Helicobacter pylori and stool tests

Gaby

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Many people have had digestive problems at some point in their lives. They've tried specific supplements, alternative remedies, and dietary changes with success. However, in this day and age, we are subjected to many environmental factors that put to the test even the most resilient.

So if symptoms persist after dedicated efforts to heal, consider consulting your health care provider to discuss the symptoms and inquire about screening stool tests:

- Hidden blood in feces: It's the screening program for colon cancer. Where I work, everyone over 50 years old is invited to participate in the program by sending a poop sample. If there's hidden blood, the person is invited for an interview to inquire about possible hemorrhoids and the like, and offered a colonoscopy. People with colon cancer in the family are even invited earlier for a colonoscopy. And some people in their 40s have shown up with colon cancer as their first disease. Keep in mind that colon cancer falls in the spectrum of insulin resistance which serves as a super fertilizer for cancer cells. Those who have metabolic syndrome or diabetes, fare worse. There is so much colon cancer nowadays, that if a person led a SAD ("standard America/Western diet") throughout their lives and are aged and never really took care of their health, I think going with the colonoscopy after a positive stool test to make an early diagnosis is worth the trouble and risk of the procedure.

- Calprotectin in feces: it helps to screen for inflammatory bowel disease.

- Helicobacter pylori antigen test in feces. It has a 98% specificity and a 94% sensitivity. Having N-acetilcysteine, antibiotics and omeprazol (proton pump inhibitors) the two weeks before will certainly alter the test (false negative). Consider also iodine on this category and other formulas that are anti-microbial.

I want to talk about this last infection because if falls under the spectrum of chronic latent infections that we discussed so extensively years ago in the following thread:


Helicobacter pylori is a spiral-shaped Gram-negative bacterium that colonizes the stomach in about 50% of all humans and is the causative factor of peptic ulcers and gastritis. Some might remember the story of how Barry J. Marshall and J. Robin Warren won the Nobel Prize in Medicine of 2005 for their discovery of how Helicobacter pylori cause these diseases because it has brought up at least a couple of times in the recommended reading of Intelligent Design.

Ever since the eradication protocols for Helicobacter pylori were introduced, medical emergencies such as bleeding peptic ulcers became a thing of the past. The last time I saw a patient who needed a surgical repair for a bleeding stomach ulcer was during the late 1990s when I was a medical student. However, recently I saw a patient with this complication because she never consulted for her digestive issues. I told her that if she had consulted, I would have asked for a stool test and made the diagnosis before she had any complication and surgical procedure. This is because eradication protocols work and then the bacteria can't do any further damage.

Signs and symptoms for H.pylori infection include:
  • Nausea
  • Vomiting
  • Abdominal pain
  • Heartburn
  • Diarrhea
  • Hunger in the morning
  • Halitosis (bad breath)
Some people end up in the emergency room thinking they have an appendicitis. Others simply have reflux and very bad breath.

These are other useful tests to detect h.pylori:

  • Carbon-13 urea breath test: Concentration of the labeled carbon is high in breath only when urease is present in the stomach, a reaction possible only with H pylori infection
  • H pylori serology: High (>90%) specificity and sensitivity; useful for detecting a newly infected patient but not a good test for follow-up of treated patients
  • Antibiogram: Useful in geographic areas with a high resistance rate against metronidazole and clarithromycin; these antibiotics should not be recommended as first-line drugs in such areas
Here's a very important Townsend Letter review on the subject:


H. pylori infection has been implicated in a variety of diseases not related to the GI tract. Skin disease association includes the following3,4:
  • Rosacea: H. pylori can increase the level of nitrous oxide in the blood or tissue contributing to the flushing and erythema of rosacea.
  • Chronic urticaria: Several studies have found a link between H. pylori and chronic urticaria. It is thought that the infection increases the permeability of the intestinal lining and exposure to allergens and also produces antibodies that may increase the release of histamine in the skin.
  • Psoriasis: H. pylori may be one of the organisms capable of triggering the inflammatory response in psoriasis.
  • Sjögren's syndrome: H. pylori may induce an autoimmune reaction to the skin and glands, causing Sjögren's syndrome.
  • Henoch-Schonlein purpura
  • Alopecia areata
  • Sweet disease
  • Systemic sclerosis
  • Atopic dermatitis
  • Behçet's disease
  • Generalized pruritus
  • Nodular prurigo
  • Immune thrombocytopenic purpura
  • Lichen planus
  • Aphthous ulceration

