Spiros P. Potamianos

Mean Platelet Volume: A Useful Marker of Inflammatory Bowel Disease Activity

OBJECTIVES:We investigated whether the mean platelet volume would be a useful marker in the evaluation of inflammatory bowel disease activity.METHODS:Complete blood count, C-reactive protein, erythrocyte sedimentation rate, serum thrombopoietin and erythropoietin, plasma β-thromboglobulin, and platelet factor 4 were measured in 93 patients with ulcerative colitis, 66 patients with Crohns disease, and 38 healthy blood donors. Disease activity was assessed by the Clinical Colitis Activity Index in patients with ulcerative colitis and by the Crohns Disease Activity Index in patients with Crohns disease.RESULTS:Mean platelet count was increased in patients with active compared to inactive ulcerative colitis (p < 0.05), and in patients with active compared to inactive Crohns disease (p = 0.0002) or healthy controls (p < 0.0001). On the other hand, mean platelet volume was significantly decreased in patients with active compared to inactive ulcerative colitis (p = 0.02) or healthy controls (p < 0.0001), and in patients with active compared to inactive Crohns disease (p = 0.0005) or healthy controls (p < 0.0001). Mean platelet volume was inversely correlated with the white blood cell count (r =−0.17, p = 0.02), C-reactive protein (r =−0.46, p = 0.009) and erythrocyte sedimentation rate (r =−0.28, p = 0.008). No significant correlations were found between mean platelet volume and serum thrombopoietin or erythropoietin levels; however, a strong negative correlation between mean platelet volume and β-thromboglobulin (r =−0.34, p < 0.0001) and platelet factor 4 (r =−0.30, p = 0.0002) was observed.CONCLUSIONS:Mean platelet volume is significantly reduced in active inflammatory bowel disease and is negatively correlated with the known inflammatory bowel disease activity markers and the platelet activation products. We propose that mean platelet volume provides a useful marker of activity in inflammatory bowel disease.

A REVIEW OF THE POSTULATED MECHANISMS CONCERNING THE ASSOCIATION OF HELICOBACTER PYLORI WITH ISCHEMIC HEART DISEASE

Since its discovery, Helicobacter pylori has been implicated in the pathogenesis of several diseases, both digestive and extradigestive. Interestingly, the majority of the extradigestive‐related literature is focused on two vascular manifestations: stroke and ischemic heart disease. Potential mechanisms for the establishment of a H. pylori‐induced ischemic heart disease have been proposed with regard to chronic inflammation, molecular mimicry, oxidative modifications, endothelial dysfunction, direct effect of the microorganism on atherosclerotic plaques as well as changes regarding traditional or novel risk factors for ischemic heart disease or even platelet‐H. pylori interactions. A positive link between H. pylori infection and ischemic heart disease has been suggested by a series of studies focusing on epidemiologic evidence, dyslipidemic alterations, upregulation of inflammatory markers or homocysteine levels, induction of hypercoagulability, oxidation of low‐density lipoprotein, causation of impaired endothelial function, detection of H. pylori DNA in atherosclerotic plaques, and participation of certain antigens and antibodies in a cross‐reactivity model. There are studies, however, which investigated the relationship between H. pylori and ischemic heart disease with regard to the same parameters and failed to confirm the suggested positive association. Further studies in the direction of interaction between H. pylori and the hosts genotype as well as a quest for evidence towards novel risk factors for ischemic heart disease such as oxidative stress, vascular remodeling, vascular calcification, or vasomotor activity, may reveal a field of great interest, thus contributing to the determination of new potential mechanisms.

Renal manifestations and complications of inflammatory bowel disease

Renal manifestations and complications are not rare in patients with inflammatory bowel disease (IBD) and may present as nephrolithiasis, amyloidosis, tubulointerstitial nephritis, and glomerulonephritis. Symptoms of renal impairment are not always specific and since the underlying bowel disease is preponderant, renal function deterioration may be underestimated. Additionally, medical treatment of patients with IBD such as aminosalicylates, cyclosporine, and tumor necrosis factor‐&agr; inhibitors can cause renal complications, although direct correlation to bowel disease is not always clear. The well‐documented renal manifestations and complications of IBD, as well as the possible renal side effects of new drugs, emphasize the need for periodic evaluation of renal function. New markers of renal function may facilitate early diagnosis and unravel the complex mechanisms responsible for kidney damage. The purpose of this review is to summarize the renal manifestations and complications as well as the markers of renal function utilized in IBD, attempting to shed more light on the pathophysiology of renal damage in IBD. (Inflamm Bowel Dis 2011;)

Angiogenin, angiopoietin-1, angiopoietin-2, and endostatin serum levels in inflammatory bowel disease.

