Biomedical subjects
Publications and source records attributed to R Cetinkaya.
Sarcoidosis is a multisystemic granulomatous disease. In the case presented, autoamputation of the distal phalanx of a little finger of the left hand was observed. The possibility of autodigital amputation as a result of sarcoidosis is discussed.
OBJECTIVE: The aim of this study was to determine the prevalence of oral lesions in 13- to 16-year-old students. METHODS: A cross-sectional survey was carried out on students in Duzce, a province in the western Black Sea region of Turkey. A total of 993 children aged between 13 and 16 from eight secondary schools were examined. Oral lesions with recurrent behavior, if observed, were recorded at the time of examination. Venous blood samples were obtained for detecting hemoglobin levels. RESULTS: Two hundred sixty adolescents (26.2%) were diagnosed with at least one oral mucosal lesion at the time of the examination. Thirteen different mucosal alterations were diagnosed, and the most common lesions were angular cheilitis (9%), linea alba (5.3%), and aphthous ulceration (3.6%). The correlation between occurrence of mucosal lesions and sex was not statistically significant (P > 0.05). Statistical evaluation of the data revealed a significant relationship only between the presence of angular cheilitis and anemia (P < 0.05). CONCLUSION: This study is the first epidemiologic study of oral mucosal lesions in adolescents in Turkey. Angular cheilitis was the only oral mucosal lesion that had a significant correlation with anemia.
The benefits of angiotensin-converting enzyme inhibitors and angiotensin II (ATII) receptor antagonist therapy of diabetic nephropathy (DNP) are thought to be largely the result of attenuation of ATII effects on proteinuria. The aim of the study was to ascertain whether there is the additive anti-proteinuric effect of enalapril plus losartan in DNP. Twenty-two patients with DNP were studied. Patients were randomly assigned to enalapril 10 mg/day (11 patients) or losartan 50 mg/day (11 patients) administered in a single oral dose in the morning for 12 weeks. and then, in 10 patients (five patients from enalapril group and five patients from losartan group), combination therapy (10 mg/day enalapril and 50 mg/day losartan) was started and continued for 12 weeks. In 12 patients, initial drugs dosages were doubled (six patients 20 mg/day enalapril and six patients 100 mg/day losartan), and monotherapy was continued for 12 weeks. Blood pressure and proteinuria were measured before and after therapy. Adverse effects were recorded at every visit. Proteinuria decreased by 33% with enalapril and losartan administered alone (p < 0.05). Co-administration of enalapril and losartan decreased proteinuria by a greater extent compared with enalapril and losartan administered alone (51%, p<0.05). This proteinuria level was significantly lower than the proteinuria level of 12 weeks therapy with enalapril and losartan alone. The decrease of proteinuria was 37% in double-dose monotherapy group (p < 0.05). Reduction of mean arterial blood pressure (MAP) in co-administration of enalapril and losartan was higher than enalapril and losartan administered alone (p < 0.05). Combination of enalapril and losartan decreased proteinuria and MAP by a greater extent compared with enalapril and losartan administered alone. We have found that proteinuria reduction induced by combined therapy is maintained throughout short-term follow-up; a greater anti-proteinuric response was observed in the patients with DNP.
AIM: In some of the patients undergoing haemodialysis, (HD) resistance might develop against recombinant human erythropoietin (rHuEPO) used for treatment of anaemia. Recently, angiotensin-converting enzyme (ACE) inhibitors that are used to treat hypertension and congestive heart failure in HD patients have been suggested to contribute to anaemia as well by inhibiting erythropoiesis. Our purpose in this study is to investigate whether or not losartan, an angiotensin II (ATII) receptor antagonist, is causing rHuEPO resistance. METHODS: In this prospective study of 12 months, we compared the effects of high dose losartan (100 mg/day) and amlodipine (10 mg/day) on rHuEPO requirement in 40 hypertensive patients receiving rHuEPO for more than 12 months on maintenance HD. Twenty normotensive rHuEPO dependent patients served as control group. Iron deficiency, hyperparathyroidism, aluminium intoxication, infections and inflammations were excluded in all patients. RESULTS: The mean haemoglobin level was found >8 g/dl in all groups. The mean weekly rHuEPO dose increased in the losartan group (p<0.0001 vs before) and remained constant in the other groups. No significant differences were found with PTH, iron status, aetiologies of renal failure in all groups. CONCLUSION: High-dose losartan increases rHuEPO requirement and should be reserved for dialysis patients with hypertension uncontrollable with other antihypertensive medications.
