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Seza Ozen

Publications and source records attributed to Seza Ozen.

At least 37 records · Page 2Linked to original sources
PubMed2004

Monocyte chemoattractant protein-1 and interleukin-8 levels in children with acute poststreptococcal glomerulonephritis.

The infiltration of leukocytes into the glomeruli is a major factor in inflammatory glomerular damage in acute poststreptococcal glomerulonephritis (APSGN). Chemokines participate in leukocyte infiltration. The aim of the present study was to investigate the role of monocyte chemoattractant protein-1 (CCL2/MCP-1) and interleukin-8 (CXL8/IL-8) in APSGN with special emphasis on their role in the clinical course of renal disease. Twenty-one children with APSGN were studied. Serum and urinary CCL2/MCP-1 and CXL8/IL-8 levels were measured by ELISA. The relationships between urinary chemokines and the degree of proteinuria were investigated. Serum and urinary CCL2/MCP-1 levels were significantly higher in the acute phase than in the resolution phase and in controls ( P<0.05). Urinary CCL2/MCP-1 levels in the control group were significantly lower than in both the acute and resolution phases ( P=0.01 and P =0.001, respectively). In the acute phase, urinary CCL2/MCP-1 correlated with the extent of proteinuria ( r=0.58, P =0.006) but not with serum CCL2/MCP-1 levels ( r=0.21, P =0.36). Urinary and serum CXL8/IL-8 levels were significantly elevated in the acute phase compared with the resolution phase and controls ( P<0.05). A consistent increase in urinary CCL2/MCP-1 was found in the acute phase of patients with APSGN, and this correlates with the degree of proteinuria. Our results emphasize the important role of locally produced chemokines in immune-mediated glomerular injury.

Acute Disease↗
PubMed2004

Effects of pentoxifylline in adriamycin-induced renal disease in rats.

Tumor necrosis factor-alpha (TNF-alpha) is a mediator of inflammation in human and animal renal disease. Pentoxiphylline (PTX) is an inhibitor of TNF-alpha. In this study we examined the effects of PTX on TNF-alpha, proteinuria, nitrite production, and apoptosis in an experimental model of Adriamycin (ADR) nephropathy in rats. Rats were divided into four groups: untreated Wistar rats (controls), PTX treatment alone, ADR treatment alone to induce nephropathy, and ADR treatment followed by PTX. ADR treatment followed by PTX treatment prevented the increase in serum TNF-alpha levels and proteinuria in rats with ADR-nephropathy ( P<0.05). Urine nitrite levels were significantly increased in the ADR-induced nephropathy group and the increase was prevented in the ADR-induced nephropathy group when they also received PTX. The urine nitrite levels were not different between the PTX-treated group and the untreated control rats. PTX prevented the rise of serum TNF-alpha in ADR nephropathy rats and a decrease in proteinuria, urine nitrite, and apoptosis in the renal tissue. These findings suggest a beneficial anti-inflammatory effect of PTX.

Animals↗
PubMed2004

Juvenile polyarteritis: results of a multicenter survey of 110 children.

OBJECTIVE: To characterize pediatric patients who had been diagnosed with polyarteritis nodosa (PAN) through necrotizing vasculitis of the small and mid-size arteries or those with characteristic findings on angiograms data were collected. STUDY DESIGN: Pediatricians were asked to classify their patients into one of the four suggested groups for juvenile PAN. Twenty-one pediatric centers worldwide participated with 110 patients. RESULTS: The girl:boy ratio was 56:54, with a mean age of 9.05 +/- 3.57 years. The cases were classified as: 33 (30%) cutaneous PAN; 5 (4.6%) classic PAN associated with hepatitis B surface antigen (HBs Ag); 9 (8.1%) microscopic polyarteritis of adults associated with antineutrophil cytoplasmic antibodies (ANCA); and 63 (57.2%) systemic PAN. Cutaneous PAN was disease confined to the skin and musculoskeletal system. All patients with HBs Ag-associated classic PAN were diagnosed with renal angiograms. Antiviral treatment was administered in most cases. Microscopic PAN patients had pulmonary-renal disease, in combination or separately. ANCA was present in 87%, and 2 patients progressed to end-stage renal failure. Patients classified with systemic PAN had multiple system involvement, almost all had constitutional symptoms, and all had elevated acute phase reactants. Corticosteroids and cyclophosphamide were the first choices of immunosuppressive treatment. The overall mortality was 1.1%. CONCLUSIONS: There were remarkable differences among pediatric patients with PAN, with different clinical manifestations and overall better survival and lower relapse rates when compared with adults.

