Risk factors promoting hypertensive crises: evidence from a longitudinal study.

BACKGROUND: Current knowledge about risk factors promoting hypertensive crisis originates from retrospective data. Therefore, potential risk factors of hypertensive crisis were assessed in a prospective longitudinal study. METHODS: Eighty-nine patients of the medical outpatient unit at the University Hospital of Bern (Bern, Switzerland) with previously diagnosed hypertension participated in this study. At baseline, 33 potential risk factors were assessed. All patients were followed-up for the outcome of hypertensive crisis. Cox regression models were used to detect relationships between risk factors and hypertensive crisis (defined as acute rise of systolic blood pressure (BP) > or =200 mm Hg and/or diastolic BP > or =120 mm Hg). RESULTS: The mean duration of follow-up was 1.6 +/- 0.3 years (range 1.0-2.4 years). Four patients (4.5%) were lost to follow-up. Thirteen patients (15.3%) experienced hypertensive crisis during follow-up. Several potential risk factors were significantly associated with hypertensive crisis: female sex, higher grades of obesity, the presence of a hypertensive or coronary heart disease, the presence of a somatoform disorder, a higher number of antihypertensive drugs, and nonadherence to medication. As measured by the hazard ratio, nonadherence was the most important factor associated with hypertensive crisis (hazard ratio 5.88, 95% confidence interval 1.59-21.77, P < 0.01). CONCLUSIONS: This study identified several potential risk factors of hypertensive crisis. Results of this study are consistent with the hypothesis that improvement of medical adherence in antihypertensive therapy would help to prevent hypertensive crises. However, larger studies are needed to assess potential confounding, other risk factors and the possibility of interaction between predictors.

Gene structure and expression of the mouse APOBEC-1 complementation factor: multiple transcriptional initiation sites and a spliced variant with a premature stop translation codon.

Editing of apolipoprotein (apo) B mRNA is mediated by an enzyme-complex that consists of the catalytic cytidine deaminase APOBEC-1 and the mRNA binding protein APOBEC-1 complementation factor or APOBEC-1 stimulating protein (ACF/ASP). Here we describe the detailed characterization of the structure, expression and splicing pattern of the mouse ACF/ASP gene. ACF/ASP mRNA is mainly expressed in mouse liver, small intestine and kidney. The deduced protein sequences of ACF/ASP from mouse and man share an identity of 93%. The mouse ACF/ASP gene consists of 12 exons and gives rise predominantly to full-length transcripts. To a minor extent (<10%) ACF/ASP mRNA with unspliced exon 8 is generated in liver, kidney and small intestine that encodes a truncated protein with a predicted molecular weight of 43 kDa. The promoter of the mouse ACF/ASP gene lacks a canonical TATA-box, but contains a cluster of Sp1 binding sites and uses multiple transcriptional initiation sites. Transfection studies demonstrated a preference of this promoter for cell lines derived from the gastrointestinal tract and proved the location of the promoter core region. The high sequence identity between man and mouse-much higher as observed for APOBEC-1-indicates a strong evolutionary constraint on the structure-function relationship of ACF/ASP, most probably due to a central role in editing and processing of apo B mRNA.