Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ANA may occur in healthy people, particularly in older people and females and is usually unrelated to present or post medication. Their presence may be due to recent virus infections or other tissue damage. In agreement with this, ANA occur significantly more often in untreated hypertensive patients and are associated with the severity of the disorder. The ANA (and other autoantibodies) seem to be markers of an ongoing vascular injury. In agreement with this, the presence of such autoantibodies increase the five-year relative risk for cardiovascular morbidity and mortality three times, both in the general population, and in patients with essential hypertension (2). Such data emphasise the importance of careful selection of control groups whenever dealing with the ANA incidence in relation to drugs. When the patient is taking a drug recognised as being associated with increased ANA incidence, it is important to identify the drug as being one which may lead to development of SLE in ANA positive patients (Table 1). If the drug is in category A, further studies are necessary. When there are symptoms consistent with the diagnosis drug-induced SLE, discontinuation of the drug results in rapid clinical improvement if the drug is the inductive factor. Where no symptoms exist, the patient should be carefully watched if SLE develops. For drugs with a high ANA incidence, but little history of inducing SLE (category B), little more has to be done.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ANA and antihypertensive drugs. Any clinical importance? 350 48

Measurements of complement split products by enzyme-linked immunosorbent assays (ELISA) are well established for the assessment of in vivo complement activation. We have combined two monoclonal antibodies (mAb) with specificities for C3b/iC3b/C3dg (mAb I3/15) and C4/C4b/C4d (mAb M4d2), respectively, in a sandwich ELISA to quantitate C4-C3 complexes as an indicator of complement activation. Serum incubated with heat aggregated IgG (HAG) was used as a standard and the C4-C3 levels expressed as microgram equivalent HAG/ml (microgram HAG-equ/ml). Normal values of C4-C3 complexes in plasma (EDTA) of healthy probands (n = 11) were 6.3 micrograms HAG-equ/ml +/- 1.5 (mean +/- 1 standard deviation (SD), with a range from 3.6 to 9.1). In patients with systemic lupus erythematosus (SLE, n = 23) C4-C3 values were clearly elevated (48.8 micrograms HAG-equ/ml +/- 52.9, range 7.5-184.7) as compared to samples from patients with idiopathic hypertension (IDH, n = 10) (6.5 micrograms HAG-equ/ml +/- 1.7, range 4.1-9.4). For SLE patients C4-C3 levels significantly correlated with values for C3b/iC3b/C3d (r = 0.69, p < 0.001) and C3 containing immune complexes (r = 0.68, p < 0.001), but not with the C4d fragment (r = 0.26). C4-C3 levels of 96% of the studied SLE patients were increased more than 2 SD above the normal mean as compared to 74% of C4d and activated C3 values, respectively. Serum treated with zymosan as an activator of the alternative pathway of complement did not exhibit higher C4-C3 values. These results demonstrate that the quantitation of in vivo generated C4-C3 complexes by ELISA provide a novel, sensitive parameter for classical pathway of complement activation.
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PMID:A novel ELISA for the assessment of classical pathway of complement activation in vivo by measurement of C4-C3 complexes. 756 Nov 48

Preeclampsia, eclampsia and HELLP syndrome are severe complications of pregnancy associated with a high morbidity and mortality for both mother and foetus. The issue of prognosis with regards to risk of relapse is therefore of upmost importance for both the patients and doctors managing their subsequent pregnancies. The overall risk of relapse is estimated to be less than 10%. The risk is especially increased in case of early onset, before the 28(th) week of amenorrhea. In such patients, an underlying renal disease, essential hypertension or secondary hypertension might be identified. A renal consultation must ensure the complete resolution of the hypertension and proteinuria, otherwise investigations need to be carried out looking for an underlying renal or vascular disease affecting the renal parenchyma or outflow. Screening for a hereditary thrombophilia is performed in the immediate post-partum period following and early onset PE, especially if associated with an IUGR, fetal death, or in an early and severe relapse. A renal biopsy is only rarely considered: it is either performed within the first post-partum days whenever a systemic disease flare-up is suspected (i.e. SLE), or late if the proteinuria failed to settle beyond 6 months post-part. Severe PE is a marker of a vascular disease of short duration, but must be considered a risk factor for later atherosclerosis with cardiovascular complications, justifying long term cardiovascular, renal and metabolic follow-up.
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PMID:[Late prognosis after preeclampsia]. 2048 49