Essentials There is a bidirectional relation between acute infections and immobilizationWe studied the impact of infection and immobilization on risk of VTE in a case‐crossover designAcute infection was a strong trigger for VTE independent of concomitant immobilizationInfection and immobilization had a synergistic effect on the VTE‐risk BackgroundA bidirectional relation exists between acute infection and immobilization, and both are triggers for venous thromboembolism (VTE). To what extent the association between infection and VTE‐risk is explained by immobilization is unknown.AimsTo investigate the impact of hospitalization with acute infection on the VTE‐risk in patients with and without concomitant immobilization, and to explore the differential impact of respiratory‐ (RTI) and urinary‐ (UTI) tract infections on the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE).MethodsWe conducted a case‐crossover study of VTE‐patients (n = 707) recruited from a general population. Hospitalizations and VTE‐triggers were registered during the 90 days before a VTE (hazard period) and in four preceding 90‐day control periods. Conditional logistic regression was used to estimate odds ratios (ORs) for VTE according to triggers.ResultsAcute infection was registered in 267 (37.8%) of the hazard periods and in 107 (3.8%) of the control periods, corresponding to a high VTE‐risk after infection (OR 24.2, 95% CI 17.2‐34.0), that was attenuated to 15‐fold increased after adjustment for immobilization. The risk was 20‐fold increased after infection without concomitant immobilization, 73‐fold increased after immobilization without infection, and 141‐fold increased with the two combined. The risk of PE was apparently higher after RTIs (OR 48.3, 95% CI 19.4‐120.0) than UTIs (OR 12.6, 95% CI 6.4‐24.7), but diminished in sensitivity analyses excluding uncertain RTI diagnoses.ConclusionsOur findings suggest that hospitalization with infection is a strong VTE‐trigger also in non‐immobilized patients. Infection and immobilization had a synergistic effect on the VTE‐risk.

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SummaryInflammation and venous thrombosis are intertwined. Only in the recent 15 years clinical epidemiological studies have focussed on inflammatory or infectious diseases as risk factors for venous thrombosis. Although a few reviews and many case reports or studies on these topic has been written, a review reporting relative or absolute risks for venous thrombosis has not been published yet. We performed a systematic review using Medline, Pubmed and Embase and found 31 eligible articles. Inflammatory bowel disease, ANCA-associated vasculitis, infections in general and more specifically, human immunodeficiency virus, pneumonia and urinary tract infections are associated with an increased risk of venous thrombosis.

Long-term, low-grade inflammation does not seem to be a risk factor for venous thromboembolism. The impact of acute inflammation, regardless of cause, on risk of venous thromboembolism is scarcely studied. We aimed to investigate the impact of acute inflammation, assessed by C-reactive protein, on short-term risk of venous thromboembolism. We conducted a case-crossover study of patients with venous thromboembolism (n=707) recruited from a general population. Information on triggers and C-reactive protein levels were retrieved from hospital records during the 90 days before the event (hazard period) and in four preceding 90-day control periods. Conditional logistic regression was used to obtain β coefficients for change in natural log (ln) transformed C-reactive protein from control to hazard periods and to determine corresponding odds ratios for venous thromboembolism. Median C-reactive protein was 107 mg/L in the hazard period, and ranged from 7 mg/L to 16 mg/L in the control periods. The level of C-reactive protein was 58% (95% CI 39-77%) higher in the hazard period than in the control periods. A one-unit increase in ln-C-reactive protein was associated with increased risk of venous thromboembolism (OR 1.79, 95% CI 1.48-2.16). The risk estimates were only slightly attenuated after adjustment for immobilization and infection. In stratified analyses, ln-C-reactive protein was associated with increased risk of venous thromboembolism in cases with (OR 1.55, 95% CI 1.01-2.38) and without infection (OR 1.77, 95% CI 1.22-2.57). In conclusion, we found that acute inflammation, assessed by C-reactive protein, was a trigger for venous thromboembolism.

This high risk in HIV co-infected TB patients suggests that standard thrombo-prophylaxis should be routinely considered in this group. However, our findings might not be generalizable due to referral bias. Further prospective studies in unselected HIV co-infected TB patients are needed to corroborate our findings.

Complex regional pain syndrome type I is a disorder of the extremities with disability and pain as the most prominent features. This paper describes the results of cognitive behavioural therapy combined with mirror box therapy in three patients with chronic complex regional pain syndrome type I. Before, during and at follow-up the following measurements were assessed: pain (visual analogue scale, 0-100), range of motion, muscle strength, and the areas of allodynia and of hyperalgesia. Furthermore, patients were asked for their feelings and thoughts about mirror box therapy and about the affected limb. Pain at rest, pain after measuring allodynia/hyperalgesia and pain after measuring strength decreased. Range of motion improved in two patients. Strength improved in one patient. The area of hyperalgesia increased for all three patients, whereas the area of allodynia remained stable in two patients and decreased in one patient. Two patients felt that their affected limb still belonged to them, one did not. Cognitive behavioural therapy combined with mirror box therapy for patients with chronic complex regional pain syndrome type I may facilitate rehabilitation. Measuring whether the affected limb still belongs in the patient's body scheme could be of prognostic value in the treatment of chronic complex regional pain syndrome type I patients.

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Cytomegalovirus is associated with hypercoagulability, and is reported to increase the risk of venous thrombosis in human immunodeficiency virus (HIV)-infected patients. Progression to AIDS, however, is also associated with hypercoagulability and venous thrombosis, and may result in more comorbidities, such as reactivation of cytomegalovirus. It is therefore unknown whether active cytomegalovirus in HIV infection results in a procoagulant state or whether hypercoagulability is the result of HIV infection itself. In this cross-sectional study of 104 consecutive HIV-infected patients, active cytomegalovirus infection was associated with hypercoagulability independently of stage of HIV disease. This finding may deserve attention in preventative recommendations for use of thromboprophylaxis in HIV-infected patients.