Comparing the efficacy of nebulizer recombinant human DNase and hypertonic saline as monotherapy and combined treatment in the treatment of persistent atelectasis in mechanically ventilated newborns

Background: The purpose of the present study was to compare the cost‐effectiveness and efficacy of nebulizer recombinant human DNase (rhDNase) and hypertonic saline (HS) as monotherapy and combined treatment in neonatal atelectasis. Methods: Eighty‐seven newborns with persistent atelectasis who did not respond to traditional treatment were studied retrospectively. Group 1 did not receive nebulizer drugs; Group 2 received 7%HS; Group 3 received rhDNase; and Group 4 received both 7%HS and rhDNase. Subjects' chest X‐ray scores, partial pressure of CO₂, respiratory rate, fraction of inspired oxygen (FiO₂) peak inspiratory pressure, atelectasis healing rate, median duration of nebulizer treatment and costs were compared. Results: Percentages of improvement in atelectasis on Day 3 of treatment in Group 1, Group 2, Group 3 and Group 4 were 27, 70, 81 and 95%, respectively, while median duration of treatment was 8.1, 3.3, 2.9 and 2.4 days, respectively. Comparison of chest X‐ray scores, partial pressure of CO₂, respiratory rate, FiO₂ and peak inspiratory pressure values before and 48 h after treatment did not yield a significant difference for the control group (P > 0.05), while a marked improvement was observed in other groups for all parameters (P < 0.05). The most distinct improvement was in Group 4, followed by Group 3. Conclusions: Although both the combined treatment with HS and rhDNase and their monotherapies are effective in the treatment of persistent atelectasis in newborns receiving mechanical ventilation, their combined use produces higher efficacy. The efficacy of rhDNase is superior to monotherapy with HS. Use of these two treatments concomitantly reduces the cost. To the best of our knowledge, the present study is the first to use HS alone or in combination with rhDNase in newborn patients.     

Fucoidin, a neutrophil rolling inhibitor, reduces damage in a rat electrical burn injury model

Background

Electrical injuries induce progressive tissue loss caused by free oxygen radicals released from neutrophil aggregates. Fucoidin, a potent inhibitor of L-selectin function, reduces the aggregation of neutrophils. The aim of this study was to evaluate the effect of fucoidin on tissue damage in rat electrical burn injury model.

Methods

Forty-two male Wistar albino rats (250–300 g) were divided into 3 groups (Group A (n = 6), control group without electrical burn injury; Groups B (n = 18) and C (n = 18), electrical burn injury groups without and with fucoidin therapy, respectively). Three separate analyses were performed at different time points on 6 out of 18 mice from Group B and C at each time point. Biochemistry (myeloperoxidase and malondialdehyde levels) and histopathology (number of neutrophils) of the skin and muscle biopsies at 1st hour; tissue edema (ratio of wet weight/dry weight of extremities) at 24th hour; and necrotic areas at 7th day after electrical injury were evaluated. The electrical burn was induced by exposing rats to 220 V AC between their left upper extremity and right lower extremity for 10 s. Fucoidin was administered as 25 mg/kg intravenous bolus injection at 15 min after electrical burn injury.

Results

Myeloperoxidase and malondialdehyde levels, number of neutrophils, tissue edema, and necrotic area were significantly less in fucoidin-applied rats than the group without fucoidin therapy.

Conclusions

Fucoidin inhibits tissue damage induced by electrical burn injury in rats by reducing necrotic area, edema and number of neutrophils.     

