An essay of reflection: Why does preeclampsia exist in humans, and why are there such huge geographical differences in epidemiology?

Robillard, Pierre‐Yves; Dekker, Gustaaf A.; Iacobelli, Simona; Chaouat, Gérard

doi:10.1016/j.jri.2015.07.001

Cited by 42 publications

(39 citation statements)

References 29 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The risk of a woman in the developing world dying from a maternal-related cause is 33 times higher than a woman in the developed world 16. Maternal mortality results from cerebral hemorrhage,17 pulmonary edema,18 acute renal failure, hepatic rupture, or DIC. Long-term effects may include chronic renal failure, cardiovascular disease,19 or cortical blindness.…”

Section: Discussionmentioning

confidence: 99%

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

Ngwenya¹

2017

IJWH

View full text Add to dashboard Cite

BackgroundSevere preeclampsia is a disorder of pregnancy characterized by high blood pressure and significant proteinuria after 20 weeks gestation. Severe preeclampsia and eclampsia have considerable adverse impacts on maternal, fetal, and neonatal health especially in low-resource countries. Hypertensive disorders of pregnancy are the third leading cause of maternal deaths in Sub-Saharan Africa. Significant avoidable maternal and neonatal morbidity and mortality may result.ObjectivesThis study aimed 1) to determine the incidence of severe preeclampsia/eclampsia in a low-resource setting; 2) to determine the maternal complications of severe preeclampsia/eclampsia in a low-resource setting; 3) to determine the perinatal outcomes of severe preeclampsia/eclampsia in a low-resource setting.MethodsThis was a retrospective descriptive cohort study carried out at Mpilo Central Hospital, a tertiary teaching referral government hospital in a low-resource setting in Bulawayo, Zimbabwe. Data were obtained from the birth registers in labor ward, intensive care unit, and neonatal intensive care unit of patients who had a diagnosis of severe preeclampsia or eclampsia for the period January 1, 2016, to December 31, 2016. The case notes were retrieved and the demographic, clinical, and outcome data were gathered.ResultsThere were 9,086 deliveries at the institution during the period January 1, 2016, to December 31, 2016. There were 121 cases of severe preeclampsia/eclampsia. The incidence of severe preeclampsia/eclampsia was 1.3% at Mpilo Central Hospital. The most common major complication was HELLP syndrome (9.1%). Maternal mortality was 1.7%. There were 127 babies born with six sets of twins, 49.6% of the babies were lost through stillbirths and early neonatal deaths.ConclusionThe incidence of severe preeclampsia/eclampsia at Mpilo Central Hospital was 1.3%. The most common maternal complication was hemolysis elevated liver enzymes low platelet syndrome. Maternal mortality was 1.7% due to acute renal failure. Nearly half (49.6%) of the babies born were lost to stillbirths and early neonatal deaths.

show abstract

Section: Discussionmentioning

confidence: 99%

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

Ngwenya¹

2017

IJWH

View full text Add to dashboard Cite

show abstract

“…In cases of stroke, infection is very common, and leads to a worse prognosis; in some cases antibiotics worsen it further (Becker et al ., ), consistent with the view that the infecting organisms were already present, and that there is an active role of LPS shedding. We note too that some molecules such as P‐type inositol phosphate glycans can act as LPS mimics (Robillard et al ., ). This is especially well established in pre‐eclampsia (e.g.…”

Section: Step 4: Microbes Can Produce and Shed Inflammagens Such As Lmentioning

confidence: 97%

“…This is especially well established in pre‐eclampsia (e.g. Dawonauth et al ., ; Kenny & Kell, ; Robillard et al ., ; Scioscia et al ., , ; Williams et al ., ) but seems to have been little investigated elsewhere.…”

