What are the potential side effects of dexamethasone in dental procedures. How can hiccups impact postoperative recovery. What is the mechanism behind drug-induced hiccups. How long do steroid-induced hiccups typically last. What are the treatment options for persistent hiccups.

Understanding Hiccups: Causes, Classification, and Mechanisms

Hiccups, medically known as singultus, are a common physiological phenomenon experienced by most people at some point in their lives. While usually brief and self-limiting, hiccups can occasionally persist and become a source of concern, particularly for postoperative patients.

What exactly are hiccups? They are sudden, involuntary contractions of the diaphragm, followed by an immediate closure of the vocal cords, producing the characteristic “hic” sound. The exact cause of hiccups remains elusive, but researchers have identified a complex neural process involving a reflex arc.

Classification of Hiccups

• Acute or transient: Lasting up to 48 hours
• Persistent: Continuing for more than 48 hours
• Intractable: Persisting for more than a month or two

While hiccups affect both males and females equally, intractable hiccups occur more frequently in men. This gender disparity in prolonged cases remains an area of ongoing research in the medical community.

The Neural Mechanism of Hiccups

The hiccup reflex arc consists of three primary components:

1. Afferent limb: Includes the phrenic and vagus nerves, along with the sympathetic chain from T6 to T12
2. Center: Located somewhere between C3 and C5 in the spinal cord
3. Efferent limb: Comprises the phrenic nerve, accessory respiratory muscles, glottis, and autonomic processes involving the medullary reticular formation and hypothalamus

Interestingly, some researchers propose that the hiccup reflex arc is actually a myoclonic action rather than a true reflex. This perspective challenges the traditional understanding of hiccups and opens up new avenues for research and potential treatment strategies.

Dexamethasone and Hiccups: A Case Study in Dental Surgery

The case study presented in the original text describes a 40-year-old male patient who developed hiccups following the administration of oral dexamethasone prior to dental implant surgery. This incident highlights the potential for corticosteroids, even in relatively low doses, to trigger hiccups in some individuals.

Key Points from the Case Study

• Patient received 8 mg oral dexamethasone approximately 1 hour before surgery
• Hiccups developed before any other medication was administered
• Hiccup rate: 5 to 7 per minute
• Oral triazolam (0.50 mg) was given, which temporarily reduced the hiccups
• Hiccups resolved completely within 42 hours after dexamethasone administration

This case underscores the importance of considering drug-induced hiccups as a potential side effect, even with commonly used medications like dexamethasone. Are there any predisposing factors that make certain individuals more susceptible to steroid-induced hiccups? Research in this area is ongoing, but factors such as individual physiology, dosage, and concurrent medications may play a role.

The Link Between Medications and Hiccups: Beyond Corticosteroids

While the case study focuses on dexamethasone, it’s important to note that various medications have been associated with triggering hiccups. Although a strict causal relationship has not been established for many drugs, clinicians often observe a correlation between certain medications and the onset of hiccups in their patients.

Medications Commonly Associated with Hiccups

• Corticosteroids (e.g., dexamethasone, prednisone)
• Benzodiazepines
• Certain antibiotics
• Chemotherapy agents
• Some antipsychotic medications

Why do these medications potentially trigger hiccups? The exact mechanisms are not fully understood, but theories suggest that they may interfere with the neural pathways involved in the hiccup reflex arc or alter neurotransmitter activity in the central nervous system.

Implications for Dental and Medical Practitioners

The occurrence of dexamethasone-induced hiccups in a dental setting raises important considerations for practitioners across various medical fields. While hiccups are generally benign, they can cause discomfort and anxiety in patients, potentially impacting the success of procedures and postoperative recovery.

Recommendations for Healthcare Providers

1. Be aware of the potential for drug-induced hiccups, especially with corticosteroids
2. Inform patients about this possible side effect
3. Monitor patients for the development of hiccups after medication administration
4. Consider alternative medications or dosing strategies if a patient has a history of drug-induced hiccups
5. Be prepared to manage hiccups if they occur during or after a procedure

How can practitioners balance the benefits of medications like dexamethasone with the risk of side effects such as hiccups? A personalized approach, taking into account the patient’s medical history, the specific procedure, and potential alternatives, is crucial in making informed decisions about medication use.