Background: Angiogenesis is a complex process, involving a great number of mediators. It is implicated in the pathogenesis of numerous diseases, holding a critical role in inflammatory bowel disease (IBD). The objective of this study was to assess serum levels of angiogenin, angiopoietin‐1, angiopoietin‐2, and endostatin in IBD patients. Methods: Measurement of all angiogenesis mediators was performed with a commercially available enzyme‐linked immunosorbent assay. Fifty‐two patients with ulcerative colitis (UC), 59 with Crohns disease (CD), and 55 healthy controls (HC) were included in the study. The values were analyzed with regard to disease and patients characteristics. Results: Angiogenin levels were significantly higher in IBD patients compared to HC (P < 0.001) and in UC and CD smoker patients compared to nonsmokers (P = 0.0121 and P = 0.005, respectively). Angiogenin levels were lower in UC patients receiving 5‐aminosalicylate (5‐ASA) alone, compared to those receiving combined therapy (P = 0.0478). Angiopoietin‐1 levels were significantly lower in IBD patients compared to HC (P < 0.0001) and increased in smokers compared to nonsmoker UC patients (P = 0.0085). IBD patients demonstrated increased angiopoietin‐2 levels compared to HC (P = 0.0131), while CD patients with disease restricted to the colon had significantly lower levels compared to other disease locations (P < 0.0001). Higher endostatin levels were recorded in UC patients with extensive colitis. Conclusions: Elevated serum angiogenin and angiopoietin‐2 levels and lower serum angiopoietin‐1 levels were shown in IBD patients, as well as a different pattern of angiogenic factor alterations related to location, treatment, smoking habits and gender. Inflamm Bowel Dis 2011

Elevated thrombopoietin serum levels in patients with inflammatory bowel disease

OBJECTIVES:Elevated platelet count is a well recognized marker of inflammatory bowel disease (IBD) activity. Thrombopoietin (TPO) is a critical cytokine in the physiological regulation of thrombopoiesis. The aim of this study was to investigate the serum levels of endogenous TPO in patients with IBD, the relationship between platelet counts and TPO levels, and the correlation of TPO with the clinical characteristics of the patients.METHODS:TPO levels in 40 patients with Crohns disease (CD), 63 patients with ulcerative colitis (UC), and in 42 healthy blood donors were assessed by ELISA. Platelet and white blood cell counts as well as C-reactive protein, and erythrocyte sedimentation rate were measured.RESULTS:TPO levels were significantly elevated in patients with CD (mean 124.3 ± SD 58.0 pg/ml, p < 0.0001) and in patients with UC (mean 152.2 ± SD 142.3 pg/ml, p < 0.0001), compared to controls (mean 53.4 ± SD 45.7 pg/ml). TPO levels remained significantly elevated in remission (mean 144.7 ± SD 131.1 pg/ml, p < 0.0001 compared to controls). Platelets were significantly elevated only in active CD, being normal in inactive disease as well as in all patients with UC. There was no significant correlation between TPO levels and various clinical characteristics of patients with IBD. No significant correlation was found between TPO levels and either platelet counts or white blood cell counts, erythrocyte sedimentation rate, and C-reactive protein.CONCLUSIONS:TPO levels are increased in IBD, irrespective of disease activity, platelet counts, and clinical characteristics of the patients. These observations indicate that TPO, apart from being a platelet producer, might have additional functions, probably related to the procoagulant state of IBD.

Downregulation of serum epidermal growth factor in patients with inflammatory bowel disease. Is there a link with mucosal damage

Background: Epidermal growth factor (EGF) is a multipotent peptide which contributes to epithelial development, inhibition of gastric acid secretion, acceleration of wound healing, and promotion of angiogenesis. The aim of this study is to evaluate serum EGF concentrations in inflammatory bowel disease (IBD) patients, with regard to disease and patients’ characteristics. Methods: EGF determination was performed by a commercially available enzyme-linked immunosorbent assay. Fifty-two patients with ulcerative colitis (UC), 59 with Crohns disease (CD), and 55 healthy controls (HC) were included in the study. Results: Mean ( ± SEM) serum EGF levels were 217.2 ( ± 30.40) pg/mL in UC patients, 324.6 ( ± 37.29) pg/mL in CD patients, and 453.1 ( ± 39.44) pg/mL in HC. Serum EGF levels were significantly lower in UC and CD patients compared to HC (P < 0.0001 and P = 0.0199, respectively). Lower serum EGF levels were observed in UC compared to CD patients (P = 0.0277). Extent of the disease was found to affect serum EGF levels in UC, demonstrating significant reduction in patients with left-sided colitis and pancolitis in comparison with those with proctitis (P = 0.0190 and P = 0.0024, respectively). EGF concentration was not influenced by other characteristics of patients and disease. Conclusions: Significantly, lower levels of serum EGF are observed in IBD patients compared to HC, while disease extent plays a key role in regulation of serum EGF in UC. Downregulation of serum EGF may be correlated with different patterns of bowel inflammation, epithelial development, and wound healing in IBD.

