Anemia in Pregnancy

Scott, Daniel E.; Pritchard, Jack A.

doi:10.1016/s0095-5108(18)31307-1

Cited by 12 publications

(14 citation statements)

References 22 publications

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“…That these systems, renin-angiotensin II-aldosterone, are operative at increased levels in early pregnancy is suggested by the findings of Scott, who has shown that plasma volume begins to increase in pregnancy as early as 6-8 wk pregnancy and rises progressively thereafter until approximately 28-30 wk of pregnancy, when the maximum plasma volume expansion is usually reached (26). It is interesting to note from the present study that in those gravidas who remained normotensive throughout pregnancy, a slight but continuing decrease in resistance to A-II pressor effects began at approximately 30 wk pregnancy, the same time that plasma volume reaches its maximal expansion.…”

Section: Introductionmentioning

confidence: 99%

“…However, while controversy exists concerning the presence of increased angiotensinase in late pregnancy, Berger and Langhans (27) [23][24][25][26] wk, while clinically normal, they became clearly defined as a separate group. At this early stage of gestation many of these subjects had become exquisitely sensitive to A-II in spite of the fact that they exhibited no clinical stigmata of pregnancy-induced hypertension (Fig.…”

Section: Introductionmentioning

confidence: 99%

“…By the 22nd wk there was a clear separation of the two groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the two groups became significant (P < 0.01) by [23][24][25][26] …”

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confidence: 99%

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A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

Gant¹,

et al. 1973

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A B S T R A C T The present study was designed to ascertain sequentially the pressor response to angiotensin II in young primigravid patients throughout pregnancy in order a) to define when in pregnancy resistance to the pressor effects of angiotensin II develops; b) to define the physiologic sequence of events leading to this resistance; and c) to ascertain whether sensitivity to infused angiotensin II could be detected before the onset of clinical signs of pregnancy-induced hypertension.With this prospective approach, two separate groups of patients were defined. The first group of patients remained normal throughout pregnancy. The second group consisted of those patients who, while clinically normotensive during the initial phase of the study, ultimately developed hypertension of pregnancy.192 patients were studied; of these, 120 patients remained normotensive and 72 developed pregnancy-induced hypertension. In both groups, vascular resistance to infused angiotensin II (more than 8 ng/kg/min required to elicit a pressor response of 20 mm Hg in diastolic pressure) was demonstrated as early as the 10th wk of pregnancy. In the group that remained normotensive, maximum mean vascular resistance occurred at 18-30 wk of pregnancy, (mean pressor dose required being 13.5 to 14.9 ng/kg/min). In those subjects who developed pregnancy-induced hypertension, the mean maximum dose required was 12.9 ng/kg/min, which was observed at the 18th wk of pregnancy. By the 22nd wk there was a clear separation of the two groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the two groups became significant (P < 0.01) by [23][24][25][26]

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

Gant¹,

et al. 1973

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“…18) Thus, Phase 1 of drug metabolism considered to be altered. 19,20) In addition, it has been reported that the renal glomerular filtration rate generally increases during pregnancy and that renal clearance of some drugs is increased. 19) The sulfotransferases (SULTs) that mainly play a role in the metabolism of ritodrine are SULT1A1 in the liver and SULT1A3 in the intestine.…”

Section: Discussionmentioning

confidence: 99%

“…19,20) In addition, it has been reported that the renal glomerular filtration rate generally increases during pregnancy and that renal clearance of some drugs is increased. 19) The sulfotransferases (SULTs) that mainly play a role in the metabolism of ritodrine are SULT1A1 in the liver and SULT1A3 in the intestine. 21) The potency ratio of the conjugation of ritodrine for SULT1A1 compared to SULT1A3 is approximately 1/5 to 1/4, with large individual differences reported for the activity of SULT1A1 in the liver.…”

Section: Discussionmentioning

confidence: 99%

Concentration of Sulfate and Glucuronide Conjugates of Ritodrine in Twin Pregnancy

Soma

Konda

Fujieda

et al. 2017

Biological & Pharmaceutical Bulletin

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Ritodrine, a drug for the treatment of threatened premature labor, is a highly selective beta-2 agonist with the major metabolites of sulfate and glucuronide conjugates. This study investigated the continuous evaluation of the concentration of ritodrine conjugates in relation to the clinical course in twin pregnancy. The subjects were 9 twin-pregnancy mothers who delivered after receiving ritodrine treatment between April 2012 and December 2013. Serum ritodrine sulfate and glucuronide conjugates were deconjugated using their specific enzymes. Ritodrine concentration was measured by liquid chromatography-tandem mass spectrometry. The continuous infusion rate of ritodrine was 2.66 0.67 (0.8-3.54) µg/min/kg, and the average concentration of unchanged ritodrine was 118.8 33.2 (63.8-194.0) ng/mL. During the study period between week 32 and week 36 of gestation, the average ratio of unchanged ritodrine concentration and sulfate ritodrine conjugate concentration for weeks 32, 33, 34, 35, and 36 were 1.7, 1.9, 1.5, 1.7, and 1.7 not significant (N.S.), respectively. The average ratio of unchanged ritodrine concentration and glucuronide ritodrine conjugate concentration were 1.8, 2.2, 1.9, 1.8, and 2.1 (N.S.), respectively. No statistical difference was identified in the ratios of unchanged ritodrine concentration and sulfate or glucuronide ritodrine conjugate concentrations. Large individual differences were shown in the concentration of sulfate and glucuronide during the gestational period. No change in the ratio of the formation of ritodrine metabolites was identified as the gestational age progressed.

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Spontaneous coronary artery dissection

Almeda

Barkatullah

Kavinsky

2004

Clinical Cardiology

101

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Summary: Spontaneous coronary artery dissection (SCAD)is an unusual cause of acute myocardial ischemia with complex pathophysiology. This paper reviews the major diagnostic and therapeutic issues of this rare but important disease. The diagnosis of SCAD should be strongly considered in any patient who presents with symptoms suggestive of acute myocardial ischemia, particularly in young subjects without traditional risk factors for coronary artery disease (especially in young women during the peripartum period or in association with oral contraceptive use). Urgent coronary angiography is indicated to establish the diagnosis and to determine the appropriate therapeutic approach. The decision to pursue medical management, percutaneous coronary intervention, or surgical revascularization is based primarily on the clinical presentation, extent of dissection, and amount of ischemic myocardium at risk.

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Anemia in Pregnancy

Cited by 12 publications

References 22 publications

A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

A Study of Angiotensin II Pressor Response throughout Primigravid Pregnancy

Concentration of Sulfate and Glucuronide Conjugates of Ritodrine in Twin Pregnancy

Spontaneous coronary artery dissection

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