Lipidmetabolism in patients with nephrotic syndrome (N.S.) and uremia under haemodialysis (H.D.) has been investigatedsince hyperlipidemia and high incidence of coronary heart disease were recognized in the both renal diseases.
In twenty patients with ischemic cerebrovascular disease fibrinopeptide A (FPA) and fibrinopeptide Bβ 15-42 (Bβ 15-42) were serially assayed in cerebrospinal fluid (CSF) and in plasma.After plasma FPA levels began to be elevated, it took a peak from 5th to 14th day after stroke (p<0.05), and gradually returned to control level. Bβ 15-42 levels in plasma were constantly elevated at least during first three weeks (Fig. 1). On the other hand, values of FPA in CSF were initially elevated and then reached to a peak on 15th to 21st day after stroke (p<0.01). However values of Bβ 15-42 in CSF remained at control level (Fig. 2).Suggestions of these results are as follows. Coagulation activity was accelerated following the onset of stroke with a short time lag. This delay of coagulation activity was considered to be due to the stroke progression, that is, continuous activation of thromdin in the ischemic regions. And it caused the elevation of FPA that released into the subarachnoid space crossing the broken blood-brain barrier. While fibrinolytic activity in plasma was continuously elevated, that in CSF was not influenced by stroke. The reason of this difference was not proven in our series.
We retrospectively examined the MR imaging (MRI) findings in 144 patients with epilepsy (31 with temporal lobe epilepsy and 113 with other epilepsies). 110 cases (76.4%) showed abnormal findings such as spotty lesions in white matter, hippocampal atrophy and/or signal change, ventricular dilatation and/or deformity, developmental lesions, brain tumors and so on. Hippocampal atrophy and/or signal change was shown in 74.1% of temporal lobe epilepsy, a remarkably high percentage (P < 0.01) compared with the other types of epilepsies (18.1%). This finding means that hippocampal lesions may play a large part in the cause of temporal lobe epilepsy. Investigation of the relationship between clinical term and abnormal findings revealed that the longer the clinical term, the larger the number of hippocampal lesions, regardless of whether it is temporal lobe epilepsy or not. Thus hippocampal lesions may occur as a result of hypoxia accompanied with seizure. Therefore we recommend horizontal and/or vertical sections of hippocampus in MR imaging of all patients with epilepsy. Even though MR findings may reflect some secondary lesions, MRI will shed some light on the proper understanding of epilepsy.
Red cell deformability was measured from the red cell filtration rate (RFR) in the patients of peripheral vascular diseases, using a 5μm Nuclepore microfilter and 20% Ht red cell suspension.In the patients of ASO, TAO and Raynaud's syndrome, the red cell deformability was cleared to be reduced significantly, comparing with age-matched controls.Furthermore, the effects of PGE1, PGI2 analogue (OP-41483) and TXA2 blockade (OKY-046) on red cell deformability in peripheral vascular disease patients were studied.PGE1 was given intravenously 11 patients (80-120μg/day, 5-14 days), and reduced red cell deformability (23.8μl/sec) was improved (47.1μl/sec) significantly (p<0.01).PGI2 analogue was also given to 16 patients (20μg, 40min) intravenously, and pre-treated value was 37.9μl/sec, while post-treated value increased to 48.8μl/sec (p<0.01).TXA2 blockade was given orally (600mg/day, 6 weeks) to 13 patients and red cell deformability was improved significantly (from 46.5 to 58.8μl/sec, p<0.01).The study showed that PGE1, PGI2 and TXA2 blockade were significantly effective on reduced red cell deformability, besides the effectiveness as an anti-platelet agent and a vasodilating agent.These prostanoids were suggested to play an important role in keeping a good microcirculation in the body.
