The effects of 8 weeks of endurance running on hepcidin concentrations, inflammatory parameters, and iron status in female runners

Exercise-associated iron deficiency is a common disorder in endurance athletes. The authors investigated the effects of long-term endurance exercise on hepcidin concentrations, inflammatory parameters, and iron status in moderately trained female long-distance runners. Eighteen runners were assigned to either an interval- or a continuous-training exercise group. The physical training consisted of two 3-week progressive overload periods, each followed by a week's recovery, and concluded with a 10- or 21-km competitive run. Samples were taken 6 times during the 8-wk training program, first at baseline (BPre), then after the first and second 3-wk training loads (TPost1, TPost2), after each recovery week (Recovery1 and Recovery2), and poststudy (BPost). Soluble transferrin receptor (sTfR) concentrations were increased in Recovery2 and BPost compared with BPre (p=.02), hemoglobin decreased in TPost1 and TPost2 (p<.001), and red blood cells decreased in TPost2 (p=.01). Hepcidin decreased with time in TPost1 and in BPost compared with BPre (p<.001) and increased in TPost2 compared with TPost1 (p<.001). No differences over time were found for high-sensitivity C-reactive protein. The main findings of the current study indicate that serum hepcidin and sTfR were affected after 8 weeks of endurance running in women. No positive relation was found with inflammation.     

Effect of Periodontal Treatment in Renal Transplant Recipients

Objective

To evaluate the effect of periodontal treatment on gingival overgrowth in a group of renal transplant patients.

Subjects and Methods

Twenty-five renal transplant recipients receiving immunosuppressive therapy with cyclosporine A (CsA) were randomly assigned to 2 groups. Group 1 (n = 15) included patients who had been specifically referred to a dental clinic to prevent gingival overgrowth and were given full periodontal therapy. Group 2 (n = 10) was comprised of patients who did not receive any professional periodontal cleaning. Patients from both groups were examined to determine their periodontal status before and after 3, 6 and 12 months in terms of their plaque index, gingival index and gingival overgrowth. During the examination, their overall health was stable.

Results

For group 1, the scores were 1.89 (baseline), 0.98 (6 months) and 0.56 (12 months), and hence there were significant reductions (p = 0.0001). The gingival indices were 1.71 (baseline), 0.76 (6 months) and 0.35 (12 months), and the reductions were also significant (p = 0.0001). A significant association was observed between poor oral hygiene and the degree of gingival overgrowth. The 1-year post-treatment follow-up showed that patients in group 1 did not develop gingival overgrowth due to the use of CsA as group 2 did without prior periodontal therapy.

Conclusion

Oral hygiene status was the most important variable related to the development and degree of gingival overgrowth due to the use of CsA.Key Words: Gingival overgrowth, Periodontal treatment, Cyclosporine     

Jugular venous `a'' wave in pulmonary hypertension: new insights from a Doppler echocardiographic study

Objective—To study the mechanisms underlying the dominant `a' wave seen in patients with primary pulmonary hypertension.

Design—Retrospective and prospective examination of the jugular venous pulse recording, flow in the superior vena cava, and Doppler echocardiographic studies.

Setting—A tertiary referral centre for both cardiac and pulmonary disease, with facilities for invasive and noninvasive investigation, and assessment for heart and heart-lung transplantation.

Patients—12 patients with primary pulmonary hypertension, most being considered for heart-lung transplantation.

Results—Two distinct patterns of venous pulse and superior vena caval flow were identified: a dominant `a' wave with no `v' wave, an absent or poorly developed `y' descent, and exclusively systolic downward flow in the superior vena cava (group 1, n = 8), and a dominant `v' wave, deep `y' descent and exclusively diastolic downward flow in the superior vena cava (group 2, n = 4). A comparison between the two groups showed age (mean (SD)) 42 (18) ν 36 (7) years, RR interval 700 (65) ν 740 (240) ms, left ventricular end diastolic dimension 3·6 (0·8) ν 3·2 (1·0) cm and end systolic dimension 2·1 (0·5) ν 2·3 (0·3) cm, right ventricular end diastolic dimension 2·6 (0·5) ν 2·8 (0·6) cm, and pressure drop between right ventricle and right atrium 60 (8) ν 70 (34) mm Hg to be similar. Duration of tricuspid regurgitation 520 (30) ν 420 (130) ms and the time interval of pulmonary closure to the end of the tricuspid regurgitant signal 140 (30) ν 110 (40) ms were longer in group 1 compared with group 2, whereas right ventricular filling time was much shorter 180 (70) ν 350 (130) ms. In seven patients from group 1, a single peak of forward tricuspid flow was present, but this pattern was seen in only one patient from group 2.

Conclusions—In patients with primary pulmonary hypertension, the apparent `a' wave seen in the venous pulse is, in fact, a summation wave. It is probably the result of large pressure changes that must underlie rapid acceleration and deceleration of blood across the tricuspid valve when the right ventricular filling time is short.

     

Statins enhance postischemic hyperemia in the skin circulation of hypercholesterolemic patients: a monitoring test of endothelial dysfunction for clinical practice?

