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61.
Bouleti C Iung B Laouénan C Himbert D Brochet E Messika-Zeitoun D Détaint D Garbarz E Cormier B Michel PL Mentré F Vahanian A 《Circulation》2012,125(17):2119-2127
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O. Debouverie P. Roblot F. Roy-Péaud C. Boinot F. Pierre O. Pourrat 《La Revue de médecine interne / fondée ... par la Société nationale francaise de médecine interne》2012
Purpose
The aim of this study was to assess the platelet count outcome during a pregnancy occurring in a series of 62 women followed for a chronic idiopathic thrombocytopenia.Methods
We studied the medical files of women who had a previous history of chronic idiopathic thrombocytopenia persistently below 150 G/L for at least 1 year, and who became pregnant over a 14-year period.Results
Sixty-two pregnancies (including 41 in women suffering from an immune thrombocytopenic purpura according to updated definition criteria) which occurred in 50 women, were analysed. At the beginning of the pregnancy, platelet count was above 150 G/L in 16% of the cases and lower than 50 G/L in 8%. Platelets decreased by more than 25% for 55% of the pregnancies, remained stable during pregnancy in 33% and improved in 12%. Platelet count remained above 50 G/L in 70% of the pregnancies and higher than 100 G/L in 27%. Mean nadir was 84 G/L at 31 weeks of gestation. A treatment was started in 40% of pregnancies, among them 64% of the cases during the last month only in order to allow locoregional anaesthesia at delivery. Platelet count was below 150 G/L at delivery in 82% of the women (116 ± 56 G/L). No bleeding occurred in 83% of the pregnancies. Neonatal mean platelet count was 225 ± 87 G/L, thrombocytopenia occurred in 17% of the babies (platelet count below 150 G/L), without any serious bleeding.Conclusion
Pregnancy worsens chronic idiopathic thrombocytopenia outcome in half of the cases, most of the time without any haemorrhagic complications. 相似文献64.
Emilie Morin France Berthelet John Weisnagel Martin Bidlingmaier Omar Serri 《Pituitary》2012,15(1):97-100
It has been suggested that treatment with adequate dose titration of pegvisomant, a GH antagonist, up to a maximum of 40 mg
daily, can achieve IGF-1 normalisation in virtually all patients with acromegaly. On the other hand, temozolomide (TMZ), an
alkylating cytostatic agent, has been reported to reduce pituitary tumour size and hormone hypersecretion in a small number
of aggressive pituitary macroadenomas. In this paper we report the case of a patient resistant to very high doses of pegvisomant
used in combination with somatostatin analogs (SSA) and to TMZ therapy. The patient, initially a 22 year-old man with an invasive
GH-secreting pituitary macroadenoma (IGF-1, 371% upper limit of normal), had active acromegaly despite a repeat transsphenoidal
surgery followed by radiotherapy and SSA (octreotide 800 μg sc daily) (IGF-1, 262% ULN). In combination with SSA, pegvisomant
was started at 20 mg daily and doses were titrated up to 60 mg daily. IGF-1 was moderately reduced and stabilized at 200%
ULN after 1 year of treatment. Serum pegvisomant level was 30,500 ng/l, the denaturalized GHBP concentration 1,120 pM and
the endogenous GH level was 220 μg/l. Pegvisomant was stopped and TMZ therapy was given for 5 cycles. However, the patient
reported an increase of acromegaly symptoms and the serum IGF-1 was raised to the same level prior to pegvisomant therapy.
Consequently, pegvisomant was tried again with doses up to 100 mg daily finally resulting in normalisation of serum IGF-1
level and improvement of acromegaly symptoms and patient well-being. We conclude that in some patients with severe acromegaly
refractory to multimodal therapy, biochemical control may be difficult to attain with conventional doses of pegvisomant or
TMZ therapy. 相似文献
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Dominique Bertrand Geoffroy Desbuissons Nicolas Pallet Alain Debure Albane Sartorius Dany Anglicheau Marie‐France Mamzer Christophe Legendre Rebecca Sberro‐Soussan 《Transplant international》2013,26(2):e4-e7
The side‐effects associated with the immunosuppressive drug sirolimus are numerous and constitute a major limitation for its use in renal transplantation. In this study, we describe two cases of renal transplant recipients treated with sirolimus who developed pericardial tamponade associated with interstitial pneumonia, proteinuria, microcytic anemia and, in one case, lymphocytic meningitidis. An extensive search for infectious agents was negative, and all symptoms disappeared after sirolimus interruption. Therefore, this case demonstrates for the first time that sirolimus can cause pericardial tamponade as well as lymphocytic meningitidis. 相似文献
67.
Abdallah Fayssoil Lee S. Nguyen Tanya Stojkovic Helene Prigent Robert Carlier Helge Amthor Jean Bergounioux Justine Zini Sebastien Damez-Fontaine Karim Wahbi Pascal Laforet Guillaume Nicolas Anthony Behin Guillaume Bassez France Leturcq Rabah Ben Yaou Nicolas Mansencal Djillali Annane Frdric Lofaso David Orlikowski 《Muscle & nerve》2022,65(1):89-95
68.
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70.
Acute systemic inflammation induces central mitochondrial damage and mnesic deficit in adult Swiss mice 总被引:1,自引:0,他引:1
Noble F Rubira E Boulanouar M Palmier B Plotkine M Warnet JM Marchand-Leroux C Massicot F 《Neuroscience letters》2007,424(2):106-110
The aim of this study was to investigate how the brain is affected during systemic inflammation. For this purpose, Swiss mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 250microg/mouse) to mimic aspects of systemic infection. Spatial learning in Y-maze test demonstrated a differential learning profile during the training test between control and LPS-treated mice, with an alteration in the latter group. We show that systemic LPS-induced inflammation and oxidative injury as assessed by reactive oxygen species (ROS) and nitrites/nitrates (NOx) production associated with reduced glutathione (GSH) depletion, cyclooxygenase-2 (COX-2) expression, and lipid peroxidation. LPS also induced a loss in mitochondrial integrity as shown by a significant decrease in membrane potential and impairment in mitochondrial redox activity. Thus, peripheral inflammation by producing brain inflammation and oxidative injury causes mnesic deficits. It remains to determine whether such events can induce neuronal dysfunction/degeneration and, with time, lead to cholinergic deficiency, amyloid deposits and cognitive impairments as they occur in Alzheimer's disease. 相似文献