A biomarker for Takayasu's disease

It was found that PTX3 levels are more accurate than CRP levels or ESR for detecting disease

 activity in selected patients with known Takayasu arteritis activity. Further studies confirming the data in a broader spectrum of patients with unknown or equivocal disease activity are needed before this marker can be used routinely as a biomarker in the clinical or research settings. Pentraxins are another possible biomarker. Pentraxins are a superfamily of proteins that are highly conserved in evolution, recognize a wide range of exogenous pathogenic substances, alter self molecules, and behave as acute-phase proteins. They are categorized as short and long pentraxins on the basis of their primary structure. C-reactive protein (CRP) and serum amyloid P are classic short pentraxins produced in the liver. Pentraxin-3 (PTX3) is a prototype of the long pentraxins. Innate immunity cells (most notably, dendritic cells and macrophages) and vascular cells produce PTX3 in response to proinflammatory signals and Toll-like receptor engagement. Pentraxin-3 plays a nonredundant role in the recognition of selected pathogens, activates the complement system, regulates cell proliferation and angiogenesis, and participates in the formation of the cumulus oophorus. This protein is synthesized locally at sites of inflammation, and increased levels are associated with vascular inflammation in different diseases affecting blood vessels; increased levels have been observed in the serum of patients with small-vessel vasculitis and in the synovial fluid of patients with rheumatoid arthritis. In future we may depending more on this marker to assess the active nature of the disease.

Longterm use of LMWH in DVT patients

Am J Med. 2011 Aug;124(8):756-65.

Long-term low-molecular-weight heparin and the post-thrombotic syndrome: a systematic review. Hull RD, Liang J, Townshend G.

Source. University of Calgary, Alberta, Canada. rdhull@ucalgary.ca

Abstract OBJECTIVE: Post-thrombotic syndrome causes considerable morbidity. The Home-LITE study showed a lower incidence of post-thrombotic syndrome and venous ulcers after 3 months of treating deep vein thrombosis with the low-molecular-weight heparin tinzaparin versus oral anticoagulation. This systematic review examined whether long-term treatment of deep vein thrombosis using low-molecular-weight heparin, rather than oral anticoagulation, reduces development of post-thrombotic syndrome. METHODS: We identified 9 articles comparing treatment of deep vein thrombosis using long-term low-molecular-weight heparin with any comparator, which reported outcomes relevant to the post-thrombotic syndrome assessed ≥ 3 months post-deep vein thrombosis. RESULTS: Pooled analysis of 2 studies yielded an 87% risk reduction with low-molecular-weight heparin in the incidence of venous ulcers at ≥ 3 months (P = .019). One study showed an overall odds ratio of 0.77 (P = .001) favoring low-molecular-weight heparin for the presence of 8 patient-reported post-thrombotic syndrome signs and symptoms. Pooled analysis of 5 studies showed a risk ratio for low-molecular-weight heparin versus oral anticoagulation of 0.66 (P < .0001) for complete recanalization of thrombosed veins.

CONCLUSION: These results support the lower incidence of post-thrombotic syndrome and venous ulcers observed in Home-LITE. Long-term treatment with low-molecular-weight heparin rather than oral anticoagulation after a deep vein thrombosis may reduce or prevent development of signs and symptoms associated with post-thrombotic syndrome. Post-thrombotic syndrome and associated acute ulcers may develop more rapidly after deep vein thrombosis than previously recognized.