Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present review examines the types of hypertension that women may suffer throughout life, their physiopathological characteristics and management. In early life, the currently used low-dose oral contraceptives seldom cause hypertension. Pregnancy provokes preeclampsia, its main medical complication, secondary to inadequate transformation of the spiral arteries and the subsequent multisystem endothelial damage caused by deportation of placental factors and microparticles. Hypertension in preeclampsia is an epiphenomenon which needs to be controlled at levels that reduce maternal risk without impairing placental perfusion. The hemodynamic changes of pregnancy may unmask a hypertensive phenotype, may exacerbate a chronic hypertension, or may complicate hypertension secondary to lupus, renovascular lesions, and pheochromocytoma. On the other hand a primary aldosteronism may benefit from the effect of progesterone and present as a postpartum hypertension. A hypertensive pregnancy, especially preeclampsia, represents a risk for cardiac, vascular and renal disease in later life. Menopause may mimic a pheochromocytoma, and is associated to endothelial dysfunction and salt-sensitivity. Among women, non-pharmacological treatment should be forcefully advocated, except for sodium restriction during pregnancy. The blockade of the renin-angiotensin system should be avoided in women at risk of pregnancy; betablockers could be used with precautions during pregnancy; diuretics, ACE inhibitors and angiotensin receptor antagonists should not be used during breast feeding. Collateral effects of antihypertensives, such as hyponatremia, cough and edema are more common in women. Thus, hypertension in women should be managed according to the different life stages.
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PMID:[Hypertension in women]. 2373 98

To detect the abnormal cortical thickness and disrupted brain resting-state functional connectivity (RSFC) in patients with systemic lupus erythematosus (SLE) without neuropsychiatric symptoms (non-NPSLE). Using T1-weighted 3D brain structural data, we first determined the regions with abnormal cortical thickness in a cohort of 33 adult female non-NPSLE patients. By taking brain regions with significantly reduced cortical thickness as the seeds, we calculated their RSFC based on the resting-fMRI data and detected the relationship between the RSFC and cortical thickness in the non-NPSLE patients. Compared to the controls, the non-NPSLE patients showed significantly cortical thinning in the left fusiform gyrus (FUS.L), left lingual gyrus (LING.L), right lingual gyrus (LING.R) and left superior frontal cortex (SFC.L). As for the RSFC, statistical analyses indicated that the abnormal cortical thickness in LING.L is associated with increased RSFC in the left posterior cingulate cortex (PCC.L), and cortical thinning in SFC.L associated with decreased RSFC in left cerebellum 6 (CRBL 6.L) in non-NPSLE patients. In addition, in non-NPSLE patients, the decreased cortical thickness in LING.L was correlated to the increased RSFC in PCC.L, and decreased cortical thickness in SFC.L was correlated to the decreased RSFC in CRBL 6.L. Our findings suggest that the cortical abnormalities may affect brain intrinsic connectivity in non-NPSLE patients.
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PMID:Cortical thickness reductions associate with abnormal resting-state functional connectivity in non-neuropsychiatric systemic lupus erythematosus. 2845 20


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