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Biomedical subjects

J J Gomez-Reino

Publications and source records attributed to J J Gomez-Reino.

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↗

The endogenous growth hormone secretagogue (ghrelin) is synthesized and secreted by chondrocytes.

Ghrelin, the endogenous ligand for the GH secretagogue receptor (GHS-R), is a recently isolated hormone, prevalently expressed in stomach but also in other tissues such as hypothalamus and placenta. This novel acylated peptide acts at a central level to stimulate GH secretion and, notably, to regulate food intake. However, the existence of further, as yet unknown, effects or presence of ghrelin in peripheral tissues cannot be ruled out. In this report, we provide clear evidence for the expression of ghrelin peptide and mRNA in human, mouse, and rat chondrocytes. Immunoreactive ghrelin was identified by immunohistochemistry in rat cartilage, being localized prevalently in proliferative and maturative zone of the epiphyseal growth plate, and in mouse and human chondrocytic cell lines. Moreover, ghrelin mRNA was detected by RT-PCR and confirmed by Southern analysis in rat cartilage as well as in mouse and human chondrocytes cell lines. Ghrelin mRNA expression has been studied in rat along early life development showing a stable profile of expression throughout. Although ghrelin expression in chondrocytes suggests the presence of an unexpected autocrine/paracrine pathway, we failed to identify the functional GH secretagogue receptor type 1A by RT-PCR. On the other hand, binding analysis with 125I ghrelin suggests the presence of specific receptors different from the 1A isotype. Scatchard analysis revealed the presence of two receptors with respectively high and low affinity. Finally, ghrelin, in vitro, was able to significantly stimulate cAMP production and inhibits chondrocytes metabolic activity both in human and murine chondrocytes. In addition, ghrelin is able to actively decrease both spontaneous or insulin-induced long chain fatty acid uptake in human and mouse chondrocytes. This study is the first to provide evidence for the presence of this novel peptide in chondrocytes and suggests novel potential roles for this newly recognized component of the GH axis in cartilage metabolism.

Animals↗

Chronic inflammation modulates ghrelin levels in humans and rats.

OBJECTIVES: The aim of this work was to investigate whether changes in plasma ghrelin, the recently discovered 28-amino acid gastric hormone that regulates growth hormone (GH) secretion and energy homeostasis, occur during inflammation in adjuvant-induced arthritis (AA) in rats. For completeness, ghrelin plasma levels were measured in rheumatoid arthritis (RA) patients. METHODS: AA was induced in male Lewis rats using Freund's complete adjuvant. Animals were monitored for weight and food intake, every 2 or 3 days, along all time-course experiments. Plasma ghrelin concentrations in 31 RA patients and 18 healthy controls, as well as in rats, were determined by a specific double-antibody radioimmunoassay. Gastric ghrelin mRNA expression was evaluated by northern blot analysis. Human GH and insulin-like growth factor (IGF)-1 were determined by quantitative chemiluminescence assay. RESULTS: Compared with controls, arthritic rats gained significantly (P < 0.01) less body weight than controls until the end of the study, when a partial recovery occurred. Ghrelin plasma levels were significantly lower at day 7 after arthritis induction than in controls (AA 7 = 91.2 +/- 5.6 pg/ml vs controls = 124.75 +/- 5.9 pg/ml), but they recovered to control levels by day 15. RA patients had ghrelin plasma levels significantly lower than healthy controls (RA = 24.54 +/- 2.57 pg/ml vs 39.01 +/- 4.47 pg/ml of healthy controls; P = 0.0041). CONCLUSION: In AA, there is a compensatory variation of ghrelin levels that relates to body weight adjustments. Recovery of ghrelin levels in the latter stage suggests an adaptive response and may represent a compensatory mechanism under catabolic conditions. In RA patients, chronic imbalance in ghrelin levels suggests that this gastric hormone may participate, together with other factors, in alterations of metabolic status during inflammatory stress.

Adult↗

The three most common CARD15 mutations associated with Crohn's disease and the chromosome 16 susceptibility locus for systemic lupus erythematosus.

