Patients with triglyceride levels over 1,000 mg/dl are at high risk of developing acute pancreatitis. This study aimed to determine the effectiveness of plasma exchange (PE) in reducing triglyceride levels during an acute attack of hyperlipidemic pancreatitis (HLP). A total of 17 hypertriglyceridemic patients with the complication of acute pancreatitis received one course of PE treatment for one or two consecutive sessions. The respective mean removal rates during a single PE for triglyceride, cholesterol, amylase, and lipase were 66.3, 62.1, 70.0, and 84.8%, respectively. An additional one exchange increased the removal rate to 83.3, 66.2, 85.5, and 87.0%, respectively. For the two-sessions of treatment, the removal rates were higher for triglyceride (P=0.0015) and amylase with a borderline statistical significance (P=0.0641). Better triglyceride clearance correlated well with lower levels of transmembrane pressure (TMP) at 90 minutes after PE (r2=0.5782, P=0.0010) and shorter plasmapheresis duration (r2=0.2241, P=0.0427). Thirteen of seventeen patients (76.5%) recovered completely, eight patients in a single-session, and five in two-sessions. Two patients developed intra-abdominal abscess, necessitating surgical drainage and two patients died due to both septic shock and multi-organ failure. No significant predictor of clinical outcome was identified. In summary, PE treatment is an effective method to clear lipids and enzymes from plasma in a single session for most HLP patients. A greater extraction of triglyceride would result in a reduced TMP and a shorter duration of PE treatment.
ContributorsGIW wrote and revised the manuscript in response to co-author comments. He finalized all the figures and tables, performed the literature search, and assisted with data interpretation. HJK critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. IBA performed the data analysis, constructed the figures and tables, and made important suggestions to improve the manuscript. H-CK assisted with the data analysis and also reviewed the manuscript. GRC critically reviewed the manuscript and made important suggestions to improve it. He assisted with data interpretation. All other authors were given the opportunity to review the manuscript and make suggestions which GIW received, either revising the paper or providing explanations. All who are not deceased were involved with approval of the manuscript.
This article represents the recommendations for the management of spontaneous intracerebral haemorrhage of the European Stroke Initiative (EUSI). These recommendations are endorsed by the 3 European societies which are represented in the EUSI: the European Stroke Council, the European Neurological Society and the European Federation of Neurological Societies.
Clinical features and anti-acetylcholine receptor (AChR) titers were compared in Chinese (n = 258) and Caucasian (n = 258) myasthenia gravis populations. The former had more early onset and ocular cases, lacked the Caucasian late onset peak, and had fewer severe cases. The distribution of anti-AChR titers was broadly similar in the two populations, and their sera reacted equally well with AChR in both races. The significantly lower (chi 2 = 14.6; p less than 0.001) median anti-AChR titer in the Chinese population can be accounted for by the higher frequency of ocular cases and lower frequency of moderate or severely affected cases.
Colchicine and 3-hydroxy-3-methy-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are well known to cause myopathy. Myotoxicity is dose-dependent in both drugs; therefore, the onset of symptoms usually takes months or years. We report the case of a patient with chronic renal failure who had been taking simvastatin for 2 years and developed acute weakness 2 weeks after the start of treatment with colchicines for recurrent gout. The electromyography and elevated muscle enzymes indicated that his symptoms were caused by myopathy. When this patient stopped taking both drugs, his weakness resolved rapidly. Acute myopathy induced by combination therapy with colchicines and simvastatin is rare. In patients with chronic renal failure, co-administration of colchicine with simvastatin may accelerate the onset of myopathy because CYP3A4 (part of cytochrome P450) is crucial in the breakdown of both drugs. When adding colchicine to a medication regimen that includes a HMG-CoA reductase inhibitor for patients with renal insufficiency, drugs that are metabolized outside the CYP3A4 system (e.g., fluvastatin and pravastatin) should be selected instead.
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