Characteristics of traditional Chinese medicine use in children with asthma: a nationwide population-based study.

Asthma is a chronic inflammatory airway disease accounting for severe morbidity and mortality in children. To determine the characteristics of traditional Chinese medicine (TCM) used to treat pediatric asthma, we conducted a nationwide population-based study by analyzing a cohort of one million randomly sampled patients from the beneficiaries of the National Health Insurance Program in Taiwan from 2002 to 2010. Children under 18 years of age with newly diagnosed asthma (ICD-9-CM code: 493, N = 45 833) were enrolled, and 57.95% (N = 26 585) of them had used TCM. The number of TCM users was significantly more than that of non-TCM users in school-age children. The most commonly prescribed TCM formula is Ding-chuan-tang, or Xing-ren (Semen Armeniacae Amarum) for the single herb. Our study is the first to reveal characteristics and prescription patterns of the use of TCM in children with asthma. Further research is needed to elucidate the efficacy and safety of these Chinese herbal products.

Molds, parental atopy and pediatric incident asthma.

UNLABELLED: To assess the independent and joint effects of parental atopy and exposure to molds on the development of asthma in childhood, the authors conducted a cohort-based, incident case-control study in 2008. The case group consisted of 188 children with new asthma, and the control group (n=376) was matched one to two for age and sex. The outcome of interest was the development of asthma during the study period. The studied determinants were parental atopy and three indicators of exposure including histories of water damage, presence of visible molds, and perceived mold odor in the home at baseline in 2002. In conditional logistic regression adjusting for confounding, parental atopy [adjusted odds ratio (aOR) 3.29, 95% CI 2.19-4.94] and the presence of mold odor (aOR 2.09, 95% CI 1.30-3.37) and visible mold (aOR 1.76, 95% CI 1.18-2.62) were independent determinants of incident asthma, and apparent interaction in additive scale was observed. Our finding suggests that the interaction between parental atopy and molds may play a role in the development of asthma in children. PRACTICAL IMPLICATIONS: Our study strengthens the evidence for the roles of indoor dampness problem and parental atopy as determinants of asthma in children. Furthermore, the interaction between parental atopy and exposure to molds suggests a role for the development of childhood asthma, i.e., the children whose parents had atopic disease and molds exposure are more susceptible to develop asthma.

Adsorption and thermal reactions of alkanethiols on pt(111): Dependence on the length of the alkyl chain.

The adsorption and thermal decomposition of alkanethiols (R-SH, where R = CH3, C2H5, and C4H9) on Pt(111) were studied with temperature-programmed desorption (TPD) and X-ray photoelectron spectroscopy (XPS) with synchrotron radiation. Dissociation of sulfhydryl hydrogen (RS-H) of alkanethiol results in the formation of alkanethiolate; the extent of dissociation at an adsorption temperature of 110 K depends on the length of the alkyl chain. At small exposure, all chemisorbed CH3SH, C2H5SH, and C4H9SH decompose to desorb hydrogen below 370 K and yield carbon and sulfur on the surface. Desorption of products containing carbon is observed only at large exposure. In thermal decomposition, alkanethiolate is proposed to undergo a stepwise dehydrogenation: R'-CH2S --> R'-CHS --> R'-CS, R' = H, CH3, and C3H7. Further decomposition of the R'-CS intermediate results in desorption of H2 at 400-500 K and leaves carbon and sulfur on the surface. On the basis of TPD and XPS data, we conclude that the density of adsorption of alkanethiol decreases with increasing length of the alkyl chain. C4H9SH is proposed to adsorb mainly with a configuration in which its alkyl group interacts with the surface; this interaction diminishes the density of adsorption of alkanethiols but facilitates dehydrogenation of the alkyl group.

Chlorobutanol, a preservative of desmopressin, inhibits human platelet aggregation and release in vitro.