Factors associated with disease evolution in Greek patients with inflammatory bowel disease.

BackgroundThe majority of Crohns disease patients with B1 phenotype at diagnosis (i.e. non-stricturing non-penetrating disease) will develop over time a stricturing or a penetrating pattern. Conflicting data exist on the rate of proximal disease extension in ulcerative colitis patients with proctitis or left-sided colitis at diagnosis. We aimed to study disease evolution in Crohns disease B1 patients and ulcerative colitis patients with proctitis and left-sided colitis at diagnosis.Methods116 Crohns disease and 256 ulcerative colitis patients were followed-up for at least 5 years after diagnosis. Crohns disease patients were classified according to the Vienna criteria. Data were analysed actuarially.ResultsB1 phenotype accounted for 68.9% of Crohns disease patients at diagnosis. The cumulative probability of change in disease behaviour in B1 patients was 43.6% at 10 years after diagnosis. Active smoking (Hazard Ratio: 3.01) and non-colonic disease (non-L2) (Hazard Ratio: 3.01) were associated with behavioural change in B1 patients. Proctitis and left-sided colitis accounted for 24.2%, and 48.4% of ulcerative colitis patients at diagnosis. The 10 year cumulative probability of proximal disease extension in patients with proctitis and left-sided colitis was 36.8%, and 17.1%, respectively (p: 0.003). Among proctitis patients, proximal extension was more common in non-smokers (Hazard Ratio: 4.39).ConclusionClassification of Crohns disease patients in B1 phenotype should be considered as temporary. Smoking and non-colonic disease are risk factors for behavioural change in B1 Crohns disease patients. Proximal extension is more common in ulcerative colitis patients with proctitis than in those with left-sided colitis. Among proctitis patients, proximal extension is more common in non-smokers.

Reduction of Radiation Doses to Patients and Staff During Endoscopic Retrograde Cholangiopancreatography

Background/Aim: Endoscopic retrograde cholangiopancreatography (ERCP) is associated with a considerable radiation exposure for patients and staff. While optimization of the radiation dose is recommended, few studies have been published. The purpose of this study has been to measure patient and staff radiation dose, to estimate the effective dose and radiation risk using digital fluoroscopic images. Entrance skin dose (ESD), organ and effective doses were estimated for patients and staff. Materials and Methods: Fifty-seven patients were studied using digital X-ray machine and thermoluminescent dosimeters (TLD) to measure ESD at different body sites. Organ and surface dose to specific radiosensitive organs was carried out. The mean, median, minimum, third quartile and the maximum values are presented due to the asymmetry in data distribution. Results: The mean ESD, exit and thyroid surface dose were estimated to be 75.6 mGy, 3.22 mGy and 0.80 mGy, respectively. The mean effective dose for both gastroenterologist and assistant is 0.01 mSv. The mean patient effective dose was 4.16 mSv, and the cancer risk per procedure was estimated to be 2 × 10-5 Conclusion: ERCP with fluoroscopic technique demonstrate improved dose reduction, compared to the conventional radiographic based technique, reducing the surface dose by a factor of 2, without compromising the diagnostic findings. The radiation absorbed doses to the different organs and effective doses are relatively low.

Optimisation of Radiation Exposure to Gastroenterologists and Patients during Therapeutic ERCP

This study intended to optimize the radiation doses for gastroenterologists and patients during therapeutic endoscopic retrograde cholangiopancreatography (ERCP) and to compare the doses based on available data obtained by other researchers. A total of 153 patients were studied in two Gastroenterology Departments, (group A, 111; group B, 42). Thermoluminescent dosimeters (TLD) were used to measure the staff and patients entrance surface air kerma (ESAK) at different body sites. The mean ESAK and effective doses per procedure were estimated to be 68.75 mGy and 2.74 mSv, respectively. Staff was exposed to a heterogonous doses. The third examiner (trainee) was exposed to a high dose compared with other examiners because no shield was located to protect him from stray radiation. Patients and examiners doses were lower compared to the lowest values found in previous studies taking into consideration the heterogeneity of patients and equipment. Staff doses during ERCP are within the safety limit in the light of the current practice.