Sema Oymak

The long‐term effects of arteriovenous fistula creation on the development of pulmonary hypertension in hemodialysis patients

The aim of this prospective study was to evaluate long‐term effects of arteriovenous fistula (AVF) on the development of pulmonary arterial hypertension (PAH) and the relationship between blood flow rate of AVF and pulmonary artery pressure (PAP) in the patients with end‐stage renal disease (ESRD). This prospective study was performed in 20 patients with ESRD. Before an AVF was surgically created for hemodialysis, the patients were evaluated by echocardiography. Then, an AVF was surgically created in all patients. After mean 23.50 ± 2.25 months, the second evaluation was performed by echocardiography. Also, the blood flow rate of AVF was measured at the second echocardiographic evaluation. Pulmonary arterial hypertension was defined as a systolic PAP above 35 mmHg at rest. Mean age of 20 patients with ESRD was 55.05 ± 13.64 years; 11 of 20 patients were males. Pulmonary arterial hypertension was detected in 6 (30%) patients before AVF creation and in 4 (20%) patients after AVF creation. Systolic PAP value was meaningfully lower after AVF creation than before AVF creation (29.95 ± 10.26 mmHg vs. 35.35 ± 7.86 mmHg, respectively, P: 0.047). However, there was no significant difference between 2 time periods in terms of presence of PAH (P>0.05). Pulmonary artery pressure did not correlate with blood flow rate of AVF and duration after AVF creation (P>0.05). In hemodialysis patients, a surgically created AVF has no significant effect on the development of PAH within a long‐term period. Similarly, blood flow rate of AVF also did not affect remarkably systolic PAP within the long‐term period.

Effects of chronic obstructive pulmonary disease on coronary atherosclerosis

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 ± 0.6 in the COPD group and 2.1 ± 0.7 in the control group (P = 0.004). The mean Extent score was 37 ± 16 in the COPD group and 23 ± 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 ± 6.3 vs 6.6 ± 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682–9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023–13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.

The Relation Between Chronic Obstructive Pulmonary Disease and Coronary Collateral Vessels

Coronary collateral vessels can provide a perfusion reserve in case of increased myocardial oxygen demand. Development of coronary collateral vessels (CCV) is triggered by the pressure gradient between the coronary bed of arteries caused by an obstruction and myocardial ischemia. Myocardial hypoxia can facilitate development of CCVs. There is a chronic hypoxemia in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the effect of COPD on CCVs. The study included 98 patients with COPD who underwent coronary angiography. Those patients in whom coronary angiography is normal or severity of coronary artery stenosis in thought not to be sufficient for the development of CCVs (<80%) were excluded from the study. A total of 98 patients (mean age, 62 ±9 years) met the criteria for the COPD group. For case-control matching, 98 consecutive without COPD patients (mean age 62 ±10) who had one or more diseased vessels with 80% or greater stenosis were included in the control group. The CCVs were graded according to the Rentrop scoring system, and the collateral score was calculated by summing the Rentrop numbers of every patient. The mean number of diseased vessels in patients with COPD and without COPD were 1.61 ±0.69 and 1.77 ±0.89 (p=0.155), respectively. The mean collateral score was 2.15 ±2.03 in the COPD group and 1.32 ±1.54 in the control group. After confounding variables were controlled for, the collateral score in patients with COPD group was significantly different from that in patients without COPD group (p=0.002). These findings suggest that CCV development is better in patients with COPD than in those patients without COPD. Thus, COPD may be an important factor affecting CCV development, which may be related to the presence of chronic hypoxemia in patients with COPD.

Transmission of Mycobacterium tuberculosis by accidental needlestick.

