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Calprotectin is a calcium binding protein with in-vitro fungitastic and bacteriostatic properties. Specifically, calprotectin is a 36kDA zinc and calcium binding protein. This protein is found in abundance in neutrophils as it accounts for 60 percent of the total cytosolic protein. Much lower concentrations of this calcium binding protein has been isolated from reactive macrophages and monocytes. The measurement of faecal calprotectin is used as a surrogate marker of the influx of neutrophils in the lumen of the bowel. Its levels act as a reliable marker for the presence of intestinal inflammation.1
So many studies support this hypothesis. Increased levels of faecal calprotectin have been found in cases of inflammatory disease, non steroidal anti-inflammatory drug treatment and colonic cancer.1,2 This suggests that the calcium binding protein is extremely sensitive for these range of conditions but it acts as a non specific marker of gastrointestinal inflammation. Inflammatory bowel diseases(1BD) constitute conditions that are responsible for a pathological inflammation of the bowel lumen. The influx of neutrophils into the lumen is a direct consequence of the inflammatory process.
The continuing reliance on faecal calprotectin measurements are driven by the poor correlation of histological and endoscopic findings with inflammatory bowel disease even though these are the primary options for clinical assessment of inflammatory disease activity.3,4 On the other hand, studies of faecal calprotectin have a positive correlation with the histological and endoscopic disease activity grading in ulcerative colitis. Even more important is that faecal calprotectin finding possess a closer correlation to histological findings than colonoscopic findings.1. This close correlation is attributable to the fact that ulcerative colitis is exclusively colonic. The faecal calprotectin measurement has a strong correlation with the levels of 111-idium labeled leukocytes which serves as the gold standard in the confirmatory diagnosis of intestinal inflammation.1 The measurement of the levels of calprotectin levels in faeces is only possible because it is entirely resistant to enzymatic degradation.
Ulcerative colitis, Crohn’s disease and neoplasms increase the levels of calprotectin but not in individuals with irritable bowel syndrome. In the latter, the levels remain normal. In summary, faecal calprotectin tests aid in the identification of organic bowel diseases against functional bowel diseases such as irritable bowel disease without the need for colonoscopy which is an invasive test. It is also important in the efficacy assessment of intestinal bowel disease treatments, prediction of flares or relapses of IBD as well as serving as an alternative diagnostic tool in patients with phobia for endoscopy or needles.
Lactose Tolerance in Infants
Lactose intolerance can be defined as a clinical symptom of specific or a general indication of the presence of abdominal pain, nausea, flatulence, diarrhea and or bloating ingestion of lactose or foods containing lactose. The magnitude of symptoms caused is dependent on the amount of lactose consumed, form of lactose containing food, or the degree of lactose deficiency, and is variable from one individual to another. In some texts, lactose intolerance is defined as lactose malabsorption that manifests when there is an imbalance between level of lactose ingestion and the inherent ability of lactase to hydrolyze the amount of lactose ingested.5
Primary lactase deficiency is solely attributable to the absolute or relative absence of lactase at the childhood development stage. It occurs in various age groups and is racially variable. In most cases it is the primary cause of lactose intolerance and or lactose malabsorption. The terms hereditary lactase deficiency, lactase nonpersistence and adult-type hypolactasia all refer to primary lactase deficiency. On the other hand, secondary lactase deficiency results from small injuries in the bowel. Such injuries can be caused by cancer chemotherapy, persistent diarrhea, acute gastroenteritis, small bowel overgrowth as well as any other cause of small injuries on the bowel wall. Even though these injuries can occur in any age group, they are more prevalent among infants.5
In comparison to primary or secondary lactase deficiency, congenital lactase deficiency is much rare. In fact, before the dawn of the 20th century children with congenital lactase deficiency could not survive due to the absence of readily accessible and nutritionally rich lactose free milk which could be used as a substitute. Another classification; developmental lactase deficiency, is used in reference to relative lactase deficiency which can be observed in preterm infants who have not achieved 34 weeks of gestation.
