Biomaterial Database

Recurrent bacterial infections associated with C3 nephritic factor and hypocomplementemia. 1983

K M Edwards, and R Alford, and H Gewurz, and C Mold

UI	MeSH Term	Description	Entries
D008297	Male		Males
D008585	Meningitis, Meningococcal	A fulminant infection of the meninges and subarachnoid fluid by the bacterium NEISSERIA MENINGITIDIS, producing diffuse inflammation and peri-meningeal venous thromboses. Clinical manifestations include FEVER, nuchal rigidity, SEIZURES, severe HEADACHE, petechial rash, stupor, focal neurologic deficits, HYDROCEPHALUS, and COMA. The organism is usually transmitted via nasopharyngeal secretions and is a leading cause of meningitis in children and young adults. Organisms from Neisseria meningitidis serogroups A, B, C, Y, and W-135 have been reported to cause meningitis. (From Adams et al., Principles of Neurology, 6th ed, pp689-701; Curr Opin Pediatr 1998 Feb;10(1):13-8)	Meningitis, Neisseria,Neisseria Meningitis,Meningitis, Meningococcal, Serogroup A,Meningitis, Meningococcal, Serogroup B,Meningitis, Meningococcal, Serogroup C,Meningitis, Meningococcal, Serogroup W-135,Meningitis, Meningococcal, Serogroup W135,Meningitis, Meningococcal, Serogroup Y,Meningitis, Meningococcic,Meningococcal Meningitis, Serogroup A,Meningococcal Meningitis, Serogroup B,Meningococcal Meningitis, Serogroup C,Meningococcal Meningitis, Serogroup W-135,Meningococcal Meningitis, Serogroup W135,Meningococcal Meningitis, Serogroup Y,Serogroup A Meningococcal Meningitis,Serogroup B Meningococcal Meningitis,Serogroup C Meningococcal Meningitis,Serogroup W-135, Meningococcal Meningitis,Serogroup W135, Meningococcal Meningitis,Serogroup Y, Meningococcal Meningitis,Meningococcal Meningitis,Meningococcal Meningitis, Serogroup W 135,Neisseria Meningitides,Serogroup W 135, Meningococcal Meningitis
D008875	Middle Aged	An adult aged 45 - 64 years.	Middle Age
D011014	Pneumonia	Infection of the lung often accompanied by inflammation.	Experimental Lung Inflammation,Lobar Pneumonia,Lung Inflammation,Pneumonia, Lobar,Pneumonitis,Pulmonary Inflammation,Experimental Lung Inflammations,Inflammation, Experimental Lung,Inflammation, Lung,Inflammation, Pulmonary,Inflammations, Lung,Inflammations, Pulmonary,Lobar Pneumonias,Lung Inflammation, Experimental,Lung Inflammations,Lung Inflammations, Experimental,Pneumonias,Pneumonias, Lobar,Pneumonitides,Pulmonary Inflammations
D012008	Recurrence	The return of a sign, symptom, or disease after a remission.	Recrudescence,Relapse,Recrudescences,Recurrences,Relapses
D003169	Complement Inactivator Proteins	Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.	Complement Cytolysis Inhibiting Proteins,Complement Cytolysis Inhibitor Proteins,Complement Inactivating Proteins,Serum Complement Inactivators,Complement Inactivators, Serum,Inactivating Proteins, Complement,Inactivator Proteins, Complement,Inactivators, Serum Complement,Proteins, Complement Inactivating,Proteins, Complement Inactivator
D003170	Complement Pathway, Alternative	Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.	Alternative Complement Pathway,Properdin Pathway,Alternative Complement Activation Pathway,Complement Activation Pathway, Alternative
D003176	Complement C3	A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.	C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D003178	Complement C3 Nephritic Factor	An IgG autoantibody against the ALTERNATIVE PATHWAY C3 CONVERTASE, found in serum of patients with MESANGIOCAPILLARY GLOMERULONEPHRITIS. The binding of this autoantibody to C3bBb stabilizes the enzyme thus reduces the actions of C3b inactivators (COMPLEMENT FACTOR H; COMPLEMENT FACTOR I). This abnormally stabilized enzyme induces a continuous COMPLEMENT ACTIVATION and generation of C3b thereby promoting the assembly of MEMBRANE ATTACK COMPLEX and cytolysis.	C3 NeF,C3 NeF IgG Autoantibodies,C3 NeF IgG Autoantibody,C3NeF IgG Autoantibodies,C3NeF IgG Autoantibody,C 3 Nephritic Factor,C3 Nephritic Factor,Complement 3 Nephritic Factor,Autoantibody, C3NeF IgG,IgG Autoantibody, C3NeF
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man