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Biomedical subjects

R E Schmidt

Publications and source records attributed to R E Schmidt.

At least 19 recordsLinked to original sources

Bias in association studies of systemic lupus erythematosus susceptibility due to geographical variation in the frequency of a programmed cell death 1 polymorphism across Europe.

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 x 10(-6)) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.

Antigens, CD↗

Differential influence of different hepatitis viruses on quality of life in HIV positive patients.

UNLABELLED: HIV-infected individuals are frequently co-infected with different hepatitis viruses. HCV has been associated with impaired quality of life in non-HIV infected patients. Little is known concerning the quality of life in HIV-infected individuals in relation to the different viral co-infections. - PATIENTS AND METHODS: We investigated 250 patients who have answered HIV-SELT and EuroQoL (EQ-5D) questionnaires assessing quality of life. Data on HBsAg, anti-HBc, anti-HCV, and GBV-C-RNA were available for 191, 188, 189, 98 patients, respectively. HCV-RNA was tested in 33 of 35 anti-HCV positive patients. - RESULTS: There was no difference in quality of life in relation to active or past HBV-infection defined by HBsAg (n = 15) and anti-HBc in the absence of HBsAg (n = 84), respectively, for both overall HIV-SELT (p = 0.66, and p = 0.43, respectively) and visual EQ-5D (p = 0.93 and p = 0.64, respectively). However, anti-HCV positivity (n = 35) was associated with significantly impaired quality of life (HIV-SELT overall p<0.001). Importantly, no difference was found in relation to HCV-viraemia in anti-HCV positive patients (p = 0.77). In multivariate analysis anti-HCV positivity, employment status, HIV viral load and GBV-C were relevant to quality of life, with GBV-C being beneficial and HCV being negative. - CONCLUSIONS: While HBV seems to play no role concerning quality of live in HIV-infected patients, the flavi-viruses HCV and GBV-C display opposing influence on quality of life. As quality of life was similarly impaired in HCV-viraemic and HCV-non-viraemic anti-HCV positive patients but better in GBV-C viraemic patients, this should be taken into account in the indication case of planned interferon therapy.

Flaviviridae Infections↗

Patients' attitude to subcutaneous immunoglobulin substitution as home therapy.

INTRODUCTION: Since 2003, immunoglobulin preparations have been approved for subcutaneous (s.c.) use in Germany. Although all our adult patients on intravenous (i.v.) substitution were offered to switch to s.c. home therapy, approximately half of them refused to change. METHODS: To evaluate patients' attitude towards s.c. home therapy, a questionnaire was developed and sent to 125 patients. Questions had to be answered by ticking numbers on a Likert scale from 1 (not at all) to 8 (very much). Four scales of the Freiburg Personality Inventory (FPI) were added. From the 70 questionnaires returned (56%), 61 could be analysed (i.v. n = 28, s.c. n = 33). RESULTS: The i.v. treated patients were afraid of being more busy with self-administration (6.9 +/- 2.1). This was not a serious concern in the s.c. treated group (3.6 +/- 1.8, p < 0.001). Many i.v. treated patients worried about severe adverse reactions at home (4.7 +/- 2.8), but patients in the s.c. group did not (1.7 +/- 1.0, p < 0.001). The statement "I dislike to puncture myself" reached 5.3 +/- 2.7 points in the i.v. treated group, but only 2.0 +/- 1.1 (p < 0.001) in the s.c. treated patients. As main reason, patients on i.v. substitution considered s.c. therapy as inconvenient (48%). Secondly, they were afraid of side effects (31%). All patients on s.c. therapy appreciated the new treatment (7.2 +/- 1.0). Main advantage for them was an increase of flexibility (6.6 +/- 1.6). The FPI displayed lower values for s.c. treated patients in the scales "Physical Complaints" and "Emotional Lability". CONCLUSION: Those patients who had changed to s.c. therapy were highly satisfied. However, others preferred to stay on i.v. treatment for different reasons. Perception of inconvenience, anxiety of side effects, but also personal traits may play a role.

Anxiety↗

Mice conditionally lacking the Wolfram gene in pancreatic islet beta cells exhibit diabetes as a result of enhanced endoplasmic reticulum stress and apoptosis.