I have a patient who was diagnosed with h.pylori after several months of debilitating stomach problems that started with diarrhea. He not only had the diarrhea, he was having a thyroiditis that took his thyroid function to its possible lowest function ability. So the following quote is relevant with this in mind:

It has been speculated that H. pylori infection may be responsible for various endocrine disorders, such as autoimmune thyroid diseases, diabetes mellitus, dyslipidemia, obesity, osteoporosis, and primary hyperparathyroidism.5

Even more important:

H. Pylori, Cognition, and Neurological Syndromes

Not only do H. pylori work on disrupting autoimmune regulation via cytokines, interleukins, humoral, and cell mediated reactions, they also play a powerful role in the modulation of hormones, neurotransmitters, demyelination, and blood - brain barrier disruption.6 This infection has been well documented to be associated with depression, schizophrenia, epilepsy, multiple sclerosis, cognitive decline, other neurological diseases, gastrointestinal motility disorders, lymphoma, and vitamin and nutrient malabsorption.

In short, it is the classical chronic latent infection creating havoc in people's health. And out of this article are the big ones: stomach cancer and lymphomas caused by an initial infection with helicobacter pylori.

Here's another article exploring the Parkinson's disease angle:


The Townsend doctor suggests this protocol to treat this infection without antibiotics:

My first interest in H. pylori aside from GI issues was rosacea. With our advantage of rapid diagnosis via EAV (electroacupuncture according to Voll) and the BioMeridian computer, it made assessment and treatment response immediately available. My favorite treatment has been with Pyloricil (Orthomolecular Products) containing mastic gum (guar gum) extract 250 mg, berberine sulfate hydrate 150 mg, bismuth citrate 125 mg, and zinc carnosine 37.5 mg per capsule. Dose is 1 capsule twice per day. If it did not test well or if the H. pylori seemed to no longer be responsive, I use mastic gum/DGL from Complementary Prescriptions with deglycyrrhizinated licorice (Glycyrrhiza glabra root and rhizome extract 300 mg) with gum mastic (Pistacia lentiscus resin extract). Chew 1 to 2 wafers as needed. I usually suggest twice per day and typically see resolution or good improvement in about 1 month. There are many other herbal and alternative treatments for H. pylori from around the world.7

Keep in mind his warning:

The depth of research in this infection is truly overwhelming, and I hope that the reader will have a higher index of suspicion in seeking and treating this universal hidden plague.

Here's Sayer Ji's suggestions to deal with h.pylori:


Keep in mind that h.pylori is super smart and sneaky though:


So in case of doubt, I would opt for the stool test, doing it after 2 weeks without any anti-microbial protocol, proton pump inhibitor or acetylcysteine to avoid false negatives. However, if you had peptic ulcers in the past, know that you are a host for helicobacter pylori.

In my experience, 10 out of 10 people experience a significant amelioration in their health after completing some sort of eradication protocol with success. Their skin might clear up, their mood is better, their energy levels are better, their digestive issues disappear, they might have less or no allergies, etc.

The super duper protocol in mainstream medicine involves pylera which is a brand name for pills containing metronidazol, tetracycline and bismuth citrate. It's a gruesome protocol with often severe Herx reactions that last throughout most of the protocol. However, Herx reactions can be palliated with a teensy bit of cortisone, i.e. prednisone 10mg. Notice how pylera contains two of the things some of us used in the autoimmune thread: metronidazol and tetracycline. Even though we didn't use tetracycline, we used an antibiotic of the same family: doxycycline. Some of us reported in that thread similar Herx reactions described by users of Pylera.

The test needs to be repeated 2-4 weeks after the eradication protocol is complemented. Again, don't use anything that could produce a false negative.

In my experience, the eradication success with pylera is 100%. Those who might not succeed might have a SAD diet and no supplement support. So in case an alternative protocol is not doing it for somebody, discussing mainstream options with a health care provider might be the way to go.

Regardless of the way a person might decide to deal with this problem, one thing is clear: don't be afraid to visit a health care provider to discuss symptoms and a possible stool test or other diagnostic tool, specially if symptoms don't go away after concerted efforts.
 
