Are sleep disorders induced by haemodialysis?
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Biomedical subjects
Publications and source records attributed to G Jean.
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Despite the absence of anti-HLA antibodies (Ab) about 10 to 20 percent of renal transplants are lost during the first months from rejection. The role of humoral rejection seems more likely than cellular rejection since they do not respond to standard anti-rejection therapy. We studied 37 patients who rejected their graft despite negative T and B lymphocytes cross-match during the first eight months (m: 59 days, range: 2-240) following kidney transplantation. These patients were compared with 57 patients who experienced a favorable outcome. The sera were tested for the presence of Ab against epidermis of a panel of 5 normal skins and against an epithelial-endothelial hybrid cell line (EA hy 926, Dr C.J.S. Edgell), expressing both endothelial and epithelial antigens. Among the 37 patients who rejected theirs grafts, 8 had anti-keratinocytes Ab, 11 had Ab against epithelial-endothelial hybrid cell line, 9 were positive for both tests. Among the 8 pts who lost their graft before 25 days, 5 were positive for at least our test. Conversely, 7 among the 57 pts with favorable outcome had Ab: 2 against keratinocytes, 5 against hybrid cell line. These data suggest that non anti-HLA Ab may play a role in graft rejection. Furthermore the detection of such Ab prior to transplantation may predict patients at risk of severe rejection. In such cases, plasma exchanges may be proposed if they develop steroid-resistant rejection.
Sixteen children, aged 2 to 5 years and ranked ASA 1, were included in this study assessing gastro-oesophageal reflux occurring under halothane anaesthesia, before and during, caudal anaesthesia. They were scheduled for surgery below the umbilicus lasting 1 to 5 h. After premedication with oral hydroxyzine (2 mg.kg-1) and intravenous atropine (10 micrograms.kg-1), induction was carried out with 3% halothane. A gastro-oesophageal pH probe was inserted via the nose after calibration at 37 degrees C. A neutral pH for the oesophageal electrode and an acid pH for the gastric one demonstrated the correct position of the probe. The pH was then registered every 4 s. The probe was left in situ until the patient left the recovery room. The caudal anaesthesia catheter was then inserted with the patient lying on his left side. Caudal anaesthesia was began with 2.5 mg.kg-1 of plain bupivacaine and 5 mg.kg-1 of plain lidocaine. When the patient was lying supine again, narcosis was maintained with 0.5% halothane and 50% nitrous oxide. A dose of 1.5 mg.kg-1 of bupivacaine was injected every 30 to 45 min. None of the children displayed any respiratory signs (coughing, dyspnoea, bronchospasm, cyanosis) during the combined anaesthetic. Two episodes of asymptomatic gastro-oesophageal reflux were revealed by this method, one lasting 7 minutes and occurring during insertion of the caudal catheter, and the other, lasting 4 minutes, during recovery. There were no pulmonary sequels. There was excellent respiratory and haemodynamic stability throughout. The two episodes seemed to have been triggered off by rapid displacement of the patient and too deep an anaesthetic.(ABSTRACT TRUNCATED AT 250 WORDS)
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In infantile cystinosis the amino acid cystine preferentially accumulates in phagocytic cells, polymorphonuclear leucocytes (PMN) and monocytes, rather than in lymphocytes. We previously described functional abnormalities in the oxidative metabolism and locomotion of cystinotic PMN and monocytes. The present study shows an abnormal lymphocyte polyclonal activation as evidenced by a decreased immunoglobulin (Ig) production and generation of Ig-containing cells (ICC) in cultures of peripheral blood mononuclear cells (PBMC) from cystinotic children upon stimulation with pokeweed mitogen and Staphylococcus aureus Cowan I. However, monocyte depletion from cystinotic PBMC fully reconstituted Ig production and ICC generation, indicating: (1) the presence of an increased monocyte-dependent suppression on lymphocyte polyclonal activation, and (2) that the intrinsic ability of cystinotic lymphocytes to respond to polyclonal stimulation was preserved. The increased cystinotic monocyte-dependent suppressive effect was not mediated by prostaglandin E2 (PGE2) since its production by cystinotic PBMC upon polyclonal activation was not different from that of controls. In addition, the sensitivity of cystinotic lymphocytes to the immunosuppressive effect of varying concentrations of exogenous PGE2 was similar to that of controls. Finally, indomethacin and 2-mercaptoethanol, two agents able to scavenge hydroxyl (.OH) radicals, restored Ig production by cystinotic PBMC, suggesting a role for reactive oxygen species in the increased cystinotic monocyte-dependent suppression.
