It has been hypothesised that colonic varices due to portal hypertension arise in patients in whom normal embryological colonic anastomoses are highly developed [36].
Hypertension arising de novo in the postpartum period in women who did not have hypertension in the antepartum period could be a non-specific phenomenon in women with no underlying disease.
Pregnancy hypertension, arising de novo from 20 weeks of gestation, is a syndrome ranging from hypertension alone (gestational hypertension) through proteinuria and multi-organ dysfunction (preeclampsia) to seizures (eclampsia) [ 10- 12] Some women with chronic hypertension develop superimposed preeclampsia.
The primary composite maternal outcome is preeclampsia arising < 37 weeks gestation, severe non-proteinuric hypertension arising < 37 weeks gestation, placental abruption, maternal stroke during pregnancy or ≤ 7 days after delivery, or maternal death during pregnancy or ≤ 7 days after delivery.
We stratified randomisation to management with automated or manual office blood pressure measurement by city to minimise possible regional differences in blood pressure measurement and management of hypertension arising from any imbalance between the groups.
The individual components of the composite maternal outcome -- preeclampsia or eclampsia arising before 37 weeks gestation, severe non-proteinuric hypertension arising before 37 weeks gestation, placental abruption, maternal stroke during pregnancy or ≤ 7 days after delivery, or maternal death during pregnancy or ≤ 7 days after delivery – are listed in Table 2.
Pulmonary hypertension often arises from the chronicity of SA or OHS, and may lead to right ventricular failure.
It also suggests that renal ischaemia and hypertension may arise via extrinsic compression from granulomatous inflammation in the absence of renal or extra-renal vasculitis.
During pregnancy a failure to meet the physiological demands will unmask impaired organ function, e.g. hypertension will arise and most often subside after delivery.
In the setting of renal sarcoidosis, our case suggests that renin-dependant hypertension may arise from renal ischaemia as a result of extrinsic compression of kidney blood vessels due to severe granulomatous inflammation.