OBJECTIVE: To test if the three most common mutations contributing to Crohn's disease on the CARD15/NOD2 gene could contribute also to genetic susceptibility to systemic lupus erythematosus (SLE), which has been found to be linked to the region of chromosome 16q13 where the CARD15 gene is located. METHODS: We obtained DNA samples from the blood of 189 SLE patients (according to the American College of Rheumatology classification criteria) and 194 controls of Spanish ancestry. Genotypes for the three CARD15 mutations (3020insC, 2722G>C and 2104C>T) were determined by hybridization with fluorescence resonance energy transfer probes on a LightCycler real-time polymerase chain reaction system. RESULTS: CARD15 genotypes were similar in SLE patients and in controls from the general population (allelic frequencies for 3020insC 0.013 in SLE patients vs 0.013 in controls; for 2722G > C 0.011 vs 0.008; and for 2104C > T 0.032 vs 0.051). CONCLUSION: We did not find evidence that the Crohn's disease-associated mutations on CARD15 contributed to SLE susceptibility.

Carrier Proteins↗

A comparison between septic bursitis caused by Staphylococcus aureus and those caused by other organisms.

Septic bursitis is an infection that usually involves olecranon and prepatellar bursae. Staphylococcus aureus is responsible for around 80% of cases. However, information regarding bursitis caused by non-Staphylococcus aureus microorganisms (NSAB) is scant. In this paper we describe the characteristics of NSAB and emphasise differences between these and Staphylococcus aureus bursitis (SAB). A retrospective study of all cases with septic bursitis seen between January 1991 and June 1998 at one university hospital was conducted. Only cases in which bursal fluid culture yielded growth of a microorganism were analysed. A literature review was conducted for completeness. Fifty-seven episodes of septic bursitis in 56 patients were studied: 47 of these were caused by Staphylococcus aureus and 11 by non-Staphylococcus aureus microorganisms. Forty-three SAB patients were male (91%). Mean age at diagnosis was 50 years (range 20-85 years). The presentation of bursitis had a seasonal trend, with a peak in the summer. Twenty-three patients (51%) had occupations involving frequent or sustained pressure on the bursae. Other risk factors were recent trauma in 11 (23%), alcoholism in six (13%), pre-existing bursal disease in five (11%), and chronic obstructive pulmonary disease in four (9%). There were 20 cases of olecranon bursitis (43%), 25 of prepatellar bursitis (53%) and two of first metatarsophalangeal bursitis. Characteristics of patients from the literature review were similar. Eight NSAB patients (73%) were male. Mean age at diagnosis was 46.9 (range 29-83 years). Two patients were plumbers and one a stonemason. Five (45%) had neither putative systemic nor local risk factors. There were five olecranon (45%), five prepatellar (45%), and one external malleolus bursitis. Infection by a mixed flora was common. Unlike SAB, the presentation of cases did not have a seasonal trend. The clinical spectrum of non-Staphylococcus aureus bursitis (NSAB) differs from that of Staphylococcus Aureus bursitis (SAB), and this should be considered in the initial diagnosis of septic bursitis.

Adult↗

Keratinocyte apoptosis and p53 expression in cutaneous lupus and dermatomyositis.

Keratinocyte apoptosis may be induced by ultraviolet-B radiation and represents a potential source of fragmented autoantigens in autoimmune diseases. This study investigates whether excessive keratinocyte apoptosis occurs in the skin lesions of cutaneous lupus (CLE) and dermatomyositis (DM) and the potential mechanisms responsible for this phenomenon. Skin biopsies have been studied from 19 patients with CLE and DM, eight with scleroderma, and five healthy controls. Apoptosis was detected by in situ end-labelling of fragmented DNA. The expression of Bcl-2, PCNA, p53, and Ki-67 proteins was studied by immunohistochemistry. In DM and CLE skin, the number of apoptotic keratinocytes was significantly increased (p=0.008) compared with normal skin. In both diseases, a large accumulation of apoptotic keratinocytes and apoptotic bodies was present in the disrupted basal zone. Unlike normal skin, a large number of keratinocytes, particularly those morphologically apoptotic, expressed p53 protein. A significant increase in the number of proliferating Ki-67 positive (p=0.0007) and PCNA-positive (p=0.0008) nuclei was also observed. In both CLE and DM, exaggerated and inappropriate keratinocyte apoptosis occurs. It is associated with increased expression of p53 and PCNA. This suggests that normal solar radiation alone or in combination with additional local factors induces DNA damage and excessive keratinocyte apoptosis in these autoimmune diseases of the skin. Apoptosis can mediate the severe epidermal lesions observed in both diseases and the release of fragmented autoantigens into the dermis.