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I know first hand the havoc that can be caused by H. Pylori overgrowth! I was plagued by recurring duodenal ulcers for 10 years before they found the culprit. This was years ago before mainstream medical practice knew of H. Pylori and its effects on ulcers. It was found using the breath test and it was “very” positive. I started on the triple antibiotic protocol but developed a bad case of thrush within 2 days. Knowing that it had to be eradicated I stopped the protocol (after consulting with my gastro doctor) and switched to Patis 30 Nano Catalytic Silver Hydrosols (from Lifesilver), 3 ounces daily for a week. Once in the morning, afternoon and night. The only ill effect I had was from candida overgrowth (probably caused by the H. Pylori) that brought on diarrhea on days 2 thru 4. After one week I went back to the gastro doctor and the breath test was negative for H. Pylori. I am posting this in case anyone else has trouble with the triple antibiotic treatment, although it should be discussed with your doctor, I am not one myself.
 
- Hidden blood in feces: It's the screening program for colon cancer. Where I work, everyone over 50 years old is invited to participate in the program by sending a poop sample.

Gaby, around here there can be seen a prolific degree of patent screening on this subject. This is to the point that specialists in colonoscopy have set up practices across from the hospitals. One thing I would like to know is do these tests (for hidden blood) come with a specific measure bar in samples (obviously they do) and what is that bar in terms of good/worse or probable of outcomes? I imaging that there is sometimes blood in stool samples for reasons (hemorrhoids or other) and if the bar is set low (like what happened with Cholesterol - they kept lowering the bar to push statin drugs) this could/would lead to over diagnosis and unnecessary intervention?
 
I know first hand the havoc that can be caused by H. Pylori overgrowth! I was plagued by recurring duodenal ulcers for 10 years before they found the culprit. This was years ago before mainstream medical practice knew of H. Pylori and its effects on ulcers. It was found using the breath test and it was “very” positive. I started on the triple antibiotic protocol but developed a bad case of thrush within 2 days. Knowing that it had to be eradicated I stopped the protocol (after consulting with my gastro doctor) and switched to Patis 30 Nano Catalytic Silver Hydrosols (from Lifesilver), 3 ounces daily for a week. Once in the morning, afternoon and night. The only ill effect I had was from candida overgrowth (probably caused by the H. Pylori) that brought on diarrhea on days 2 thru 4. After one week I went back to the gastro doctor and the breath test was negative for H. Pylori. I am posting this in case anyone else has trouble with the triple antibiotic treatment, although it should be discussed with your doctor, I am not one myself.

Yeah, it's brutal. I got the yeast thing on day three but Gaby prescribed an antifungal pill and that took care of it right away, so I continued on. It's been about two weeks, I've been taking probiotics to repopulate, and I tell ya, my whole digestion seems to be re-booted.
 
I imaging that there is sometimes blood in stool samples for reasons (hemorrhoids or other) and if the bar is set low (like what happened with Cholesterol - they kept lowering the bar to push statin drugs) this could/would lead to over diagnosis and unnecessary intervention?

I guess it depends on the country and its system. In this sense and in general, a public system would only want to do the necessary colonoscopies. I know that I've seen up to 50 or more red blood cells in a result, and they will report it negative.

There is so much colon cancer and cancer in general, that literally every single family seems to be dealing with it in one way or another.

I've seen a good deal of early diagnosis made from this simple test, so I think it's worth it for the average person with a typical Western lifestyle. There are those who don't do the tests, and then they consult a doctor when there is already metastatic cancer. Ideally, a person should be taking care of their health though and not waiting until the last minute.
 
Regarding diet:

There is so much colon cancer nowadays, that if a person led a SAD ("standard America/Western diet") throughout their lives and are aged and never really took care of their health, I think going with the colonoscopy after a positive stool test to make an early diagnosis is worth the trouble and risk of the procedure.

See that some discussion has taken place here with Keyhole's Oxalate subject, and Oxalate is something to be aware of. From following the Oxalate threads, how Oxalate's form (from the foods high in them) and move through the gut or blood, it is something to take note of that could be producing blood in stools (while causing havoc generally).
 