Adolescent↗
PubMed2004

Beneficial role of intravenous calcitriol on bone mineral density in children with severe secondary hyperparathyroidism.

OBJECTIVES: In this prospective study, the effect of calcitriol therapy on bone mineral density and osteopenia in patients with severe secondary hyperparathyroidism has been investigated. MATERIALS AND METHODS: The study was carried out on 24 chronic dialysis patients consisting of 13 boys and 11 girls, aged between 8-18 years. Patients were divided into 3 groups according to the severity of hyperparathyroidism and therapy regimens. Group I consisted of 5 patients with normal parathormon levels who did not receive calcitriol therapy. In group II and III, there were patients with secondary hyperparathyroidism. Group II consisted of 10 patients receiving oral calcitriol therapy. Group III consisted of 9 patients receiving intravenous (i.v.) calcitriol. Bone mineral density was measured by dual energy x-ray absorptiometry. Osteopenia was defined as a Z-score worse than -2. Bone mineral density was assessed as baseline and at the end of one year. RESULTS: A significant improvement was observed in Z-score in the group III whereas the mean value of Z-score tended to be worse in group I and it was not significantly different in group II from the initial values. The better Z-score in group III was associated with more effective stabilization of alkaline phosphatase level and bone specific alkaline phosphatases (BAP) concentrations. CONCLUSION: Significant improvement of Z-score in group III suggested the beneficial role in i.v. administration of calcitriol in chronic dialysis patients.

Administration, Oral↗
PubMed2004

Noonan syndrome and systemic lupus erythematosus: presentation in childhood.

Noonan syndrome is a relatively common disorder which is usually diagnosed in childhood because of the presence of distinctive facial features, short stature and cardiac anomalies. Previous clinical studies of Noonan syndrome have suggested that autoimmune disorders may be another possible manifestation and there have been two recent reports of Noonan syndrome patients with systemic lupus erythematosus. In this report we present an 11-year-old boy with Noonan syndrome and systemic lupus erythematosus, supporting the previous observations of an association between these two conditions.

Autoimmune Diseases↗
PubMed2004

Influence of Serum Amyloid A (SAA1) and SAA2 gene polymorphisms on renal amyloidosis, and on SAA/C-reactive protein values in patients with familial mediterranean fever in the Turkish population.

OBJECTIVE: To evaluate the effect of serum amyloid A (SAA) 1 and SAA2 gene polymorphisms on SAA levels and renal amyloidosis in Turkish patients with familial Mediterranean fever (FMF). METHODS: SAA1 and SAA2 gene polymorphisms and SAA levels were determined in 74 patients with FMF (39 female, 35 male; median age 11.5 yrs, range 1.0-23.0). All patients were on colchicine therapy. SAA1 and SAA2 gene polymorphisms were analyzed using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). SAA and C-reactive protein (CRP) values were measured and SAA/CRP values were calculated. RESULTS: The median SAA level was 75 ng/ml (range 10.2-1500). SAA1 gene polymorphisms were: a/a genotype in 23 patients (31.1%), a/beta genotype in 30 patients (40.5%), a/g genotype in one patient (1.4 %), beta/beta genotype in 14 patients (18.9%), beta/g genotype in 5 patients (6.8 %), and g/g genotype in one patient (1.4%). Of the 23 patients who had a/a genotype for the SAA1 polymorphism, 7 patients had developed renal amyloidosis (30.4%) compared to only one patient without this genotype (1/51; 2.0%); p < 0.001. SAA2 had no effect on renal amyloidosis. SAA1 and SAA2 genotypes had no significant effect on SAA levels. SAA/CRP values were significantly lower in patients with the SAA1a/a genotype, compared to other SAA1 genotypes: 0.16 (0.025-1.96) versus 0.23 (0.012-28.20), p < 0.05. CONCLUSION: SAA1a/a genotype is one genetic factor that confers a significant risk for amyloidosis in the Turkish FMF population. Neither the SAA1 nor SAA2 genotypes had a significant effect on SAA level.

Adolescent↗
PubMed2003

Low serum apolipoprotein AI levels in amyloidosis related to familial Mediterranean fever.

