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Objectives: To evaluate the extent of delay in the diagnosis of pulmonary embolism (PE) in primary care, and to identify determinants that are associated with such diagnostic delay. Design: Retrospective observational study. Setting: 6 primary care practices across the Netherlands. Participants: Data from patients with an objectively confirmed diagnosis of PE (International Classification of Primary Care (ICPC) code K93) up to June 2015 were extracted from the electronic medical records. For all these PE events, we reviewed all consultations with their general practitioner (GP) and scored any signs and symptoms that could be attributed to PE in the 3 months prior to the event. Also, we documented actual comorbidity and the diagnosis considered initially. Primary and secondary outcome measures: Delay was defined as a time gap of >7 days between the first potentially PE-related contact with the GP and the final PE diagnosis. Multivariable logistic regression analysis was performed to identify independent determinants for delay. Results: In total, 180 incident PE cases were identified, of whom 128 patients had 1 or more potential PE-related contact with their GP within the 3 months prior to the diagnosis. Based on our definition, in 33 of these patients (26%), diagnostic delay was observed. Older age (age >75 years; OR 5.1 (95% CI 1.8 to 14.1)) and the absence of chest symptoms (ie, chest pain or pain on inspiration; OR 5.4 (95% CI 1.9 to 15.2)) were independent determinants for diagnostic delay. A respiratory tract infection prior to the PE diagnosis was reported in 13% of cases without delay, and in 33% of patients with delay (p=0.008). Conclusions: Diagnostic delay of more than 7 days in the diagnosis of PE is common in primary care, especially in the elderly, and if chest symptoms, like pain on inspiration, are absent. [ABSTRACT FROM AUTHOR]

Joint damage due to (recurrent) joint bleeding in haemophilia causes major morbidity. Although the exact pathogenesis has not been fully elucidated, a central role for iron is hypothesised. Likewise, in hereditary haemochromatosis joint destruction is caused by iron overload. A comparison between these types of arthropathy could provide more insight in the influence of iron in inducing joint damage. A literature review was performed to compare both disorders with respect to their clinical and histological characteristics, and preclinical studies on the influence of iron on different joint components were reviewed. Similarities in the features of arthropathy in haemochromatosis and haemophilia are cartilage degeneration, subchondral bone changes with osteophyte and cyst formation, and osteoporosis. In both disorders synovial inflammation and proliferation are seen, although this is much more explicit in haemophilia. Other substantial differences are the age at onset, the occurrence of chondrocalcinosis radiographically and calcium pyrophosphate dihydrate deposition disease in haemochromatosis, and a rapid progression with joint deformity and neovascularisation in haemophilia. Preclinical studies demonstrate detrimental effects of iron to all components of the joint, resulting in synovial inflammation and hyperplasia, chondrocyte death, and impaired osteoblast function. These effects, particularly the synovial changes, are aggravated in the presence of a pro-inflammatory signal, which is prominent in haemophilic arthropathy and minimal in haemochromatosis. Additional research is needed to further specify the role of iron as a specific target in treating these types of arthropathy. [ABSTRACT FROM AUTHOR]