Yeah, it's brutal. I got the yeast thing on day three but Gaby prescribed an antifungal pill and that took care of it right away, so I continued on. It's been about two weeks, I've been taking probiotics to repopulate, and I tell ya, my whole digestion seems to be re-booted.
I am with you Laura, took probiotics for a month after I was rid of H. Pylori. I have not had a problem with my stomach or intestines since, been about 10 years now. I love that I can eat spicy foods again as they are one of my favorites. Glad you are on the mend and feeling better!
 
Like anything else, context seems to be the most important factor in H.Pylori.

For some people, it is clearly a problem. Although on the other hand, it seems to be protective for others? My question is - does the immune system facillitate the overgrowth of the bacteria to provide a "helping hand"?

Protective effects of Helicobacter pylori against gastroesophageal reflux disease may be due to a neuroimmunological anti-inflammatory mechanism.

There is some evidence that Helicobacter pylori infection has a protective effect against gastroesophageal reflux disease (GORD) and its complications such as Barrett's oesophagus and oesophageal adenocarcinoma. In this paper, we propose that a neuroimmunological mechanism is responsible for the protective effect of H. pylori on GORD. H. pylori infection of the gastric mucosa induces a T helper1-like immune response and production of pro-inflammatory cytokines. These cytokines can inhibit local sympathetic tone, whereas they increase systemic sympathetic tone. Increased sympathetic tone can induce an anti-inflammatory milieu, which in turn can inhibit inflammation in the oesophagus and lower oesophageal sphincter (LOS). Furthermore, H. pylori infection may stimulate the cholinergic anti-inflammatory pathway. It has been suggested that reflux-induced oesophageal inflammation plays an important role in the pathogenesis of reflux oesophagitis. Reduction of oesophageal inflammation by increased systemic sympathetic tone and vagal activity may lead to a decrease in reflux-induced oesophageal injury and LOS dysfunction in GORD.


Helicobacter pylori: A Beneficial Gastric Pathogen?

GERD and H. pylori: A good example of beneficial effects
Gastroesophageal reflux disease (GERD) incidence has been increased mostly in developed communities where H. pylori infection is almost effectively eradicated (27, 28). GERD is the main risk factor for Barrett’s esophagus, and it has been associated with another deadly gastroduodenal carcinoma called “esophageal adenocarcinoma” (3, 5). However, the relationship between GERD and H. pylori remains incompletely defined (29). Several studies suggested that eradication of H. pylori infection in the setting of duodenal ulcer disease would result in an increase in GERD symptoms (3, 30). In other words, an inverse association of H. pylori infection with decreased rate of this sort of disease was a challenging topic in new gastroenterology (14, 3133). Of note, GERD and its sequelae, which include Barrett’s esophagus and esophageal adenocarcinoma, is decreasing in countries in which most individuals are infected by H. pylori (15, 34, 35).

Actually, not only has worldwide H. pylori prevalence changed in recent decades but also other environmental factors affecting on human health such as socioeconomical levels, diet, and vaccination were drastically changed (10, 17). If so, H. pylori is confronting with different situation rather than before. Remarkably, H. pylori can undergo drastic genetic change through each generation, while human genes do not change frequently. As a result, frequent genetic changes in H. pylori helped the bacterium to adapt quickly (18). Remarkably, slower adaptation in humans deteriorates longtime established equilibrium between H. pylori and human. Because of this, elimination of H. pylori as permanent resident of human microbiome would not be the first option to deal with gastroduodenal diseases. According to what explained about GERD and H. pylori as a protective effect, the long cohabitation in our stomach calls for more deep studies to elucidate microbiota and human health. GERD is the best example of disease, which became more frequent after starting the H. pylori treatment (34). Indeed, after antibiotic usage against H. pylori and, of course, its eradication in Western countries, a constant equilibrium between H. pylori and human health disappeared.


Interestingly, in Northeastern Malaysia, the low prevalence of H. pylori infection was frequently reported (3638). As general rule, one expects that frequency of diseases such as asthma and GERD should be relatively low rather than the findings of expected inverse association were not found (3941). Actually, the association between H. pylori infection and certain diseases such as GERD and asthma risk can be affected by geographical and genetic differences (37, 41). As a result, there is a complex and mostly undetermined associations between human microbiome and health; accordingly, all attempts to change this arranged biological system can exacerbate certain diseases. Undoubtedly, we need to eradicate virulent H. pylori in people with adverse clinical manifestations, but this conclusion cannot be generalized to all H. pylori positive subjects.

