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.
Diagnosis
Stages
There are 4 stages of disease, with stage 4 being the rarest and most severe. Stage 1 Cells infiltrate the periphery of the flap, without involving central cornea. Stage 2 Peripheral cells migrate to the center of the cornea, and impair vision; presentation is usually 2 to 3 days after surgery. Stage 3 Cells at the central cornea form clumps of dense cell aggregates. Stage 4 Otherwise known as central toxic keratopathy, stage 4 characteristically has no inflammatory cells at the anterior chamber or cornea, but there is central stromal necrosis, and the cornea becomes opacified; onset is usually 3 to 9 days after refractive surgery. Treatment
Depending on severity, therapies may range from topical or oral anti-inflammatories to irrigation and surgical repair. References


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