Adult↗

Cyclooxygenase-1 and -2 are expressed by human T cells.

In vitro, prostaglandins (PG) have strong inhibitory effects on T cell activation and proliferation and inhibitors of PG synthesis (NSAID) increase proliferation and activation of T cells. Although most studies have failed to demonstrate cyclooxygenase (COX) activity in lymphocytes, there is contradictory evidence on the synthesis of different PG. We have studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot the expression of COX-1 and -2 mRNA and protein in resting and activated peripheral blood or Jurkat T cells. Cells were activated by T cell receptor triggering with OKT3 antibodies and activation confirmed by flow cytometric analysis of surface CD69. COX enzymatic activity was measured by determination of arachidonic acid (AA)-induced PG synthesis. Both peripheral blood and Jurkat T cells expressed COX-1 and -2 mRNA and protein. COX-1 was constitutively expressed and did not change after OKT3 stimulation. COX-2 was inducible upon OKT3-induced activation. In spite of the presence of COX mRNA and immunoreactive protein, AA-induced PG synthesis was not detected at the EIA detection (pM) level. The potential role of cyclooxygenases in T cells deserves further study, since no PG of the studied series seem to be synthesized by T cells.

Antibody Specificity↗

Risk of thrombosis in patients with antiphospholipid antibodies and factor V Leiden mutation.

OBJECTIVE: Antiphospholipid antibodies (aPL) are thrombophilic risk markers in patients with systemic lupus erythematosus (SLE) or primary antiphospholipid syndrome (APS). The risk factors for recurrent venous or arterial thrombosis and indications for longterm anticoagulation therapy are debated. We hypothesized that carrying a second thrombophilic defect, factor V Leiden mutation, would increase the risk for thrombosis in patients with aPL. METHODS: Seventy-five patients with primary APS and 83 with SLE and aPL with or without thrombosis followed at 2 university hospitals were studied. Factor V mutation rate was analyzed in patients and in 200 healthy blood donors by polymerase chain reaction analysis. RESULTS: The prevalence of factor V Leiden mutation in patients with SLE and aPL or primary APS was similar to controls. Patients with deep vein thrombosis or arterial thrombosis did not have a significantly increased rate of factor V mutation compared to controls or to patients with aPL without thrombosis. CONCLUSION: Factor V Leiden mutation is not significantly associated with vein thrombosis in patients with aPL. However, due to the sample size we cannot rule out synergy between both factor V Leiden and aPL. A trend toward increased risk for thrombosis was detected in patients with the mutation and this should be analyzed in a larger study.

Adult↗

Muscle dysfunction in elderly individuals with hip fracture.

OBJECTIVE: To investigate muscle metabolism in elderly people with hip fracture. METHODS: Free carnitine, carnitine esters, and respiratory chain enzyme activity were measured in muscle tissue from 54 patients over 65 years who underwent surgery for hip fracture, and from 40 healthy controls. RESULTS: Eighty-five percent of patients older than 85 have either abnormal carnitine distribution or defects in the respiratory chain. CONCLUSION: Elderly patients with hip fracture have muscle metabolic alterations that may contribute to neuromuscular impairment and be amenable to therapy.

Age Factors↗

Detection of COX-1 and COX-2 isoforms in synovial fluid cells from inflammatory joint diseases.

OBJECTIVE: To investigate the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in cells from synovial fluid (SF) of patients with acute or chronic arthritis. METHODS: SF was obtained from eight patients with acute crystal-induced arthritis, nine with rheumatoid arthritis and four with psoriatic arthritis. COX-1 and COX-2 gene expression was studied by reverse transcriptase-polymerase chain reaction (RT-PCR). Protein expression was detected by Western blotting and immunocytochemistry. RESULTS: There was expression of COX-1 mRNA in all and COX-2 mRNA in most of the SF samples from acute or chronic arthritis. By immunocytochemistry, both COX-1 and COX-2 immunoreactivity was restricted to a variable fraction of mononuclear cells. COX-1 staining was observed in 10-fold more cells than COX-2. By Western blotting, COX-1 protein was detected in 60% of the SF samples and COX-2 in none. There were no differences in the pattern of COX-1 and COX-2 expression between chronic and acute SF samples. CONCLUSION: In arthritis, both COX-1 and COX-2 isoforms are expressed by SF cells. COX-1 is the most abundant isoform. Since the strong COX-1 immunostaining observed in a fraction of mononuclear SF cells is not observed in peripheral blood leucocytes, it may be the result of either the activation or recruitment of a subset of mononuclear cells with a high COX-1 expression level.

