Diagnosis is by renal biopsy, and treatment parallels the underlying IBD.Amyloidosis (see endocrinological involvement) secondary to Crohns disease has been described and is known to affect the kidneys.Pancreatic
Pancreatitis may be associated with both UC and CD. The most common cause is iatrogenic and involves sensitivity to medications used to treat IBD (3% of patients), including sulfasalazine, mesalamine, 6-mercaptopurine, and azathioprine. Pancreatitis may present as symptomatic (in 2%) or more commonly asymptomatic (8–21%) disease in adults with IBD.Cardiovascular and Circulatory
Children and adults with IBD have been rarely (<1%) reported developing pleuropericarditis either at initial presentation or during active or quiescent disease. The pathogenesis of pleuropericarditis is unknown, although certain medications (e.g., sulfasalazine and mesalamine derivatives) have been implicated in some cases. The clinical presentation may include chest pain, dyspnea, or in severe cases pericardial tamponade requiring rapid drainage. Nonsteroidal anti-inflammatory drugs have been used as therapy, although this should be weighed against the hypothetical risk of exacerbating the underlying IBD.In rare cases, cardiomyopathy, endocarditis, and myocarditis have been described.Crohns disease also increases the risk of blood clots; painful swelling of the lower legs can be a sign of deep venous thrombosis, while difficulty breathing may be a result of pulmonary embolism. Respiratory
Laryngeal involvement in inflammatory bowel disease is extremely rare. Only 12 cases of laryngeal involvement in Crohn disease have been reported until now. Moreover, only one case of laryngeal manifestations in ulcerative colitis has been reported so far.
Ostomy-related complications
Common complications of an ostomy (a common surgery in Crohns disease) are: Mucosal edema, Peristomal dermatitis, Retraction, Ostomy prolapse, Mucosal/skin detachment, Hematoma, Necrosis, Parastomal hernia, and Stenosis. Etiology
The etiology of Crohns disease is unknown. Many theories have been disputed, with four main theories hypothesized to be the primary mechanism of Crohns disease. In autoimmune diseases, antibodies and T lymphocytes are the primary mode of inflammation. These cells and bodies are part of the adaptive immune system, or the part of the immune system that learns to fight foreign bodies when first identified. Autoinflammatory diseases are diseases where the innate immune system, or the immune system we are genetically coded with, is designed to attack our own cells. Crohns disease likely has involvement of both the adaptive and innate immune systems. Autoinflammatory theory
Crohns disease can be described as a multifactorial autoinflammatory disease. The etiopathogenesis of Crohns disease is still unknown. In any event, a loss of the regulatory capacity of the immune apparatus would be implicated in the onset of the disease. In this respect interestingly enough, as for Blaus disease (a monogenic autoinflammatory disease), the NOD2 gene mutations have been linked to Crohns disease. However, in Crohns disease, NOD2 mutations act as a risk factor, being more common among Crohns disease patients than the background population, while in Blaus disease NOD2 mutations are linked directly to this syndrome, as it is an autosomal-dominant disease.