Biomedical subjects

P Economopoulos

Publications and source records attributed to P Economopoulos.

18 recordsLinked to original sources

PubMed2003

Localised gastrocnemius myositis in Crohn's disease.

A19-year-old woman presented with pain and tenderness in both calves associated with pyrexia and neutrophil leukocytosis. Gastrocnemius muscle biopsy showed a non-specific lymphocytic myositis and she was found to have positive c-ANCA, in the absence of other evidence of systemic vasculitis. Subsequent investigation of her gastrointestinal tract revealed extensive Crohn's disease. The myositis responded promptly to treatment with prednisolone 0.5 mg/kg. A review of the literature showed that localised calf pain in the setting of Crohn's disease can be caused by non-specific myositis, granulomatous myositis or vasculitis. It is proposed that the "gastrocnemius myalgia syndrome" be included in the typical - albeit rare - extraintestinal manifestations that may herald the appearance of inflammatory bowel disease.

Adult↗

PubMed2001

The effect of human platelet alloantigen polymorphisms on the in vitro responsiveness to adrenaline and collagen.

A number of clinical studies have suggested that carriage of the low frequency allele (b) of the human platelet antigen 1 (HPA-1) system is a risk factor for coronary thrombosis. We have examined the effect of a series of HPA biallelic polymorphisms (systems -1, -2, -3 and -5) on the in vitro platelet aggregation in response to adrenaline and collagen in 30 healthy volunteers. There was a significantly higher prevalence (10 out of 18) of carriers of the HPA-1b polymorphism among subjects showing a > 50% aggregation response to adrenaline ('responders') than the prevalence (1/12) in 'non-responders' (P < 0.05). Platelets heterozygous for the HPA-1b polymorphism showed a significantly higher rate (slope) and greater extent (%) of adrenaline-induced aggregation than platelets not carrying the HPA-1b allele (P < 0.05). A greater extent of collagen-induced aggregation was also demonstrated in HPA-1ab platelets (P < 0.05). Inhibition of adrenaline-induced aggregation following incubation with aspirin was greater (P < 0.01) in HPA-1ab than in HPA-1aa platelets. Collagen-induced aggregation was slower in carriers of the HPA-5b allele than in HPA-5aa subjects (P < 0.05). Polymorphisms of the HPA-2 and HPA-3 systems were not associated with different aggregation responses to either adrenaline or collagen. These results support the clinical observation that polymorphism HPA-1b may predispose to increased platelet thrombogenicity and suggest that the presence of polymorphism HPA-5b might render the platelet less reactive to collagen.

Adult↗

PubMed1996

Glucocorticoids stimulate prostaglandin H synthase type-2 (PGHS-2) in the fibroblast cells in human amnion cultures.

The human amnion may be an important source of prostaglandins involved in the onset of labour. Glucocorticoids are possible regulators of amnion prostaglandin synthesis and have been shown to stimulate the PGE2 output and prostaglandin H2 synthase (PGHS) activity of human amnion cells maintained in primary monolayer culture. There are two known isoforms of PGHS: the constitutively expressed PGHS-1 and the inducible PGHS-2. Recent studies have shown that the latter isoform is induced by glucocorticoids. The amnion consists of a single layer of epithelial cells beneath which lies a mesenchymal layer containing fibroblasts and it is not known which cell types are responding to glucocorticoids in this manner. In the present study, we demonstrate that although both cell types are present in culture, PGHS-2 protein and mRNA levels increase exclusively within the fibroblasts in response to dexamethasone, while PGHS-1 protein and mRNA levels remain unaffected in both cell types. These results suggest that the stimulation of PGE2 in cultured amnion cells by glucocorticoids is due to an upregulation of PGHS-2 gene transcription in fibroblasts, and that these previously overlooked cells may have important roles to play in the synthesis of prostaglandins involved in labour.

Amnion↗

PubMed1977