Several factors have been reported to affect faecal calprotectin levels. Some of these factors have been investigated in this study through the survey. Referring to Figure 3.1, 34% participant are aged between 50-59 years. From this study, a correlation between age and calprotectin level is positive, meaning that, as age of participant increases, calprotectin level increases (p <0.05; R=0.249) (Table 3.6). Another study also reported that calprotectin level increases with age in adults [103]. The increase in faecal calprotectin with age can possibly due to failing immune function [94].
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Socioeconomic status is another factor which is thought to impact on calprotectin level. Figure 3.2 shows that 48.86% participants were from medium socioeconomic status. From Table 3.7, the correlation between socioeconomic status and calprotectin level was statistically significant (p< 0.05). The Correlation coefficient R is -0.215, implying that in Mauritius, as socioeconomic status decreases, calprotectin level increases. This implies that participants from low socioeconomic status had higher calprotectin levels as compared to participants from high socioeconomic status who had low calprotectin levels. Another study reported that low socioeconomic status is associated with significantly elevated levels of biomarkers of inflammation (IL-6, CRP and TNF-α) as compared to high socioeconomic status [99].
The health status of participants was divided in 3 subcategories: healthy, unhealthy, and quite healthy. From Figure 3.3, 66% participants stated that they are healthy while 20% were unhealthy. Referring to Table 3.8, no positive correlation exists between health status and calprotectin level (p>0.05). This implies that health status of the individual does not affect calprotectin level.
47 % participants judged that they were moderately stressed (Figure 3.6). Stress has long been implicated in the pathogenesis of several GI conditions. Stress profile is known to contribute to GI inflammation. From this study, a statistically significant correlation does not exist between calprotectin and stress level (p>0.05) (Table 3.10). This demonstrates that as stress level rises; calprotectin does not increase accordingly, implying that according to the test, GI inflammation is not observed accordingly. This is refuted by findings of another study, reporting that stress is a potent modulator of the inflammatory response in the gut [104].
Among other lifestyle factors which can affect calprotectin level and thus GI inflammation is undoubtedly alcohol consumption. Excessive alcohol consumption often results in intestinal damage, mediated by inflammatory processes [105]. Figure 3.7 shows that only 4.55% participants consumed alcohol regularly. Statistical analysis demonstrates no correlation between alcohol consumption and calprotectin level (p> 0.05; Table 3.11). Another study also reported that faecal calprotectin level in active-drinking alcoholics are not significantly different, compared with controls. These results may suggest the absence of a subclinical intestinal inflammation involving neutrophils in the alcoholics [105].
Cigarette smoking is another factor likely to cause GI inflammation and thus, affecting calprotectin level. With reference to Figure 3.8, 20.45% participants smoke. Table 3.12 shows that the correlation coefficient is 0.073, however, it is not significant (p>0.05). There is no linear relationship between smoking and calprotectin level. However, literature suggests that smoking modifies pro/anti-inflammatory cytokines, which can contribute to inflammation [78]. Cigarette smoke and nicotine can aggravate colon and stomach inflammation [79]. However, this study concludes that no correlation exists between cigarette smoking and calprotectin level.
Genetic influences can also alter the probability of suffering from GI inflammation. The study reveals that 40.91% participants (Figure 3.9) have family history of GI inflammation. Using the Mann Whitney test, a statistically significant correlation is seen between calprotectin level and family history of GI inflammation (p < 0.05) (Table 3.13).
Literature suggests that GI surgery may have a protective or detrimental effect on GI inflammation. From Figure 3.11, 12.50% participants had undergone different types of GI surgery. The R2 value for GI surgery and calprotectin level is 0.037 (Table 3.16), implying that no linear relationship exists between calprotectin level and GI surgery. There is only 3.7% chance of having a linear relationship between calprotectin concentration and GI surgery. With reference to Table 3.15, it can be depicted that the correlation between calprotectin concentration and GI surgery is not statistically significant (p>0.05).
Consumption of different types of food may have different types of outcome on the GIT. Some food can have a protective role on the GIT while others have detrimental effects. Table 3.2 shows that 62.5% participants consume fruits & vegetables daily while 50% consume meat & dairy products every day. A correlation between consumption of fruit & vegetables and calprotectin level is statistically significant (R=0.236, p<0.05) (Table 3.17). This means that with the consumption of fruits and vegetables, calprotectin level increases. No such correlation was noticed with other classes of food. However, literature suggests that there is an inverse relationship between calprotectin level and vegetable consumption [94]. The effects of dietary constituents on faecal calprotectin may be via their effects on colonic bacteria. In the colon, dietary fibre is fermented by bacteria causing changes to the species distribution of the bacterial flora. A diet low in fibre and vegetables may promote the growth of more unfavourable microbial species [94].
Referring to Figure 3.12, it can be seen that 65.91% participants took antibiotics in the last 6 months while 34.09% did not. The Mann Whitney test suggests that there is no correlation between antibiotic intake and calprotectin level (p>0.05) (Table 3.18).
