ABSTRACT
A 17-year-old woman presented with a 3-year history of recurrent, severe abdominal pain with spontaneous resolution within a few days. An ultrasound revealed nothing more than free fluid within the pelvis. An MRI of the small bowel was done within 24 hours of abdominal pain onset, which revealed extensive submucosal oedema associated with moderate volume ascites. A repeat MRI of the small bowel after 72 hours showed near-complete resolution of these changes. Checking C1 inhibitor levels confirmed a diagnosis of hereditary angio-oedema with an abdominal presentation. This is a rare cause of recurrent abdominal pain and, to our knowledge, the first case in which MR images have been obtained during and after an acute attack.
Subject(s)
Angioedemas, Hereditary , Abdominal Pain/etiology , Adolescent , Angioedemas, Hereditary/diagnostic imaging , Ascites , Edema/diagnostic imaging , Edema/etiology , Female , Humans , Magnetic Resonance ImagingSubject(s)
Adenosine Deaminase/deficiency , Bone Marrow Failure Disorders/genetics , Intercellular Signaling Peptides and Proteins/deficiency , Lymphopenia/genetics , Mutation , Neutropenia/genetics , Adenosine Deaminase/blood , Adenosine Deaminase/genetics , Adult , Amino Acid Sequence , Bone Marrow Failure Disorders/blood , Bone Marrow Failure Disorders/enzymology , Bone Marrow Failure Disorders/pathology , Female , Humans , Intercellular Signaling Peptides and Proteins/blood , Intercellular Signaling Peptides and Proteins/genetics , Lymphopenia/blood , Lymphopenia/enzymology , Middle Aged , Neutropenia/blood , Neutropenia/enzymology , PedigreeSubject(s)
Azepines/chemistry , Gene Expression Regulation, Neoplastic , Interleukin-6/metabolism , Lipopolysaccharides/chemistry , Multiple Myeloma/metabolism , Triazoles/chemistry , Aged , Aged, 80 and over , Antibodies, Monoclonal/chemistry , Cell Survival , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Protein Structure, Tertiary , Real-Time Polymerase Chain ReactionABSTRACT
Galectin-1, the prototype of a family of beta-galactoside-binding proteins, has been implicated in a wide variety of biological processes. Data presented herein show that galectin-1 stimulates monocyte migration in a dose-dependent manner but is not chemotactic for macrophages. Galectin-1-induced monocyte chemotaxis is blocked by lactose and inhibited by an anti-galectin-1 antibody but not by nonspecific antibodies. Furthermore, galectin-1-mediated monocyte migration was significantly inhibited by MEK inhibitors in a rapid, time-dependent manner suggesting that MAP kinase pathways are involved in galectin-1. Migration was also almost completely blocked by pertussis toxin implying G-protein involvement in the galectin-1-induced chemotaxis. These results demonstrate a role for galectin-1 in monocyte chemotaxis which differs from galectin-3 in that macrophages are nonresponsive. Furthermore, our observations suggest that galectin-1 may be involved in chemoattraction at sites of inflammation in vivo and may contribute to disease processes such as atherosclerosis.