Therapeutic preparations of desmopressin for parenteral use contain the preservative chlorobutanol (5 mg/ml). We show here that chlorobutanol is a potent inhibitor of platelet aggregation and release. It exhibited a significant inhibitory activity toward several aggregation inducers in a concentration- and time-dependent manner. Thromboxane B2 formation, ATP release, and elevation of cytosolic free calcium caused by collagen, ADP, epinephrine, arachidonic acid and thrombin respectively were markedly inhibited by chlorobutanol. Chlorobutanol had no effect on elastase-treated platelets and its antiplatelet effect could be reversed. It is concluded that the antiplatelet effect of chlorobutanol is mainly due to its inhibition on the arachidonic acid pathway but it is unlikely to have a nonspecific toxic effect. This antiplatelet effect of chlorobutanol suggests that desmopressin, when administered for improving hemostasis, should not contain chlorobutanol as a preservative.

Brachial plexus compression due to subclavian pseudoaneurysm from cannulation of jugular vein hemodialysis catheter.

Jugular venous cannulation is generally safer than subclavian cannulation. The traumatic complications associated with jugular vein hemodialysis catheters are rare. A jugular vein, therefore, has become the preferred site for hemodialysis catheter insertion. We describe the first case of brachial plexus compression attributable to delayed recognition of a right subclavian pseudoaneurysm as a complication of jugular venous cannulation of hemodialysis catheter. We advocate that any neck swelling, new bruit, and the symptoms of brachial plexopathy after jugular venous cannulation warrant an intensive investigation to exclude arterial injury. Because delayed diagnosis may lead to a worsened prognosis in patients with brachial plexus palsy, physicians should exercise vigilance to detect and manage early the potentially serious and fatal complications of subclavian artery pseudoaneurysm and brachial nerve injury.

Chorea induced by thiamine deficiency in hemodialysis patients.

Thiamine deficiency is mainly encountered in alcoholics or food faddists, but it may complicate chronic dialysis because of low intake and accelerated loss of thiamine in dialysis patients. We report here 2 hemodialysis (HD) patients who developed chorea induced by thiamine deficiency. We propose that thiamine deficiency, with a consequent dysfunction of the basal ganglia, may induce chorea in HD patients.

8-hydroxy-2'-deoxyguanosine of leukocyte DNA as a marker of oxidative stress in chronic hemodialysis patients.

In contrast to proteins and lipids, oxidative damage to DNA has not been well studied in patients undergoing hemodialysis (HD). We hypothesized that phagocytes are activated after blood-membrane contact during HD, and oxidants from metabolic activation can damage leukocyte DNA. To test this hypothesis, the 8-hydroxy-2'-deoxyguanosine (8-OHdG) content of leukocyte DNA was measured by high-performance liquid chromatography electrochemical detection method in 35 age- and sex-matched healthy subjects, 22 undialyzed patients with advanced renal failure, and 109 HD patients to assess the relation between oxidative DNA damage and complement-activating membranes, blood antioxidants, and iron status. Dialysis membranes were classified into complement-activating (cellulose; n = 55) and non-complement-activating (polymethylmethacrylate [PMMA]; n = 35; polysulfone [PS]; n = 19) membranes. We found increased oxidative stress in undialyzed and HD patients based on a decrease in plasma levels of ascorbate and alpha-tocopherol adjusted for blood lipid (alpha-tocopherol/lipid), serum albumin, and reduced glutathione levels in whole blood and an increase in oxidized glutathione levels in whole blood compared with controls (P < 0.001). The greatest 8-OHdG level in leukocyte DNA was in HD patients, followed by undialyzed patients and healthy controls (P < 0.001), and was significantly greater in HD patients using cellulose membranes than those using PMMA or PS membranes (P < 0.001). 8-OHdG levels correlated with plasma alpha-tocopherol/lipid (r = -0.314; P < 0.005), serum iron (r = 0. 446; P < 0.001), and transferrin saturation values (r = 0.202; P < 0.05) in the analysis of all HD patients. In a 6-week crossover study, 8-OHdG levels significantly decreased after the switch from cellulose to synthetic membranes for 2 weeks and increased after the shift from synthetic to cellulose membranes (P < 0.05). Iron metabolism indices and plasma alpha-tocopherol/lipid values did not change significantly in the study period. We conclude that 8-OHdG content in leukocyte DNA is a biomarker of oxidant-induced DNA damage in HD patients. Oxidative DNA damage is a consequence of uremia, further augmented by complement-activating membranes.

Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients.

Patients with end-stage renal disease undergoing regular dialysis are prone to encephalopathy, but the cause is often unclear. Dialysis patients are at risk for thiamine deficiency, which may mimic many uremic complications, including encephalopathy. To determine whether unexplained encephalopathy in regular dialysis patients is associated with thiamine deficiency, we conducted a prospective study that enrolled 30 consecutive dialysis patients with altered mental status admitted to a referred hospital during a 1-year period. A complete history, physical and neurological examinations, laboratory investigations, and computed tomographic scans or magnetic resonance imaging of the brain were obtained for each subject. In 10 of the 30 patients, diagnoses remained obscure after the initial workup. Manifestations included confusion, chorea, acute visual loss, rapidly progressive dementia, myoclonus, convulsions, and coma. Intravenous thiamine was administered to these 10 patients. All 10 patients had thiamine deficiency confirmed by a marked response to thiamine supplementation and/or a low serum thiamine concentration (35.3 +/- 6.0 nmol/L; normal, >50 nmol/L). Nine patients recovered, but one patient failed to respond because of delayed treatment. We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency. This condition is fatal if unrecognized and can be successfully treated with prompt thiamine replacement.

Erythropoietin hyporesponsiveness: from iron deficiency to iron overload.

Iron deficiency is the most frequently encountered cause of suboptimal response to recombinant human erythropoietin (rHuEPO). Carefully assessing iron status is of paramount importance in chronic renal failure patients prior to or during rHuEPO therapy. Because there is great need for iron in the EPO-stimulated erythroid progenitors, it is essential that serum ferritin and transferrin saturation levels should be maintained over 300 microg/liter and 30%, respectively. Investigators have shown that oral iron is unlikely to keep pace with the iron demand for an optimal rHuEPO response in uremics. Therefore, patients with iron deficiency will always require intravenous iron therapy. The early and prompt iron supplementation can lead to reductions in rHuEPO dose and hence cost. After the iron deficiency has been corrected or excluded, we must remember all of the possible causes of hyporesponsiveness in every rHuEPO-treated patient. As dose requirements vary, it is not clear which dose of rHuEPO causes this hyporesponsiveness. However, if the patient with iron repletion does not respond well after the induction period, the major causes blunting the response to rHuEPO should be investigated. Most factors are reversible and remediable, except resistant anemia associated with hemoglobinopathy or bone marrow fibrosis, which requires a further increase in the rHuEPO dose. By means of early detection and correction of the possible causes, the goal of increasing therapeutic efficacy can be achieved. Iron overload may lead to an enhanced risk for infection, cardiovascular complication, and cancer. Over-treatment with iron should be avoided in dialysis patients, despite the fact that the safe upper limit of serum ferritin to avoid iron overload is not clearly defined. On the other hand, functional iron deficiency may develop even when serum ferritin levels are increased. Controversy remains as to whether intravenous iron therapy can overcome this form of hyporesponsiveness in iron-overloaded patients. Moreover, a treatment option of iron supplementation is not warranted in these patients, as the potential hazards of iron overload will be worsened. We demonstrated that the mean hematocrit significantly increased from 25.1+/-0.9% to 31+/-1.2% after eight weeks of intravenous ascorbate therapy (300 mg three times a week) in 12 hemodialysis patients with serum ferritin levels of more than 500 microg/liter. The enhanced erythropoiesis paralleled with a rise in transferrin saturation (27.8+/-2.5% vs. 44.8+/-9.5%, P < 0.05) and reductions in erythrocyte zinc protoporphyrin (130+/-32 vs. 72+/-19 micromol/mol heme, P < 0.05) and monthly rHuEPO dose (24.2+/-4.5 vs. 16.8+/-3.4 x 10(3) units, P < 0.05) at the end of study. It is speculated that ascorbate supplementation not only facilitates the iron release from storage sites and its delivery to hematopoietic tissues, but also increases iron utilization in erythroid cells. Our study provides a more complete understanding of the pathogenesis of iron overload-related anemia and the development of an adjuvant therapy, intravenous ascorbic acid, to the existing treatments.

