Serial studies on circulating immune complexes in post-streptococcal sequelae.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Fillit.
Explore the source record for details and available documents.
We had a patient with primary acquired hypogammaglobulinemia (PAH), nodular lymphoid hyperplasia, giardiasis, and the subsequent development of regional enteritis (RE). The case is of interest because the development of regional enteritis in a patient with PAH has not been previously reported, to our knowledge. The interaction of hypogammaglobulinemia and RE is discussed from an immunologic point of view. The report adds RE to the many known bowel diseases associated with PAH.
Alzheimer's disease is a dementing disorder affecting increasingly large numbers of individuals in the aging population. The characteristic neuropathologic changes of Alzheimer's disease are the deposition of extracellular amyloid plaques, neurons containing neurofibrillary tangles, and neuronal cell loss. The A4 amyloid peptide is the major constituent of senile plaques. In addition to the A4 peptide, senile plaques contain a variety of molecular species, including proteoglycans and inflammatory components. The presence of proteoglycans in the amyloid deposits of Alzheimer's disease and of systemic amyloidoses suggests that these molecules play an active role in the pathogenesis of amyloidosis. However, the molecular mechanisms that lead to the codeposition of amyloid peptide with proteoglycans is still unknown. Recent evidence suggests that the metabolism of proteoglycans is altered in Alzheimer's disease patients. The acute-phase response observed in the brain of patients affected by Alzheimer's disease may be responsible for this effect. In this article, we discuss the role of proteoglycans in Alzheimer's disease, and the possible interactions between factors involved in brain inflammatory mechanisms and proteoglycans in the pathogenesis of Alzheimer's disease.