The effect of dialytic modalities on clinical outcomes in ESRD patients with familial Mediterranean fever

BACKGROUND: Familial Mediterranean fever (FMF) is an autosomal recessive disease seen primarily in Sephardic Jews, Turks, and Armenians. The disease manifests as recurrent attacks of fever and serositis. The most important complication of FMF is the development of renal failure due to AA type amyloidosis. There has not been extensive experience with renal replacement therapy in FMF amyloidosis. Nevertheless, there may be a concern about the possibility of higher rates of morbidity and mortality in amyloidotic patients maintained on chronic hemodialysis. Moreover, there is not enough experience regarding patients on chronic peritoneal dialysis. As a result, the best treatment modality of end-stage renal disease (ESRD) in these circumstances still remains unclear. This study aimed to compare the effect of hemodialysis and peritoneal dialysis modalities on clinical outcomes in ESRD patients associated with FMF amyloidosis. METHODS: Forty FMF patients with ESRD due to amyloidosis were retrospectively analyzed. All 40 patients were on renal replacement therapy, 20 on hemodialysis (HD), 20 on peritoneal dialysis (PD). Peritoneal solute transport rates, weekly mean creatinine clearance, and daily mean ultrafiltration (UF) of the patients on chronic peritoneal dialysis were evaluated. Weekly dialysis durations, dialysis membrane properties, Kt/V values, interdialytic weight gains, and frequency of hypotension during dialysis were evaluated on hemodialysis patients. All of the patients were examined according to their demographic characteristics, laboratory results, duration time on dialysis, erythropoietin requirements, frequencies of infectious complications requiring hospitalization, and the two renal replacement modalities mentioned above were compared in terms of these parameters. RESULTS: Serum albumin levels of the patients with FMF amyloidosis who were maintained on peritoneal dialysis treatment were lower (2.87 vs 3.45) and the frequency of infections of the same group was higher (4.2 vs 0.5) than the patients with ESRD secondary to other diseases in the CAPD group. CONCLUSIONS: This retrospective analysis showed that peritoneal dialysis may have some disadvantages in amyloidotic patients. Due to the high frequency of hypoalbuminemia and infectious complications seen in this group, peritoneal dialysis is widely accepted as an alternative choice of treatment when hemodialysis is not appropriate.     

Reno-vascular hypertension in childhood: a nationwide survey

Renovascular disease accounts for 8–10% of all cases of paediatric hypertension, whereas, in adults, its incidence is approximately 1%. The Turkish Paediatric Hypertension Group aimed to create the first registry database for childhood renovascular hypertension in Turkey. Twenty of the 28 paediatric nephrology centres in Turkey responded to the survey and reported 45 patients (27 girls, 18 boys) with renovascular hypertension between 1990 and 2005. The age at presentation ranged from 20 days to 17 years. The mean blood pressure at the diagnosis was 169/110 mmHg. Chief complaints of symptomatic patients were headache (38%), seizure (18%), epistaxis (4%), growth retardation (4%), cognitive dysfunction (4%), polyuria (2%), palpitation (2%), and hemiplegia (2%). Renovascular hypertension was found incidentally in 11 children. The diagnosis of renovascular hypertension was established with conventional angiography in 39 patients, MR angiography in three, CT angiography in two, and captopril diethylene triamine penta-acetic acid (DTPA) scintigraphy in one patient. Twenty-one children had bilateral renal artery stenosis and 24 had unilateral renal artery stenosis. Of these, 14 (31%) had fibromuscular dysplasia; 12 (27%) Takayasu’s arteritis; six (13%) neurofibromatosis; two (5%) Williams syndrome; one (2%) Kawasaki disease; one (2%) mid-aortic syndrome; one (2%) extrinsic compression to the renal artery, and eight (18%) unspecified bilateral renal artery stenosis. Hypertension was controlled with antihypertensive drugs in 17 patients. Percutaneous transluminal angioplasty (PTRA) or surgery had to be performed in 28 patients: PTRA in 16 patients, PTRA + surgery in one patient and surgery in 11 patients (four nephrectomies). The importance of vasculitic disease, especially Takayasu’s arteritis, should not be underestimated in children with renovascular hypertension.     