Pancreatic enzymes in uremic patients with or without dialysis.

One hundred thirty blood samples from 87 patients with renal failure, but without abdominal pain, were analyzed for blood urea nitrogen (BUN), creatinine, amylase, p-isoamylase, and lipase simultaneously. We found that 74, 78, and 80% of the patients had hyperamylasemia, hyperisoamylasemia, and hyperlipasemia. None had amylase higher than five times the upper limit. A few patients (2.3%) had lipase elevated to more than 10 times the upper limit. No significant change of pancreatic enzyme level was noted as a result of hemodialysis, but a significant amount of amylase was removed from the circulation in patients receiving intermittent peritoneal dialysis. Significantly lower pancreatic enzyme levels were observed in patients with less impairment of renal function. We conclude that elevation of pancreatic enzymes in uremic patients is more frequent and more extensive than most articles indicate, and that the extent of increase is related more to renal function than to the modalities of dialysis the patients received.

Assessment of neurotoxicity induced by oral administration of chlordecone (Kepone) in the mouse.

Neurotoxicity in the mouse was produced following oral administration of chlordecone at 10, 25 and 50 mg/kg/day in corn oil vehicle. Hyperexcitability and tremors were observed on the 1st, 4th and 9th day after the administration of chlordecone at 50, 25 and 10 mg/kg/day, respectively, and mortality occurred on the 5th, 7th and 13th day after daily administration of the respective doses. In all cases, the cumulative LD 50 for chlordecone was estimated between 180 and 200 mg/kg. Daily oral administration of chlordecone caused loss of body weight, and the loss of body weight was greatest at the onset of tremor. The effect of chlordecone on food and water consumption varied depending on the dose. A recovery in body weight, and food and water consumption were observed upon the termination of chlordecone treatment. In terms of neurotoxic responses, the effect of chlordecone on motor coordination in the mouse was dose-dependent, both during treatment and during recovery after terminating treatment. The threshold for pentylenetetrazol-induced seizures was significantly reduced in chlordecone treated animals. This study may provide essential basic information for studying the biochemical mechanisms of chlordecone-induced neurotoxicity in the mouse.

Home treatment of uremia with gastrointestinal dialysis.

Twenty patients with end-stage renal disease and a creatinine clearance of less than 5 ml/min were tre ated with oral gastrointestinal (GI) dialysis. The dialyzate contained an electrolyte solution with 180-220mmoles/l of mannitol. In fasting state in the morning the self-prepared 7 liters of dialyzate was drunk at a rate of one glass every 5 minutes for about 3 hours. Intermittent diarrhea with passage of watery fluid occurred during the whole period. After each treatment the average drop in BUN in individual patients was 11--22%, but no significant decrease in serum creatinine. With twice to thrice weekly GI dialysis uremic symptoms such as anorexia, nauseal and vomiting were usually improved with slight prolongation of life. However, treatment is usually difficult when the patient becomes oliguric or anuric, so its value in long-term management of chronic uremia is limited. Most of our patients either died or shifted to hemodialysis within a few months of institution of the therapy.

The removal index for evaluation of dialysis.

OBJECTIVES: To find an index of adequacy that takes into consideration the effect of the decreasing concentration of urea nitrogen in hemodialysis (HD) and can be used before treatments to quantitate the prescriptions with the same criterion for both HD and continuous ambulatory peritoneal dialysis (CAPD). DESIGN: The removal index was obtained through mathematical theories and then compared with the urea index (KT/V) values of the sample patients. PATIENTS: Thirty-two HD and 21 CAPD patients were included. All patients were dialyzed with optimal urea index values and had been stable for at least one year. RESULTS: The removal index in HD (xi HD) for each dialysis was O.62 +/- 0.07, and the normalized removal index in CAPD (xi CAPD) was 0.59 +/- 0.11. There was no statistical significance. This result is consistent with the fact that no difference of morbidity or mortality exists between these two modalities. CONCLUSION: After mathematical manipulation, the removal index in HD can be presented in the form of the urea reduction ratio, which is a retrospective measure to estimate the performance of hemodialysis. This study implies that the removal index is able to facilitate the prescriptions for adequate dialysis. The removal index can also be used to explain the reason why the urea index values are always larger in HD than in CAPD.