Managing Drug-Induced Hiccups: Strategies and Interventions

When faced with drug-induced hiccups, healthcare providers have several options for management. The approach often depends on the severity and duration of the hiccups, as well as the underlying cause.

Treatment Options for Transient Hiccups

• Reassurance and monitoring, as most cases resolve spontaneously
• Physical maneuvers (e.g., holding breath, drinking water from the opposite side of the glass)
• Breathing exercises or techniques to interrupt the hiccup cycle
• Mild sedation, if appropriate and necessary

Interventions for Persistent or Intractable Hiccups

• Pharmacological treatments (e.g., baclofen, gabapentin, metoclopramide)
• Adjustment or discontinuation of the suspected causative medication
• Nerve blocks or stimulation techniques
• In rare cases, surgical interventions may be considered

What factors should guide the choice of treatment for drug-induced hiccups? The decision should be based on the individual patient’s circumstances, the underlying medical condition, and the potential risks and benefits of each intervention.

The Impact of Hiccups on Patient Care and Outcomes

While often considered a minor nuisance, persistent hiccups can have significant implications for patient care, especially in postoperative settings. Understanding these potential impacts is crucial for healthcare providers to ensure optimal patient outcomes.

Potential Consequences of Prolonged Hiccups

• Disruption of sleep patterns
• Interference with proper nutrition and hydration
• Increased anxiety and stress
• Potential complications in wound healing or recovery processes
• Negative impact on overall patient satisfaction and well-being

How can healthcare providers mitigate the impact of hiccups on patient care? Proactive management, clear communication with patients about potential side effects, and prompt intervention when hiccups persist are key strategies to minimize negative outcomes.

Future Directions in Research and Clinical Practice

The case of dexamethasone-induced hiccups in a dental setting highlights the need for continued research and awareness in this area. As our understanding of drug-induced hiccups evolves, several avenues for future investigation and improvement in clinical practice emerge.

Areas for Future Research

• Mechanisms underlying drug-induced hiccups, particularly for corticosteroids
• Genetic or physiological factors that may predispose individuals to drug-induced hiccups
• Development of predictive models to identify patients at higher risk
• Novel interventions or preventive strategies for drug-induced hiccups
• Long-term impacts of recurrent drug-induced hiccups on patient health and quality of life

How can clinicians contribute to advancing knowledge in this field? Careful documentation of cases, participation in clinical studies, and sharing experiences through case reports and professional forums can all play a crucial role in expanding our understanding of drug-induced hiccups.

Improving Clinical Practice

1. Enhanced patient education about potential side effects of medications
2. Development of standardized protocols for managing drug-induced hiccups
3. Integration of hiccup risk assessment into preoperative evaluations
4. Collaborative approaches between different medical specialties to address complex cases
5. Incorporation of lessons learned from case studies into medical and dental education curricula

What role can technology play in advancing our understanding and management of drug-induced hiccups? The integration of artificial intelligence and machine learning algorithms could potentially help identify patterns and risk factors that are not immediately apparent to human observers, leading to more personalized and effective prevention and treatment strategies.

As we continue to explore the complex relationship between medications and hiccups, it’s clear that a multidisciplinary approach, combining insights from neurology, pharmacology, and various clinical specialties, will be essential in developing comprehensive solutions to this challenging side effect. By remaining vigilant and open to new evidence, healthcare providers can ensure that they are well-equipped to manage drug-induced hiccups effectively, ultimately improving patient care and outcomes across a wide range of medical and dental procedures.

Transient Hiccups Associated with Oral Dexamethasone

Case Rep Dent. 2013; 2013: 426178.