Amyloidosis (A) related to familial Mediterranean fever (FMF) causes serious morbidity and mortality in children. Our study evaluates serum levels of apolipoprotein (Apo) AI, AII, B, and E and Apo AII/AI ratios as a non-invasive diagnostic tool for amyloidosis in children with FMF and FMF-A. Results were compared with those of patients with childhood nephrotic syndrome (NS) and healthy children (controls). Significantly lower serum levels of Apo AI (90.20+/-28.30 mg/dl) were documented in patients with FMF-A than in all other groups (FMF 126.89+/-51.07 mg/dl, NS 140.38+/-33.73 mg/dl, and controls 134.67+/-12.73 mg/dl) ( P<0.01). Diagnostic sensitivity, specificity, and predictive value for this test were 85%, 80%, and 85%, respectively. Apo AII/AI ratio results were essentially equal in all groups ( P>0.05). It is concluded that a decreased Apo AI serum level, but not Apo AII/AI ratio, is a useful, non-invasive test for the early diagnosis of FMF-A in children.

Adolescent↗
PubMed2003

Familial Mediterranean fever and glomerulonephritis and review of the literature.

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent and self-limited attacks of fever usually accompanied by polyserositis. Amyloidosis is its most common renal complication. A number of reports have shown vasculitic diseases such as polyarteritis nodosa and Henoch-Schönlein purpura affecting the kidney in FMF. Here we present a patient with FMF and membranoproliferative glomerulonephritis and analyze the data published on these two entities.

Adult↗
PubMed2003

Familial mediterranean fever: revisiting an ancient disease.

UNLABELLED: Familial Mediterranean fever (FMF) is an auto-inflammatory disease characterised by periodic attacks of fever and serositis. Recent genetic and epidemiological research have highlighted the importance of this disease. FMF is the most frequent periodic fever syndrome and is transmitted in an autosomal recessive fashion. The disease is caused by mutations in the gene on the short arm of chromosome 16, coding for the protein "pyrin". Pyrin is mainly expressed in neutrophils and monocytes and is among the proteins involved in the interleukin-1 inflammatory pathway. The recurrent attacks of fever are accompanied by severe abdominal pain, arthritis and/or chest pain along with a marked increase in acute phase reactants. Among these, serum amyloid A protein is especially important since it is the precursor of the amyloid A fibrils deposited in secondary renal amyloidosis. Renal amyloidosis has a grave prognosis. Differential diagnosis from other periodic fever syndromes is especially important in western European countries. Among these hyper IgD syndrome is common in Netherlands and the tumour necrosis factor receptor-associated periodic syndrome is especially common among Scottish and Irish families. Mutation analysis of the gene may be helpful in diagnosing FMF; however, if this is not possible, a trial of colchicine is a helpful diagnostic tool. The indications for life-long colchicine treatment should be discussed with the family. CONCLUSION: Familial mediterranean fever and other auto-inflammatory syndromes should be suspected in children with recurrent febrile attacks. Early diagnosis will save the child from unnecessary work-up and kidney involvement.

Colchicine↗
PubMed2003

Successful renal transplantation in a child with ANCA-associated microscopic polyangiitis.

Crescentic glomerulonephritis (CGN) is a clinicopathologic entity which is characterized by severe renal dysfunction of rapid onset with glomerular crescents. Type III CGN is associated with the absence of glomerular immune complex deposition (pauci-immune) and is associated with antineutrophil cytoplasmic antibody (ANCA). Microscopic polyangiitis and idiopathic pauci-immune necrotizing glomerulonephritis (NCGN) are strongly associated with ANCA directed against myeloperoxidase (anti-MPO). We describe here an unusual pediatric patient with MPO-ANCA-associated rapidly progressive glomerulonephritis (RPGN), emphasizing the management and outcome of the disease.

Anti-Glomerular Basement Membrane Disease↗
PubMed2003

Urinary glycosaminoglycans in the course of familial Mediterranean fever.

UNLABELLED: Familial Mediterranean fever (FMF) is characterised by recurrent fever and serositis. The most important complication of the disease is amyloidosis. Cheap and non-invasive methods would be important in predicting or establishing the early diagnosis of amyloidosis. For this purpose, we studied the role of urinary glycosaminoglycans (GAG). The study group included 123 FMF patients without an attack and 11 patients with FMF associated amyloidosis. Ten healthy children and ten patients with primary nephrotic syndrome served as controls. In patients with amyloidosis, urinary GAG were lower than in patients with FMF, patients with nephrotic syndrome and controls (median and range: 8.54 mg hexuronic acid/g creatinine (1.87-25.5), 5.8 (1.7-17.26), 23.12 (8.74-28.06) and 19.25 (14.2-26.9) respectively, P<0.01). There was a significant negative correlation between the duration of the disease and urinary GAG ( r= -043, P=0.002). In 49 FMF patients with a low GAG, urinary GAG increased significantly after an increase in the colchicine dose (median and range: 6.64 mg hexuronic acid/g creatinine (1.77-19.39) and 9.45 mg hexuronic acid/g creatinine (2.36-28.9), P<0.01). CONCLUSION: These results suggest that urinary glycosaminoglycan levels may be a predictor of amyloidosis in patients with familial Mediterranean fever. We also suggest that effective colchicine doses may be monitored by following urinary glycosaminoglycan excretion.

