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T Pettersson

Publications and source records attributed to T Pettersson.

At least 37 records · Page 2Linked to original sources
PubMed1998

Evaluation of an ELISA test for determination of the serum transferrin receptor. Demonstration of discordance between results obtained with two methods.

We undertook this study to evaluate a recently introduced ELISA kit for determining serum transferrin receptor (TfR) concentration (TfR, Ramco Laboratories, Inc.), to produce reference values for healthy adults, and to compare the results with another commercially available reagent system. The mean (SD) recovery of added TfR was 88% (6%). In dilution studies, the ratio between the measured and expected values was 0.98 (0.11). The intra-assay and interassay coefficients of variation were from 5% to 7% and from 6% to 9% in a physiological and a supraphysiological concentration range, respectively, and from 13% to 16% in a subnormal concentration range. In healthy adults between 20 and 60 years of age, we observed no age- or sex-related differences in TfR values. Thus, the same reference interval, 3.0-8.2 mg l(-1), may be used for this population. The correlation between the results obtained with the Ramco TfR test and the Amgen Diagnostics Clinigen test was satisfactory (r=0.79). The Ramco TfR test produced higher values (Tf=0.40 (-0.45-1.25)+1.46 (1.16-1.75)* Clinigen). The number of samples that fell within the same concentration interval with both methods (low, normal or high in relation to the respective reference interval) was only 45% (27/60). The Ramco TfR test had fewer values falsely suggesting iron deficiency than the Clinigen test. Serum TfR methods need to be uniformly standardized.

Adult↗
PubMed1998

Rheumatic features of sarcoidosis.

Signals from alveolar macrophages in concert with T helper 1 cell-derived cytokines are likely to account for the development of lymphocytic alveolitis, the earliest event in pulmonary sarcoidosis. At the least, a subgroup of patients with pulmonary sarcoidosis has an oligoclonal local expansion of T cells, suggesting an ordered antigen-driven immune response. The clinical features of sarcoidosis may mimic those of many rheumatic diseases and sarcoidosis may coexist with autoimmune diseases. Patients with sarcoidosis have an abnormal regulation of 1,25-dihydroxycholecalciferol, with higher serum levels in the summer season. Although acute sarcoid arthritis does not lead to joint destruction, musculoskeletal pain may sometimes be protracted and recurrence of arthritis may occur. Corticosteroid therapy is effective in controlling symptoms in sarcoidosis, but relapse is much more common after corticosteroid-induced remission than after spontaneous remission.

Adrenal Cortex Hormones↗
PubMed1998

Serum homocysteine and methylmalonic acid in patients with rheumatoid arthritis and cobalaminopenia.

OBJECTIVE: To analyze the significance of cobalaminopenia (< 200 pmol/l) in patients with severe rheumatoid arthritis (RA). METHODS: We studied 42 patients with RA and cobalaminopenia (incidence 4%). Most patients had severe and longstanding disease. Concentrations of homocysteine, methylmalonic acid (MMA), gastrin, and pepsinogen 1 were analyzed in sera that had been stored frozen. A capillary gas chromatographic mass spectrometric technique was used to determine homocysteine and MMA. RESULTS: As a group, patients had significantly higher levels of serum homocysteine and serum MMA than laboratory reference probands (p < 0.0001 and p < 0.005, respectively). Individually, 20 of 39 patients had elevated serum levels of homocysteine (> 15 micromol/l). In 12 of 39 patients serum levels of MMA were elevated (> 0.37 micromol/l). Twenty of 42 patients had biochemical signs of disturbed gastric function. CONCLUSION: Our findings were compatible with the hypothesis that cobalaminopenia is one of several biochemical signs of gastrointestinal dysfunction in patients with severe RA. It is suggested that the hyperhomocysteinemia associated with vitamin B12 deficiency, folate deficiency, vitamin B6 deficiency, and impaired renal function may have a role in promoting high cardiovascular morbidity in patients with RA.

Adult↗
PubMed1997

Rheumatic features of sarcoidosis.