Published online 2013 Oct 9. doi: 10.1155/2013/426178

Author information Article notes Copyright and License information Disclaimer

Hiccups, or singulata (hiccup is singultus), are commonly experienced by most people at one time or another and are usually brief and self-limiting. Although pharmacotherapeutic agents are not generally considered causal in the etiology of hiccups, many clinicians empirically associate episodic hiccups in their patients as being drug induced. The two classes of drugs most often cited as causing hiccups are corticosteroids and benzodiazepines. This report involved a patient who was given preoperative dexamethasone and developed hiccups before anesthesia and surgery commenced. He at no time was in distress, and the surgical procedure was completed without complication. By the second postsurgical day his hiccups were resolved completely. Although the association may be anecdotal, many clinicians consider hiccups a potential side effect of steroid therapy, especially high doses of steroids. Of interest in this case is the relatively low dose of corticosteroid used, albeit apparently linked to his hiccups. Practitioners should be aware of this potential condition.

Hiccups, or singulata (hiccup is singultus), are very common and are experienced by most people at one time or another. They are usually brief and self-limiting but may become prolonged in some patients [1]. Hiccups that linger on for some time may become worrisome to the postoperative patient, thus hindering their nutritional and sleep needs [2, 3].

Hiccups are sudden, uncontrolled contractions of the diaphragm, followed by immediate inspiration and closure of the glottis over the trachea, producing the “hiccup” sound [4]. The classification of hiccups is as follows: up to 48 hours, acute or transient; longer than 48 hours, persistent; and more than a month or two, intractable [5]. The frequency of hiccups in males and females is equivalent, although intractable hiccups occur at a much higher rate in men [6, 7]. The exact etiology of the hiccup is unknown, but the neural process involves the reflex arc consisting of the afferent limb, the center, and the efferent limb [8, 9]. The afferent limb contains the phrenic and vagus nerves together with the sympathetic chain from T6 to T12. The center is linked to the afferent and efferent limbs and occupies a nonspecific location somewhere between C3 and C5. The efferent limb includes the phrenic nerve, accessory respiratory muscles, the glottis, and autonomic processes involving the medullary reticular formation and hypothalamus [4, 10]. One review proposed that the hiccup reflex arc is a myoclonic action and not a true reflex [11].

Medical conditions that have been associated with the development of hiccups include gastrointestinal, neurological, pulmonary, psychogenic, cardiovascular, metabolic, anesthesia related, and drug induced conditions [3, 4, 8, 12, 13]. Using a strict standard, drugs have not been proven to be a common cause of hiccups [7, 14]. Nevertheless, many clinicians have alluded to various medications as triggering the hiccup reflex [1, 3, 6, 13, 15–24]. The following case describes a patient who experienced transient hiccups following oral presurgical administration of dexamethasone.

A 40-year-old male with an unremarkable medical history presented for surgery to place an implant. He was in excellent health, did not take any medications, and was not allergic to any drugs. The patient had taken a single prophylactic dose of 8 mg oral dexamethasone approximately 1 hour earlier. After presurgical vital signs were taken, and before any other medication (sedation, local anesthesia) was administered, the patient developed intermittent bouts of hiccups at a rate of roughly 5 to 7 per minute. He was in no distress and wanted to continue the procedure. Oral triazolam 0.50 mg was given, and by the time the surgery started, the episodic hiccups were reduced greatly allowing the implant to be placed uneventfully. By the time the patient was ready to be escorted from the clinic, the hiccups had returned at about the same rate they occurred preoperatively. He was given postoperative instructions and reassurances and followed up telephonically the next day, where he reported that by late afternoon (32 hours) the rate of hiccup episodes was reduced. The patient’s hiccups resolved completely by 42 hours after he took the dexamethasone. At the 1-week postoperative appointment, the incident was reviewed with the patient and counseling was given on the suspected drug-induced cause of the transient hiccups for his future reference/benefit.

