Characterization of Malignant Portal Vein Thrombosis with Contrast-Enhanced Ultrasonography

We prospectively evaluated the effectiveness of contrast-enhanced ultrasonography (CEUS) for differentiation of benign versus malignant portal vein thrombosis (PVT). We studied a total of 43 patients with chronic liver disease, hepatocellular carcinoma-suggestive nodules and confirmed PVT, in whom the nature of the PVT was confirmed by follow-up imaging (US, computed tomography and/or magnetic resonance imaging) performed up to 6 mo after CEUS. PVT was assessed by US, Doppler US and CEUS with respect to vessel wall disruption and/or invasion, color Doppler vascularization, pulsed Doppler vascularization pattern and CEUS enhancement and vascularization pattern, and thrombi were classified as benign or malignant based on these findings. Follow-up studies revealed malignant PVT in 22 of the 43 patients (51%) and benign PVT in 21 patients (49%). CEUS findings were consistent with follow-up studies in 41 of the 43 patients (95%), with κ?=?0.903 (p < 0.0001), sensitivity?=?91% and specificity?=?100%, indicating that CEUS can be confidently used to differentiate benign from malignant portal vein thrombosis in the setting of chronic liver disease.     

Mitochondrial encephalomyopathies: biochemical approach.

Thanks to recent advances in the molecular genetics of mitochondrial encephalomyopathies, we can now begin to correlate genetic lesions with biochemical defects. In the fatal infantile myopathy due to cytochrome c oxidase (COX) deficiency, an autosomal recessive condition, immunocytochemical studies have shown an isolated defect of subunit VIIa, which is 1 of the only 2 tissue-specific subunits of human COX. In muscle biopsies from patients with Kearns-Sayre syndrome, a multisystem disorder characterized by deletions of the mitochondrial DNA (mtDNA), the activities of all mitochondrial enzymes containing mtDNA-encoded subunits are decreased. The results of Northern analysis, in situ hybridization, and immunocytochemistry in muscle, and of mitochondrial protein synthesis in cultured fibroblasts suggest that partially deleted mtDNAs are transcribed but not translated, probably due to lack of indispensable tRNAs.     

Manifestations of insulin-dependent diabetes mellitus in the periodontium of young Brazilian patients

The periodontal condition of patients with insulin-dependent diabetes mellitus was evaluated in terms of plaque, gingival indices, pocket depth, and alveolar bone loss. Thirty male and female diabetic patients aged 5 to 18 years were compared with 30 non-diabetic subjects and correlated with sex and age. Statistical analyses of the data showed that the mean plaque index was significantly higher (P less than 0.01) among the diabetic patients (1.23) than among the control subjects (0.81). The plaque index was significantly higher (P less than 0.01) among diabetic females (1.34) than among diabetic males (1.10), whereas no sex differences were observed in the control group. The arithmetic means obtained for gingival index were statistically higher (P less than 0.01) for the diabetics (0.58) when compared with the controls (0.15), but no significant differences were obtained when the values were correlated with sex and age. Pocket depth did not differ statistically between groups. When pocket depth was correlated with sex, a statistically significant difference (P less than 0.05) was observed only for the palatal region, with a depth of 2.1 mm in female patients and 1.92 mm in male patients. When pocket depth was correlated with age, a positive correlation (P less than 0.01) was detected in the diabetic group for all regions investigated, whereas the correlation was not significant in the control group. Mean alveolar bone loss was higher in the anterior upper (1.94 mm) and anterior lower (1.87 mm) regions of the diabetic group when compared to the controls (1.52 and 1.37 mm respectively), the difference being significant at the 5% level of probability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mitochondrial myopathy of childhood associated with depletion of mitochondrial DNA.

We have studied five children with mitochondrial myopathy manifesting within or soon after the first year of life. Muscle biopsies showed ragged-red fibers and decreased respiratory chain activity. All five patients had a severe decrease (2 to 34% of normal) in the amount of muscle mitochondrial DNA (mtDNA). The depletion of mtDNA correlated with absence of mtDNA-encoded translation products and with loss of cytochrome c oxidase enzyme activity in individual muscle fibers. This mitochondrial myopathy of childhood illustrates one phenotypic expression of a novel pathogenetic mechanism in mitochondrial diseases, the specific depletion of mtDNA in affected tissues.