Our understanding of the pathogenesis of sarcoidosis has recently been improved by studies elucidating the interaction between alveolar T lymphocytes and macrophages. It is particularly the activated CD4+ T helper 1 cells that in concert with macrophages produce a cascade of cytokines and chemotactic factors, which results in lymphocytic alveolitis succeeded by the granulomatous lesions. The accumulation in the alveoli of a specific subpopulation of T lymphocytes with a restricted expression of gene segments for the variable portion of the T cell receptor suggests that the process is antigen driven. The clinical features of sarcoidosis may mimic those of many rheumatic diseases and coexistence of sarcoidosis with autoimmune diseases is reported with increasing frequency. Musculoskeletal manifestations of sarcoidosis include acute and chronic arthritis, chronic myopathy, acute polymyositis and muscle nodules, and cystic osseous lesions. Acute sarcoid arthritis represents a relatively common form of acute oligoarthritis in young adults. For patients with chronic or refractory musculoskeletal sarcoidosis, low-dose methotrexate may be a therapeutic alternative.

Humans↗
PubMed1997

A two-site delfia immunoassay for measurements of the N-terminal peptide of pro-atrial natriuretic peptide (nANP).

A rapid, sensitive and reliable two-site immunoassay for measurements of the N-terminal peptide of pro-atrial natriuretic peptide (nANP) is presented. The method uses one monoclonal antibody, directed against the N-terminal part of nANP, as catcher antibody and another monoclonal antibody, directed against the C-terminal part of nANP, as detector antibody. The catcher antibody is biotinylated and is bound to streptavidin pre-coated microtiter strips. The detector antibody is labelled with Europium, which is measured in a Wallac DELFIA time-resolved fluorometer. Blood collected in plain Vacutainer tubes gave same measured amounts of nANP as blood collected in heparinised tubes. Blood collected in tubes containing EDTA gave same measured amounts of nANP as the plain tubes, provided that a 2-step assay protocol was used. Based upon 100 healthy blood donors, a reference interval was calculated to < 450 pmol/L. Within the reference group there was a significant increase of serum nANP with age. Based on 42 patients with different degree of impaired renal function, a significant correlation of nANP and serum creatinine was found. Assay performance, given as total assay variation was 12%, 10% and 9% respectively at serum levels of 140, 970 and 3500 pmol/L. It is concluded that this method is fast, sensitive and reliable for clinical measurements of nANP.

Adult↗
PubMed1996

Cathepsin G and elastase in synovial fluid and peripheral blood in reactive and rheumatoid arthritis.

The purpose of the study was to evaluate the involvement of serine proteinases cathepsin G and elastase on pathomechanisms in synovial fluid (SF) of patients with reactive (ReA) and rheumatoid, (RA) arthritis. Cathepsin G, elastase, and their endogenous inhibitors alpha1-antichymotrypsin (alpha1-ACT) and alpha1-proteinase inhibitor (alpha1-PI) were identified immunohistochemically from SF and peripheral blood (PB) of patients with ReA and RA. Cathepsin G and elastase activities in SF and PB were measured spectrophotometrically. Dot-immunostaining was used to identify cathepsin G, elastase, but also alpha1-ACT and alpha1-PI from SF and PB. Cathepsin G and elastase-like activities (IU/I) were slightly elevated in ReA SF compared to the corresponding peripheral blood values (11.4 +/- 9.2 vs 4.8 +/- 1.7, NS, and 5.1 +/- 2.8 vs 2.3 +/- 2.2, NS), which was similar to what was seen in RA (16.4 +/- 6.2 vs 0.53 +/- 0.4, p < 0.05, and 6.51 +/- 1.8 vs 1.22 +/- 0.58, p < 0.05). Although some samples did not contain cathepsin G and/or elastase-like activities, all samples contained immunoreactive enzyme, but also alpha1-ACT and alpha1-PI. In ReA SF, in contrast to monocytes, all polymorphonuclear (PMN) cells contained cathepsin G and elastase. Cathepsin G and elastase activities correlated with each other (r = 0.78, p < 0.05) suggesting PMN / primary granules as their likely source. There was a closer association between the cathepsin G or elastase and SF leukocyte count in ReA than in RA. In ReA and RA SF elevated cathepsin G and elastase activities are detected compared to activity levels in PB suggesting local production mainly from PMNs. The co-existence of highly cellular SF and cathepsin G and elastase activity in the documented presence of endogenous inhibitors in ReA SF together with the, known, usually self-remitting clinical course of ReA, suggest a brisk and even exaggerated local PMN serine proteinase release; sparing of joints does not seem to be due to lack or inhibition of PMN responses but rather to a successful down-regulation or cessation of the responses initially elicited.

Adult↗
PubMed1996

Spinal pseudoarthrosis complicating ankylosing spondylitis: a report of two patients.