There are few reports in the literature on dexamethasone-induced hiccups and none in the dental literature [6, 15, 18, 23, 24]. Other cases of corticosteroid-induced hiccups have been reported [1, 25], and Dickerman et al. have described the first cases of anabolic steroid-induced hiccups [16, 17]. The only other adverse reaction to steroids found in the dental literature was a case of episodic psychiatric disturbance (cognitive dysfunction) in an 18-year-old female who had taken dexamethasone briefly [26]. The author would be remiss not to mention another suspected dexamethasone-induced transient hiccups case he came across years earlier, but, because other drugs were also given intravenously at the same time, it could not be confirmed.

Corticosteroids and benzodiazepines are the drug groups referenced most frequently in the literature as being associated with hiccups (see the following list), although Thompson and Landry state that there is not sufficient proof that any drug can be considered as definitely causing hiccups [14]. Souadjian and Cain reviewed 220 cases of protracted hiccups and did not mention any medication in the etiology of hiccups [7]. Garvey, who looked at postoperative cases of hiccups, came to the logical conclusion that the etiologic factor was probably drug related [3]; however, she also recounted that the intubation itself may be a contributing factor [27].

Drugs Possibly Associated with Triggering Hiccups:

•  

  Steroids (dexamethasone, methylprednisolone, oxandrolone, and progesterone)

•  

  Benzodiazepines (midazolam, lormetazepam, and lorazepam)

•  

  Barbiturates (methohexital)

•  

  Antibiotics (azithromycin)

•  

  Phenothiazines (perphenazine)

•  

  Opioids (hydrocodone)

•  

  Alcohol.

The case described here was mild and short term and, even though somewhat inconvenient to the patient, was in practice, clinically insignificant. Hiccups that become persistent or intractable however can interfere with a patient’s daily activities and cause them to seek medical assistance. There are various reports in the literature of different treatments for protracted hiccups, including pharmacologic agents [4, 5, 8, 18, 22, 28–34]. Chlorpromazine is at present the only medication approved by the FDA for the treatment of hiccups, although many practitioners have reported less than desirable results with this drug [6, 17, 29].

Baclofen has been shown to successfully treat chronic hiccups [3, 4, 19, 30, 34], and promising results have been attained with the use of gabapentin alone [31] or as an add-on to combination therapy [5, 32].

The evidence for medication-induced hiccups may be empirical, yet for many the association is strong enough that clinicians should take notice. This is especially true for treatments involving steroids [35], drugs that are commonly used in medicine, including dental medicine. Being able to recognize the potential “drug-hiccup link” will better prepare health care practitioners manage any unexpected complications.

There are many uses for steroids in medicine and dentistry, and clinicians should be attentive to any possible side effects of medications prescribed. This paper and case explain the correlation between hiccups and steroid treatment in the perioperative setting. Although drug-induced hiccups have not been absolutely confirmed with controlled studies, the incidence is sufficient enough to raise questions by many practitioners. Fortunately, most cases of corticosteroid-related hiccups appear to be transient and usually end after the drug is withdrawn.

The authors declare that they have no conflict of interests.

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Hiccups: Causes, treatments, and complications

Hiccups happen when a person’s intake of air becomes momentarily blocked. Possible causes include having gas in the stomach, eating spicy food, and having an underlying health condition.

When a hiccup forms, it is because of a sudden, involuntary contraction of the diaphragm at the same time as a contraction of the voice box, or larynx, and the total closure of the glottis, which is where the vocal cords are located. As a result, there is a sudden rush of air into the lungs, accompanied by the familiar “hic” sound.

Hiccups are medically known as synchronous diaphragmatic flutter or singultus. They can occur individually or in bouts. They are often rhythmic, meaning that the interval between each hiccup is relatively constant.

Most people have hiccups from time to time, and they usually resolve without treatment within a few minutes.

Rarely, there may be prolonged or chronic hiccups, which can last for a month or longer. Hiccups that last for longer than 2 months are known as intractable hiccups.

If a bout of hiccups lasts for longer than 48 hours, this is considered persistent, and the person should contact a doctor. This tends to be more common in men than women and could signify a more serious medical condition.

