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Experiments conducted by Goldblatt and colleagues 1 on the effects of renal-artery constriction in animals led to the recognition that renal-artery stenosis may cause hypertension. Initially, surgical revascularization was the only treatment for renal-artery stenosis, 2 , 3 but percutaneous transluminal balloon angioplasty, 4 with or without stent placement, later supplanted surgery as the preferred treatment. 5 In uncontrolled, retrospective studies of balloon angioplasty, 36 to 100 percent of patients with hypertension had some reduction in blood pressure, with the highest rates of response in patients with fibromuscular dysplasia, 6 but in few patients, however, was blood pressure restored to normal levels. In two small, randomized . . .

To the Editor: The review by Russell (Oct. 19 issue) 1 recommends the protocol used by Rivers et al. 2 and adopted in the Surviving Sepsis Campaign guidelines 3 for the initial resuscitation in severe sepsis. Although others 4 have warned against the use of this protocol, this warning did not receive the attention we think it deserves. Estimates of intravascular volume based on any given level of filling pressure do not reliably predict the response to fluid administration. In addition, patients with sepsis have characteristically high central venous oxygen saturation because of decreased oxygen extraction. The initial mean central venous oxygen saturation of . . .

Pro- and antiinflammatory cytokines and mediators were measured in 39 patients with acute life-threatening meningococcal infections classified into 3 groups: A, meningitis without shock (n = 20); B, meningitis with shock (n = 9); and C, shock without meningitis (n = 10). The plasma concentrations of proinftammatory endotoxin, tumor necrosis factor-a (TNF-α), interleukin (IL)-6, and IL-8 and antiinflammatory cytokines and mediators IL-1 receptor antagonist, IL-10, and soluble TNF receptors p55 and p75 were strongly associated with this classification; the highest concentrations were in group C. IL-4 was not measurable. IL-1β was increased only in rapidly fatal cases. In addition, cerebrospinal fluid (CSF) was analyzed in 21 patients for TNF-α and its soluble receptors. In CSF, these compounds were mainly increased in group A, reflecting an intrathecal compartmentalized cytokine production. It is concluded that both pro- and antiinflammatory mediators are simultaneously increased and are strongly associated with a classification based on simple clinical parameters.

To the Editor: Dickens et al. (July 28 issue) 1 describe a patient who underwent directional coronary atherectomy with an excimer laser. The procedure was complicated by chest pain and the acute onset of blurred vision. Funduscopic examination revealed a white plaque in the left eye, occluding the inferior hemiretinal artery. This was interpreted as a fibrin embolus. After therapy, the visual acuity improved from 20/80- to 20/40, but the visual-field defect remained. Unfortunately, there is no mention of the treatment given. Even in the concluding remarks, in which the authors stress the need for immediate therapy in retinal-artery occlusion, the . . .

We report the case of an 18-year-old man with meningococcal meningitis and low serum concentrations of mannose-binding lectin (MBL). His mother and grandfather, who had also had meningitis in early adulthood, also had low concentrations of MBL in their serum.

Circulating concentrations of tumor necrosis factor-α (TNF), interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and soluble TNF receptors p55 (sTNFr-55) and p75 (sTNFr-75) and ex vivo production ofTNF, IL-1, IL-6, and IL-1ra using a whole blood culture system were measured during the acute and convalescent stages of meningococcal infection. Circulating TNF and IL-1 were below detection level, whereas IL-6 and IL-1ra, sTNFr-55, and sTNFr-75 were increased at admission. The ex vivo production of proinflammatory cytokines TNF, IL-1, and IL-6 was suppressed at admission and restored gradually during recovery. On the contrary, the production of the antiinflammatory IL-1ra was increased at admission. The elevated concentrations of both IL-1ra and sTNFr early in the course of infection suggest a regulatory role for these antiinflammatory compounds. The observed down-regulation of the ex vivo production of TNF, IL-1, and IL-6 and up-regulation of the production of IL-1 ra in the acute stage may indicate a protective regulation mechanism.

A 73-year-old man underwent cemented total hip arthroplasty for left femoral head necrosis. 3 h after surgery, he complained of dyspnoea and chest pain. He rapidly developed respiratory distress and was intubated and ventilated. A chest radiograph showed extensive consolidations particularly in the right lung (inset).

In 39 patients with acute meningococcal infections, the plasma concentrations of tumor necrosis factor-α (TNF) and its soluble receptors (sRs) TNFsR-p55 and TNFsR-p75 were measured from admission till recovery. At admission, patients with shock had significantly higher TNF, TNFsR-p55, and TNFsR-p75 values than patients without shock. In addition, during the first 24 hours, patients with shock had higher TNFsR-p75 to TNFsR-p55 ratios, indicating that in shock the increase of TNFsR-p75 exceeds that of TNFsR-p55. TNF measured more than 12 hours after admission failed to differentiate between shock and nonshock because TNF concentrations normalized within 12–24 hours. However, because concentrations of TNFsRs remained elevated for 5–6 days, at that time plasma TNFsRs still differentiated between shock and nonshock. Plasma exchange or whole blood exchange (PEBE), performed in 20 patients with shock, accelerated the decrease of plasma TNFsRs. However, because of a rebound after each PEBE session, the overall half-lives of both TNFsRs were not affected by PEBE.

The regulation of tumor necrosis factor-α (TNF) and interleukin-1β (IL-1β) production was studied in patients with meningococcal disease. Circulating TNF and IL-1β normalized within 1 day. TNF mRNA and IL-1β mRNA in white blood cells decreased over 3-4 days. During the acute stage, TNF and IL-1β production in stimulated whole blood cultures was down-regulated. After 4-5 days, this production was restored. The down-regulation was unlikely to be caused by circulating IL-6 and IL-10, as these cytokines normalized within 2-3 days. TNF mRNA in stimulated cultures during the acute stage, with down-regulated production, did not differ from that at recovery, with restored production. In contrast, the down-regulated production of IL-1β was associated with significantly lower IL-1β mRNA levels. Thus, TNF and IL-1β production are differentially regulated. Whereas TNF production is regulated posttranscriptionally, IL-1β production is also regulated at the mRNA level.