The nutritional effects of low-protein diets are difficult to assess in humans. Normal and uraemic growing rats were therefore fed: a moderately low-protein (12%) reference diet (diet R), two 5% casein diets, one supplemented with essential amino acids (AA) (diet A) and the other with their keto acids (diet K), and a 7% casein diet isonitrogenous with diet K (diet L). Appetite and growth of both uraemic and control rats were identical on diets R and A and were reduced on diets K and L. Stunting was prominent in rats fed diet L and more severe than in those on diet K. Diet K induced marked anorexia in controls. This effect was smaller in uraemic rats, which were all anorectic, regardless of the diet. Plasma essential AA were similar in rats on diets R and A but low in control rats fed diets L and K. In particular, diet K did not improve the branched-chain AA levels although it produced better growth than diet L. Plasma and muscle threonine were surprisingly elevated in rats on the semi-synthetic diets A and K, despite identical or lower consumptions. Regardless of the diet, uraemia resulted in unchanged or increased plasma essential AA, despite reduced appetite and stunting. Uraemia caused a marked rise in some non-essential AA. Muscle essential AA, except for threonine, were essentially unaltered and did not correlate with growth or uraemia.
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Data on cystine leukocyte content are analyzed in cystinotic patients receiving cysteamine as a depleting agent of cellular cystine. During 2 years, 63 measurements of cystine leucocyte content were performed in 15 cystinotic patients, aged 20 months to 22 years, taking daily 40 to 65 mg/kg of cysteamine. An original method was used to measure leukocyte cystine: a binding protein assay with a specific cystine-binding protein from E. coli. Results were taken individually because of various clinical situations in patients. In 8 patients taking cysteamine regularly, 6 hours after a dose, cystine leukocyte content was between 1 and 2 nmol 1/2 cystine/mg protein, about 10 times less than basal values without treatment and 5 to 10 times more than control subjects. In less compliant patients, cystine leukocyte content was close to basal values without treatment (3 to 25 nmol/mg). Some variability was observed between individuals receiving cysteamine: pharmacokinetic parameters may need further investigation. This sensitive and specific assay helped in controlling compliance and adjusting dosage regimen in each patient. The aim was to maintain a minimum effective dosage in order to avoid toxic side effects of cysteamine.
The monoclonal antibody OKT3, administered for 2 to 3 weeks in a dosage of 0.1 mg/kg, in combination with azathioprine and prednisone, proved more effective than conventional antilymphocyte serum for the prevention of renal transplant rejection. Side effects were less marked with OKT3 than with antilymphocyte serum. Infectious complications, especially viral, occurred with the same incidence in both groups. In the long term, following discontinuation of OKT3 or antilymphocyte serum, incidence of rejection episodes and graft survival rates were identical in both groups. OKT3 in a lower dosage of 0.05 mg/kg was less effective, with several patients developing rejection during treatment, and induced more common and earlier anti-OKT3 immunization.
We compared nonbronchoscopic bronchoalveolar lavage (NB-BAL) with open lung biopsy to determine the etiological diagnosis of lung infiltrates in patients requiring mechanical ventilation. NB-BAL was performed via a cuffed reusable 7F catheter generally used for right heart catheterization (BAL-C). In 13 patients, BAL-C and open lung biopsy were performed in the same lobe immediately after death when the ventilator was still functioning. No organism was cultured from BAL-C cultures when histopathologic examination of the lung showed no pneumonia and lung culture isolated no organism. Among the 10 positive BAL-C cultures, lung biopsy showed histologic pneumonia in 9 cases. Among these 9 pneumonia cases, 14 organisms were isolated in lung cultures and BAL-C correctly identified the causative agent in 13 cases. BAL-C appears to be an effective and safe procedure in the diagnosis of pulmonary infections in patients under mechanical ventilation who have previously received antibiotic therapy.
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Forty-two male patients with alcoholic liver disease were studied for iron status by indirect hematological assays, including red cell ferritin (RCF), and histochemical estimations. Serum iron and ferritin, total iron-binding capacity levels were unrelated to iron deposits, whereas RCF concentration was a good index of iron stores as detected by direct assessment on bone marrow and liver biopsy specimens. A relatively high proportion of alcoholics (19%) were iron-deficient. Alcoholic patients with cirrhosis exhibited higher RCF values than patients with alcoholic hepatitis. However, this increase was apparently unrelated to cirrhosis per se. In alcoholics we found that RCF was mainly related to levels of bone marrow iron. The increased RCF values observed in patients with hepatic siderosis was mediated by marrow iron stores. RCF can therefore be regarded as a useful test to distinguish patients with liver siderosis and normal values of bone marrow iron.
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