Arthritis, Gouty↗

Prospective study of serum and urinary nitrate levels in patients with systemic lupus erythematosus.

OBJECTIVE: To study prospectively whether serum and urinary nitrate levels are related to lupus activity. METHODS: Fifty patients with systemic lupus erythematosus (SLE) were studied prospectively for 2 yr. Every 4 months, the SLE Disease Activity Index (SLEDAI) was administered to the patients, and blood and 24 h urine samples were obtained; 88 healthy controls were also studied. Nitrate levels were measured by the Greiss method. Statistical analyses were performed using standard parametric and non-parametric tests, and analysis of serial measurements. RESULTS: Twelve patients suffered infections, 12 active nephritis and 17 episodes of non-renal activity. By analysis of serial measurements, serum and urinary nitrate levels did not correlate with SLEDAI. C-Reactive protein (CRP) levels, presence of infection and creatinine clearance weakly influenced nitrate levels. CONCLUSIONS: In SLE, serum and urinary nitrate levels do not parallel lupus activity. Other variables, related or not to SLE, seem to affect these levels.

Adolescent↗

Apoptosis and proliferation of fibroblasts during postnatal skin development and scleroderma in the tight-skin mouse.

Tight-skin (Tsk) is a dominant gene mutation that causes a fibrotic skin disease in mice, similar to human scleroderma. Both conditions are characterized by increased numbers of dermal fibroblasts containing high levels of procollagen mRNA. Whether this fibroblast population arises from fibroblast growth or fibroblast transcriptional activation is debated. Proliferation and apoptosis of fibroblasts of normal and Tsk mice were studied in skin sections before, at onset, and in established fibrosis. Tissues sections were immunostained with proliferating cell nuclear antigen (PCNA) as proliferation marker. Apoptosis was investigated by in situ end-labeling of fragmented DNA and nuclear staining with propidium iodide. The expression of the apoptosis inhibitor Bcl-2 was investigated by immunohistochemistry. We demonstrate differences in fibroblast proliferation and apoptosis related to postnatal skin growth and development. Neonatal skin exhibits the highest levels of proliferation and apoptosis in fibroblasts. In contrast, low proliferation and absence of apoptosis characterizes adult fibroblasts. Skin fibroblasts express Bcl-2 only in newborns, and at other ages Bcl-2 was restricted to epithelial cells. Our results also suggest that neither increased fibroblast proliferation nor defective apoptosis accounts for the fibrotic phenotype of Tsk. Therefore, transcriptional activation of extracellular matrix genes appears more relevant in the pathogenesis of Tsk fibrosis.

Animals↗

Antiphospholipid antibodies in patients with eosinophilia myalgia and toxic oil syndrome.

OBJECTIVE: To explore whether antiphospholipid antibodies (aPL) are markers of vascular related damage or merely evidence of toxic related autoimmunity, we investigated the presence of different aPL in patients with toxic oil syndrome (TOS) and compared the profile with patients with eosinophilia myalgia syndrome (EMS). METHODS: Reactivity against cardiolipin, P-serine, P-inositol, and P-choline was investigated by ELISA in the blood of 266 patients with acute and chronic TOS, 25 healthy relatives of TOS patients, and 48 patients with EMS. RESULTS: 32% of TOS and 13% of EMS patients had IgG antibodies against cardiolipin and other polyanions. 20% of both TOS and EMS patients presented IgM antibodies against anionic and zwitterionic phospholipids. 36% of TOS healthy relatives had IgM antibodies against differently charged phospholipids. Among 200 patients with chronic TOS, there was no significant association between antibodies and clinical manifestations. CONCLUSION: aPL with different specificity are present in a high percentage of patients with TOS and EMS. The significance of these antibodies remains unclear.

Antibodies, Antiphospholipid↗

Abnormal carnitine distribution in the muscles of patients with idiopathic inflammatory myopathy.

