DP w2 antigen in Japanese patients with Graves' disease and hypothyroidism due to blocking TSH-R Ab, and we proposed a new concept of autoimmune TSH receptor disease within autoimmune thyroid disease and emphasized possible critical roles of HLA-DP. Recent evidence of restricted usage of the Ig VH gene in cloned B lymphocytes from Graves' patients producing TSH-R Ab has also been presented.

Autoimmune Diseases↗

PubMed2000

Management of reactive arthritis in a juvenile gorilla (Gorilla gorilla gorilla) with long-term sulfasalazine therapy.

A juvenile western lowland gorilla (Gorilla gorilla gorilla) experienced recurrent fever, lethargy, diarrhea, and/or arthritis starting at age 6 mo. During an episode at age 15 mo, Shigella sp. was isolated from diarrheic feces. At age 41 mo, reactive arthritis was diagnosed. In addition, the gorilla's growth was retarded. All arthritic attacks were managed symptomatically prior to age 4 yr, at which time a severe episode precipitated the implementation of therapy with sulfasalazine, an arthritis suppressive medication. Examination 27 mo later revealed cessation of progressive joint pathology although the animal exhibited decreased range of motion in most joints. The gorilla has been on sulfasalazine therapy for 4 yr without lameness. Growth has resumed, and there has been no radiographic evidence of progressive joint degeneration. Immunogenetic analysis of whole blood obtained at age 68 mo identified the gorilla major histocompatibility class I allele, Gogo-B*0101, which has limited nucleotide sequence similarity to HLA-B27, an allele associated with postinfection reactive arthritis in humans. Sulfasalazine therapy effectively managed reactive arthritis in this gorilla and should be considered for similarly frequently affected animals. Juvenile gorillas, in populations with a history of clinical shigellosis and/or postdiarrhea arthritis, may benefit from prophylactic sulfasalazine therapy after episodes of bacterial enterocolitis. Sulfasalazine therapy should be considered in all gorillas, juvenile and adult, experiencing confirmed Shigella sp.-associated enterocolitis.

Animals↗

PubMed1991

Anti-Ro(SSA) and anti-La(SSB) antibodies in lupus erythematosus and Sjögren's syndrome.

Anti-Ro(SSA) and La(SSB) antibody determinations have become important serologic tests in the evaluation of lupus erythematosus and Sjögren's syndrome patients. These antibodies appear to identify a group of lupus patients with prominent skin diseases. Although much of the initial investigations regarding the value of these antibodies has been performed in the United States and Europe, preliminary studies suggest that the frequency of these antibodies in Japanese and other Oriental patients may be double that seen in American patients. This article will briefly review our knowledge of the molecular, immunogenetic and clinical features of the anti-Ro(SSA) and anti-La(SSB) antibody responses.

Antibodies, Antinuclear↗

PubMed1990

The mouse as a model of experimental autoimmune uveoretinitis (EAU).

An EAU model has been developed in the mouse using the retinal soluble antigen (SAg), and the interphotoreceptor retinoid-binding protein (IRBP). Immunogenetic studies indicate that sensitivity to disease is H-2 dependent, but some data suggest that non-MHC genes may also contribute to the regulation of EAU. IRBP was a more potent uveitogen than SAg. Ability to mount lymphocyte and antibody responses was exhibited both by EAU-susceptible and by EAU-resistant strains, and could not be used as a predictive parameter. Dependence of disease induction on variables of immunization was studied in B10.A mice (I-Ak) immunized with IRBP. Use of Bordetella pertussis as additional adjuvant was a prerequisite for successful disease induction. Use of purified pertussis toxin (PTX), rather than a suspension of pertussis bacteria, allowed reduction of the immunization protocol to a single dose of IRBP in CFA. Severity and incidence of disease, as well as its clinical course, were directly affected by the dose of antigen and PTX, and could be controlled by varying their respective doses. A spectrum of disease, from hyperacute to chronic, could be obtained. The chronic type of EAU tended to relapse, with lesions reappearing after a brief period of essential quiescence. The special advantages of the murine EAU model for the study of ocular autoimmunity are discussed.

Animals↗

PubMedDate not supplied

On research subsystems and their integration in the computer-supported part of hospital information systems.

Taking as an example the special research programme ('Sonderforschungsbereich') in leukemia research and immunogenetics (SFB120) of the University of Tübingen, we intend to discuss how research subsystems should be built up, which functions they should take over and which network architecture is suitable. Furthermore, we examined to what extent research subsystems can be integrated in the computer-supported part of hospital information systems. It can easily be seen that no general solution exists for the structuring. The structure depends rather upon the specific problems and information requirements of individual research units. The clinical environment must be taken into account if research subsystems are to be integrated into the computer-supported part of a hospital information system. Especially in regard to the data protection aspect, we must keep in mind that the connection between subsystems must not necessarily result in the setup of a network for the corresponding computer systems.

