39 research outputs found
Clinical practice: Protein-losing enteropathy in children
Protein-losing enteropathy (PLE) is a rare complication of a variety of intestinal disorders characterized by an excessive loss of proteins into the gastrointestinal tract due to impaired integrity of the mucosa. The clinical presentation of patients with PLE is highly variable, depending upon the underlying cause, but mainly consists of edema due to hypoproteinemia. While considering PLE, other causes of hypoproteinemia such as malnutrition, impaired synthesis, or protein loss through other organs like the kidney, liver, or skin, have to be excluded. The disorders causing PLE can be divided into those due to protein loss from intestinal lymphatics, like primary intestinal lymphangiectasia or congenital heart disease and those with protein loss due to an inflamed or abnormal mucosal surface. The diagnosis is confirmed by increased fecal concentrations of alpha-1-antitrypsin. After PLE is diagnosed, the underlying cause should be identified by stool cultures, serologic evaluation, cardiac screening, or radiographic imaging. Treatment of PLE consists of nutrition state maintenance by using a high protein diet with supplement of fat-soluble vitamins. In patients with lymphangiectasia, a low fat with medium chain triglycerides (MCT) diet should be prescribed. Besides dietary adjustments, appropriate treatment for the underlying etiology is necessary and supportive care to avoid complications of edema. PLE is a rare complication of various diseases, mostly gastrointestinal or cardiac conditions that result into loss of proteins in the gastrointestinal tract. Prognosis depends upon the severity and treatment options of the underlying disease
Conversion and identity in early colonial perspectives Friars and indians in Mesoamerica, 1545-1679
SIGLEAvailable from British Library Document Supply Centre- DSC:D60309 / BLDSC - British Library Document Supply CentreGBUnited Kingdo
Das kulturelle gedächtnis mesoamerikas im kulturvergleich zum alten China : rituale im spiegel von schrift und mündlichkeit
The use of nitrofurantoin for children with acute cystitis caused by extended-spectrum Β-lactamase–producing Escherichia coli
The ideological manipulation of Hebrew literature in English translation in the 1970s and 1980s
A case of Lemierre’s syndrome complicated by clival osteomyelitis and bilateral cranial nerve XII palsy
Learning from poor single women’s autonomous households in Mexico in the sixteenth and seventeenth centuries
Mycobacterium simiae Infection in Two Unrelated Patients with Different Forms of Inherited IFN-ÎłR2 Deficiency
Interferon-Îł receptor 2 (IFN-ÎłR2) deficiency is a rare primary immunodeficiency characterized by predisposition to infections with weakly virulent mycobacteria, such as environmental mycobacteria and BCG vaccines. We describe here two children with IFN-ÎłR2 deficiency, from unrelated, consanguineous kindreds of Arab and Israeli descent. The first patient was a boy who died at the age of 4.5 years, from recurrent, disseminated disease caused by Mycobacterium simiae. His IFN-ÎłR2 defect was autosomal recessive and complete. The second patient was a girl with multiple disseminated mycobacterial infections, including infection with M. simiae. She died at the age of 5 years, a short time after the transplantation of umbilical cord blood cells from an unrelated donor. Her IFN-ÎłR2 defect was autosomal recessive and partial. Autosomal recessive IFN-ÎłR2 deficiency is life-threatening, even in its partial form, and genetic diagnosis and familial counseling are therefore particularly important for this condition. These two cases are the first of IFN-ÎłR2 deficiency associated with M. simiae infection to be described