Fast facts on hiccups

• The exact cause of hiccups remains unclear, but experts have linked chronic hiccups to a wide range of conditions, including stroke and gastrointestinal problems.
• Most cases resolve without treatment, but prolonged hiccups can lead to complications such as insomnia and depression.
• If hiccups last for longer than 48 hours, the person should contact a doctor, who may prescribe muscle relaxants.
• Avoiding alcohol and not eating too quickly can reduce the chance of experiencing hiccups.

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The National Organization for Rare Disorders describes hiccups as “an involuntary spasmodic contraction of the muscle at the base of the lungs (diaphragm) followed by the rapid closure of the vocal cords. ”

A wide range of underlying conditions can trigger chronic or persistent hiccups.

Exactly how or why short bouts of hiccups happen remains unclear, but experts have linked some factors to a higher chance of experiencing them. The sections below look at some of these factors in more detail.

Lifestyle factors

The following may trigger hiccups:

• eating hot or spicy food that irritates the phrenic nerve, which is located near the esophagus
• having gas in the stomach that presses against the diaphragm
• eating too much or causing stomach distension
• drinking sodas, hot liquids, or alcoholic drinks, especially carbonated drinks
• experiencing stress or strong emotions

Some medications — such as opiates, benzodiazepines, anesthesia, corticosteroids, barbiturates, and methyldopa — can also cause hiccups.

Medical conditions

Often, hiccups occur unexpectedly, and neither the person nor the doctor can identify their likely cause.

However, doctors have linked chronic hiccups to several conditions. These include:

• gastrointestinal conditions, such as inflammatory bowel disease, a small bowel obstruction, or gastroesophageal reflux disease (GERD)
• respiratory conditions, such as pleurisy of the diaphragm, pneumonia, or asthma
• excessive and habitual consumption of alcohol
• conditions that affect the central nervous system, such as a traumatic brain injury, encephalitis, a brain tumor, or a stroke
• conditions that irritate the vagus nerve, such as meningitis, pharyngitis, or goiter
• psychological reactions, including grief, excitement, anxiety, stress, and shock
• conditions that affect metabolism, including hyperglycemia, hypoglycemia, and diabetes
• liver and kidney problems
• cancer, either as a result of damage caused by the condition or as a side effect of the treatment, such as chemotherapy
• conditions of the autonomic nervous system, which also affects breathing, sweating, the heartbeat, hiccups, and coughing

Other conditions that may be related to hiccups include bladder irritation, liver cancer, pancreatitis, pregnancy, and hepatitis. Surgical procedures and lesions may also be risk factors.

Infants may experience hiccups more frequently during or after feeding, as they may swallow food too quickly or overfeed. Hiccups could also be a sign of an infant being full. Therefore, pediatricians typically recommend short feeds with burping breaks.

Hiccups may also occur due to an infant’s breathing and swallowing not yet being in sync. In turn, this can cause an infant to draw breath and swallow, which can produce a hiccup.

Hiccups in infants may also result from changes in stomach temperature. For example, this may be the case if they consume a cold drink then have something warm to eat.

Generally, hiccups tend to be a sign of healthy growth and development. However, frequent hiccups may also result from GERD, which is a common and easily treatable condition in infants.

Hiccups alone are not a sign of reflux. Some other possible symptoms in infants with suspected GERD include:

• crying more frequently
• arching the back excessively during or after feeds
• spitting up more often than usual

Parents and caregivers should consult a pediatrician if they notice that their infant is experiencing several symptoms and suspect that reflux may be causing them.

Prolonged hiccups can lead to complications such as:

• Weight loss and dehydration: If the hiccups are long term and occur at short intervals, it can become difficult to eat.
• Insomnia: If prolonged hiccups persist during the sleeping hours, it can be hard to fall asleep or stay asleep.
• Fatigue: Prolonged hiccups can be exhausting, especially if they make it hard to sleep or eat.
• Communication problems: It can be difficult for the person to speak if they have hiccups.
• Depression: Long-term hiccups can increase the risk of developing clinical depression.
• Delayed wound healing: Persistent hiccups can make it harder for post-surgical wounds to heal, thereby increasing the risk of infections or bleeding after surgery.