The need for second-generation antihepatitis C virus testing in uremic patients on continuous ambulatory peritoneal dialysis.

OBJECTIVE: To assess the prevalence and clinical relevance of a hepatitis C virus (HCV) infection in continuous ambulatory peritoneal dialysis (CAPD) patients by first- (Ortho) and second-generation (Abbott and UBI) HCV antibody enzyme immunoassays. DESIGN: Thirty-two serum samples tested by first-generation HCV antibody enzyme immunoassays (EIA's) were reevaluated using two second-generation HCV antibody EIA's. Basic demographic data, history of blood transfusions, and duration of hemodialysis and CAPD were reviewed. Results were analyzed by chi square analysis, Wilcoxon rank sum, and the paired t-test. SETTING: The medical college's affiliated teaching hospital. RESULTS: The prevalence of the antibody anti-HCV increases with the duration of previous hemodialysis, but not with the duration of CAPD. The positive detection of anti-HCV by second-generation HCV antibody EIA's was higher than first-generation EIA's (25% and 34.4% vs 12.5%). CONCLUSION: The prevalence and clinical relevance of HCV infection can be more accurately studied using the second-generation assays in uremic patients.

Absence of modulating effects of cytokines on antioxidant enzymes in peritoneal mesothelial cells.

OBJECTIVE: To investigate the modulation of superoxide dismutase, glutathione peroxidase, and catalase by cytokines and endotoxin in human peritoneal mesothelial cells. DESIGN: Cultured human peritoneal mesothelial cells were treated with various concentrations of interleukin-1 alpha, tumor necrosis factor-alpha (TNF-alpha), interleukin-6, interleukin-8, transforming growth factor-beta (TGF beta), and lipopolysaccharide. Cell morphology was observed and the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed. The antioxidant enzyme activities of human peritoneal mesothelial cells were also compared with those of human liver and kidney tissues. RESULTS: Interleukin-1 alpha, TNF alpha, TGF beta, and lipopolysacharide caused dose-dependent cytotoxicities in mesothelial cells. The activities of these three antioxidant enzymes did not change after treatment with cytokines and endotoxin. The total superoxide dismutase activity of confluent human peritoneal mesothelial cells was found to be greater than that of human liver and kidney tissues and was composed mostly of manganese superoxide dismutase activity. Furthermore, glutathione peroxidase and catalase activities of human peritoneal mesothelial cells were lower than those of human liver and kidney tissues. CONCLUSION: In human peritoneal mesothelial cells, lack of induction of antioxidant enzymes by inflammatory cytokines, as well as high superoxide dismutase activity accompanied by insufficient glutathione peroxidase and catalase activities may both contribute to the susceptibility of these cells to oxidative damage. Therefore, appropriate management to decrease oxidative injury to the peritoneum should be taken into consideration when treating long-term continuous ambulatory peritoneal dialysis patients.

Significance of nitrogen removal mass in uremic patients on different modalities of dialysis therapy.