Computer Communication Networks↗

PubMed2000

How to outfox mother nature--autoimmunity: moving from shadows to sunshine.

The morbidity and disability associated with autoimmune diseases represent a significant health problem. One in 31 people have one form or another of an autoimmune disease. Despite the avalanche of molecular data, immunogenetic definitions and improvements in serologic diagnosis, we are still far from discovering the etiologies of these diseases. For some autoimmune diseases, there may be a very long latency period between disease onset and clinical presentation. Existing therapies tend to be only partially successful and often accompanied by a variety of serious side effects. However, even in the absence of a complete understanding of the underlying genetic, environmental and coincidental factors that confer susceptibility to autoimmune diseases, we believe that it is possible to devise successful therapies by interfering with one or more of the pathways of destruction characteristic of a specific autoimmune disease. We have prepared a futuristic look at the treatment of autoimmune disease by extrapolation of current research directions as well as thoughts on new methods of delivery of recombinant monoclonal antibodies. We predict that we will "cure" autoimmune pathology long before we understand the etiology. In the case of inflammatory bowel disease, as a model, and taking advantage of what is known on animal studies, we illustrate the progress that has been made in elucidating these pathways of destruction and speculate about possible therapeutic approaches.

Animals↗

PubMedDate not supplied

Psoriatic arthritis--pathogenesis and epidemiology.

Psoriatic arthritis (PsA), recognised for over 100 years, is common representing the second most frequent diagnostic category after RA and occurring in up to 10% of patients with skin psoriasis. The pathogenic connection between psoriasis and arthritis is not yet clear although our understanding of the mechanisms of disease has progressed significantly in recent years. Factors including immunogenetics, infection, autoimmunity, angiogenesis, trauma and the nervous system are implicated in the pathogenesis of PsA. Organ involvement is largely restricted to the connective tissue of the skin and joints, including both the synovial tissue and sites of entheseal attachment. This restricted inflammatory response suggests that either a common antigen driving the immune response or that antigenic proteins or cells are present at these sites only having migrated the or arising de novo. The epidemiology of Psoriasis has been extensively examined since the 1960's, however there have been few large epidemiological studies of PsA. In addition, the lack of diagnostic criteria for the diagnosis of PsA until 1973, and the diffuse clinical manifestations of this condition have hindered meaningful conclusion regarding the epidemiology of this form of arthritis.

Arthritis, Psoriatic↗

PubMed1992

Juvenile rheumatoid arthritis, juvenile chronic arthritis, and juvenile spondyloarthropathies.

Immunogenetics are supporting the marked heterogeneity of chronic arthritis in children. Thus DRw13-DRw18 and DQw6-DQw18 were associated with persistent pauciarticular disease in children with an early onset of disease. Several studies have shown DPw2 as an additional susceptibility factor in this subgroup. Standardization of diagnostic criteria for juvenile onset spondyloarthropathy and psoriatic arthritis is necessary; various studies are in progress, and although HLA-B27 provides the common marker, this may only apply to a small group of juvenile psoriatics who have spondyloarthropathy. In the management of juvenile rheumatoid arthritis, methotrexate in moderate doses has been shown to be superior to lower doses of methotrexate and placebo in controlling polyarthritis. Methotrexate may be of particular value in treating the polyarthritis that follows a pauciarticular onset. The possible value of sulfasalazine in a B27 group with persistent polyarthritis has been suggested. Highlights of corticosteroid therapy were intra-articular injections, particularly in pauciarticular disease, the suggestion that deflazacort has a calcium sparing effect, and the possible role of intravenous methylprednisone in the management of severe disease.

Adrenal Cortex Hormones↗

PubMed1991

Immune reactions in allergic alveolitis.