There is no routine test to evaluate the activity of Behçet's disease (BD). Ferritin as a serum predictor of iron storage is an important acute phase reactant. In this study, we assessed serum ferritin levels in patients with active BD and compared them with those of patients with inactive BD. We aimed to show the relationship between ferritin and BD. The patients with BD were subdivided into two groups according to disease activity: active (24 patients; 18 men and 6 women, average age 36.5 +/- 4.9 [28-45] years), and inactive (20 patients; 16 men and 4 women, average age 37.2 +/- 5.2 [30-49] years). Twenty healthy volunteers (15 men and 5 women; average age 38.2 +/- 4.6 [30-47] years) served as controls. Patients with active BD had significantly higher serum ferritin levels (p=0.0001) than the inactive and control groups. Ferritin levels in patients with inactive BD did not differ significantly from healthy control subjects (p=0.687). We concluded that in patients with active BD, serum ferritin levels are increased and do not reflect serum iron levels.
AA amyloidosis is a relatively rare disease which complicates chronic inflammatory diseases, chronic infections, familial Mediterranean fever (FMF) and malignant diseases. Although amyloid deposition may be found in many organs, renal involvement dominates the clinical picture. We reviewed 63 patients with AA amyloidosis who presented to our nephrology department between 1995 and 2000. Prognostic markers, detailed history, physical examination and laboratory tests were evaluated. The causes of AA amyloidosis were as follows: FMF 42 (66.6%), pulmonary tuberculosis 9 (14.2%), chronic osteomyelitis 4 (6.3%), bronchiectasia 4 (6.3%), rheumatoid arthritis 1 (1.5%), juvenile idiopathic arthritis 1 (1.5%), inflammatory abdominal aortic aneurysm 1 (1.5 %), unknown aetiology 1 (1.5%). The diagnosis was made on renal biopsies in 63.4% of the patients, while the remaining 36.6% were diagnosed as a result of rectal biopsies. Sixteen patients died. A low serum albumin, high creatinine and high 24-hour urine albumin excretion were associated with high mortality.
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Alkaptonuria is a rare, autosomally recessive, metabolic disorder caused by a deficiency in homogentisic acid oxidase. It results in accumulation and deposition of homogentisic acid in cartilage, eyelids, forehead, cheeks, axillae, genital regions, nail beds, buccal mucosa, larynx, tympanic eardrum, and the tendons. We report a 33-year-old woman who presented with alkaptonuria and ochronotic pigment deposited in articular cartilage and cartilage of the ear and sclera.
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Secondary amyloidosis (AA amyloidosis) is a well known cause of nephrotic syndrome and renal failure. Several studies in patients with nephrotic syndrome have suggested a beneficial effect of angiotensin-converting enzyme inhibitors (ACEI). Angiotensin II (ATII) receptor antagonists effect on the long term is not known. In this study, we intended to study the effect of losartan, as an ATII receptor antagonist, on proteinuria and renal functions in patients with normotensive secondary amyloidosis. In total 44 patients with biopsy proven AA amyloidosis associated with nephrotic proteinuria were included. The first group of patients (n=22) was treated with losartan 50 mg/day. The second group of patients (n=22) did not receive any specific antiproteinuric treatment. Urinary protein loss was effectively lowered by losartan from 4.38 +/- 1.0 to 2.8 +/- 0.61 g/day (p<0.0001), whereas the control group showed a slight fall in proteinuria as 4.21 +/- 1.06 to 4.12 +/- 1.07 g/day (p = 0.176). Hypoalbuminemia improved significantly from 2.52 +/- 0.69 to 2.78 +/- 0.46 g/dl (p = 0.004), in the losartan group, whereas serum albumin had fallen in the control group from 2.44 +/- 0.57 to 2.27 +/- 0.41 (p = 0.041). Serum creatinine increased in the control group from 1.52 +/- 0.42 to 2.39 +/- 0.51 mg/dl (p<0.0001), and in the losartan group from 1.59 +/- 0.50 to 1.84 +/- 0.6 mg/dl (p<0.001), after 24 months of treatment. The ATII receptor blocker losartan is effective in protecting against the progression of nephropathy due to AA amyloidosis. Symptomatic treatment of proteinuria with losartan is therefore to be considered, especially with severe proteinuria even in normotensive patients.
Familial Mediterranean fever (FMF) is characterized by recurrent attacks of fever and serositis. Typical attacks of FMF last 3 to 5 days. Fever and myalgia are not always improved by colchicine therapy and sometimes require steroid therapy. We present two cases of severe prolonged febrile myalgia where steroid therapy was needed.