Adolescent↗
PubMed2003

Th1 polarization in familial Mediterranean fever.

OBJECTIVE: Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by fever and serosal inflammation accompanied with an outburst of acute phase inflammatory products and cytokines. We studied the role of T helper (Th) 1 and 2 cells in FMF to elucidate the character of the inflammation. The cytokine products of Th1 and Th2, interferon-g (IFN-g) and interleukin 4 (IL-4), respectively, were analyzed by intracellular cytokine staining and FACS analysis. METHODS: We studied 34 Turkish patients with FMF (18 asymptomatic, 8 during an attack, and 8 with amyloidosis) and 14 age matched controls, as well as 11 parents of the patients who were accepted as heterozygotes for MEFV (Familial Mediterranean gene) mutations. Peripheral blood mononuclear cells were isolated and stained with monoclonal antibodies for IFN-g and IL-4. The percentage of IL-4 positive T cells was not significantly different between the groups. However, the percentage of IFN-g positive T cells in FMF patients experiencing an attack (median 25.8%, range 8.9-50.5%) was significantly higher than asymptomatic FMF patients (median 12%, range 0.1-70.7) (p = 0.04) and age matched controls (n = 7, median 0.4%, range 0-3.9%) (p = 0.0001). The percentage of IFN-g positive T cells in asymptomatic FMF patients was also significantly higher than age matched controls (p = 0.008). Heterozygotes for FMF had significantly higher IFN-g production (median 2.6%, range 0-42.4%) compared to age matched controls (n = 7, median 0.2%, range 0-1.4) (p = 0.001). IFN-g production in FMF patients with secondary amyloidosis was also markedly increased but had a large range of variation. CONCLUSION: Inflammation in FMF shows a Th1 polarization. We suggest that in patients with FMF the IFN-g concentrations may remain higher because the defective pyrin is not able to inhibit this Th1 mediated inflammation.

Adult↗
PubMed2003

Mutations in the gene for familial Mediterranean fever: do they predispose to inflammation?

OBJECTIVE: To analyze 70 individuals who were found to have the Mediterranean fever (MEFV) gene for the presence of definite familial Mediterranean fever (FMF) and to assess if they were prone to clinical and laboratory inflammation. We also prospectively evaluated 72 patients with childhood rheumatic diseases for the presence of MEFV mutations. METHODS: Seventy patients with one MEFV gene mutation were reevaluated for the presence of a clinical FMF phenotype using a new set of criteria. They were also questioned for the presence of musculoskeletal symptoms and rheumatic diseases. They were sampled for erythrocyte sedimentation rates and C-reactive protein levels. A second group with childhood rheumatic diseases were diagnosed according to international criteria. RESULTS: Median age of the 70 heterozygous individuals was 12 years. About 1/3 (34.3%) were classified with clinical FMF phenotype according to the suggested criteria. Fifteen (21.4%) were classified as normal and 3 (4.3%) had recurrent abdominal pains but did not fulfill all criteria for clinical FMF. Overall, 28 (40.0%) had some form of rheumatic complaint and 15 (21.4%) had developed a rheumatic disease including Behçet's disease, a vasculitis, or acute rheumatic fever. The mean ESR and CRP levels were 45.47 +/- 33.05 mm/h and 4.00 +/- 6.73 mg/dl, respectively. Among the 72 patients with rheumatic diseases of childhood, 22 (30.5%) carried one or 2 mutations of the MEFV gene. The mutated allele frequency among patients with rheumatic diseases was significantly higher than those in controls (p < 0.05). Within this group, among the 59 patients with juvenile idiopathic arthritis 15 had mutations in the heterozygous or homozygous form. CONCLUSION: We confirm the acute phase response in the carriers for MEFV mutations. We suggest that these patients may have a tendency to develop certain manifestations due to an increased baseline of inflammation, and the presence of these mutations may affect their disease course when they develop rheumatic disease.

Adolescent↗