This article discusses newer cellular immunological and immunoregulatory events operative in the pathogenesis of "allergic alveolitis" (aa). An early increase in neutrophils and chemotactic factors followed by an influx of macrophages and lymphoid cells with ultimate production of granulomas have been demonstrated in the bronchoalveolar lavage (BAL) fluids of experimental animals and of man in aa. Transfer of specifically sensitized lymph node and spleen cells intraperitoneally followed by antigen challenge via the respiratory tract route has resulted in production of pulmonary lesions closely resembling those observed in human aa in several animal species. Activated alveolar macrophages and T-cells, local lymphokine production, and elevated immunoglobulin levels in BAL fluid have also been demonstrated repeatedly in experimental animal models of these diseases. High levels of interleukin-1 have also been demonstrated in aqueous extracts prepared from pulmonary granulomatous lesions. Other studies have indicated a role for macrophage-derived lipoxygenase products in production of experimental pulmonary granulomatous inflammation. Mononuclear cell pulmonary infiltrates have been inhibited by corticosteroids, the use of antimacrophage serum, neonatal thymectomy, cobra factor venom, and cyclosporin. A T suppressor factor and other suppressor factors from adherent cell populations have also been shown to dampen or modulate experimental granuloma formation. Appropriately sensitized animals which demonstrate chronic pulmonary granulomatous inflammation can also become "desensitized" following a series of antigen challenges. The desensitization produced is immunospecific and nontransferable with immune serum. Studies of bronchoalveolar lavage fluids in man have demonstrated a very high percentage of lymphocytes in BAL fluids. The percentage of suppressor cytotoxic T-cells is usually above 40% and CD4:CD8 ratios are reversed. Evidence also suggests that suppressor lymphocytic alveolitis is a chronic event in patients with aa. Immunogenetic studies of granulomatous pneumonitis resembling aa in different strains of mice have shown that certain high-responder strains develop intense granulomas after inoculation with killed bacille Calmette-Guérin (BCG), whereas other low-responder strains do not. The intensity of the pulmonary granuloma formation in this model has been shown to be a dominant and polygenic trait and to be linked to the immunoglobulin heavy chain locus (IgH). Strains that develop intense, chronic granulomatous inflammation have usually proved to be anergic, and the anergy also appears to be under genetic control.(ABSTRACT TRUNCATED AT 400 WORDS)

Alveolitis, Extrinsic Allergic↗

PubMed1991

Psoriasis and psoriatic arthritis associated with human immunodeficiency virus infection.

It has been well established that psoriasis, psoriatic arthritis, and Reiter's syndrome can occur in patients with HIV infection. These arthocutaneous diseases tend to occur in temporal proximity to the development of AIDS and ARC, and their clinical manifestations are unusually severe. The appearance or exacerbation of psoriasis, arthritis, or Reiter's syndrome in a high-risk person should alert the clinician to possible underlying HIV infection. Treatment should be dictated by the severity of the skin and musculoskeletal disease as well as by the status of the immune system. Zidovudine appears to be effective in many diseases, especially psoriasis, and nonsteroidal antiinflammatory drugs are the mainstay for arthritis. Immunosuppressive agents such as methotrexate and azathioprine are contraindicated because they exacerbate immunodeficiency and promote infections. Epidemiologic studies suggest that the prevalence of these diseases, especially Reiter's syndrome, may be higher in HIV-positive populations than previously thought, especially in those patients with AIDS and ARC. Immunogenetic factors like HLA-B27 are important in the predisposition to Reiter's syndrome associated with HIV infection; however, it is not clear what role they play in HIV-associated psoriasis. Mechanisms underlying these observations remain unclear, although potential insights into the pathogeneses of psoriasis and Reiter's syndrome may be gained through future studies. Already it seems likely that CD4-positive helper T-cells, the target of HIV, are not necessary for the expression of psoriasis or Reiter's syndrome, and because of HLA class I associations, a role for CD8 positive cytotoxic T lymphocytes can be suspected. Infections, promoted by the profound immunodeficiency of AIDS, seem to be the most plausible explanations for the cutaneous and articular complications of HIV infection.

Arthritis, Psoriatic↗

PubMed1990

[Preparation of vaccines].

A historical review on the preparation and use of vaccines is presented. The example of smallpox vaccination in man is interesting, as it affords an insight into the development of the principle of vaccination, the improvement of the vaccine and the eradication of the disease. Moreover, the various stages of vaccinology were described. Initially, vaccines were prepared on the basis of the attenuated or inactivated pathogens. After the introduction of animal cell culture techniques among others it became possible to realise an amplification of the preparation of virus vaccines. Since the introduction of recent biotechnological methods, including monoclonal antibodies and recombinant DNA technology, the development and preparation of well characterised and purified vaccines became possible. Immunology, including the development of adjuvants and the immunogenetic aspects, is essential in the further development of vaccines. Furthermore, it should be stressed that in using vaccines, the control aspects of the new generation of vaccines including the application of so-called Good Manufacturing Practice (GMP), directives for their preparation should be strictly adhered to.

Adjuvants, Immunologic↗

PubMed1977

[Transplantation antigens: the individual in biology and psychology].