AIMS/HYPOTHESIS: Wolfram syndrome is an autosomal recessive disorder characterised by childhood diabetes mellitus, optic atrophy and severe neurodegeneration, resulting in premature death. The aim of this study was to investigate the mechanisms responsible for the phenotype of carbohydrate intolerance and loss of pancreatic beta cells in this disorder. MATERIALS AND METHODS: To study the role of the Wolfram gene (Wfs1) in beta cells, we developed a mouse model with conditional deletion of Wfs1 in beta cells by crossing floxed Wfs1 exon 8 animals with mice expressing Cre recombinase under the control of a rat insulin promoter (RIP2-Cre). Complementary experiments using RNA interference of Wfs1 expression were performed in mouse insulinoma (MIN6) cell lines (WfsKD). RESULTS: Male knockout mice (betaWfs(-/-)) began developing variable and progressive glucose intolerance and concomitant insulin deficiency, compared with littermate controls, by 12 weeks of age. Analysis of islets from betaWfs(-/-) mice revealed a reduction in beta cell mass, enhanced apoptosis, elevation of a marker of endoplasmic reticulum stress (immunoglobulin heavy chain-binding protein [BiP]), and dilated endoplasmic reticulum with decreased secretory granules by electron microscopy. WfsKD cell lines had significantly increased apoptosis and elevated expression of the genes encoding BiP and C/EBP-homologous protein (CHOP), two markers of endoplasmic reticulum stress. CONCLUSIONS/INTERPRETATION: These results indicate that (1) lack of expression of Wfs1 in beta cells was sufficient to result in the diabetes mellitus phenotype; (2) beta cell death occurred by an accelerated process of apoptosis; and (3) lack of Wfs1 was associated with dilated endoplasmic reticulum and increased markers of endoplasmic reticulum stress, which appears to be a significant contributor to the reduction in beta cell survival.

Animals↗

Association of multiple sclerosis with ILT6 deficiency.

Multiple sclerosis (MS) is an autoimmune disorder of multifactorial etiology. Family studies have shown strong genetic contributions. Linkage analyses have revealed several regions harboring risk genes including chromosome region 19q13. ILT6 is one of the most interesting candidate genes, since ILTs are involved in the generation of immunological tolerance. There is an absence/presence of variability of the ILT6 gene comprising several exons, thus incapacitating the gene function. In the present study, we examined the association of ILT6 deletion with MS. Using PCR typing, deficiency of ILT6 was examined in 607 blood donors and in 751 Caucasian German, as well as 89 French MS patients. Homozygous ILT6 deficiencies were significantly more prevalent in MS patients (7.1%) than in blood donors (3.8%; P=0.009). ILT6 deficiency is associated with MS in the German population and hence a likely risk factor for autoimmune disorders.

Chromosomes, Human, Pair 19↗

Association of killer cell immunoglobulin-like receptors with scleroderma.

OBJECTIVE: Scleroderma is an autoimmune disorder of unknown etiology. A genetic contribution has been demonstrated, and genes influencing activation of the immune system have been potentially identified as candidate genes in this process. The repertoire of killer cell immunoglobulin-like receptors (KIRs) that are involved in the activation of T cells and natural killer cells is highly variable. Recently, an association of KIR2DS2 with vasculitis in patients with rheumatoid arthritis has been reported. Because scleroderma is characterized by an involvement of the vascular system, we sought to determine whether KIR2DS2 is associated with scleroderma. METHODS: We typed 9 KIR genes in 102 patients with scleroderma and in 100 blood donors, using polymerase chain reaction on genomic DNA. RESULTS: Twelve patients with scleroderma, compared with only 2 blood donors, had KIR phenotypes characterized by the presence of the activating KIR2DS2 and the absence of the corresponding inactivating KIR2DL2 (P = 0.005). CONCLUSION: The genetic combination of KIR2DS2+ and KIR2DL2- is associated with scleroderma.

Genetic Predisposition to Disease↗

[Immune restoration inflammatory syndromes].

Increase of prevalence of certain immunodeficiencies is caused by more frequent use of immunosuppresive treatment, by advances in supportive care of immunodeficient individuals and by the pandemic spread of HIV-infection respectively. Highly active antiretroviral treatment (HAART) is able to reconstitute the impaired immunity in the HIV-infected individual and therefore to reduce morbidity and mortality. On the other hand paradoxical exacerbation of inflammatory or opportunistic diseases may develop during immunoreconstitution. By their distinct pathophysiological, clinical and therapeutic particularities these disease have been summarized as Immune Restoration Inflammatory Syndromes (IRIS). This review summarizes the variety of immunoreconstitution disorders and describes possible diagnostic pitfalls. Potential therapeutic options and an algorithm for the classification of the syndrome are proposed.

Algorithms↗

GB virus C infection and quality of life in HIV-positive patients.