4.2 Central obesity and GI inflammation
One aim of this study is to determine whether centrally obese males are more susceptible to GI inflammation or not. 44 participants (50%) were centrally obese while 44 (50%) had a normal waistline (Figure 3.4). The BMI of participants was also assessed. From Figure 3.5, it can be concluded that 56.82% participants had normal BMI (18.5-24.9 kg/m2), 36.36% were overweight (25.0≤BMI≤29.9) and 6.82% participants were obese (BMI≥30.0). It should be noted that an individual with central obesity does not necessarily mean that he is obese. Centrally obese participants can have normal BMI as well.
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Using the Spearman’s correlation, a statistically significant correlation between central obesity and calprotectin level was not found (p> 0.05) (Table 3.9). Moreover, there is no statistically significant correlation between BMI and GI inflammation (Table 3.9). Calprotectin is described as a novel marker of obesity [106]. Literature suggests that central obesity correlates more strongly with disease states compared with total body fat [7]. Another study reported that faecal calprotectin level is normally elevated in individuals with increased BMI [107]. In addition, obesity-relaed systemic changes can create conditions predisposing to gut inflammation [108]. One study reported that though patients have high faecal calprotectin level, which is characteristic of GI inflammation, they may not necessarily have associated symptoms [7]. This provides evidence that there can be increased inflammatory activity in normal subjects associated with obesity.
4.3 Drug use and GI inflammation
The main objective of this study is to investigate drug use and GI inflammation. Referring to Table 3.21, a statistically significant correlation was not noted between drug use and calprotectin level (p>0.05). It should be noted that in this study, none of the participants had calprotectin levels higher than 620 pg/ mL, which is the cut off point for this ELISA kit. This implies that no participant suffered from GI inflammation. With reference to Table 3.5, the maximum calprotectin level recorded is 300pg/mL. The mean calprotectin level is 97.3 pg/mL.
Referring to Table 3.4, 10.2% participants consume hypoglycaemic drugs while 9.1% use both hypoglycaemic and antihypertensive drugs. Yet, no correlation was found between drug use and GI inflammation (Table 3.21). With reference to Figure 3.19, 39.77% participants use drugs daily. However, no statistically significant correlation was noted between duration of therapy and calprotectin level (p > 0.05) (Table 3.22). This suggests that duration of drug therapy does not influence calprotectin level and hence GI inflammation. Other factors such as frequency of therapy with a given drug or whether the drug is brand or generic also do not affect calprotectin levels (Table 3.22).
One study reported that low-dose aspirin treatment does not increase faecal calprotectin levels, although the use of NSAIDs might cause a rise in calprotectin concentrations due to NSAID-induced enteropathy in patients without IBD [39]. This study shows that aspirin does not increase calprotectin level; however, it also demonstrates that NSAIDs do not increase calprotectin level as no participant taking NSAIDs had calprotectin level above the cut off value.
4.4 Signs and symptoms of GI inflammation and calprotectin level
With reference to Figure 3.13, 37.50% of the participants stated that they have suffered from GI inflammation in the past. Among those who have suffered from inflammation in the past, 17.05% suffered from gastritis while 11.36% suffered from inflammation of the intestine (Figure 3.14).
Some participants have recently suffered from signs and symptoms of GI inflammation such as abdominal pain. Referring to Table 3.3, it can be seen that 27.3% participants suffered from no signs and symptoms of GI inflammation. Another 27.3% stated that they suffered from diarrhoea, abdominal pain and flatulence recently. These are clinical symptoms of GI inflammation. However, despite this fact, no statistically significant correlation was noted between signs & symptoms of GI inflammation and calprotectin level (p>0.05) (Table 3.20). Despite this fact that participants clinically suffered from signs and symptoms of GI inflammation, no calprotectin level above the cut-off point of 620 g/mL (Table 3.5) was detected. Although clinical signs & symptoms of GI inflammation were present, the calprotectin level might not have risen to a concentration high enough to be detected by the ELISA kit. This may account for calprotectin levels below the cut-off value.
In addition, among those suffering from signs and symptoms of GI inflammation, 29.55% of them ultimately took drugs to alleviate these symptoms (Figure 3.15). Furthermore, Figure 3.16 depicts that among those suffering from signs & symptoms of GI inflammation, in 57.95% cases, they were acute while in 13.64% cases, these signs and symptoms were chronic. These two factors might have contributed to the fact that no correlation is seen between calprotectin level and signs of GI inflammation as these drugs might have attenuated the inflammation, if ever present, which could have resulted in calprotectin levels below the cut-off point. Moreover, since the inflammation they suffered from was mostly acute, this might imply that the calprotectin level might not have reached a concentration high enough to be detected by the ELISA kit.
4.5 Calprotectin level
With reference to Table 3.5, it can be seen that the minimum calprotectin level recorded was 20pg/mL while the maximum level recorded is 300pg/mL. The table also demonstrates that 15.9% of participants had calprotectin level of 80pg/mL. However, we can conclude that none of the participants suffered from GI inflammation because in no case, the calprotectin level exceeded 620pg/mL, which is the cut-off point for this ELISA kit. Only values above 620pg/mL indicate that GI inflammation is detected. Otherwise for all values below 620pg/mL, it suggests that GI inflammation is absent. Another study reported that the normal range for calprotectin is 52.8-352.9 μg/mL, meaning that levels of calprotectin above 352.9 μg/ mL should be considered positive for GI inflammation [109]. This shows that there is inter-kit variation for cut-off points for calprotectin level.
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