Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Rheumatology (Oxford) ; 40(3): 290-6, 2001 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-11285376

RESUMO

BACKGROUND: Primary fibromyalgia syndrome (PFS) is a chronic disorder commonly seen in rheumatological practice. The pathophysiological disturbances of this syndrome, which was defined by the American College of Rheumatology in 1990, are poorly understood. This study evaluated, in 30 patients, the hypothesis that PFS is a pain modulation disorder induced by deregulation of serotonin metabolism. OBJECTIVES: To compare platelet [(3)H]imipramine binding sites and serotonin (5-HT) levels in plasma-rich platelets (PRP) of PFS patients with those of matched healthy controls and to compare the levels of biogenic amine metabolites in the cerebrospinal fluid (CSF) of PFS patients with those of matched controls. METHODS: Platelet [(3)H]imipramine binding sites were defined by two criteria, B(max) for their density and K(d) for their affinity. PRP 5-HT and CSF metabolites of 5-HT (5-hydroxyindoleacetic acid, 5-HIAA), norepinephrine (3-methoxy, 4-hydroxy phenylglycol, MHPG) and dopamine (homovanillic acid, HVA) were assayed by reversed-phase high-performance liquid chromatography with coulometric detection. RESULTS: [(3)H]Imipramine platelet binding was similar (P=0.43 for B(max) and P=0.30 for K(d)) in PFS patients (B(max)=901+/-83 fmol/mg protein, K(d)=0.682+/-0.046) and in matched controls (B(max)=1017+/-119 fmol/mg protein, K(d)=0.606+/-0.056). PRP 5-HT was significantly higher (P=0.0009) in PFS patients (955+/-101 ng/10(9) platelets) than in controls (633+/-50 ng/10(9) platelets). When adjusted for age, the levels of all CSF metabolites were lower in PFS patients. The CSF metabolite of norepinephrine (MHPG) was lower (P:=0.003) in PFS patients (8.33+/-0.33 ng/ml) than in matched controls (9.89+/-0.31 ng/ml) and 5-HIAA was lower (P=0.042) in PFS female patients (22.34+/-1.78 ng/ml) than in matched controls (25.75+/-1.75 ng/ml). For HVA in females, the difference between PFS patients (36.32+/-3.20 ng/ml) and matched controls (38.32+/-2.90 ng/ml) approached statistical significance (P=0.054). CONCLUSION: Changes in metabolites of CSF biogenic amines appear to be partially correlated to age but remained diagnosis-dependent. High levels of PRP 5-HT in PFS patients were associated with low CSF 5-HIAA levels in female patients but were not accompanied by any change in serotonergic uptake as assessed by platelet [(3)H]imipramine binding sites. These findings do not allow us to confirm that serotonin metabolism is deregulated in PFS patients.


Assuntos
Aminas Biogênicas/líquido cefalorraquidiano , Plaquetas/metabolismo , Fibromialgia/sangue , Fibromialgia/líquido cefalorraquidiano , Imipramina/farmacocinética , Serotonina/metabolismo , Plaquetas/efeitos dos fármacos , Dopamina/metabolismo , Feminino , Fibromialgia/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Norepinefrina/metabolismo , Trítio/farmacocinética
2.
Ann Fr Anesth Reanim ; 11(5): 587-91, 1992.
Artigo em Francês | MEDLINE | ID: mdl-1335704

RESUMO

Two cases of thrombocytopenia due to a low molecular weight heparin (Fraxiparine) are reported. The first case was a 35-year-old alcoholic man with acute mild pancreatitis. After having been treated with Fraxiparine for 12 days to prevent venous thrombosis, routine laboratory studies revealed a thrombocytopenia (49 G.l-1). At the same time, a minor haemorrhage occurred in the nasogastric tube. Prothrombin time, partial thromboplastin time, fibrin degradation products and D-dimers remained normal. There were no soluble fibrin monomers. Fraxiparine was discontinued. The thrombocyte count continued to decrease (12 G.l-1) up to the thirteenth day, it raised 3 days later to 110 G.l-1, and returned to normal after 9 days more (395 G.l-1). The second patient was a 58-year-old man given prophylactic Fraxiparine between the 5th and 16th days after admission for a severe asthma attack. Here again, after 12 days of treatment, the thrombocyte count decreased to 74 G.l-1. There were no other abnormalities, neither clinically nor in laboratory findings. Heparin administration was discontinued and the thrombocytopenia had resolved 3 days later. In both patients, the diagnosis of thrombocytopenia elicited by low molecular weight heparin was confirmed by finding, in vitro, a platelet aggregating factor in the presence of Fraxiparine. The literature concerning this topic is reviewed and discussed.


Assuntos
Heparina de Baixo Peso Molecular/efeitos adversos , Trombocitopenia/induzido quimicamente , Adulto , Humanos , Masculino , Pessoa de Meia-Idade , Agregação Plaquetária/efeitos dos fármacos , Contagem de Plaquetas , Trombocitopenia/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...