HELLP syndrome, a syndrome of hemolysis, elevated liver enzymes and low platelets may occur in pregnancy with pre-eclampsia/eclampsia, and its a significant complication is acute renal failure (ARF). The aim of study was to determine frequency and outcome of HELLP syndrome complicated by ARF. Thirty-nine patients with pregnancy-related ARF were treated between Jan 1, 1989 and Jan 1, 1999. In these patients, the most frequent causes were HELLP syndrome (n = 14; 36%), postpartum hemorrhage (n = 10; 26%), pre-eclampsia/eclampsia (n = 6; 15%) and abruptio placenta (n = 4; 10%). Seven of the patients with HELLP syndrome had impairment of consciousness during hospitalization. Of these patients, coma in 5, stupor in 1, confusion in 1 were diagnosed. Twelve of the patients with HELLP syndrome and 14 of the other patients were treated by dialysis. Mann-Whitney U test and chi2 test(corrected by Yates and Fisher exact) were used for statistical analysis. Although serious clinical findings, with supportive treatment, 12 patients with HELLP syndrome and 21 other patients were fully recovered. One patient both with and without HELLP syndrome could not recovered due to diffuse cortical necrosis. Moreover, one patient with HELLP syndrome and 3 other patients were died. Mortality rate of the patients with HELLP syndrome was not found different from those of the other patients (p = 0.544). The causes of death were cerebral hemorrhage in patient with HELLP syndrome and disseminated intravascular coagulation (n = 1), cerebral emboli (n = 1), adult respiratory distress syndrome (n = 1). Fetal death occurred in 4 patients with HELLP syndrome (28.5%) and 7 other patients (28%), and rates were similar (p > 0.5). Finally, HELLP syndrome was the most frequent cause leading to ARF in pregnancy and their prognosis was not different from those of the other patients.
In literature, there was little data about frequency and outcome of ARF with two or more causes in etiology. Therefore, the aim of this study was to search this issue. This series included 339 patients with ARF from Jan 1,1987 to Jan 1,1999. Fourty-six (30 males) of all patients (13.5%) had two or more causes in etiology of ARF. Of these patients, causes were prerenal and renal in 26 (56%), prerenal, renal and postrenal in 12 (26%), renal and postrenal in 4 (9%), and prerenal and postrenal in 4 (9%). The most frequent cause is diarrhea and vomiting in prerenal, gentamycin usage in renal and prostate hypertrophy in postrenal. Of these patients, there was oliguria in 32 (70%), anuria in 8 (17%) and non-oliguria in 6 (13%). Treatment modalities of patients was only medical in 19 (41%), dialysis in addition to medical therapy in 27 (59%). In spite of treatment, 5 (10.8) of patients with two or more causes in etiology died. Causes of death were uremic coma in 2, cardiac disorders in 2 and septic shock in 1. Three (11.2%) of other patients with one cause died. Mortality rates were not different (chi2: 0.0298, p > 0.5). Cortical necrosis was diagnosed in one patient with multiple etiology and 2 of other patients. Finally, frequency of ARF with two or more etiologic causes was 13.5%, and most frequent causes were hypovolemia and nephrotoxic drugs. Outcome of these patients was similar to other patients with one cause.
Management of renal transplant patients requires periodic measurement of renal function, which is usually assessed by measuring the glomerular filtration rate (GFR). The most commonly used marker for GFR is serum creatinine, although muscle wasting and tubular secretion may lead to overestimation of the actual GFR. Serum concentrations of the low-molecular-weight proteins, cystatin C and beta(2)-microglobulin (B(2)M), may afford useful markers to determine a reduced GFR. We investigated whether these molecules provide reliable indicators of renal function in 75 renal transplant patients. Cystatin C and B(2)M correlated significantly with creatinine (r =.648, P <.05 and r =.578, P <.05, respectively). Inverse serum creatinine was superior to inverse cystatin C and inverse B(2)M when renal function equations were used (r =.95, P <.05, according to MDRD; r =.87, P <.05, according to Cockroft-Gault). Receiver operating characteristic (ROC) analysis was performed to quantitate the accuracy of the different markers to detect reduced GFR using a cutoff value of 70 mL/min. No significant difference between the areas under the ROC curves comparing cystatin C and B(2)M was observed; however, serum creatinine demonstrated a significantly greater value than cystatin C (.981 vs.724, P =.001). We conclude that serum creatinine is a more efficacious marker than serum cystatin C to assess renal function.
