Available evidence suggests that fracture prediction with bone densitometry may improve when used on people at high risk of osteoporotic fractures. The objectives of this literature review were: (1) to identify risk factors for fracture that are associated with the development of a low bone mass for both men and women; (2) to describe and assess the relationship between these factors and the risk of fracture; and (3) to classify them according to the strength of their association with fracture incidence. Studies were identified from MEDLINE (1982-1997), HealthSTAR (1975-1997) and The Cochrane Library (1997) databases. Pre-stated inclusion criteria (original analytic studies assessing risk factors for osteoporotic fractures in men and women) and methodologic quality were assessed by two independent investigators. Information on the study design and analysis, characteristics of participants, exposure (risk factor) and outcome measures (relative risk and odds ratios for fracture incidence), control for potential confounding factors and risk estimates was extracted using a standardized protocol. Qualitative and meta-analytic techniques were used for data synthesis. As a result, risk factors were classified into three groups according to their strength of association with fracture: high risk (RR > or = 2), moderate risk (1 < RR < 2) and no risk or protective (RR < or = 1). Of approximately 80 risk factors identified from 94 cohort and 72 case-control studies, 15% were classified in the high-risk group, including low body weight, loss of weight, physical inactivity, the consumption of corticosteroids or anticonvulsants, primary hyperparathyroidism, diabetes mellitus type 1, anorexia nervosa, gastrectomy, pernicious anemia, and aging (> 70-80 years). Eighteen percent and 8% of risk factors were classified in the moderate and no risk group respectively, whereas 60% showed either a lack of scientific evidence confirming their association with fracture or contradictory results. An efficient strategy for bone densitometry provision may thus be its selective use in those individuals who present with several strong or moderate risk factors for fracture related to bone mass loss.

Background: To determine the effect of aspirin on ulcer healing rate in patients with chronic venous insufficiency, and to establish prognostic factors that influence ulcer evolution. Methods: Between 2001 and 2005, 78 patients with ulcerated lesions of diameter >2 cm and associated with chronic venous insufficiency were evaluated in our hospital. Of these, 51 patients (22 men, 29 women) with mean age of 60 years (range: 36e86) were included in a prospective randomized trial with a parallel control group. The treatment group received 300 mg of aspirin and the control group received no drug treatment; in both groups, healing was associated with standard compression therapy. During follow-up, held weekly in a blinded fashion, there was ulcer healing as well as cases of recurrence. Results were analyzed by intention-to-treat approach. Cure rate was estimated using KaplaneMeir survival analysis, and the influence of prognostic factors was analyzed by applying the Cox proportional hazards model. Results: In the presence of gradual compression therapy, healing occurred more rapidly in patients receiving aspirin versus the control subjects (12 weeks in the treated group vs. 22 weeks in the control group), with a 46% reduction in healing time. The main prognostic factor was estimated initial area of injury (P ¼ 0.032). Age, sex, systemic therapy, and infection showed little relevance to evolution. Conclusions: The administration of aspirin daily dose of 300 mg shortens the healing time of ulcerated lesions in the chronic venous insufficiency (CVI). The main prognostic factor for healing of venous ulcerated lesions is the initial surface area of the ulcer.

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We describe a patient with Horner's syndrome caused by an extensive intraparietal hematoma in the wall of the internal carotid artery confused with an arterial dissection. Detection of such pathology instead of dissection or arteritis is important as the management is different. As far as the authors know, it is the first case in which a haematoma within an atherosclerotic plaque is clinically related Horner's syndrome. A 81-year-old man presented with acute right hemiplegia and loss of vision of the left eye due to a central retinal artery occlusion. The patient underwent a computerised angiotomography which demonstrated left internal carotid artery occlusion with recanalisation after carotid bifurcation. Clinically, the patient developed a syndrome of Claude-Bernard Horner which replaced the diagnosis on the suspicion that it was a carotid artery dissection. The patient had miosis and ptosis of left eye. In the magnetic resonance angiography, an intramural of a possible hematoma was observed. It was decided to perform surgical treatment of the carotid lesion. As this clinical case shows, there are symptomatic courtships that must be studied in detail so as not to confuse the carotid dissection with critical stenosis of the internal carotid artery.

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