Section: Step 4: Microbes Can Produce and Shed Inflammagens Such As Lmentioning

confidence: 99%

No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

Kell

2018

Biological Reviews

108

View full text Add to dashboard Cite

Since the successful conquest of many acute, communicable (infectious) diseases through the use of vaccines and antibiotics, the currently most prevalent diseases are chronic and progressive in nature, and are all accompanied by inflammation. These diseases include neurodegenerative (e.g. Alzheimer's, Parkinson's), vascular (e.g. atherosclerosis, pre‐eclampsia, type 2 diabetes) and autoimmune (e.g. rheumatoid arthritis and multiple sclerosis) diseases that may appear to have little in common. In fact they all share significant features, in particular chronic inflammation and its attendant inflammatory cytokines. Such effects do not happen without underlying and initially ‘external’ causes, and it is of interest to seek these causes. Taking a systems approach, we argue that these causes include (i) stress‐induced iron dysregulation, and (ii) its ability to awaken dormant, non‐replicating microbes with which the host has become infected. Other external causes may be dietary. Such microbes are capable of shedding small, but functionally significant amounts of highly inflammagenic molecules such as lipopolysaccharide and lipoteichoic acid. Sequelae include significant coagulopathies, not least the recently discovered amyloidogenic clotting of blood, leading to cell death and the release of further inflammagens. The extensive evidence discussed here implies, as was found with ulcers, that almost all chronic, infectious diseases do in fact harbour a microbial component. What differs is simply the microbes and the anatomical location from and at which they exert damage. This analysis offers novel avenues for diagnosis and treatment.

show abstract

“…primarily maternal pre-eclampsia might not be linked with a defective trophoblastic invasion in the first weeks of gestation but rather to a maternal predisposition for inflammation (notably, obesity, food inflammation, chronic hypertension) and/or vascular problems (thrombophilias, obesity, diabetes, antiphospholipid syndrome, dyslipidemia, insulin resistance etc…). This distinction between LOP and EOP also triggered the epidemiological observation that LOP is clearly the predominant phenotype: 90% of cases in developed countries, in contrast to only approximately 70% in developing areas (Robillard et al, 2016; Iacobelli et al, 2016). In other words, in developing areas this 30% incidence of early onset PE (EOP) pose a tremendous epidemiological challenge concerning maternal and neonatal morbidities.…”

mentioning

confidence: 94%

Historical evolution of ideas on eclampsia/preeclampsia: A proposed optimistic view of preeclampsia

Robillard

Dekker

Chaouat

et al. 2017

Journal of Reproductive Immunology

Self Cite

View full text Add to dashboard Cite

Eclampsia (together with epilepsy) being the first disease ever written down since the beginning of writings in mankind 5000 years ago, we will make a brief presentation of the different major steps in comprehension of Pre-eclampsia. 1) 1840. Rayer, description of proteinuria in eclampsia, 2) 1897 Vaquez, discovery of gestational hypertension in eclamptic women, 3) In the 1970’s, description of the “double” trophoblastic invasion existing only in humans (Brosens & Pijnenborg,), 4) between the 1970’s and the 1990’s, description of preeclampsia being a couple disease. The “paternity problem” (and therefore irruption of immunology), 5) at the end of the 1980’s, a major step forward: Preeclampsia being a global endothelial cell disease (glomeruloendotheliosis, hepatic or cerebral endotheliosis, HELLP, eclampsia), inflammation (J. Roberts. C Redman, R Taylor), 6) End of the 1990’s: Consensus for a distinction between early onset preeclampsia EOP and late onset LOP (34 weeks gestation), EOP being rather a problem of implantation of the trophoblast (and the placenta), LOP being rather a pre-existing maternal problem (obesity, diabetes, coagulopathies etc…). LOP is predominant everywhere on this planet, but enormously predominant in developed countries: 90% of cases. This feature is very different in countries where women have their first child very young (88% of world births), where the fatal EOP (early onset) occurs in more than 30% of cases. 7) What could be the common factor which could explain the maternal global endotheliosis in EOP and LOP? Discussion about the inositol phospho glycans P type.

show abstract

An essay of reflection: Why does preeclampsia exist in humans, and why are there such huge geographical differences in epidemiology?

Cited by 42 publications

References 29 publications

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

No effects without causes: the Iron Dysregulation and Dormant Microbes hypothesis for chronic, inflammatory diseases

Historical evolution of ideas on eclampsia/preeclampsia: A proposed optimistic view of preeclampsia

Contact Info

Product

Resources

About