BACKGROUND AND PURPOSE: While most nephrologists use Kt/V values for dialysis prescriptions, some researchers are beginning to view the role of solute removal mass as an indicator of adequate dialysis. This study, using nitrogen as a surrogate for solute removal, probed whether solute removal mass can be used as the target of adequate dialysis. Mathematical formulas for easy bedside calculation of nitrogen removal mass were used to avoid the problems associated with direct measurement. METHODS: The weekly removal mass of urea nitrogen (M) and the urea generation rate (G) of 32 conventional hemodialysis (HD) and 21 continuous ambulatory peritoneal dialysis (CAPD) patients were calculated. All the patients were anuric, clinically stable, and under adequate dialysis pursuant to either the criterion of the urea index, Kt/V, or clinical requirements. RESULTS: The difference in MHD (MHD = 41.9 +/- 9.5 g/week, MCAPD = 38.8 +/- 11.9 g/week) and G (GHD = 3.90 +/- 1.02 mg/min, GCAPD = 3.85 +/- 1.21 mg/min) between the two groups was statistically insignificant (p = 0.119 and p = 0.868, respectively). When protein nitrogen leaking through the peritoneal membrane was considered and added to MCAPD, nitrogen removal in CAPD patients (M'CAPD = 42.3 +/- 13.0 g/week) approached that in HD patients (p = 0.886). There was no correlation between dialysis dosage and urea removal mass in either the CAPD or HD groups. CONCLUSIONS: Urea nitrogen removal mass is similar to the protein catabolic rate (PCR) in stable patients. It is meaningful in dialysis evaluation only when it is used simultaneously with blood urea nitrogen measurement. However, because M changes at the inception of dialysis, it more significant than PCR in the evaluation of unstable patients.

Low molecular weight heparin in diabetic and nondiabetic hypercholesterolemic patients receiving long-term hemodialysis.

Dyslipidemia is a major factor associated with cardiovascular disease, which is the leading cause of death in hemodialysis patients. Low molecular weight heparin (LMWH) is superior to conventional unfractionated heparin in treating hyperlipidemia in nondiabetic long-term hemodialysis patients and has fewer side-effects. Only a few reports have addressed the influence of LMWH on serum lipids in diabetic patients, although dyslipidemia is common among this population. We investigated the effect of LMWH on serum lipids in 12 nondiabetic and eight diabetic hypercholesterolemic patients receiving long-term hemodialysis. Patients had been receiving hemodialysis with unfractionated heparin for a minimum of 6 months before beginning the study. Continuous LMWH infusion during hemodialysis was administered to all patients for 2 months, followed by unfractionated heparin administration for 2 months. During LMWH treatment, plasma anti-factor Xa activity increased from 0.06 +/- 0.04 IU/mL before dialysis to 0.49 +/- 0.25 IU/mL after 3 hours. Serum total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), and apolipoprotein B (Apo B) in both nondiabetic and diabetic patient groups and lipoprotein (a) (Lp(a)) in patients with higher initial values (> or = 15 mg/mL) decreased significantly after LMWH treatment (TC from 6.38 +/- 1.14 to 5.07 +/- 1.09 mmol/L, LDL-C from 3.08 +/- 0.93 to 2.15 +/- 0.88 mmol/L, Apo B from 100 +/- 18 to 78 +/- 18 mg/dL, all p < 0.01; Lp(a) from 41.8 +/- 34.5 to 28.5 +/- 22.8, p < 0.05). They rebounded to pre-LMWH levels after the 2 months on unfractionated heparin (TC 5.72 +/- 1.11 mmol/L, LDL-C 2.97 +/- 1.01 mmol/L, Apo B 98 +/- 20 mg/dL, Lp(a) 38.1 +/- 29.0 mg/dL). We conclude that continuous infusion of LMWH during dialysis reduces serum total cholesterol, low-density lipoprotein-cholesterol, and apolipoprotein B concentrations in both diabetic and nondiabetic hypercholesterolemic hemodialysis patients, and does not increase the risk of bleeding compared with unfractionated heparin.

Reduction of serum calcium by sodium sulfonated polystyrene resin.

Sodium resin has been clinically administered against hyperkalemia widely, but its effects of lowering the serum calcium has never been documented. In our study, 7 patients with chronic renal failure were chosen at random to take sodium resin 30 g per day for 3 days. The sodium resin not only lowered the serum potassium level (p less than 0.05) but also brought down the level of serum calcium (p less than 0.05). The reduced ability of patients with chronic renal failure to absorb calcium from the gastrointestinal tract is well recognized, so its effects of lowering calcium will be more likely to aggravate the serum calcium imbalance further. If sodium resin has to be used for the maintainance of serum potassium in patients with chronic renal failure the serum calcium should be monitored closely in order to lighten the osteodystrophy and secondary hyperparathyroidism.