 
Protective Role of Helicobacter pylori Infection in Prognosis of Gastric Cancer: Evidence from 2454 Patients with Gastric Cancer

Background
A number of studies have investigated the association between Helicobacter pylori (H. pylori) infection and the prognosis of gastric cancer (GC), with inconsistent and inconclusive results. We performed a meta-analysis to derive a more precise estimation of the association.
Methodology/Principal Findings
A systematic search of PubMed, EMBASE, Cochrane and Chinese wanfang databases was performed with the last search updated on February 19, 2013. The hazard ratio (HR) and its 95% confidence interval (95%CI) were used to assess the strength of association. A total of 12 studies including 2454 patients with GC were involved in this meta-analysis. The pooled HR was 0.71 (95%CI: 0.57–0.87; P = 0.001) for OS and 0.60 (95%CI: 0.30–1.18; P = 0.139) for DFS in GC patients, respectively. The protective role of H. pylori infection in the prognosis of GC was also observed among different subgroups stratified by ethnicity, statistical methodology, H. pylori evaluation method and quality assessment. There was no evidence of publication bias.
Conclusions/Significance
This meta-analysis suggests a protective role for H. pylori infection in the prognosis of GC. The underlying mechanisms need to be further elucidated, which could provide new therapeutic approaches for GC.

 
Not only does H.Pylori seem to be (perhaps sometimes) protective against GERD and gastric cancer, but it also appears to be protective against other diseases (autoimmune etc).

This is why in some of my patients, if I see H.Pylori on a stool DNA sequence analysis, yet they are asymptomatic, I am cautious about discussing killer approaches. After delving into this topic a while ago, I decided that it might not be the best idea for reasons laid out in the following paper.

This paper talks about some of the surprising associations:

Helicobacter pylori: beneficial for most?

Negative assocciation with inflammatory bowel disease

Epidemiological studies indicate that inflammatory bowel disease (IBD) is more prevalent in areas with lower rates of H. pylori colonization, such as the USA [8]. On the other hand, there is a steady rise in the incidence of IBD in H. pylori-endemic regions that corresponds to the beginning of anti-H. pylori therapy for peptic ulcer disease [9]. These observations have led to a number of studies investigating the association between H. pylori infection and IBD.

Our laboratory recently published a meta-analysis showing a negative correlation with IBD: 27.1% of IBD patients showed evidence of H. pylori infection compared with 40.9% patients in the control group [10]. These data suggest that there are protective benefits of H. pylori infection against the development of IBD. However, long-term studies investigating the effect of eradication of H. pylori on the development of IBD are warranted.

Like the asthma and obesity studies, there existed no mechanistic studies to explain this correlation. Commonly cited as the explanation for this negative association is the hygiene hypothesis: cleaner conditions early in life lead to a higher incidence of autoimmune diseases later in life by suppressing natural development of the immune system. H. pylori infection is more prevalent in developing parts of the world with poor hygiene. Since poor sanitary conditions are thought to play a role in the lower rates of IBD in these parts of the world, H. pylori infection is widely believed to be a marker of poor hygiene in one’s birthplace, and not a direct contributor to protection against IBD.

Mechanisms
Helicobacter pylori infection triggers a unique inflammatory response in which the infection persists despite the activation and recruitment of T and B lymphocytes, phagocytic cells and other immune cell populations [11]. This suggests that H. pylori infection may induce immune tolerance, favoring its persistence in the stomach. To investigate further the H. pylori–IBD connection, the direct influence of H. pylori infection on the host immune system needs to be elucidated. This cannot be performed in the clinical setting given that environmental hygiene is a strong confounding factor. Thus, we carried out this study in a mouse model of H. pylori infection and experimental colitis. We first showed that H. pylori infection can protect against Salmonella typhi-induced experimental colitis [12]. Higher IL-10 in the mesenteric lymph nodes could explain the protective mechanism. We employed a mouse model of H. pylori infection and showed that induction of Tregs by H. pylori appears to be a major adaptation to evade host immunity [13]. H. pylori alters the dendritic cell-polarized Th17/Treg balance toward a Treg-biased response, resulting in suboptimal Th17 response and failure to eradicate the offending pathogen. This mechanism may also explain the negative correlation that exists between H. pylori infection and the incidence of IBD, a condition in which Th17 may play a pivotal role.

