Food malabsorption/intolerance complaints triggered by primary epiploic appendagitis

Primary epiploic appendagitis (PEA) is an uncommon and self-limiting cause of acute or subacute abdominal complaints. The diagnosis of PEA, with its characteristic appearance, is made with computed tomography (CT). This report describes a patient seven months after a CT-confirmed diagnosis of PEA. Because of persistent and recurring, functional, non-specific abdominal complaints, food intolerance/malabsorption was investigated. Fructose malabsorption combined with histamine intolerance was found. A registered dietician helped develop an individually-tailored diet to address the problem. Within four days of beginning the fructose-free and histamine-reduced diet, the patient’s complaints resolved. In conclusion, abdominal symptoms caused by fructose malabsorption and histamine intolerance may have been triggered by PAE in this patient

Patent abdominal subcutaneous veins caused by congenital absence of the inferior vena cava: a case report

<p>Abstract</p> <p>Introduction</p> <p>Patent paraumbilical and abdominal subcutaneous veins are found frequently as collaterals in patients due to portal hypertension mainly in liver cirrhosis.</p> <p>Case presentation</p> <p>For evaluation of portal hypertension in a 72-year-old Caucasian man without liver cirrhosis, magnetic resonance imaging with gadolinium contrast-enhancement was performed and demonstrated a missing inferior vena cava. A blood return from the lower extremities was shown through enlarged collateral veins of the abdominal wall, vena azygos and hemiazygos continuation, and multiple liver veins emptying into the right cardiac atrium. We describe a rare case of abdominal subcutaneous wall veins as collaterals caused by a congenitally absent infrarenal inferior vena cava with preservation of a hypoplastic suprarenal segment.</p> <p>Conclusion</p> <p>Knowledge of these congenital variations can be of clinical importance and it is imperative for the reporting radiologist to identify these anomalies as they can have a significant impact on the clinical management of the patient.</p

Thoracic CT findings of novel influenza A (H1N1) infection in immunocompromised patients

The goal of this study is to describe the spectrum of initial and follow-up CT findings of novel influenza A (H1N1) infection in a series of immunocompromised patients. Eight immunocompromised patients with documented novel influenza A (H1N1) had CT imaging at our institution between May 2009 and August 2009. A total of 20 CTs (initial and follow-up) were reviewed for the presence, severity, and distribution of the following: ground glass opacity, consolidation, interlobular septal thickening, mosaic perfusion, airway wall thickening, airway dilatation, nodules, cysts, pleural effusion, pericardial effusion, lymphadenopathy, and air trapping. The most common findings were airway thickening/dilatation, peribronchial ground glass opacity, centrilobular nodules, and tree-in-bud opacities. Peripheral consolidation involving the lower lobes was also a common pattern. Findings frequently involved all lobes and were closely associated with either large or small airways. Two patients presented with atypical CT findings including focal lobar consolidation and patchy lower lobe consolidation with soft tissue centrilobular nodules. Most survivors showed near complete resolution of findings within 35 days. CT scans in immunocompromised patients with novel influenza H1N1 commonly show a strong airway predominance of findings or peripheral areas of consolidation involving the lower lobes. A subset of patients with novel influenza A (H1N1) will show findings not typical of viral infection

Hyper-IgG4 disease: report and characterisation of a new disease

BACKGROUND: We highlight a chronic inflammatory disease we call 'hyper-IgG4 disease', which has many synonyms depending on the organ involved, the country of origin and the year of the report. It is characterized histologically by a lymphoplasmacytic inflammation with IgG4-positive cells and exuberant fibrosis, which leaves dense fibrosis on resolution. A typical example is idiopathic retroperitoneal fibrosis, but the initial report in 2001 was of sclerosing pancreatitis. METHODS: We report an index case with fever and severe systemic disease. We have also reviewed the histology of 11 further patients with idiopathic retroperitoneal fibrosis for evidence of IgG4-expressing plasma cells, and examined a wide range of other inflammatory conditions and fibrotic diseases as organ-specific controls. We have reviewed the published literature for disease associations with idiopathic, systemic fibrosing conditions and the synonyms: pseudotumour, myofibroblastic tumour, plasma cell granuloma, systemic fibrosis, xanthofibrogranulomatosis, and multifocal fibrosclerosis. RESULTS: Histology from all 12 patients showed, to varying degrees, fibrosis, intense inflammatory cell infiltration with lymphocytes, plasma cells, scattered neutrophils, and sometimes eosinophilic aggregates, with venulitis and obliterative arteritis. The majority of lymphocytes were T cells that expressed CD8 and CD4, with scattered B-cell-rich small lymphoid follicles. In all cases, there was a significant increase in IgG4-positive plasma cells compared with controls. In two cases, biopsies before and after steroid treatment were available, and only scattered plasma cells were seen after treatment, none of them expressing IgG4. Review of the literature shows that although pathology commonly appears confined to one organ, patients can have systemic symptoms and fever. In the active period, there is an acute phase response with a high serum concentration of IgG, and during this phase, there is a rapid clinical response to glucocorticoid steroid treatment. CONCLUSION: We believe that hyper-IgG4 disease is an important condition to recognise, as the diagnosis can be readily verified and the outcome with treatment is very good