Differential diagnosis
Other diseases may cause an increased excretion of fecal calprotectin, such as infectious diarrhea, untreated coeliac disease, necrotizing enterocolitis, intestinal cystic fibrosis and neoplastic pediatric tumor cells.Conditions with similar symptoms as Crohns disease includes intestinal tuberculosis, Behçets disease, ulcerative colitis, nonsteroidal anti-inflammatory drug enteropathy, irritable bowel syndrome and coeliac disease.Conditions with similar symptoms as ulcerative colitis includes acute self-limiting colitis, amebic colitis, schistosomiasis, Crohns disease, colon cancer, irritable bowel syndrome, intestinal tuberculosis and nonsteroidal anti-inflammatory drug enteropathy.Liver function tests are often elevated in inflammatory bowel disease, and are often mild and generally return spontaneously to normal levels. The most relevant mechanisms of elevated liver functions tests in IBD are drug-induced hepatotoxicity and fatty liver. Classification
The chief types of inflammatory bowel disease are Crohns disease and ulcerative colitis (UC). Inflammatory bowel diseases fall into the class of autoimmune diseases, in which the bodys own immune system attacks elements of the digestive system.Accounting for fewer cases are other forms of IBD, which are not always classified as typical IBD:
Microscopic colitis subdivided into collagenous colitis and lymphocytic colitis
Diversion colitis
Behçets disease
Early Onset IBD
Indeterminate colitisNo disease specific markers are currently known in the blood, enabling the reliable separation of Crohns disease and ulcerative colitis patients. The way doctors can tell the difference between Crohns disease and UC is the location and nature of the inflammatory changes. Crohns can affect any part of the gastrointestinal tract, from mouth to anus (skip lesions), although a majority of the cases start in the terminal ileum.
Both subtypes are autosomal recessive disorders, meaning that a mutant allele must be inherited from both parents in order to cause disease.Subtype I: Neutral Lipid Storage Disease with Myopathy (NLSD-M), is caused by a mutation in the PNPLA2 gene, which reduces the normal expression orfunction of the ATGL protein. PNPLA2 is located on chromosome 11. ATGL is an enzyme involved in catabolism of triglycerides (long-term fat storage) into fatty acids (short-term fat storage) within the body In the absence of fully functional ATGL, triglycerides accumulate in the bloodstream and bodily tissues. Interestingly, individuals with NLSD are not typically obese. It has been proposed that the assimilation, rather than degradation of triglycerides is the main factor in fat accumulation in adipose cells. In the absence of functional ATGL, triglycerides accumulate in the bloodstream and bodily tissues. Interestingly, individuals with NLSD are not typically obese. It has been proposed that the assimilation, rather than degradation of triglycerides is the main factor in fat accumulation in adipose cells. Patients with NLSD-M display progressive skeletal myopathy and severe cardiomyopathy in ~40% of cases. The pathophysiology and mechanistic basis of myopathy arising from deficits is lipid metabolism is not yet known.Subtype II:  Neutral Lipid Storage Disease with Ichthyosis (NLSD-I), or Chanarin-Dorfman syndrome, is caused by a mutation in the CGI-58 protein. CGI-58 is a coactivator of ATGL, and together these proteins sustain blood lipid levels between meals.