Other potential complications include an irregular heartbeat and GERD.

Hiccups that last for under 48 hours do not usually need any medical attention because they typically resolve on their own. If they persist for longer than this, the person should consult a doctor.

The doctor may ask:

• when the hiccups began
• how often they occur
• if they are happening all the time
• what the person was doing before the hiccups started

They will likely perform a general physical examination and a neurological exam to check the person’s:

• reflexes
• balance
• coordination
• eyesight
• sense of touch
• muscle strength
• muscle tone

If an underlying condition may be the cause, the doctor may order the following tests:

• blood tests to check for infections, kidney disease, or diabetes
• imaging tests — such as an X-ray, CT scan, or MRI scan — to assess for any anatomical irregularities that may be affecting the phrenic or vagus nerves or the diaphragm
• an endoscopic test, in which a healthcare professional passes an endoscope — which is a flexible tube with a small camera at the end — down the person’s throat to check the windpipe or esophagus
• en electrocardiogram to check for heart-related conditions by measuring electrical activity in the heart

Some causes of hiccups are preventable. A few ways to reduce the chance of experiencing hiccups include:

• avoiding sudden changes in temperature
• not drinking alcohol or sodas
• eating moderately and not too quickly

Most hiccups are brief and go away after a short while. However, if they persist or cause worrying symptoms, the person should contact a doctor.

Drug-induced esophagitis

The first case of drug-induced esophagitis was described in 1970 by J. Pemberton [1]: ulcers of the esophageal mucosa were found in a patient taking potassium chloride [2]. Since that publication, a number of articles have appeared with reports of the development of drug-induced esophagitis against the background of the use of many drugs (drugs) from different pharmacological groups, they are summarized in table . In total, about 100 drugs have been identified that may be the cause of the development of drug-induced esophagitis [3]. Esophagitis associated with the use of antibiotics, antiretroviral and antitumor drugs, non-steroidal anti-inflammatory drugs (NSAIDs) is the best studied [4]. Drug-induced lesions of the esophagus occur as a result of the direct toxic effect of drugs and their effect on the nervous system (lower pressure in the lower esophageal sphincter, difficulty in emptying the stomach, etc.) [2, 4]. Drugs can also cause or exacerbate the course of gastroesophageal reflux disease (GERD) and, as a result, esophagitis [2, 4]. Drug-induced lesions of the esophagus significantly reduce the patient’s quality of life.

Table . Drugs associated with the development of drug-induced esophagitis [1-6, 9, 11, 12, 15-21, 23-29]

