IBD and IBS are among important intestinal diseases which considered as challenge of health-care systems with continually increasing incidence. Numerous factors play a role in the occurrence of IBD such as aberrant and continuing immune response to the microbes in the gut, genetic susceptibility and environmental factors[13]. Like with IBD, the cause of IBS is not fully understood. Researchers believe that while stress can aggravate IBS, the syndrome is actually caused by a disturbance between the brain and the gut[14].
Oxidative stress, inflammation, anemia, and malnutrition often are common factors in active IBD and IBS[15]. In these regard, our data showed that MDA as main marker for oxidative stress, was increase in IBD and IBS significantly in comparison with controls. Moreover, we found a significant imbalance antioxidant and oxidant blood system in IBD patients (ratio of se/MDA and Zn/Cu). Moreover, there are a multitude of risk factors in IBD and IBS for micronutrient deficiencies. It seems that reduced food intake is one of the most important mechanisms for malnutrition in IBD and IBS. In addition, because in both diseases, intestinal tissue are involved, the patient may be deficient in nutrients, which may be due to impaired absorption of nutrients in the intestine[16]. In this study, we examined important nutritional, oxidative stress and inflammation related factors such as iron, zinc, selenium and copper, and also evaluated some proteins that carry these nutritional factors, namely ferritin, transferrin and ceroplasmin in IBD and IBS patients.
Our results showed reduction zinc levels in both groups of IBD and IBS in male and female patients compared to the control group. However, this decrease was higher in IBD group and this difference was statistically significant between IBD and IBS. Zinc is an abundant and essential trace mineral and enzymes such as metalloproteinases required zinc for catalytic activity. Moreover, zinc is important in immune function. Absorption of zinc was taken in length of the small intestine but the transport procedure isn’t well described [17]. Like our results, in IBD patients, a number of studies have reported low plasma zinc levels in IBD patients [12, 18, 19]. Because of very little zinc is present in the serum, interpretation of this results is difficult.
Selenium is another necessary component of vital enzymes with antioxidant role as cofactor of glutathione peroxidase and thioredoxin reductase[20]. As oxidative stress is one of the main factor in IBD and IBS pathogenesis, so selenium levels are investigated as anti-oxidant factor. There have been studies to date, in which selenium levels were found to be significantly lower in both IBS and IBD patients, compared with controls [21–23]. Our results showed that the amount of selenium in the group IBD decreased and IBS increased, although these changes were not significant compared to the control group. Moreover, our results exposed that reduction in selenium level was significant in IBD male patient in comparison with IBS and control group.
It seems that the imbalance of oxidants and antioxidant were more pronounced in men. In contrast to selenium, copper showed increase in IBD and IBS group, but like selenium, these changes were not significant compared to the control group. Copper is a trace element with diverse function in electron and oxygen transportation[24]. Although a recent study reported 84% of patients show reduction in copper[18], but other studies have failed to show this and one study of IBD patients, was found serum copper level, to be similar to controls, and elevated in IBD patients in two studies[12, 23]. Because, copper does not exist as a free ion in the body, the interpretation of copper results in these patients must be done very carefully and special attention should be paid to these points that serum copper and ceruloplasmin in determining body copper stores have limitations, as both may also be acute phase reactants. Serum copper may also influence via certain renal diseases, with prolonged inflammation, and due to increased iron or zinc intake[25].
Our result confirmed the reduction in Fe, ferretin and transferrin levels in IBDs but not in IBS in comparison with control group, however this difference was only significant in transferrin level Fe is involved in several complex biological processes, including, but not restricted to many enzymes, and the immune system, which are not yet fully understood[26, 27]. Low ferritin was associated with increased risk for IBD [28]. There are several possible causes of iron deficiency among IBD patients include bleeding, reduced iron uptake, insufficient dietary intake because of avoidance of food due to gastrointestinal symptoms[29]. In accordance with our data, one Canadian and Swedish studies reported decrease in iron and ferretin leves in IBD patients [28, 30].
Another point in assessing Fe in IBD patients was that Fe reduction reported in female more than men. In along with our study, Spanish and Swedish study reported iron deficiency is more prevalent in females compared to males [31, 32]. Transferrin is an iron deficiency marker and is a negative acute phase reactant as well and as such decreases in response to inflammation. Moreover, via trapping iron and suppressing free radical production, transferrin is an important component of serum antioxidant defense [33]. Along with our results, Malgorzata Matusiewicz et.al reported the reduction in transferrin concentrations in IBD patients[26]. Reduce transferrin concentrations occurred in active IBD and therapeutic approaches which trigger TNF lead to enhancement of Fe and transferrin levels[34].
Ceruloplasmin as an acute-phase plasma protein that elevated plasma level of ceruloplasmin can be observed in inflammation, trauma, or infection. Ceruloplasmin is a ferroxidase with important function in Fe metabolism via converting Fe2 + to Fe3+, and inhibition of ferrous ion-mediated production of ROS[35]. In our study IBS patients have increase in ceruloplasmin level in comparison with control and IBD patients, however the observation was not significant. Intestinal ceruloplasmin mediate absorption of Fe. It seems that the increase in ceruloplasmin expression in the IBS patients is a compensatory mechanism to increase Fe absorption in IBS patients, but in IBD patients with severe condition, no difference in ceruloplasmin levels was observed with controls.
Our study examined the differences between IBD and IBS diseases in nutritional oxidative status factors. The study also had a control group that strengthens the process and data. As the results show, it seems that the IBD group shows more differences with healthy and control individuals in the invistigated parameters. It seems that the IBS is the initial stage of IBD that is gradually becomes more severe. More IBD and IBS are two different diseases but with over overlap factors.