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Can H. pylori cause pre-eclampsia?

H. pylori and pre-eclampsia

H. pylori and pre-eclampsia is taken from my e-book, How H. pylori Causes Fertility and Pregnancy Problems, which you can download here for free.

H. pylori––especially the CagA strain––can induce pre-eclampsia by triggering inflammation in the vascular system and by altering the immune response.

Since PE is a potentially devastating condition, it’s essential to consider H. pylori in this context.

Other microbes may also play a role in pre-eclampsia, but like H. pylori, these are not generally recognised by the medical system.

What is pre-eclampsia (PE) ?

Pre-eclampsia is a pregnancy syndrome characterized by high blood pressure and the appearance of protein in the mother’s urine after Week 20 of gestation.

It affects about 2%-8% of all pregnancies and remains a primary cause of maternal or fetal mortality and morbidity worldwide.

It’s not something to take lightly.

Evidence that H. pylori causes pre-eclampsia (or at least contributes)

When the World Journal of Gastreoenterology published a 2014 paper on H. pylori, reproduction and pregnancy, at least three studies had shown that H. pylori is detected more frequently in mothers with pre-eclampsia compared with women with uneventful pregnancies.

The authors of the WJG papers were directly studying the association between H. pylori and PE. They wrote this in their review paper:

“We also showed a strong association between the onset of PE and CagA-positive H. pylori strains infection, which are more virulent and therefore more likely to elicit the generalized inflammation and the subsequent vascular damage typical of PE.”

They also stated:

“Recently, we found that CagA/VacA dual seropositivity is specifically associated with PE and, in particular, with “placental PE”. Interestingly, Franceschi et al (2012) demonstrated that antibodies against the H. pylori virulence factor CagA cross-react in vitro with placental tissue reducing its invasiveness ability and it is well known that these antibodies recognize antigens localized on the surface of endothelial cells. Therefore infection with CagA-positive strains could contribute not only to the exacerbated maternal inflammatory response leading to all forms of PE but also to the abnormal placentation typical of “placental PE.”

It has been a common theme in my research that CagA and VacA H. pylori strains are more strongly connected with serious health problems involving the cardiovascular system.

It appears that PE is no exception.

H. pylori influences endothelial inflammation and general inflammation markers such as c-reactive protein. It can increase blood pressure, raise blood homocysteine and alter cholesterol, insulin and blood sugar levels.

Unfortunately, doctors working with patients at “ground level” are completely oblivious to H. pylori’s potential role in these cardiovascular problems.

Because pre-eclampsia is to all intents and purposes an inflammatory condition affecting the cardiovascular system, it’s important to acknowledge the potential role of H. pylori, as the WJG authors point out:

“H. pylori could be involved in the pathogenesis of PE mainly by inducing inflammation and oxidative stress and consequently generalized endothelial dysfunction. In fact, it was observed that H. pylori seropositive PE subjects are characterized by a more severe inflammatory status compared to the inflammatory response characterizing normal pregnancy, since pre-eclamptic women showed higher levels of C-reactive protein, tumour necrosis factor (TNF)-alpha and maternal leukocytes count. Interestingly, pre-eclamptic patients, had higher H. pylori seropositivity rate and serum malondialdehyde levels, a common marker of lipid peroxidation, compared with healthy pregnant women. Furthermore, the subgroup of seropositive PE mothers had higher serum levels of total cholesterol and low-density lipoprotein (LDL)-C compared to seronegative PE women.”

Since the 2014 WJG paper, a number of additional studies have been performed on H. pylori and PE. In 2017, di Simone et al concluded their study by writing:

“Our data show, for the first time, an association between Hp infection and PE with abnormal uterine arteries Doppler velocimetry, suggesting a role for Hp infection in impairing placental development and increasing the risk to develop PE. This study opens the new perspective of a potential screening and treatment for Hp infection in pregnancy.”

Helicobacter. 2017 Apr;22(2). doi: 10.1111/hel.12347. Epub 2016 Aug 3.

Another 2017 paper by den Hollander et al concludes with the statement:

“Our data suggest that H. pylori colonization may be a risk factor for PE and SGA (small for gestational age). If these associations are confirmed by future studies and shown to be causal, H. pylori eradication may reduce related perinatal morbidity and mortality.”

Helicobacter. 2017 Apr;22(2). doi: 10.1111/hel.12364. Epub 2016 Oct 27.

A further paper from 2017 by Nourollahpour Shiadeh et al suggests that H. pylori may not be alone in contributing to the pathological process leading to PE, by including other microbes such as Chlamydia pneumonia and viruses in the picture:

“The literature review revealed that many bacteria including Helicobacter pylori, Chlamydia pneumonia, and those are involved in periodontal disease or urinary tract infections (UTIs) and some viral agents such as Cytomegalovirus, herpes simplex virus type-2, human immunodeficiency virus, and some parasites especially Plasmodium spp. and Toxoplasma gondii can be effective in development of PE… Inflammation responses against infections has major role in the inducement of PE. The shift of immunological cytokine profile of Th2 toward Th1 and high levels of pro-inflammatory cytokines (TNF-ɑ, IL-12, IFN-γ, etc.), increase of oxidative stress, increase of anti-angiogenic proteins, increase of vascular endothelial growth factor receptor 1 (sVEGFR1), and complement C5a are the main potential mechanisms related to infections and enhanced development of PE. Thus, early diagnosis and treatment of bacterial, viral, and parasitic infections could be an effective strategy to reduce the incidence of PE.”

Where does this leave you?

If you’re having difficulty with pregnancy-related disorders and your doctors are at a loss regarding what might be going on, I strongly suggest you take a look at your gut.

Digestion affects everything. More and more research is released each week showing how gut microbes, inflammation, nutrient absorption and other factors contribute to body-wide symptoms and diseases.

When your gut is inflamed, other organs become inflamed and/or starved of the nutrients they require. This can all be assessed and properly tested.

Most of the testing can be done from the comfort of your own home!

Key Points on H. pylori and pre-eclampsia

  • H. pylori––especially the CagA subtype––can induce pre-eclampsia by triggering inflammation in the vascular system and by altering the immune response.
  • Since PE is a potentially devastating condition, it’s essential to consider H. pylori in this context.
  • Other microbes may also play a role in PE.

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