The persistent defense of biological individuality is explained on the basis of the concept that "foreign" and "self" are complementary phenomena. Since it is the T-lymphocyte of the immune system which recognizes "foreign", its receptor must represent "self". How is this accomplished in immunogenetic terms? An intriguing possibility would be the somatic reduplication and amplification of "self" through random combinatorial principles by means of exclusion: all receptors are formed, but those directed against "self" suppressed while the others (including those identical with "self") remain at disposition. In this way, HLA gene products, rather than representing immune receptors themselves, would prime the formation of the immunological repertoire indirectly. The concept that "self" plays the role of a template copied by the actual recognition system is supported by elementary information theory. Analogies to other, higher biological information systems such as the brain are drawn. Moreover, since neuroscience and psychology are in fact inseparable, the analogies reach even much further. A common blueprint can be traced from primitive cell to cell interactions through molecular immunology to neurochemistry, psychology and philosophy. Particularly Jung's concept of psychological individuation as the never-ending struggle of the human individual for consciousness would precisely fit the role of "molecular individuation" as a means of acquiring the immunological repertoire. In psychological terms "foreign" corresponds not only to the outer world (antigens( but also to our own unconscious (antiidiotypic set) resulting in a similar network of mutual interactions between conscious and unconscious much as between idiotypes and anti-idiotypes.

B-Lymphocytes↗

PubMed1978

[Atopy and RAST. Diagnostic, therapeutic and standardization problems. Experimental contribution (allergy to antibiotics)].

The authors outline the immunological and immunogenetic bases of atopy, as well as the radioimmunological techniques employed in the allergological diagnosis and purification as well as standardization of the allergens. The latest trends of the allergological immunotherapy are examined, covering fundamentally two wide fields: the possibility to elicit an aspecific immunological tolerance (soluble suppressor substances of IgE response; Asp-Ser-Asp-Pro-arg pentapeptide, D-GL copolimer conjugated aptens) or the specific induction of "suppressor" mechanisms (allergoids, modified allergens). The preliminary results obtained on sera of patients with a symptomatology highly indicative of penicillin allergy, employing RAST Penicilloil G and Penicilloil V, are also reported.

Allergens↗

PubMed1984

Inflammatory disorders of muscle. Immunological aspects.

Immunological abnormalities associated with inflammatory disorders of muscle have the potential for diagnostic utility but current data suggest that there is considerable heterogeneity with overlap between many of the conditions considered in the differential diagnosis. Immunogenetic factors may influence the expression of disease. For example, D-penicillamine may induce myasthenia gravis and/or polymyositis, depending on the HLA antigens of the recipient.

Antibodies↗

PubMed1977

Complete HLA and Bf typing in families. I. Analysis of MLC responses and LD typing.

A triple normalization protocol for the analysis of MLC responses was evaluated using data obtained in more than 1700 triplicate reactions between the members of 17 families. The results show the method to be consistent with immunogenetic expectations. Typing responses to HTC, however, may have values identical with those of some weak one-haplotype responses and often can only be resolved by segregationanalysis.

Epitopes↗

PubMed1995

[Prognostic criteria for the clinical course of systemic lupus erythematosus].

To develop some individual prognostic criteria of SLE clinical course the Wald's analysis of immunogenetic markers (HLA) was used. The obtained summarized diagnostic coefficients allow predicting a subacute or chronic pattern of the disease, the rate of generalization and the most frequent location of the process in certain organs. The constant character of HLA-typing results and the simplicity of the given prognostic tables made the proposed diagnostic method convenient for medical practice.

Acute Disease↗

PubMedDate not supplied

D-penicillamine induced myasthenia gravis: clinical, serological and genetic findings.

Eight cases of D-penicillamine (DP) induced myasthenia gravis (MG) are presented. Seven patients were being treated for rheumatoid arthritis (RA) and one for scleroderma. The mean duration of DP treatment until the myasthenic symptoms developed ranged from 2-8 months. The DP dose reached 500 mg daily. It was found that the clinical and immunological findings were almost similar to those of idiopathic MG, but were less severe. All patients had increased titers of acetylcholine receptor antibodies in their sera. Discontinuation of D-penicillamine resulted in the complete resolution of myasthenic symptoms after 2-6 months. One patient required ventilation, immunosuppressive therapy and plasma exchange. No association was found between DP related MG and the various autoantibodies tested. Immunogenetic analysis showed that three patients had HLA-DR1, two HLA-DR3, one HLA-DR4 and one HLA-DR5. In conclusion, the clinical presentation of DP-induced MG seems similar to idiopathic MG. DP-related MG is relatively benign, although it sometimes can cause life-threatening muscle weakness requiring aggressive therapy. The relatively small number of patients included in this study, however, does not permit any firm conclusions regarding the HLA associations of DP-related MG.

Adult↗