OBJECTIVE: To analyze the levels of free carnitine and carnitine esters in the muscles of patients with inflammatory myopathies. METHODS: Six men and 7 women with inflammatory myopathy and 25 age-matched healthy controls were studied. Free carnitine and carnitine esters in muscle homogenates were measured by a radiochemical procedure. Muscle histochemical staining and measurement of respiratory chain enzyme activity were also performed. RESULTS: Eleven patients had muscle carnitine insufficiency. Five of them had subsarcolemmal oxidative accumulations, 5 had lipid droplets, and 4 had defects of the respiratory chain enzyme complexes. CONCLUSION: Abnormal distribution of muscle carnitine is present in patients with inflammatory myopathies and could impair muscle function. Coexistent mitochondrial dysfunction may contribute to carnitine insufficiency.

Adolescent↗

Outcome of silent lupus nephritis.

To analyze the long-term outcome in patients with silent lupus nephritis, we retrospectively studied 20 patients with systemic lupus erythematosus without clinical renal involvement who had renal biopsies in our unit between 1978 and 1986 and reviewed 193 cases reported between 1957 and 1995. Two patients of the current series were lost to follow-up. Mean follow-up in the other 18 was 13 +/- 3 years (range, 2 to 17). On kidney biopsy, nine had class I, six class II, one class IV, and two class V disease (WHO classification). Three patients with prior normal renal function died of nonrenal causes. During the study, the remaining 15 patients had normal renal function and urinalysis. Most patients from the literature had "mild" histologic lesions, but 30 had diffuse proliferative glomerulonephritis. Over an average of 46 months of follow-up from biopsy, renal survival rate and patient survival rate were 98% and 91%, respectively. Three patients died of end-stage renal failure. In conclusion, end-stage renal failure in patients with silent lupus nephritis is rare regardless of the histopathological renal lesions. Patients survival depends on nonrenal causes.

Adolescent↗

Frequencies of HLA-A24 and HLA-DR4-DQ8 are increased and that of HLA-B blank is decreased in chronic toxic oil syndrome.

The cause of toxic oil syndrome (TOS) has not yet been definitively determined, but some genetic susceptibility factors (certain HLA antigens and female sex) have been identified in 236 patients. Similarities with genetic factors for scleroderma and hydralazine-induced lupus (i.e. in TOS female sex and HLA-A24, Pcorrected = 0.00001 and DR4, Pcorrected = 0.04, respectively) may provide a clue to the responsible xenobiotic and its pathogenesis, and may also help in understanding the basis of the related eosinophilia-myalgia syndrome associated with tryptophan ingestion. In this paper it is also established that a human class I antigen (HLA-A24) and, independently, an HLA class II haplotype (DR4-DQ8, Pcorrected = 0.04) and arginine 52 in the alpha-DQ chains (Pcorrected = 0.03) are associated with TOS susceptibility, similarly to insulin-dependent diabetes. This further supports the classification of TOS as an autoimmune disease. Also, the increased frequency of a particular set of low-frequency HLA class I antigens in chronic TOS patients (i.e. B27, B37, B38 and B49) and the probable decrease in the frequency of HLA-B homozygotes in surviving patients (Pcorrected = 0.008) may provide an objective model to explain the maintenance of the HLA polymorphism: less frequent HLA alleles may be more advantageous in the event of unexpected human contact with unusual xenobiotics (not only microbes); however, other mechanisms working together to preserve and generate HLA polymorphism may coexist.

Fatty Acids, Monounsaturated↗

Autoantibodies in sera from patients with L-tryptophan-associated eosinophilia-myalgia syndrome. Demonstration of unique antigen-antibody specificities.

The purpose of this study was to determine whether specific autoantibodies could be identified that are associated with eosinophilia-myalgia syndrome (EMS). Sera from 44 patients with EMS were tested by indirect immunofluorescence, immunodiffusion against calf thymus extract, and immunoprecipitation from HeLa cell extract. Antinuclear antibodies were detected in the sera of 24/39 patients with EMS (61.5%) by indirect immunofluorescence against HEp-2 cells. Seven patients (16%) were demonstrated to have specific autoantibodies by immunoprecipitation in which at least two shared patterns were noted. In three sera immunoprecipitation identified a similar 63-kDa band (Ab-1). An additional four sera shared a pattern of bands consisting of a strong 110-kDa protein and a weak 95-kDa protein (Ab-2). Absorption of HeLa extract with a strongly positive Ab-2 serum confirmed that the four patients shared the same antibody. In conclusion, the detection of these autoantibodies provides evidence of autoimmunity in EMS, and may distinguish this syndrome from clinically related conditions.

Autoantibodies↗