It was recently shown that GBV-C infection is associated with prolonged survival of HIV-infected individuals. The GB virus C is the closest known relative of hepatitis C virus in man. The latter has been associated with significant impairment in quality of life, independent from the associated liver disease. We were thus interested in the impact of GB virus C infection on quality of life in HIV-infected individuals. We retrospectively analyzed a cohort of HIV-positive patients who previously answered the 'HIV-SELT' and the 'EQ-5D' questionnaires assessing quality of life and for whom data on GB virus C RNA status were available. In this study we identified no adverse effect of GB virus C on quality of life, but, in contrast, GB virus C viraemic patients showed better quality of life in all parameters for the scores in comparison to GB virus C-negative HIV-infected patients. HIV-positive patients with a GB virus C infection showed superior quality of life. These data further support the favourable course of HIV disease in GB virus C-positive patients.

Adult↗

Lack of mutations in LMNA, its promoter region, and the cellular retinoic acid binding protein II (CRABP II) in HIV associated lipodystrophy.

Familial partial lipodystrophy (FPL) and lipodystrophy observed in HIV-1 infected patients receiving highly active antiretroviral therapy (HAART) share multiple clinical and metabolic features. Recently, missense mutations of LMNA encoding lamin A/C have been described in FPL providing evidence for a pivotal role of lamin A/C in the regulation of adipocytes. Moreover, the cellular retinoic acid binding protein (CRABP) has been suggested to be involved in HAART associated lipodystrophy. In this study, we excluded mutations within the complete coding region and the promoter of LMNA and the CRABP II gene in HIV-1 infected patients with lipodystrophy and also any correlation of the nucleotide polymorphism at codon 566 in exon 10 of LMNA with metabolic abnormalities. Protease inhibitors including indinavir have been shown to reduce adipocyte cell differentiation and increase apoptosis of adipocytes in vitro. Indinavir leads to altered retinoic acid signaling most likely by an activation of the RAR/RXR heterodimer, perhaps by displacing all-trans-retinoic acid from CRABP. Since LMNA is regulated by a retinoic acid responsive element (L-RARE) in the promoter region, we propose that indinavir impairs retinoic acid homeostasis and/or interact via the L-RARE within the LMNA promoter. This results in altered LMNA expression and subsequent impaired adipocyte differentiation, lipodystrophic body habitus, and metabolic disturbances in HIV infected patients receiving HAART.

Amino Acid Sequence↗

[Lipodystrophy syndrome. Therapeutic progress is still pending].

A common problem seen with the long-term use of highly active antiretroviral therapy (HAART) is the HIV-associated lipodystrophy syndrome. Clinical signs include a loss of peripheral subcutaneous fatty tissue, an increase in visceral or local fat, and altered glucose and lipid metabolism. The physical changes frequently impair quality of life, and the patient's adherence to treatment regimens. Metabolic changes may possibly represent cardiovascular risks with incalculable consequences over the long term. Although the lipodystrophy syndrome was first described in 1998. It still lacks a definition. So far, therapeutic strategies have remained ineffective or have had only limited success. Proposed treatments include general recommendations (diet, physical exercise, etc.), changing the antiretroviral therapy, and treatment with metabolically active medication.

Anti-HIV Agents↗

[Immune reconstituted inflammatory syndrome. Pitfalls of antiretroviral therapy].

The pandemic HIV infection, the more frequent use of immunosuppressive treatment, and the improved long-term prognosis of immunocompromised patients due to better supporting therapies have resulted in an increase in the prevalence of immunodeficiencies. Highly active antiretroviral therapy (HAART) can improve immunocompetence in HIV patients, even when the immunodeficiency is far advanced. This has resulted in an impressive and lasting lowering of the morbidity and mortality associated with HIV infection. However, immune reconstitution may exacerbate subclinical opportunistic infections or autoimmune diseases, or result in an unexpected, paradoxical aggravation of intercurrent inflammatory diseases. The atypical inflammatory conditions have a number of synonymous names: immune restoration disease (IRD), immune reconstitution syndrome (IRS), or immune reconstitution inflammatory syndrome (IRIS). In the light of specific differential therapeutic consequences, it is important to distinguish the clinical presentation from that of corresponding opportunistic infections. However, diagnostic and therapeutic standards for IRIS have not yet been worked out. The present overview also points to possible diagnostic pitfalls, and makes suggestions for a possible classification of the condition and the therapeutic options.

Acquired Immunodeficiency Syndrome↗

[Immunologic control of HIV-1 infection. Fantasy or soon reality?].

