Crohn's disease and Takayasu's arteritis: An uncommon association

Takayasu’s arteritis(TA)and Crohn’s disease(CD)are two rare autoimmune disorders;however some reports describe the presence of both diseases in the same patient.This finding has suggested the possibility that both diseases could share some common etiologic origin.We describe a case of a 13-year-old male affected by CD characterized by fever,diarrhea,weight loss,abdominal pain and elevation of inflammatory markers.Clinical and histological features from colonic specimens were consistent with CD.Treatment with steroids and azathioprine was started,however disease flared every time steroids were tapered.One year later,while still on treatment,he came back to our attention for dyspnea at rest and at night,tiredness and weakness.At physical examination a diastolic heart murmur was found as well as a left carotid artery bruit.A transthoracic echocardiography showed mild aortic valve insufficiency,left ventricular hypertrophy and a dilated ascending aorta with same findings at the aortic arch.A computed tomography scan showed abdominal aortathickening,dilated thoracic aorta and the presence of a thoracic aortic aneurysm.TA associated with CD was diagnosed and medical treatment with cyclophosphamide,steroids and aminosalicylic acid was started,with good clinical response at 6 mo follow-up.We discuss the presence of possible common causes for the two diseases and the importance of differential diagnosis in those patients characterized for intractable disease.

Heterozygous nucleotide-binding oligomerization domain-2 mutations affect monocyte maturation in Crohn's disease

AIM： To investigate the function of monocytes in Crohn＇s disease （CD） patients and to correlate this with disease- associated nucleotide-binding oligomerization domain-2 （NOD2） gene variants. METHODS： Monocytes from 47 consecutively referred CD patients and 9 healthy blood donors were cultured with interleukin （IL）-4 and granulocyte-macrophage colony-stimulating factor （GM-CSF）, and stimulated with lipopolysaccharide （LPS） or muramyldipeptide （MDP）, the putative ligand of NOD2. RESULTS： We found that monocytes from CD patients differentiated in vitro to mature dendritic cells （DCs）, as determined by immunophenotype and morphology. IVOD2 genotype was assessed in all subjects, and we observed high CD86 expression on immature and LPS-stimulated DCs in IVOD2 mutated CD patients, as compared with wtlVOD2 CD patients and controls. By contrast, CD86 expression levels of DCs induced to maturity with MDP derived from IVOD2-mutated subjects were comparable to those of normal subjects. The amount of IL-12p70 in patient-cell cultures was larger than in controls aEer LPS treatment, but not aEer treatment with MDR CONCLUSION： Our results suggest that DCs obtained from patients with mutations in the IVOD2 gene display an activated phenotype characterized by high CD86 expression, but have a diminished response to MDP when compared to the terminal differentiation phase. We speculate that the altered differentiation of monocytes might lead to an imbalance between inflammation and the killing ability of monocytes, and may be relevant to the pathogenesis of CD.