OBJECTIVES: The present study aims to investigate whether laser Doppler flowmetry can be used to monitor improvements in vascular function during statin therapy. BACKGROUND: Endothelial dysfunction is an early feature of atherosclerosis in hypercholesterolemic patients and can be improved by statins. There are several methods to assess endothelial function in vivo, none of them being feasible in everyday practice. METHODS: Skin perfusion, measured by laser Doppler flowmetry, was assessed at rest and during reactive hyperemia. Nineteen hypercholesterolemic patients (age 42 to 73 years, total cholesterol 5.4 to 9.6 mmol/l) were studied before and during statin therapy. To further investigate the mechanisms, postischemic skin hyperemia was measured before and after intradermal injection of the nitric oxide synthase inhibitor L-NAME and its inactive isoform D-NAME (0.5 micromol/10 microl each). On a separate day, the healthy volunteers were reexamined before and 2 h after 1,000 mg aspirin. RESULTS: Postischemic skin blood flow was markedly reduced in hypercholesterolemic patients (45 +/- 11%) compared with healthy controls (238 +/- 20%, p < 0.0001) and improved after statin therapy (113 +/- 15%, p = 0.0005 vs. pre-treatment). In the healthy volunteers, the hyperemic responses were not significantly different after L-NAME and D-NAME. Aspirin reduced hyperemia from 274 +/- 49% to 197 +/- 40% (p = 0.025). CONCLUSIONS: Reactive hyperemia of the skin microcirculation can be easily and reproducibly assessed by laser Doppler flowmetry. Vasodilator prostaglandins are the major mediators of postischemic skin hyperemia, which is impaired in hypercholesterolemic patients and can be enhanced by cholesterol-lowering therapy. Thus, laser Doppler flowmetry may represent a tool to assess and monitor vascular function during therapy in everyday practice.     

Capecitabine cardiotoxicity--case reports and literature review

This study presents 3 case reports of patients who experienced anginous pain during treatment with capecitabine. The interruption of capecitabine and sublingual or intravenous nitroglycerine treatment lead to recovery. Rechallenge of capecitabine with dose reduction of 30% lead to repeated anginous pain in 2 patients. Treatment with capecitabine had been replaced with weekly bolus 5FU-LV, without further cardiotoxicity. The literature contains data from about 50 patients who experienced cardiotoxicity during capecitabine treatment. The most frequent manifestations of capecitabine cardiotoxicity included: anginous pain in 38/53 (71.7%), arrhythmia in 6/53 (11.3%), myocardial infarction in 6/53 (11.3%). Cardiotoxicity of capecitabine lead to death in 6/53 (11.3%) patients. Risk factors for cardiotoxicity are associated with the grade 4 and the fatal outcome of cardiotoxicity (p = 0.035, p = 0.015), but not with the symptom recurrence upon capecitabine rechallenge (p = 0.18). The combination chemotherapy regimens are associated with the grade 4 of cardiotoxicity (p = 0.048), but not with the fatal outcome (p = 0.3). Rechallenge of capecitabine lead to symptoms recurrence in 10/16 patients. Neither the dose reduction of capecitabine (p = 0.18) nor the additional medical prophylaxis (p = 0.37) were important for the outcome of capecitabine rechallenge.     

Impact of vasoactive intestinal polypeptide and gastrin-releasing peptide on small bowel microcirculation and mucosal injury after hepatic ischemia/reperfusion in rats

Background and aims Alterations in microvascular perfusion of the intestine after hepatic ischemia/reperfusion have been suggested as an important cause of postoperative septic complications. We therefore investigated small bowel microcirculation and mucosal injury after liver ischemia/reperfusion in a rat model. Furthermore, we analyzed the effects of the regulatory peptides vasoactive intestinal polypeptide and gastrin-releasing peptide for their splanchnic vasoactivity.Methods Hepatic ischemia was induced by clamping of the left hepatic artery and vein for 40 min, followed by 60 min of reperfusion. The control group was treated similarly, but without clamping of the liver vessels. Ten minutes after clamping of the hepatic vessels, vasoactive intestinal polypeptide or gastrin-releasing peptide, respectively, were continuously infused intravenously in the experimental groups. Small bowel microcirculation and mucosal injury were assessed using intravital microscopy and the Chiu-score, respectively.Results The functional capillary density of the small intestine following ischemia and reperfusion of the left hepatic lobe significantly decreased compared to normal controls in both the mucosa and the smooth intestinal muscle. Red blood cell velocity decreased, whereas leukocyte–endothelium adherence, stasis index and the mucosal injury score increased. Administration of vasoactive intestinal polypeptide resulted in an increase of functional capillary density in the mucosa and of the red blood cell velocity and a decrease in the stasis index. The mucosal injury score was significantly higher in reperfused animals without treatment. The application of gastrin-releasing peptide resulted in an isolated increase of the red blood cell velocity. Leukocyte adherences could not be altered by the regulatory peptides.Conclusion We conclude that hepatic ischemia/reperfusion injury leads to significant alterations of small bowel microcirculation and mucosal injury. Vasoactive intestinal polypeptide and gastrin-releasing peptide attenuate the damage in a different manner.