The human immunodeficiency virus-1 (HIV-1) preferentially infects CD4+ cells, leading to their destruction. In contrast to other viral infections, the immune system is unable to keep the HIV infection under permanent control in most cases. This failure ultimatively results in immunodeficiency with occurrence of AIDS-defining diseases. In recent years, highly active antiretroviral therapy (HAART) has become available, and the number of AIDS cases and deaths have decreased dramatically. However, limitations of HAART become more apparent, demanding greater emphasis on search for alternative approaches. Stimulation and modulation of the immune response to HIV are new and promising strategies. A prerequisite, however, is the knowledge about immunologic defense mechanisms against HIV. In this article, the major factors of innate and acquired immune responses to HIV are described.

AIDS Vaccines↗

Enhanced frequency of a PTPRC (CD45) exon A mutation (77C-->G) in systemic sclerosis.

A point mutation in exon A (C to G transversion at position 77) of human PTPRC (CD45) has recently been associated with the development of multiple sclerosis (MS) for at least a subgroup of patients. In the present report, we studied the frequency of the 77C-->G transversion in two other autoimmune diseases namely systemic sclerosis (SSc) and systemic lupus erythematosus (SLE). The mutation was found with significantly enhanced frequency in patients suffering from SSc suggesting that PTPRC could play a role as susceptibility gene not only in MS but also in other autoimmune diseases. Further understanding of the mode of interaction of mutant PTPRC with other susceptibility genes may uncover mechanisms common in various autoimmune disorders.

Exons↗

CD8beta/CD28 expression defines functionally distinct populations of peripheral blood T lymphocytes.

Peripheral blood CD8+ T lymphocytes generally express the CD8 coreceptor as an alphabeta heterodimer. On these cells, the CD8beta chain is present either at high (CD8betahigh) or low density (CD8betalow). CD8betahigh cells are CD28+, whereas CD8betalow cells are CD28+ or CD28-. Therefore, three subpopulations of CD8+ T cells can be described: (i) CD8betahighCD28+ (ii) CD8betalowCD28+, and (iii) CD8betalowCD28- cells. Phenotypic and functional characterization of these CD8+ T cell subsets revealed significant differences. CD8betahighCD28+ cells predominantly express CD45RA. In contrast, CD8betalowCD28+ cells frequently express CD45R0 and the activating NK receptor CD161. CD8betalowCD28- cells frequently revert to the CD45RA phenotype. In addition, these cells express CD16, CD56, CD94, and the killer-inhibitory receptors NKB1 and CD158a. Intracellular IL-2 was frequently detected in CD8betahighCD28+ cells and CD8betalowCD28+ cells, but not CD8betalowCD28- cells. CD8betalowCD28+ cells and CD8betalowCD28- cells frequently stained positive for IFN-gamma. In addition, these cells contain intracellular perforin and granzyme A. Expression of Fas (CD95) as well as susceptibility to apoptosis is markedly increased in CD8betalowCD28+ and CD8betalowCD28- cells as compared to CD8betahighCD28+ cells. In vitro activation of peripheral blood lymphocytes triggered expansion of CD8betahighCD28+ cells as well as a development into CD8betalowCD28+ and CD8betalowCD28- cells. Similarly, activation of CD8betahighCD28+ cord blood cells resulted in the appearance of CD8betalowCD28+ and CD8betalowCD28- cells. These data suggest that CD8betahighCD28+ cells can differentiate into CD8betalowCD28+ and CD8betalowCD28- cells upon TCR stimulation. Therefore, the CD8beta/CD28 subsets in peripheral blood may reflect distinct stages of post-thymic CD8+T cell development.

Adult↗

[Economic aspects of ambulatory and inpatient treatment of HIV positive patients].

Highly active antiretroviral therapy (HAART) was introduced in the midst of the 1990s. The sustained declin of morbidity and mortality by HAART has been proven to be cost effective despite high expenditures for regular administration of cost intensive antiretroviral drugs. Yearly direct treatment costs are estimated as high as [symbol: see text] 20,000 to [symbol: see text] 30,000 per case in Germany. Approximately two third of all direct costs are caused by the use of antiretrovirals. Despite rising use of HAART and increasing drug prices, general costs for treatment decreased in the last years. This is explained by declining costs for hospitalisation and by increasing use of less expensive drug combinations. In addition deferment of initiation of HAART to slightly more advanced stages of immunodeficiency is recommended in recent treatment guidelines and leads to further reduction of direct costs. Modified treatment concepts with presumed cost saving effects, like periods of antiretroviral treatment interruption, are currently under investigation.

Ambulatory Care↗