Study of the usefulness of optic fundi examination of patients with hypertension in a clinical setting.

The purpose of this study was to evaluate the usefulness of direct opthalmoscopy by non-opthalmologists in patients with hypertension. In a cross-sectional survey, we analysed the association between optic fundi abnormalities, individually and according to the criteria of Keith and Wagener (KW), with blood pressure and duration of known hypertension in 400 non-diabetic hypertensive patients. The optic fundi abnormalities were more frequent in patients with diastolic blood pressure (DBP) > 105 mm Hg (P = 0.002), SBP > 180 mm Hg (P < 0.0001) and with a duration of known hypertension > 3 years (P = 0.002). The severity of hypertension did not vary in parallel with the KW classes I and II: 34.5% of patients classified as KW I had a diastolic pressure of > 105 mm Hg compared with only 25.3% of those classified as KW II. Class III abnormalities were infrequent (2.5% of the whole cohort). In a logistic regression model, diffuse arteriolar narrowing was associated with DBP (P = 0.002) and age (P < 0.001). Abnormalities of the arteriovenous crossings were associated with SBP (P = 0.001) and duration of disease (P = 0.008). The positive predictive value of any fundoscopic abnormality to estimate the severity of hypertension was 59% and the negative value was 60%. The results of this study demonstrate that optic fundi examination by internists and cardiologists does not give an accurate assessment of the severity of hypertension in most patients, and that the Keith-Wagener classification of retinopathy has a limited applicability.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of succinate dehydrogenase and beta-hydroxybutyrate dehydrogenase activities by methylmalonate in brain and liver of developing rats.

The effects of methylmalonate (MMA) on succinate dehydrogenase (SDH) and beta-hydroxybutyrate dehydrogenase (HBDH) activities in brain and liver of 15-day-old rats were studied. The apparent Km of SDH for succinate was 0.45 mmol/L in brain and 0.34 mmol/L in liver. MMA inhibited the enzyme activity in both tissues with Ki values of 4.5 mmol/L and 2.3 mmol/L in brain and liver, respectively, and the inhibition was of the reversible competitive type. The calculated Km for HBDH with beta-hydroxybutyrate as substrate was 1.26 mmol/L in brain and 0.36 mmol/L in liver. MMA inhibited the enzyme with a Ki value of 0.015 mmol/L in brain and 0.275 mmol/L in liver. These results are probably relevant to our understanding of cerebral metabolism in methylmalonic acidaemic children, especially during ketoacidotic and hypoglycaemic crises, and may be related to the pathogenesis of cerebral dysfunction of methylmalonic acidaemia.