[The clinical and radiological characteristics and evolution of incidentally diagnosed pulmonary thromboembolism]. / Diagnóstico casual de tromboembolismo pulmonar: descripción de las características clínicas y radiológicas y su evolución.

OBJECTIVES: To evaluate the cases of pulmonary embolism (PE) detected incidentally in our hospital, the associated risk factors, clinical and radiological characteristics, and evolution. MATERIAL AND METHODS: We retrospectively reviewed the reports of routine contrast-enhanced chest CT examinations performed during a 19-month period to detect cases in which PE was diagnosed incidentally. We found 18 cases of incidentally diagnosed PE and we reviewed the clinical histories and CT images of these patients to analyze the risk factors, clinical presentation, radiological characteristics, treatment, and evolution of PE in these cases. RESULTS: We found 18 patients (9 men and 9 women; mean age: 61 years) with incidentally detected PE. The main risk factor for developing PE was the presence of a neoplasm (n = 16). No PE-related symptoms were present in 12 patients. A multidetector CT scanner was used for the examination in most cases (n = 16). PE was centrally located in 16 patients. Five patients were not treated with anticoagulation and no embolic events occurred in these patients. Two of the remaining patients died because of PE. CONCLUSIONS: The incidental finding of PE can be common in oncological patients. Multidetector CT probably has a greater capacity for the incidental detection of PE in these patients. The outcome of incidentally detected PE can vary from death to remaining stable to spontaneous resolution.

p53 abnormalities in CLL are associated with excess of prolymphocytes and poor prognosis.

To determine the role of the p53 gene in chronic lymphocytic leukaemia (CLL) and its possible involvement in the pathogenesis of a progressive form of CLL characterized by > 10%, prolymphocytes (CLL/PL), we selected 32 cases, 17 with typical morphology and 15 CLL/PL. The extent of inactivation of p53 was examined by assessing loss of heterozygosity (LOH) at 17p13.3, by sequencing the highly conserved region (exons 5-9) of the p53 gene and by analysing p53 protein expression. LOH was detected in 8/28 (29%) cases, p53 mutations in 5/32 (16%) cases and p53 expression in 5/27 (19%) cases. Overall 11 cases (30%) had p53 abnormalities of which eight cases had CLL/PL. There was a significant association between CLL/PL and p53 abnormalities (P=0.05); 75% of cases with LOH, 80% of p53 mutations and 80% of cases positive for p53 protein had CLL/PL. Thus, p53 inactivation is the first gene abnormality identified so far to be involved in the development of CLL/PL. All the cases with typical CLL and p53 abnormalities had only one allele affected whereas 4/6 CLL/PL had both alleles inactivated. This difference in the extent of p53 inactivation suggests that accumulation of p53 abnormalities may be associated with progression of CLL to CLL/PL. CLL cases with p53 abnormalities were characterized by a higher incidence of stage C (P<0.025), a higher proliferative rate (P=0.05), short survival (P<0.005) and resistance to first-line therapy (P<0.02) but not to nucleoside analogues. Analysis of the correlation between p53 status and incidence of trisomy 12 by fluorescence in situ hybridization (FISH) showed that trisomy 12 was more frequent in cases without p53 abnormalities, suggesting that trisomy 12 and p53 may represent different pathways of transformation in CLL.