A practical means of evaluating the prognosis of acute pancreatitis, as measurement of carotid artery intima-media thickness.

BACKGROUND AND STUDY AIMS: Factors such as age, obesity, diabetes mellitus and hyperlipidemia that cause adverse prognosis in acute pancreatitis also cause an increase in carotid intima-media thickness. In this study, we aimed to investigate the usability of the measurement of carotid intima-media thickness, which is an easy to apply, cost-effective means of measurement applied to the patients, in predicting AP prognosis, apart from the criteria currently utilized to predict AP prognosis. PATIENTS AND METHODS: 101 patients diagnosed with acute pancreatitis were prospectively enrolled into the study. Right and left common carotid artery intima-media thickness, right and left internal carotid artery intima-media thickness were measured with ultrasonographic images performed within the first 24 hours of hospitalization. local or systemic complications and organ failure development were monitored in the follow-up of the patients. RESULTS: After the ROC analysis was performed and the threshold value was determined. The patients with main and internal carotid artery intima-media thickness above 0.775 mm were seen to have a more severe AP (p = 0.000). Local and systemic complications and organ failure were also more common in these patients. CONCLUSIONS: Measurement of carotid intima-media thickness is a non-invasive method that can be used to predict the prognosis in patients with acute pancreatitis at presentation.

A case of treacher collins syndrome.

Treacher Collins syndrome (TCS) is an autosomal dominant disorder of craniofacial development with an incidence of 1/50,000 live births. Mutations of the TCOF1 gene have been found to be responsible for most cases of this mandibulofacial disorder. Here we report TCS in an individual who has a heterozygous c.1021_1022delAG deletion in exon 7 of the TCOF1 gene (NG_011341.1). This is the second Turkish patient with a severe TCS phenotype resulting from a de novo c.1021_1022delAG mutation.