Two middle-aged men with long-standing ankylosing spondylitis presented with recurrence of back symptoms after minor traumas. Clinical and radiographic findings were suggestive of spinal pseudoarthrosis at the L2/L3 and T11/T12 level, respectively, but the possibility of infectious spondylitis remained a concern. On granulocyte scintigraphy, the affected regions were distinguished by showing decreased activity. Magnetic resonance imaging clearly demonstrated the extent of the lesions and, in one of the patients, revealed spinal canal compression, which necessitated surgical treatment. The other patient gradually improved on conservative therapy.

Adult↗
PubMed1996

Amyloidosis.

Developments concerning amyloidosis associated with rheumatic diseases or often causing musculoskeletal symptoms are reviewed. The pathogenesis, clinical manifestations, diagnosis, and therapy of amyloid A, amyloid light-chain, and amyloid beta 2-microglobulin amyloidosis are discussed from the standpoint of a clinical rheumatologist. The biology of the precursor protein serum amyloid A (SAA) has been extensively studied, and a new assay for SAA has been developed. In amyloid beta 2-microglobulin amyloidosis, modified beta 2-microglobulin may function as a pathogenic factor that initiates an inflammatory reaction in which macrophages produce cytokines that induce osteoclastogenesis and bone resorption. Further experience with serum amyloid P component scintigraphy in the diagnosis and monitoring of amyloidosis has accumulated. Guidelines for the dosage of colchicine in the treatment of amyloidosis associated with familial Mediterranean fever have been published. In amyloid light-chain amyloidosis, intensive chemotherapy in combination with bone marrow transplantation or autologous stem-cell infusion has potential therapeutic significance.

Amyloidosis↗
PubMed1996

Neurone-specific enolase levels in pleural effusions in patients with rheumatoid arthritis.

BACKGROUND: High pleural fluid levels of neurone-specific enolase (NSE) have been reported, not only in patients with small cell lung cancer but also in those with chronic inflammatory diseases. METHODS: NSE concentrations were determined in pleural fluid and serum from 342 patients with pleural effusions including 17 with rheumatoid arthritis. RESULTS: The median NSE concentration in pleural fluid was higher in rheumatoid effusions than in any other condition studied. The median pleural fluid:serum NSE ratio was highest in patients with rheumatoid arthritis (11.6) and about unity in all other diseases including small cell lung cancer (0.9). In patients with rheumatoid arthritis pleural fluid concentrations of NSE correlated inversely with pleural fluid glucose concentrations and the pH of the pleural fluid. CONCLUSIONS: A high pleural fluid:serum NSE ratio was found consistently in pleural effusions from patients with rheumatoid disease.

Arthritis, Rheumatoid↗
PubMed1996

Pleural fluid beta-2-microglobulin and angiotensin-converting enzyme concentrations in rheumatoid arthritis and tuberculosis.

Concentrations of beta 2-microglobulin (B2M) and angiotensin-converting enzyme (ACE) were measured in pleural fluid (Pf) and serum (S) of 364 patients with pleural effusions. Eleven patients had rheumatoid arthritis (RA), 36 verified tuberculosis (TB), 15 suspected TB, 120 cancer, 21 empyema, 34 pneumonia, 33 various defined diseases, 67 effusions of unknown aetiology and 27 congestive heart failure. The median concentrations of Pf-B2M and Pf-ACE were significantly higher in patients with RA than in patients with any other disease (p < 0.005). Tuberculous effusions contained higher Pf-ACE concentrations than any other type of non-rheumatoid effusion (p < 0.05). With sensitivities of 91%, the specificity of Pf-B2M and Pf-ACE for the diagnosis of RA was 86% and 55%, respectively. Local cellular immune events probably account for the abundance of B2M and ACE in rheumatoid and tuberculous pleural effusions. Pf-B2M and Pf-ACE determinations may aid in the differentiation of rheumatoid and tuberculous pleurisy from other types of pleural disease.

Arthritis, Rheumatoid↗
PubMed1996

Pleural fluid interferon-gamma and tumour necrosis factor-alpha in tuberculous and rheumatoid pleurisy.

