The virus removal of protein A affinity chromatography, inactivation capacity, acid pH and a combination of high temperature with a chaotropic agent was determined in this work. The model viruses studied were sendaivirus, human immunodeficency virus (HIV-IIIb), human poliovirus type-II, human herpesvirus I and canine parvovirus. The protein A affinity chromatography showed a maximum reduction factor of 8 logs in the case of viruses larger than 120 nm size, while for small viruses (18-30 nm) the maximum reduction factor was about 5 logs. Non viral inactivation was observed during the monoclonal antibody elution step. Low pH treatment showed a maximum inactivation factor of 7.1 logs for enveloped viruses. However, a weak inactivation factor (3.4 logs) was obtained for DNA nonenveloped viruses. The combination of high temperature with 3 M KSCN showed a high inactivation factor for all of the viruses studied. The total clearance factor was 23.1, 15.1, 13.6, 20.0 and 16.0 logs for sendaivirus, HIV-IIIb, human poliovirus type-II, human herpesvirus I and canine parvovirus, respectively.
The metabolic response to sepsis is characterized by increased proteolysis and gluconeogenesis, reduced protein synthesis, and negative nitrogen balance. The effects of a solution with a high proportion of branched-chain amino acids (BCAA) on the nutritional state of septic patients were evaluated. Eighty patients with peritonitis were divided into two groups of 40 patients; group 1 was administered a solution with 22.5% BCAA and group 2 with 45% BCAA. The following parameters were evaluated: anthropometrics, creatinine/height index, urinary 3-methylhistidine, nitrogen balance, stress index, albumin, prealbumin, transferrin, retinol binding protein, lymphocytes, delayed cutaneous sensitivity tests, studies of hepatic function, and plasma aminogram. In group 2 a more positive nitrogen balance, a greater drop in the stress index, a rise in plasma prealbumin and retinol binding protein levels, an increase in the creatinine/height index, and a more marked fall in the urinary excretion of 3-methylhistidine were found. When solutions with a high BCAA content were administered, there was an increase in the plasma concentrations of these amino acids in the BCAA/aromatic amino acid quotient and a decrease in the aromatic amino acids. Plasma concentrations of leucine and valine achieved very high, potentially toxic, levels at 15 days when solutions with high BCAA content were used. It is concluded that solutions with BCAA are advisable for use in the septic patient in the increased protein catabolic phase, where positive nitrogen balance, a reduction in muscle protein catabolism, and faster recovery of muscle and visceral protein were obtained.
losartan and treatment with oral prednisolone 50 mg/day, the angioedema cleared within 3 days. The symptoms of the transient ischemic attack cleared within 1 day, leaving only a residual minimal mimic paresis of the facial nerve (slight hanging of the right mouth angle) for about a week. As antihypertensive treatment, a calcium antagonist was given instead of losartan. No relapse of the angioedema had occurred within 4 months of follow-up. Because of the risk, no attempt of re-exposure to losartan was made.There was no hint of an atopic disposition.No nonsteroidal antiphlogistic drugs had been taken. C1-esterase inhibitor (amount and function), C3, and C4 were normal. As no other cause could be identi®ed, losartan was probably the cause of the angioedema.Angioedema has been found to be due both to conventional angiotensin-converting enzyme inhibitors (1) and, in some cases, to angiotensin II receptor antagonists (2, 3).Recently, increased plasma bradykinin concentrations have been measured during episodes of angioedema caused by an angiotensin-converting enzyme inhibitor, supporting the hypothesis that the wellknown interference with the bradykinin system is part of the underlying pathogenetic mechanism in these adverse drug reactions (4).However, angiotensin II receptor antagonists do not interfere with the kallikrein-kinin system (5); therefore, these ®ndings cannot be applied to losartan. Until now, the pathogenetic mechanism of angioedema due to losartan has remained unclear.Cerebral manifestations and transient ischemic attacks have been reported in association with angioedema of unknown cause (6) or angioedema caused by C1-esterase inhibitor de®ciency (7). To our knowledge, this case is the ®rst described case of angioedema due to an angiotensin II receptor antagonist associated with a transient ischemic attack.
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