Diagnosis of Lactose Intolerance
Children suspected of lactose intolerance can be diagnosed partly on the basis of the presenting symptoms. Abdominal distention, abdominal cramping, flatulence and diarrhea are directly correlated to the amount of lactose ingested but independent of the cause of the malabsorption. These symptoms may or may not have any correlation with the degree of the deficiency of lactase. Amounts as little as 12g can cause chronic abdominal pain hence the physician should try to determine the nature of the infants’ food intake. Moreover, malabsorption of lactose increases the levels of lactose in colon.
These excesses are metabolized by intestinal bacteria to produce gases and volatile acids hence the flatulence. These same intestinal gases stimulate the intestinal nerves causing visceral cramps and intestinal distention. By keeping a good clinical history of the infants food intake and the presentation of symptoms, followed by an administration of a lactose free diet(basically for two weeks) and symptoms observation, the physician can be able to conclusively diagnose lactose intolerance. Should the lactose tolerance test fail to achieve diagnosis, stool examination can be done to determine any presence of parasites such as Cryptosporidia species of Giardia lamblia in the upper gastrointestinal tract. Lactose breath tests and breath hydrogen tests augment each other and they are more reliable that clinical history.5
Role of Breath Tests in the Investigation of the Gastrointestinal Tract
Breath tests can be used in the diagnosis of lactose intolerance. In this case, the biochemical test is performed by administering a standard amount of lactose such as 2g/kg-25g/kg after overnight fasting and measuring the concentration of hydrogen in expiration over a two to three hour duration. Should the concentration of hydrogen increase by >20ppm in expired air after approximately one hour, the results are positive for lactose malabsorption. However, false, positive and false negative results may be produced by the absence of hydrogen producing bacterial flora(10-15% of the population), recent usage of antimicrobial agents affecting bacterial activity, intestinal motility disorders, limited bacterial overgrowth and consumption of diets with high fiber content prior to the test. 5
Urea breath test is also useful in the diagnosis of H. pylori infection. The test is dependent on urease activity of the microorganism in the detection of active infection. The patient is made to ingest either 13C or 14C labeled urea and urease. If the microorganism is present, it will hydrolyze urea into isotypically labeled CO2 and ammonia. The carbon dioxide expired from the gastrointestinal tract can then be trapped and quantified. This test is commonly employed to identify patients with active infection. It also forms the basis for the establishment o a more effective treatment regimen.6
Calculation of Faecal Osmotic Gap and its Influence on Clinical Decisions
Briefly, the faecal electrolytes and osmotic gap test is used to differentiate between osmotic and secretory diarrhea. It is important to note that the faecal electrolytes test is only feasible in the presence of liquid faecal samples since it is a measurement specifically in the water phase of the samples. The specimen for this test is usually liquid faeces. The laboratory request is faecal potassium and faecal sodium. A direct measure of the faecal osmolality is normally unhelpful and it is normally assumed that its value is 300mmol/kg water. However, if measured, the results are normally < 300 as a result of the breakdown of non absorbed carbohydrates by bacteria following defecation. 7
The faecal osmotic gap is then calculated as;
Faecal osmotic gap = 300 – 2(Na + K)
The results are interpreted as;
Faecal sodium < 60 mmol/L and an osmotic gap > 100 mmol/kg suggests osmotic diarrhea. Faecal sodium > 90 mmol/L and an osmotic gap < 50 mmol/kg suggests secretory diarrhea, or osmotic diarrhea due to sodium containing laxatives. 7, 8
Diagnosis of Cardiac Disease
Cardiac failure presents as hypotension, but there are variable definitions. The most commonly accepted diagnostic procedures include the systolic blood pressure(SBP) which is less that 90mmHg, mean arterial blood pressure(MAP) which is less than 60mmHg. These determinants of blood pressure are useful in determining the pathophysiology of hypertension. For instance, according to Ohm’s law;
Pressure = Flow x Resistance, thus,
MAP ≈ CO x SVR
This implies that MAP is directly proportional to cardiac output CO and can be used to determine the systemic vascular resistance(SVR). Cardiac Output is determined by the stroke volume(SV) and heart rate(HR), hence;
MAP ≈ HR x SV x SVR
Stroke volume is in turn determined by myocardial afterload, preload and contractility, hence,
MAP ≈ HR x Preload x Afterload x Contractility.
In essence therefore, MAP is proportional to HR and measures of myocardial contractility, preload and afterload and hence hypotension can only occur when there is a decrease in HR, preload, afterload and contractility.9