If you’ve been following the news, you’re aware that the COVID-19 pandemic has continued to change and evolve, with new symptoms being presented by different variants.
Fatigue, shortness of breath, cough, and other respiratory symptoms, joint pain, muscle pains, memory issues, problems concentrating or brain fog, heart palpitations, sleep issues, loss of or changes in smell or taste, depression, anxiety, fever, and fatigue are some of the most commonly reported symptoms.
Other common symptoms noted were laryngo-pharyngeal (LPR) difficulties such as a sore throat, throat clearing, globus, and dysphonia, in addition to the classic heartburn esophageal type symptoms (husky voice).
The emergence of these symptoms frequently coincided with a positive PCR test and a diagnosis of COVID-19, sometimes in conjunction with other symptoms that may or may not have been a manifestation of COVID, and sometimes in isolation, with patients otherwise remaining well.
In one case report published in the Journal of Gastroenterology, a patient acquired heartburn symptoms following anti-reflux surgery with no evidence of surgical complications or relief with drugs. The timing of both SARS-CoV-2 exposure and symptom start helped doctors diagnose COVID-19-related esophageal hypersensitivity.
The occurrence of gastric reflux, though not prevalent at the time, was already documented in China during the early days of the COVID-19 epidemic.
Surprisingly, some of the new emergent BA.2 subvariants, such as the BA.2.12 and, more specifically, the BA.2.3 and BA.2.3.4 subvariants, are suspected of having a tropism for the gastrointestinal system and producing a range of gastrointestinal disorders, including acid reflux. Media reports in Alberta, Canada, where these variants are common, reveal an increase in gastrointestinal problems.
Gastric reflux is also becoming more common in Long COVID, according to many specialists.
Gastric reflux symptoms are a developing gastrointestinal concern in many Post-COVID-19 patients, according to a Harvard Gastric Reflux – COVID-19 study.
COVID-19 is now widely recognized as a systemic disease with a wide range of clinical manifestations. Every system in the body is vulnerable, and neurological consequences have long been known.
Encephalitis and encephalomyelitis, as well as illnesses induced by peripheral nerve injury, such as Guillain-Barré syndrome, have all been linked to the central nervous system.
According to a Wuhan research, up to a third of hospitalized patients had neurological problems. However, as the outbreak developed in 2020, clinicians and patients realized that loss of smell and taste were among the most common symptoms.
According to an epidemiological meta-analysis, up to 20% of COVID patients experience loss of smell (hyposmia) and loss of taste (hypogeusia).
The facial nerve (cranial nerve VII), which provides fibres to the anterior two-thirds of the tongue, the glossopharyngeal nerve (cranial nerve IX), which provides fibres to the posterior third of the tongue, and the vagus nerve (cranial nerve X), which provides fibres to the epiglottis region, are the three cranial nerves that mediate taste. The olfactory (I) nerve is responsible for smell.
Other cranial nerves, such as facial paralysis and Bell’s palsy (VII), abducens nerve palsy (VI), and optic nerve (II) sheath enhancement, have also been reported in COVID patients, as detected by clinical examination and/or magnetic resonance imaging (MRI).
The mechanism by which SARS-CoV-2 induces these symptoms, however, is unknown. It’s been proposed that the smell and taste difficulties could be caused by a direct infection of the nasal and pharyngeal mucosa, such as the so-called “olfactory cleft syndrome,” in which the olfactory cleft is blocked, causing conductive loss. Certainly, much of the systemic damage induced by COVID is due to well-documented inflammatory mediated responses, but additional systemic mechanisms such as hypoxia and coagulopathy may also be present. However, there appears to be some indication that the virus might directly reach the central nervous system or peripheral nerves, and the olfactory bulb is a well-known route for viral entrance into the central nervous system.
The angiotensin converting enzyme 2 (AGE2) is directly targeted by the SARS-CoV-2 virus via its spike protein, and their proteases are expressed in the olfactory epithelium. The COVID virus can pass across the respiratory epithelial barrier, into the blood and lymphatic system, and finally into the central nervous system via the blood-brain barrier. ACE2 receptors are also found in the neurological system, and viral RNA has been found in the cerebro-spinal fluid of certain patients, as well as case studies describing brain abnormalities on MRI that point to direct viral involvement.
As a result, while the mechanism is unknown, COVID can certainly cause symptoms linked with cranial nerve dysfunction.
Many of you are probably wondering how all of this relates to reflux.
To begin, several complicated neurological reflexes mediate the functioning of the upper and lower esophageal sphincter mechanisms that protect the airway against gastro-esophageal reflux. The vagus and glossopharyngeal cranial nerves, as well as the phrenic nerve that supplies the diaphragm, are all involved.
There have already been reports of phrenic nerve palsy in COVID patients.
Thus, it appears reasonable to speculate that viral damage to one or more of the nerves involved in these neurological reflexes, either directly or indirectly, disrupts these reflexes, resulting in gastro-esophageal reflux.
Many patients’ reflux symptoms have slowly faded, which is unusual in primary gastro-esophageal disease but consistent with temporary neurological injury and the usual slow recovery of taste and smell dysfunction following SARS-CoV-2 infections, according to some clinicians.
There are many additional possible mechanisms that should be explored.
Changes in the gut microbiome have been discovered to produce reflux symptoms.
According to research released last year, 60% of patients seeking anti-reflux surgery have Small Intestinal Bacterial Overgrowth (SIBO). This syndrome is linked to the use of proton pump inhibitors (PPIs) and antibiotics, as well as a disruption in gastrointestinal motility.
Although it is unknown if COVID causes intestinal neurological injury, gastrointestinal symptoms are well characterized in COVID, and the gut is densely packed with angiotensin receptors. The fermentation of sugars by microorganisms in the small bowel, which is normally rather sterile, results in the production of intra-luminal gas and, as a result, excessive belching. Reflux symptoms are thought to be caused by the spewing of aerosolized stomach contents into the esophagus and throat.
SARS-CoV-2 has been linked to gut microbiome dysbiosis in numerous studies.
Gastric reflux can be triggered by gut microbiome dysbiosis.
Many of the patients examined had been prescribed antibiotics to address various forms of COVID and even higher dosages of PPIs when GP services were being supplied remotely, which should be recognized as simply anecdotal evidence. The majority of these patients said they were mostly ineffective.
Many of these individuals were diagnosed with SIBO using lactulose hydrogen breath tests, and their symptoms often disappeared after eradication.
Is it possible that a percentage of these individuals’ symptoms are all caused by SIBO?
Many of these topics remain unsolved, and it’s likely that reflux symptoms are caused by multiple causes.
Physicians, on the other hand, are confident that COVID has been linked to reflux symptoms in some of the patients they’ve seen in recent months, whether directly or indirectly.
More research is needed to find answers, particularly to learn how COVID affects the neurological system and cranial nerves in general, as well as the neural reflexes that ordinarily prevent gastro-esophageal reflux in particular.
In the meantime, doctors recommend that patients with reflux symptoms be evaluated for their entire symptom profile, including those caused by COVID and SIBO, and that long-term usage of PPIs that don’t provide symptomatic relief be avoided.
Image Credit: Getty
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