Tuberculous and rheumatoid pleural effusions show features suggesting a strong local cellular immune response. Pleural fluid (Pf) from patients with tuberculosis, rheumatoid arthritis (RA) and other diseases were compared with respect to interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha). Immunoassays were used to determine Pf-IFN-gamma and Pf-TNF-alpha in 102 patients, including 11 with RA, 31 with verified tuberculosis, 23 with suspected tuberculosis, 11 with pneumonia, 14 with lung cancer and 12 with congestive heart failure. Measurable Pf-IFN-gamma occurred exclusively in patients with verified (median 1.8 ng x mL-1; 95% confidence interval (95% CI) 0.63-4.0 ng x mL-1) or suspected (0.37 ng x mL-1; 95%CI 0-0.7 ng x mL-1) tuberculosis. The highest median Pf-IFN-gamma was observed in those patients who showed a positive pleural fluid culture for Mycobacterium tuberculosis. In pleural effusions due to other diseases, including RA, IFN-gamma was undetectable. The highest Pf-TNF-alpha occurred in verified tuberculosis (median 198 ng x L-1; 95% CI 169-222 ng x L-1) and RA (210 ng x L-1; 95% CI 147-231 ng x L-1). Pleural fluid interferon-gamma is a highly useful marker for diagnosing tuberculous pleurisy. Although tuberculous and rheumatoid pleural effusions share several biochemical features, they are strikingly different with respect to interferon-gamma.

Arthritis, Rheumatoid↗
PubMed1996

Similar pleural fluid findings in pleuropulmonary tularemia and tuberculous pleurisy.

Biochemical and cellular characteristics of pleural fluid from two patients with pleuropulmonary tularemia and 39 patients with tuberculous pleurisy were compared. High pleural fluid concentrations of adenosine deaminase, lysozyme, and beta 2-microglobulin occurred in both diseases. As is the case with tuberculous pleural effusions, pleural fluid in tularemia showed an abundance of lymphocytes, predominantly CD4-positive T lymphocytes. The similar pleural fluid findings suggest analogous local pathogenetic mechanisms in tularemia and tuberculosis. In the diagnostic evaluation of a lymphocyte-rich exudative pleural effusion with a high adenosine deaminase concentration, a possible cause to consider is tularemia.

Aged↗
PubMed1996

Circulating transferrin receptor during erythropoietin medication of anemic patients with rheumatoid arthritis.

Serum levels of the transferrin receptor (TfR) were monitored in 12 anemic patients with rheumatoid arthritis (RA) undergoing treatment with recombinant human erythropoietin (rHuEPO) for a 24-week period. Measurement of TfR was performed using an enzyme immunoassay. Compared to a mean pretreatment level of 4.2 mg/l (range 2.1-6.1 mg/l), there was an increase in the mean TfR concentrations from 2 weeks of treatment onwards to a maximum of 7.7 mg/l (range 2.1-12.3 mg/l) at 12 weeks (p < 0.01). Nine of the 12 patients responded to rHuEPO with an increase in blood hemoglobin concentration of 15 g/l or more. An increase in TfR levels was documented not only in the responders but also in the 3 nonresponders. We conclude that in anemic RA patients exogenous erythropoietin induces a swift and sustained increase in the serum concentration of TfR, which probably reflects increased expression of TfR on erythroblasts. This sustained elevation of TfR seems to occur even in patients who do not have an increase in their hemoglobin level.

Adult↗
PubMed1995

Lutein associated with a transthyretin indicates carotenoid derivation and novel multiplicity of transthyretin ligands.

Transthyretins isolated from different species bind hydrophobic compounds and are often obtained in a yellow form. Such a transthyretin from chicken serum was purified by chromatography using Sepharose-coupled human retinol-binding protein. The yellow chromophore was extracted with methanol and purified by reverse phase HPLC followed by normal-phase chromatography on a nitrile column. Ultraviolet-visible absorbance and mass spectrometry identified the yellow compound as lutein, i.e. xanthophyll, (all-trans)-beta, epsilon-carotene-3,3'-diol, estimated to constitute 10-30% of associated colourless compounds. These components are different from the yellow component isolated from human transthyretin and establish that carotenoid-derived pigments can be associated with transthyretins.

Animals↗
PubMed1995

A yellow component associated with human transthyretin has properties like a pterin derivative, 7,8-dihydropterin-6-carboxaldehyde.

Transthyretin (TTR) in plasma is associated with yellow compounds. Their properties differ, and in the chicken protein a major yellow compound has recently been identified as a carotenoid, lutein, also called xanthophyll. We now show that the major yellow component extracted from human TTR has properties like a pterin derivative, 7,8-dihydropterin-6-carboxyaldehyde (2-amino-4-hydroxy-6-formyl-7,8-dihydropteridine). The human TTR derivative has chromatographic and spectral properties identical to a yellow photochemical degradation product of biopterin and a spectrum like that of the pterin aldehyde.

Choroid Plexus↗