Deterioration of gas exchange in patients with severe thrombotic thrombocytopenic purpura with respiratory failure during therapeutic plasma exchange

Therapeutic plasma exchange (TPE) is a procedure performed on patients suffering from various disorders, including thrombotic thrombocytopenic purpura (TTP). As we noted a frequent transient deterioration in respiratory function when the procedure was performed on intensive care unit (ICU) patients, we studied retrospectively the incidence of respiratory deterioration during and shortly after TPE and looked for a probable correlation with a change in the white blood cell (WBC) counts. Over a period of 10 months six patients with TTP, five of whom had parenchymal lung disease due to different medical reasons, underwent TPE. The oxygen saturation was measured continuously before, during, and after TPE; additionally, the WBC and differential counts were measured pre‐ and post‐TPE. The ratio of the oxygen saturation by pulse oxymetry (SpO₂) to the fraction of inspired oxygen (FiO₂) was calculated before, during and after TPE. In these five patients with lung disorders, there was a consistent trend of a decreasing SpO₂/FiO₂ quotient during and within 2 h post TPE compared to the pre‐TPE value. The decrease in SpO₂/FiO₂ range was 0.20–0.89 with an average of 0.56. In the same 5 patients there was an increase in the WBC count in the range of 2.3–19.7 × 10⁹/L with an average increase of 9.3 × 10⁹/L. The percent neutrophils of the total WBC counts also increased following most of the sessions, this increase was in the range of 1–15 % with an average of 7%. The effect of TPE on the SpO₂/FiO₂ ratio and the correlation to the WBC count and to a possible neutrophil activation has not been previously reported. We postulate that TPE can accentuate respiratory deterioration in patients with TTP who already have acute lung injury. This may be due to the priming and activation of the leukocytes that could lead to the release of cytokines and inflammatory mediators during the procedure. Thus, it is important to be aware of the possible deterioration in respiratory function and gas exchange while administering TPE to patients with pre‐existing parenchymal lung injury. J. Clin. Apheresis. 16:143‐147, 2000. © 2001 Wiley‐Liss, Inc.     

Effectiveness of maternity support belts in reducing low back pain during pregnancy: a review

Aims. This article aims to review the literature published to date on the types, current use, the biomechanical effects and adverse effects of maternity support belts for low back pain during pregnancy, to identify future research directions. Background. Lumbar/pelvic support belts are frequently recommended for the prevention and treatment of low back pain during pregnancy. Design. Systematic review. Methods. MEDLINE, CINAHL, the Cochrane Library and patents databases were electronically searched. Results. Maternity support belts belong to one of the four main types of maternity support garments, which are widely commercially‐available. Current research showed limited evidence in support of the commercial maternity products regarding the effectiveness in the prevention and/or treatment of low back pain during pregnancy, other than that from the manufacturers. However, potential stabilisation effect of maternity support belt was demonstrated in some studies. Adverse effects reported include increased pain, fetal heart rate changes, skin irritation and discomfort. Conclusions. There is insufficient scientific evidence to conclude that wearing maternity support belts reduces pregnancy‐related low back pain and/or pelvic girdle pain. Future research directions in the area of biomechanics and physiology are recommended. Relevance to clinical practice. This review provides comprehensive understanding of the effectiveness of maternity support belts for the relief of low back pain during pregnancy which will facilitate healthcare professionals in providing evidence‐based advice to their patients.     

Tranexamic acid, an inhibitor of plasminogen activation, reduces urinary collagen cross-link excretion in both experimental and rheumatoid arthritis

The plasminogen activation system is one of the enzyme systems held responsible for bone and cartilage degradation in rheumatoid arthritis (RA). In this study, we evaluated the effect of tranexamic acid (TEA), an inhibitor of plasminogen activation, on urinary collagen cross-link excretion and radiological joint damage in rat adjuvant arthritis (AA) and on urinary collagen cross-link excretion in patients with RA. In the animal study, adjuvant arthritis was induced in male Lewis rats. From day 7 onward, high-dose TEA (500 mg/kg body weight, once daily) or placebo was administered orally. Study groups consisted of TEA-treated normal rats (C + TEA), placebo-treated normal rats (C + plac), AA rats treated with TEA (AA + TEA) or with placebo (AA + plac). To monitor joint destruction, urinary collagen cross-link excretion (pyridinoline, HP; deoxypyridinoline, LP) was measured by high-performance liquid chromatography at days 14 and 21. Radiological evaluation of joints was performed at day 21. In the patient study, TEA was administered to nine patients with RA as adjuvant medication (approximately 20 mg/kg body weight, three times daily) for 12 weeks. Urinary HP and LP excretion levels were measured before and during TEA treatment, and 4 weeks after the cessation of TEA treatment. In AA + TEA rats, a significant reduction of HP and a tendency towards a reduction of LP excretion were found compared with AA + plac rats (P < 0.05), at day 14, whereas the HP/LP ratio did not change. No difference was observed in HP, LP excretion, HP/LP ratio and radiological damage score between the TEA- and placebo-treated AA rats at day 21. In RA patients, a significant reduction of HP and LP excretion was found during the TEA treatment period (P < 0.05). After the cessation of TEA treatment, HP and LP excretion increased towards baseline levels. No effect on disease activity was observed. The plasmin antagonist TEA reduced the excretion of collagen pyridinoline cross-links in both experimental and rheumatoid arthritis. As such, this study not only supports the involvement of the plasminogen activation system in the destructive phase of arthritis, but also suggests a beneficial effect of therapeutic strategies directed against inhibition of matrix proteolysis.      

Somatic hypermutation in low-grade mucosa-associated lymphoid tissue- type B-cell lymphoma

The origin of low-grade mucosa-associated lymphoid tissue (MALT)-type B- cell lymphoma is still unclear. Using a novel two-step procedure, we have sequenced the Ig VH genes expressed by cells from four patients with gastric low-grade MALT-type lymphoma. The nucleotide sequences of the complementarity determining region 3 (CDR3) of the genomic DNA were first amplified using consensus oligonucleotide primers, then sequenced. Based on the CDR3 sequence amplified from each MALT lymphoma, individual tumor-specific primers were synthesized and used directly in the polymerase chain reaction (PCR) to analyze the sequences of their Ig heavy-chain variable region. When compared with the germ-line sequence, many nucleotide substitutions, mainly in the CDRs, were found in the variable gene sequences of the four MALT lymphomas. The mutations showed a high replacement-to-silent ratio and were distributed in a way which suggested that the tumor cells had been positively selected through their antigen receptor. Our findings indicate that the MALT-type lymphoma B cells are hypermutated postgerminal center lymphocytes that have undergone antigen selection.