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Results for “complex diseases”

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At least 451 records · Page 25Linked to original sources
PubMed1980

Virus-induced immune complex disease: specific anti-viral antibody and C1q binding material in the circulation during persistent lymphocytic choriomeningitis virus infection.

Mice of several strains persistently infected with lymphocytic choriomeningitis virus (LCMV) mount continuous anti-LCMV immune responses leading to the formation and tissue deposition of immune complexes. Such mice carry infectious virus-immunoglobulin (presumably anti-LCMV antibody) complexes in the circulation. We have now determined that anti-LCMV antibody both complexed and free is found in the circulation of mice persistently infected with LCMV. This antibody reacts specifically against the three main LCMV structural polypeptides: nucleoprotein, 63,000 m.w. and two glycopeptides, GP-1 and GP-2 with m.w. of 45,000 and 35,000, respectively. A C1q binding assay was developed and found to be effective in measuring C1Q binding substances (presumably virus-anti-viral Ig complexes) in the circulations of several strains of mice persistently infected with LCMV. With different strains of mice, the levels, time of formation, and fate of C1q binding materials varied markedly. Formation of antibodies to LCMV was correlated with the detection of C1q binding materials. Mice (SWR/J) persistently infected with lactic dehydrogenase virus also form infectious virus-Ig in their sera but deposit minimal amounts of complexes in their tissues. In such mice, C1q binding substances did not form in the circulation.

Animals↗
PubMed1990

The seborrheic disease complex. An approach to underlying causes and therapies.

Seborrhea is a multifaceted disease, and it is a common presentation in the small animal practice setting. This article addresses the considerations to be aware of in approaching the diagnosis of this complex entity. Emphasis is placed on recent advances of diseases that cause seborrhea and on appropriate therapy. A simplified practical approach to topical antiseborrheic shampoo therapy is presented.

Animals↗
PubMedDate not supplied

Secretory otitis media. An immune complex disease.

The purpose of our paper is to propose a possible mechanism involving an immune-mediated disease process. A microbiological, biochemical and immunological approach to substantiate such a mechanism is presented.

Adolescent↗
PubMed2001

Locating the genes underlying a simulated complex disease by discriminant analysis.

The purpose of this study was to propose and evaluate a novel multivariate approach for genetic mapping of complex binary human diseases. This approach uses the application of either of two methods of standard (stepwise) discriminant analysis to detect linkage based on the differential marker identity-by-descent distributions among the three affection groups of sib pairs (concordantly affected, discordant, and concordantly unaffected). One of the advantages of this approach is that it allows for simultaneously testing all markers, as well as other genetic and environmental factors, in a single multivariate setting. We have explored its properties and behaviors via an application to the simulated data in Genetic Analysis Workshop 12.

Chromosome Mapping↗
PubMed1998

Peliosis of the spleen: an immune-complex disease?

AIMS: To determine the pathogenesis of splenic peliosis by further morphological and immunohistochemical examination. METHODS AND RESULTS: Histological, electron microscopic and immunohistochemical examination revealed evidence for an inflammatory genesis of splenic peliosis with destruction of reticular fibres and local deposits of IgG and activated complement C3. CONCLUSION: Our findings indicate that the peliotic lesion in the spleen may be mediated by immune-complex deposits.

Female↗
PubMed2005

HEMICENTIN-1 (FIBULIN-6) and the 1q31 AMD locus in the context of complex disease: review and perspective.

Age-related macular degeneration (AMD) is the most common blinding disorder in the Western world. Similar to other common diseases in which age is a risk factor (e.g., type II diabetes or Alzheimer's disease), AMD is thought to have a complex etiology. Previously, a Gln5345Arg mutation in HEMICENTIN-1 was found to segregate with AMD in a large family. However, the population frequency of this allele is inconsistent with the large proportion of families shown by linkage studies to map near this gene at 1q31. This review summarizes current knowledge regarding the role of HEMICENTIN-1 in AMD, the results of association studies for the Gln5345Arg mutation, and the linkage evidence for an AMD locus on 1q31. The data can be reconciled through proposing both additional variants in HEMICENTIN-1 and a second genetic risk factor for AMD in the region.

Aging↗
PubMed2000

Drug-Drug interactions of clinical significance in the treatment of patients with Mycobacterium avium complex disease.

Therapeutic and prophylactic regimens directed specifically against Mycobacterium avium complex (MAC) are increasingly being used in patients infected with the human immunodeficiency virus (HIV). Several of the drugs used in the management of MAC have been associated with significant drug interactions involving the cytochrome P450 (CYP) enzyme system. This enzyme system is also highly influenced by other drugs used in the management of patients with HIV, particularly the protease inhibitors, non-nucleoside reverse transcriptase inhibitors (NNRTIs) and azole antifungals. This article reviews the published concentrations or subtherapeutic concentrations of other drugs have been described. In particular, concurrent use of rifabutin with clarithromycin or fluconazole has resulted in increased concentrations of rifabutin and an accompanying increase in the incidence of rifabutin toxicities, including uveitis and leucopenia. Similar results have been seen when rifabutin is combined with protease inhibitors or delavirdine. The macrolides, clarithromycin and azithromycin, have also been associated with significant drug interactions. Clarithromycin has a higher affinity for CYP than azithromycin and, thus, is more frequently associated with clinically significant drug interactions. Clarithromycin is an inhibitor of CYP and may result in toxic concentrations of other drugs metabolised by this enzyme system. Such interactions have been described with rifabutin and the statin lipid-lowering agents. In addition, nevirapine and efavirenz have been shown to significantly reduce clarithromycin concentrations, whereas the protease inhibitors and delavirdine may increase clarithromycin concentrations. Other drugs used in the management of patients with MAC are not metabolised by CYP and thus have a lower incidence of interactions, although the absorption of ciprofloxacin may be impaired when it is given with products containing multivalent cations, such as didanosine. However, clinicians must remain vigilant for drug interactions when reviewing a patient's medication profile, keeping in mind both interactions that have been described in the literature and those that may be predicted based upon known pharmacokinetic profiles.

Azithromycin↗
PubMed1982

Leukocytoclastic vasculitis. A cutaneous expression of immune complex disease.

Thirty-nine patients with clinical, histologic, and immunofluorescence evidence of leukocytoclastic (necrotizing) vasculitis were studied for the presence of circulating immune complexes. These patients were selected prospectively during a three-year interval from patients seen in a dermatology clinic. Clinical and serologic data are summarized and representative cases are presented. This large series of patients with leukocytoclastic vasculitis emphasizes both the frequency of this disorder and the varied disease settings within which it may manifest. The immunopathologic data presented support an immune complex-mediated pathogenesis for this disease process.

Adolescent↗
PubMed1979

Rheumatoid arthritis, immune complex disease, and hypereosinophilic syndrome. Report on a case.

A patient with typical rheumatoid arthritis is presented. After a short period of the disease a hyperosinophilic syndrome (HES) developed with vasculitis, pulmonary fibrosis, and thrombosis, and the disease took a malignant course. The patient died within a year after the diagnosis of HES. High titres of rheumatoid factor were manifested and total complement (CH50) was very low, indicating an active immune disease. As HES has been suggested to have an autoimmune aetiology, these findings are interesting, as positive rheumatoid serology has very rarely been reported in patients with this syndrome.

Arthritis, Rheumatoid↗