Serial peritoneal macrophage function studies in CAPD patients with peritonitis.

Continuous ambulatory peritoneal dialysis, peritoneal macrophage, IL-1, IFN-r, TNF, phagocytosis. Peritoneal macrophages (PM) perform first-line defense activity against peritonitis, the most important complication in CAPD therapy. Our longitudinal study compared the PM function in 14 patients in a low peritonitis occurrence group (LPOG) and 6 in a high peritonitis occurrence group (HPOG) before and during peritonitis; all started CAPD therapy after January 1988. The results show that at the onset of peritonitis, PM function including bactericidal killing (BA) activity, phagocytosis index (PI), H2O2 release, interleukin-1 (IL-1) and tumor necrosis factor (TNF) secretion can increase rapidly in the LPOG. However, this was absent in the HPOG. Both groups had a decrease of PM immunological function in the initial 7 to 10 days after onset of peritonitis, then PM functions began to return toward their pre-peritonitis state. However, in the HPOG, the recovery of PM function was very slow, resulting in significantly lower PM functions. In vitro, when normal PM were put into peritonitis dialysate, IL-1, TNF production and PI, BA activity of PM were decreased. This suppressor activity was absent in the peritonitis-free dialysate. These results suggest a suppressor factor(s) in the HPOG peritoneal dialysate may decrease the function of PM rather than cause easy peritonitis development.

Persistent transforming growth factor beta 1 expression may predict peritoneal fibrosis in CAPD patients with frequent peritonitis occurrence.

The efficiency of continuous ambulatory peritoneal dialysis (CAPD) depends on the permeability of the peritoneal membrane. Peritoneal fibrosis (PF) causes the loss of dialytic function. Several studies have indicated that PF is closely related to the proliferation of peritoneal fibroblasts and the deposition of extracellular matrix (ECM). Transforming growth factor beta 1 (TGF beta 1) plays a major role in stimulating ECM deposition. Frequent peritonitis occurrence may cause persistent TGF beta 1 mRNA expression. In an attempt to search for a factor related to PF, we designed a longitudinal study to measure TGF beta 1 levels in dialysate and TGF beta 1 mRNA expression in peritoneal mononuclear cells (PMNCs) from peritoneal dialysate before, at the onset of and once a week during peritonitis and after peritonitis in patients with high peritonitis occurrence (HPO) and patients with low peritonitis occurrence (LPO). Fifteen patients with a LPO rate and 5 patients with a HPO rate were followed up longitudinally. Meanwhile, TGF beta 1 levels and TGF beta 1 mRNA expression were augmented in peritoneal dialytic fluid before, during, and after the episodes of peritonitis. Peritoneal permeability was evaluated by the peritoneal equilibration test (PET). The results revealed that in the LPO group, TGF beta 1 and TGF beta 1 mRNA were detectable at early stages of peritonitis, but the levels decreased rapidly and were undetectable 2 weeks after peritonitis. On the other hand, in the HPO group, TGF beta 1 and TGF beta 1 mRNA persisted for a long time. We could detect TGF beta 1 and TGF beta 1 mRNA in dialytic fluid and PMNCs even 2, 3, and 4 weeks after episodes of peritonitis. When compared with that of the first or second episode of peritonitis, peritoneal function evaluated with the PET was found to obviously deteriorate at the third episode of peritonitis. These findings were confirmed by an in situ hybridization technique to evaluate the relationship between TGF beta 1 mRNA expression and PF from biopsied peritoneal specimens. These findings suggest that the high TGF beta 1 levels in the dialysate are related to an increased expression of TGF beta 1 in the peritoneum. Persistent TGF beta 1 expression in the peritoneum may serve as a useful parameter in predicting PF in CAPD patients with frequent peritonitis occurrence.