Transmission by airbone spread of infected respiratory secretions from person to person is the main route of dissemination of tuberculosis infection [1]. In addition, tubercle bacilli may enter the body from the gastrointestinal tract following ingestion of contaminated foods and from skin through a recent cut or abrasion on exposed surfaces [2]. Herein, an unusual case of tuberculosis lymphadenitis resulting from accidental needle stick is presented. The patient is a 37-year-old female medical doctor. She was accidental exposed to a needle stick injury while performing a pleura biopsy by using Cope’s biopsy needle on a patient with culture-positive and biopsy-proven tuberculous pleurisy. During the removal of the biopsy material from Cope’s needle using a syringe needle, the needle got stuck in her middle finger of the left hand. Three weeks later, a small, hard, purple-colored papule appeared at the injury point and disappeared spontaneously in the next 6 months. Eight months later, the patient became aware of a lymphadenopathy in the left supraclavicular region. Physical examination of the patient revealed bilaterally a multinodular goitre, a BCG scar on the left deltoid region and a left supraclavicular mobile, hard, and painless lymphadenopathy (1 ! 1 cm in diameter). The remaining part of physical examination findings was unremarkable. Her laboratory findings were within normal limits except for a mildly increased C-reactive protein level (8 mg/dl). Her chest radiograph and lung computed tomography showed no abnormality. An intradermal test with 5 units of PPD showed a positive reaction with a 40-mm induration in diameter at 48 h. The patient’s previous PPD skin test was found to be negative 4 years ago. The lymph node was excised surgically and histopathologic examination showed granulomatous lymphadenitis and caseation necrosis consistent with tuberculosis. Staining of the biopsy material with the Ziehl-Neelsen procedure revealed acid-fast bacilli in histiocytes (fig. 1). The patient was treated with isoniazid, rifampin, ethambutol, pyrazinamide in the first 2 months and, isoniazid and rifampin thereafter without any adverse effect. Accidental needle stick is a very well-known route of transmission of viral infections such as human immunodeficiency virus, hepatitis B and hepatitis C viruses. Not only blood but also other infected body fluids may also cause transmission of infectious agents [3]. Primary skin tuberculosis usually results from introduction of MycobacFig. 1. Histologic section of supraclavicular lymph node biopsy demonstrating acid-fast bacilli in histiocytes. Ziehl-Neelsen. !1,000.

Does arterio-venous fistula creation affects development of pulmonary hypertension in hemodialysis patients?

Background: Pulmonary arterial hypertension (PAH) is a common complication in hemodialysis (HD) patients and its pathogenesis is not explained clearly. Arterio-venous fistulas (AVFs) creation may contribute to the development of PAH because of increased pulmonary artery blood flow. However, it was not prospectively evaluated that effect of AVF on the development of PAH. Aim: We aimed to evaluate the effects of AVF on PAH and the relationship between blood flow rate of AVF and pulmonary artery pressure (PAP) in HD patients. Patients and Method: The prospective study included 50 patients with end-stage renal disease. Before an AVF was surgically created for hemodialysis, the patients were evaluated by echocardiography. Then, an AVF was surgically created in the patients. After mean 76.14 ± 11.37 days, the second evaluation was performed by echocardiography. Results: Before AVF creation, 17 (34%) out of 50 patients had PAH. The systolic PAP was significantly higher in the patients with PAH compared with patients without PAH (47.82 ± 9.82 mmHg vs. 30.15 ± 5.70 mmHg, respectively, p = 0.001). In the second evaluation, 19 (38%) out of 50 patients had PAH. The systolic PAP values were significantly higher in the patients with PAH compared with patients without PAH (47.63 ± 8.92 mmHg vs. 25.03 ± 7.69 mmHg, P = 0.001, respectively). There was no relationship between the blood flow rate of AVF and PAP. Conclusion: PAH is a common problem in HD patients. AVF has no significant effect on the development of PAH within a short period. Similarly, blood flow rate of AVF also did not affect remarkably the systolic PAP.

The Influence of Anemia on Mortality in Patients with Chronic Obstructive Pulmonary Disease

Yöntemler: KOAH tanısı ile 01 Ocak 2004 31 Aralık 2008 tarihleri arasında izlenen hastalar, ICD-10 kodları kullanılarak hastane bilgi işlem sistemi veri tabanı aracılığıyla saptandı. Anemi tanısı Dünya Sağlık Örgütü kriterlerine göre konuldu. Hastalarda KOAH evrelemesi GOLD kriterlerine uygun olarak FEV 1 /FVC değerlerine göre yapıldı. Mortalite 1 Ocak 2004 ile 1 Ocak 2010 tarihleri arasında herhangi bir tarihte yaşamın kaybedilmesi olarak tanımlandı.