Arnold et al. provided more evidence that H. pylori infection enhances the Treg response and thus limits the severity of asthma in a mouse model [14].
In subsequent studies we further demonstrated that H. pylori DNA decreases proinflammatory cytokine production by dendritic cells and attenuates dextran sodium sulfate-induced colitis in mice.

We showed that H. pylori DNA, which has been found in the colon and stool of infected patients [15,16], has immunoregulatory properties [17]. H. pylori DNA suppresses type 1 interferon and IL-12 production from mouse bone marrow-derived dendritic cells, possibly owing to its high immunoregulatory sequence to immunostimulatory sequence ratio. This may explain why the systemic levels of type 1 interferon were found to be lower in H. pyloricolonized patients than noncolonized controls [17].

We also showed that the administration of isolated H. pylori DNA significantly ameliorated the severity of experimental colitis in mice.

Clinical implications

Clinical studies clearly demonstrate that eradication of H. pylori infection significantly reduces the incidence of peptic ulcer disease and its complications. This supports the recommendation by the NIH that H. pylori is harmful to a small subset of patients and should be appropriately treated. However, because of immune tolerance conferred by H. pylori infection, its elimination from the body in asymptomatic patients may not be a good idea. Up to 50% of patients may experience mild side effects associated with antibiotic treatment [18]. Furthermore, treatment fails in approximately 25% of patients [19], so widespread use of antibiotics may result in future antibiotic-resistant strains. Therefore, we recommend that only symptomatic patients or asymptomatic family members of gastric cancer patients should be tested and treated. Unless treatment is considered, if the result is positive, physicians should not test the patient for H. pylori

Research implications
We know that H. pylori causes ulcers, but do all strains of H. pylori cause ulcers? Most people count all H. pylori strains as ‘bad’, but it is possible that some strains are more harmless than others. More research needs to be conducted on differences between strains before we blacklist all of them. In addition, we know that Asian populations have an especially high incidence of gastric cancer, but no convincing theory exists as to why. If we can understand why some people experience symptoms while others remain asymptomatic, then we may be more efficient at treating the infection and even providing H. pylori-based treatments for chronic inflammatory conditions.

Conclusion
It is good to recognize that H. pylori causes serious symptoms in 15% of those infected, but it is also essential to consider the remaining 85% of H. pylori carriers: quite possibly, the bacterium is protecting these people from chronic inflammation, a burgeoning problem in today’s steadily advancing society.

Before eradicating the bacteria, the beneficial effects of H. pylori and differences between strains need to be examined more thoroughly to make sure we are not eliminating a potential, albeit hidden, ally that has lived with us for more than 58,000 years.
By treating those who are unaffected, we could be unwittingly breeding susceptibility to a host of serious chronic inflammatory problems; however, by properly harnessing H. pylori’s veiled benefits (i.e., its DNA), we may be able to obtain all the advantages without any of the complications. If we look at H. pylori as a good bacterium with bad side effects as opposed to a bad bacterium with good side effects, perhaps we can gain something from this bug.

 
All fine and good, but I'm experiencing a host of symptom relief with just this one protocol. It's been like a revelation. A lifetime of stomach and bowel and autoimmune type problems as well as a boatload of food sensitivities... seem to be just kind of not there now. Not that I'm 100%, but the improvement is rather dramatic.
 
Notice how my posts highlight those who are very symptomatic and whose health is seriously affected after concerted efforts to regain health. I don't think that systematic eradication for all is called for and not even mainstream sources recommends that. Those who are very symptomatic after trying various things should consider consulting to discuss a diagnostic test and a treatment. Of those treated, there is always improvement. Context is everything. Above all, common sense.
 
Thanks for posting Gaby. I'll be getting a test and will be interested to see if this could be related to my chronic hives.

If anyone is looking to do a test in the US I found this site:


It's $139 for the H Pylori stool test. They submit a doctors order to a local lab that you go to for the test. Looks like they have access to thousands of labs in the US.
 
Thank you Gaby for the post. I had a colonoscopy last year and doctor said every thing good. I had peptic ulcer once 20 years back. I will order the test Renaissance posted to check any issues.
Finally, I got the results of the test and it is negative.
 
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