NPHS2 (podicin) mutations in Turkish children with idiopathic nephrotic syndrome

The podocin (NPHS2) gene encodes podocin protein, which has an important role in glomerular ultrafiltration and controlling slit membrane permeability. The detection of an NPHS2 mutation affects the treatment plan for children with nephritic syndrome (NS). The frequency and spectrum of podocin mutations in the Turkish population have remained largely unknown. The aim of this study was to screen for podocin mutations in Turkish patients with steroid-resistant NS (SRNS) and to compare it with other published series. There were 295 children with SRNS, originating from Turkey, included in this study. Forty-one patients (13.8%) had familial NS and 254 patients (86.2%) had sporadic NS. Mutation analysis was performed in all eight exons of the NPHS2 gene with the direct DNA sequencing method. There were 53 different pathogenetic NPHS2 mutations detected, including 37 novel mutations. The mutation detection rate was 24.7% for all patients, 29.2% for familial, and 24% for sporadic SRNS. The most common mutated exon was exon 5 (52 allele). The presence of mutations in exon 4 was found to increase the risk of end-stage renal disease (ESRD). Among patients with mutations, the rates of renal failure and/or ESRD (26%) were significantly higher than in those without mutations (12.6%). The mean time of progression to renal failure and ESRD in patients with mutations (1.8 ± 2.5 years) was significantly shorter than in patients without mutations (3.7 ± 4.0 years). Additionally, in patients with heterozygote mutations, fewer cases (13.6%) progressed to renal failure and/or ESRD than in with patients who had homozygote/compound heterozygote mutations (31.3%). In conclusion, podocin mutations are responsible for some of both familial and sporadic SRNS cases in Turkey. The mutations in this gene should be searched for in every child after presentation with the first episode of NS.     

Increased plasma homocysteine and allantoin levels in coronary artery disease: possible link between homocysteine and uric acid oxidation

OBJECTIVE: Homocysteine increases the damage to the cardiovascular system in different ways, one of them is the formation of reactive oxygen species resulting from the auto-oxidation of homocysteine.At the same time, uric acid is one of the major antioxidants in the plasma and protects the cells towards increased ROS activity. In humans, allantoin is only formed from non-enzymatic oxidation of uric acid by free radicals. We aimed to determine the levels of homocysteine, uric acid and allontoin in patients with coronary artery diseases, and to evaluate the possible correlation between homocysteine and allantoin. METHODS AND RESULTS: Plasma total homocysteine, uric acid and allantoin levels of 50 patients with coronary artery diseases and 23 healthy controls were determined by HPLC methods. Commercial diagnostic kits were used for the determination of other biochemical parameters.We obtained higher homocysteine, uric acid and allantoin levels in patients than in controls (p < 0.0001). Homocysteine levels were positively correlated with uric acid (r = 0.435, p < 0.0001) and allantoin (r = 0.583, p < 0.0001) levels in the whole study population.This correlation was persistent between allantoin and homocysteine after adjustment of these parameters for age, sex and creatinine. We accepted 15.0 micromol/l as a cut-off value between normal and mildly elevated homocysteine levels for patients and controls. Twenty-five patients showed moderate hyperhomocysteinaemia. The mean allantoin and uric acid values of the moderate hyperhomocysteinaemic group were significantly higher than that of the group having lower homocysteine levels than this cut-off value (p < 0.0001 for allantoin, p < 0.02 for uric acid). CONCLUSION: Results imply that there is increased allantoin production resulting from uric acid oxidation by free radicals in hyperhomocysteinaemic patients with coronary artery disease. The possible significance of the relationship between homocysteine and allantoin warrants further study.     

The importance of cytokines, chemokines and nitric oxide in pathophysiology of migraine

The certain etiology migraine is unknown. The study was aimed at determining to the efficiency of cytokines, chemokines and nitric oxide (NO) to the pathophysiology of migraine. The levels of cytokines, chemokines and NO in serum of 25 patients with migraine during attacks and attack-free periods and 25 healthy controls were investigated. The levels of cytokines and chemokines were determined by enzyme-linked immunosorbent assay. NO concentrations were determined by a nitrate/nitrite colorimetric assay kit. In attack groups, IL-10 levels were found higher than in attack-free groups and healthy controls (p<0.05). IL-6 levels in migraine patients were significantly higher than in healthy controls. The levels of RANTES were high in attacks groups. There was an increase NO concentrations in migraine attacks. The study's results reflect that the etiology of migraine is multifactorial and probably related to immunological changes.