Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic arteritis is a rare complication in systemic lupus erythematosus (SLE). Information about its clinical manifestations is still very limited. Elevated serum r-glutamyl transpeptidase and alkaline phosphatase levels, but without elevated bilirubin and transaminase levels, were found in the present report to be the clinical presentation of hepatic arteritis. This clinical picture originally suggested a disease of the biliary tree. Hepatic arteritis must be included in the differential diagnosis of biliary tract disorders in SLE.
Lupus 1995 Apr
PMID:Clinical manifestations of hepatic arteritis in systemic lupus erythematosus. 779 21

Antiphospholipid syndrome (APS) is defined by the presence of aPL antibodies in patients with thromboembolic phenomena. Some antiphospholipid (aPL) antibodies, such as those directed against beta2-glycoprotein I (beta2GPI), are associated with thromboembolism, possess Lupus Anticoagulant (LA) activity and recognize their target antigen only when bound to specific surfaces or to phospholipids (PL). To ascertain whether both free and antibody-bound beta2GPI circulate in APS, we set up an ELISA to detect [IgG anti-beta2GPI-beta2GPI] immune complexes. In this system, rabbit anti-human beta2GPI antibodies were adsorbed onto plastic plates, incubated with patient plasma, and bound complexes were detected by means of alkaline phosphatase-labeled goat anti-human IgG; each assay was stopped when positive controls consisting of in vitro generated immune complexes reached an Optical Density (OD) of 0.5 at 405 nm. Plasma from 16 patients with APS showed a mean OD405 of 0.291 (range 0.115-0.558), not statistically different from the mean obtained for 15 age- and sex-matched healthy volunteers (mean OD405 = 0.169, range 0.066-0.264). Surprisingly, levels of immune complexes in 14 patients with other autoimmune diseases and no circulating anti-beta2GPI antibodies were statistically higher (mean OD405 = 0.552, range 0.204-0.991) than those of healthy subjects and patients with APS. These data indicate that while autoantibodies to beta2GPI are mainly unbound in plasma of patients with APS, they are complexed with their antigen in patients with other autoimmune diseases, possibly reflecting a higher binding affinity.
Lupus 1999
PMID:[Anti-beta2 glycoprotein I-beta2 glycoprotein I] immune complexes in patients with antiphospholipid syndrome and other autoimmune diseases. 1019 6

The aim of this study was to assess the skeletal metabolism in a murine model of systemic lupus erythematosus (SLE). MRL/n and MRL/l mice (respectively representing a benign and a malignant form of the disease) were observed from 1.5 to 6.5 months of life. The monthly follow-up included: biochemical and histomorphometrical studies of the femoral bone, serum biochemistry, immunoglobulins and osteocalcin, and histological evaluation of the kidney tissue. The results showed a higher femoral weight (+11.5%), calcium (+4.4%) and protein bone content (+11.4%) and a significantly higher (+77%) phosphorus bone content in the MRL/n group; significantly lower (-48.9%) bone alkaline phosphatase enzymatic activity, lower bone alkaline/acid phosphatase enzymatic activities ratio (-40.8%) and lower (-38.4%) serum osteocalcin values in the MRL/l group (which might suggest reduced bone formation in these animals); markedly smaller trabecular bone volume (BV/TV) in the femoral head (-36.2%) and femoral neck (-39.8%), and smaller cortical and femoral areas in the mid-femoral shaft (-38.8% and -38.1% respectively) in the MRL/l group; higher serum immunoglobulins, increased serum blood urea nitrogen (BUN) and creatinine and a higher index of activity in the kidney histology in the MRL/l group, indicating increased activity of the disease in this substrain. The MRL mice, through their two substrains, may serve as a valuable laboratory animal model for study of the skeletal changes in SLE and of the influence of the disease activity on the skeletal metabolism.
Lupus 2001
PMID:Osteoporosis in murine systemic lupus erythematosus--a laboratory model. 1143 79

We describe a 24-year old male patient with systemic lupus erythematosus (SLE) with the gastrointestinal manifestations of protein-losing enteropathy (PLE) and primary sclerosing cholangitis (PSC). He presented with periorbital, scrotal and lower limb oedema. PLE was diagnosed because of hypoalbuminaemia together with an elevation of alpha-1-antitrypsin stool clearance and absence of proteinuria. PSC was diagnosed on the basis of an elevated serum alkaline phosphatase and lymphocytic and fibrous cholangitis. His disease was also complicated by neuropsychiatric lupus and hypogonadism. All the manifestations of SLE resolved with systemic corticosteroids and pulsed cyclophosphamide treatment. This case report documents the unusual association of SLE with PLE and PSC, and this relationship suggests that autoimmunity underlie the pathogenesis of these conditions.
Lupus 2006
PMID:Systemic lupus erythematosus with concurrent protein-losing enteropathy and primary sclerosing cholangitis: a unique association. 1653 81

A case of a genetically HLA-B27 patient fully investigated by molecular analyses, following a holistic vision and an anamnestic assessment of multi-site ecosystems is repeated. VDRL, Lupus anti-coagulant (LAC) and Widal-Wright (WWR), resulted positive. The antibodies (IgG/IgA anti-Ct) against chronic Chlamydia trachomatis inflammation were positive. In the context of all the enzymatic activities in reference range, the AMS and the ALP enzymatic activities showed an increasing trend and a time course augment depending respectively. Cultures, parasitological, digestibility tests and molecular analyses were then performed to investigate the different human ecosystems. Parasitological research and digestibility test were performed, resulting a latent chronic bowel inflammation, including certain enteroinvasive pathogens, such as, Salmonella, Shigella, Yersinia and Campylobacter (Enteric Pathogens Group, EPG) and Escherichia Coli pathogens (Escherichia Coli Pathogens Group, ECPG). The Salmonella typhi-DNA resulted positive, while 90% of the total microbic charge (TMC) was represented by C. freundi in culture analyses. Interpreting the VDRL positive test as early triggering of autoimmune disease, a few acute phase proteins as a pauci-symptomatic chronic phlogistic process, the amylase and alkaline phosphatase alterations as tissue markers of early intestinal inflammation, the Widal's reaction positivity together with the precocious clinical and faecal manifestations, this study suggests the prime triggering role of these atypical pathogens to cause a chronic low grade autoimmune response against the tissue/organ susceptible target, causing inflammaging phenomenon in young patient with chronic latent infection by Salmonella typhi, leading to Reiter's syndrome, in HLA-B27 positive patient.
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PMID:Can latent synergism of intestinal pathogens be responsible for inflammaging process causing Reiter's syndrome in a young patient HLA-B27 infected by atypical pathogens? A holistic view and clinical biochemical reinterpretation. 2324 Nov 24