Noncompliance with regard to diet, medications and routine physician visits is frequently observed among some patient groups. This results in late graft dysfunction and behavior loss. In the present study, we defined compliance as attendance at 80% or more outpatient visits. The study included 63 cadaveric and 158 living-related renal transplant recipients namely, 150 men and 76 women of 8 to 70 years of age (median 38 +/- 12) who were operated between 1986 and 2001. Demographic data, number of visits attended per month, cigarette smoking, and alcohol intake were probed with a questionnaire that was delivered to the patients, 8 of whom died; hemophagocytic syndrome (n = 4), cardiovascular disease (n = 2), Kaposi' sarcoma (n = 1), and cerebrovascular bleeding (n = 1). Twenty-three patients had lost their graft. Compliance among men was lower than among women, a result that trended toward statistical significance (P =.087). Compliance was not related to marital status (P =.297), but tended to increase with educational background (P =.059). Graft loss (P =.546) and aging (P =.509) were not related to compliance. There was no relationship between compliance and mortality rate (P =.526). Interestingly, living-related kidney transplant recipients showed lower compliance than cadaveric kidney recipients, a result that was statistically significant (P =.04). Noncompliance was also related to cigarette smoking during the pre- and posttransplant periods (P =.008 and P =.03, respectively), as well as alcohol intake (P =.000). In conclusion, male gender and living-related donation are related to noncompliance, but (in contrast with literature) not young age, graft loss, or mortality. Compliance increases with educational status of the patients. Smoking and alcohol intake are closely related to noncompliance.
In this study we investigated the influence of a tacrolimus (TAC) plus mycophenolate mofetil (MMF) immunosuppressive regimen on the acute rejection rate and side effect profile in renal transplant recipients. The study included 80 living-related and 40 cadaveric donor renal transplant recipients (82 men, 38 women) of mean age 35 +/- 10 years (range, 16 to 58) who were operated between August 1999 and September 2002. The mean HLA mismatches was 3 +/- 1 (range, 0 to 5). All patients received prednisolone, MMF (2 g/d for the first 14 days posttransplant and then 1 g/d) plus TAC (0.2 mg/kg/d). They were followed for the development of rejection attacks and side effects. Diabetes mellitus developed in 13 patients (9 men, 4 women; 10.8%). Initially, patients required insulin therapy but after 6 months, 5 recipients no longer needed insulin therapy and were switched to oral hypoglycermic agents and diet control. Hypertension was diagnosed in 58 patients (48.3%). Neither gender nor donor origin (P =.14; P =.79, respectively) produced a significant difference in diabetes mellitus development. Biopsy proven acute rejection episodes were observed in 16 out of 120 patients (13.3%). Six out of 120 patients lost their grafts throughout the study period including one death because of suicide, one because of cytomegalovirus disease and hemophagocytic syndrome, one due to posttransplant lymphoproliferative disease and two to a cardiac arrhythmia. Only one patient lost his graft due to acute accelerated vascular rejection. Biopsy-proven chronic rejection appeared in one patient. In conclusion, although the incidence of insulin-dependent diabetes mellitus during posttransplant 6 months, seems high it decreased to 1.6% upon reduction of the TAC dosage. TAC plus MMF immunosuppression seems effective and safe in terms of acute rejection rates and side effect profiles.
Iron deficiency is an important factor in the management of anemia in both dialysis and transplant patients. Serum ferritin and transferrin saturation (TS) may be influenced by the presence of inflammation. Recently, the soluble transferrin receptor (s-TfR) has been considered to be a marker of functional iron stores. In this study, parameters of the iron state were investigated in terms of agreement (assessed by kappa) with the diagnosis of iron deficiency and with inflammation. The study was performed in 38 hemodialysis, 31 continuous ambulatory peritoneal dialysis, and 21 anemic renal transplant patients. CRP and amyloid A protein (AAP) were studied as markers of inflammation. Iron deficiency was defined as ferritin <100 mg/L, TS <20%, or s-TfR >1.76 mg/mL. We observed that s-TfR levels were significantly related to both dialysis duration (r = 0.28 in dialysis and r = 0.60 in transplant patients, both P <.05) and PTH levels (r = 0.23 in dialysis and r = 0.55 in transplant patients, both P <.05). Among the transplant group, ferritin and TS, as well as TS and s-TfR were significantly related (r = 0.84 and r = -0.64, respectively), but not s-TfR and ferritin. Among the dialysis group, ferritin and TS, and also TS and s-TfR, were significantly related (r = 0.35 and r = -0.30, respectively), whereas s-TfR and ferritin were not. In the transplant group, the kappa value for agreement between ferritin and TS in the diagnosis of iron deficiency was 0.76 (P =.006), and 0.33 (P =.04), respectively. Among patients with CRP levels <0.3 mg/L or AAP levels <6.4 mg/L, the relation between parameters of iron state was more robust. The kappa value for agreement between ferritin and s-TfR was 0.49 (P =.006) in the dialysis group and 1 (P =.002) for that between ferritin and TS in the transplant group. Our results suggest that PTH levels may influence s-TfR levels. Discordance between ferritin, TS, and s-TfR as markers of iron deficiency might be explained by the effects of inflammation.