9002 3

Group of medicines

90 023

Bleomycin

Cytarabine

Dactinomycin

Daunorubicin

Fluorouracil

Methotrexate

Vincristine

900 23

Calcium channel blockers

900 39

Drug	Mechanism	Level of evidence
Antibiotics	Clindamycin Doxycycline Penicillin Rifampicin Tetracycline Erythromycin Amoxicillin Metronidazole Ciprofloxacin Cloxacillin	Direct mucosal injury esophagus or decrease its resistance to reflux	b/c
Antitrevirus	NELFINAVIR Zidacitabin Zidovudin	9000 6
Glucocorticoids	–	Lower esophageal sphincter pressure reduction	A
Non-steroidal anti-inflammatory drugs	Aspirin® Ibuprofen Naproxen Aceclofenac Acetaminophen Phenylbutazone	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	A/B
Chemotherapy drugs	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	B/C
Hormones and their derivatives	Estrogen Progesterone	Pressure reduction in the lower esophageal sphincter	A
Antiarrhythmics	Quinidine	Direct mucosal injury esophagus or decrease in its resistance to reflux	B
Anticoagulants	Dabigatran Warfarin	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	B
Nifedipine Amlodipine Felodipine	Difficulty emptying the stomach, decreased pressure in the lower esophageal sphincter	B
Nitrates	Isosorbide dinitrate 9 0005	Decreased pressure in the lower esophageal sphincter	A
Adenosinergic	Theophylline	Lower esophageal sphincter pressure reduction	A
Anticholinergics	Emepronium bromide	Direct damage to the mucosa of the esophagus	A
Sahazesiya	Glimepiride	The mechanism is unknown 9,0005	C
Bisphosfonat 0026	Alendronate Ethronate Pamidronate Medak Ibandronate	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	B depressants	Amitriptyline Dotypine Lofepramine Clomipramine	Lower esophageal sphincter pressure reduction	B
Anxiolytics	Alprazolam	Mechanism unknown	C
Benzodiazepines0005 Zolpidem	Lower esophageal sphincter pressure reduction	A
Antiepileptics 9000 5	Phenytoin	Mechanism unknown	C
Vitamins	Ascorbic acid	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	C
Macro- and microelements	Iron sulfate Potassium chloride	Direct damage to the mucosa of the esophagus or reduction of its resistance to reflux	C
Other drugs	Pinaveria bro mid Thiropramide	Mechanism unknown	C

Evidence level: A – one or more randomized, controlled clinical trials; B – non-randomized clinical trials, prospective observational studies, cohort studies, retrospective studies, case-control studies, meta-analyses and/or post-marketing surveillance; C – the presence of one or more published cases or a series of cases.

Epidemiology

The incidence of drug-induced esophagitis is not completely known, but there are separate regional studies. For example, in Sweden, the incidence of drug-induced esophagitis is 4 cases per 100,000 population per year. Drug-induced esophagitis is more common in women aged 18–70 years, as well as in the elderly [4].

Classification and pathogenetic mechanisms

Drugs, the use of which is associated with the development of drug-induced esophagitis, can be divided into three groups according to their effect on the mucosa of the esophagus [4, 5]. The drugs of the first group cause temporary damage to the mucous membrane due to the low pH when dissolved in water. Localized discrete ulcers appear, which, after discontinuation of the drug, heal on their own without the formation of esophageal strictures. This group of drugs includes doxycycline, tetracycline, clindamycin, emepronium bromide, ascorbic acid and ferrous sulfate (II). Drugs of the second group cause permanent damage to the mucous membrane of the esophagus. These include quinidine, potassium chloride, and bisphosphonates. Drugs of the third group, causing permanent damage to the mucosa of the esophagus with strictures, include NSAIDs [4, 5]. According to one of the studies, the number of cases of esophagitis caused by the drugs of the first group is 65.8%, the drugs of the second group – 12.4%, the third group – 21.8% [5].

Drug-induced esophagitis occurs as a result of a combination of three main components of pathogenetic mechanisms: the action of drugs, the characteristics of the esophagus and exogenous factors [4, 6]. Drugs can cause esophagitis by direct or indirect effects on the mucosa of the esophagus [4]. The direct effect is the formation of caustic compounds (acids, alkalis, etc.), the indirect effect is the induction of a systemic reaction that can damage the mucosa (for example, the induction of acid reflux by calcium channel antagonists) [4]. In addition, the following characteristics of the drug are important: drug coating, duration of contact with the esophagus, release rate, size and shape.

Morphological and functional disorders such as esophageal achalasia, strictures, reflux, diverticula and hernias of the esophagus, cardiomegaly may increase the risk of drug-induced esophagitis due to a concomitant decrease in pressure in the distal esophagus. However, drug-induced esophagitis can also occur against the background of the normal state of the esophagus [4]. Exogenous factors that depend on the patient include body position when taking drugs, the amount of water taken with the drug, the time of taking the drug and the amount of saliva [6].

Pathophysiological mechanisms of development of drug-induced esophagitis against the background of individual drugs are presented in table .

Risk factors

Risk factors for the development of drug-induced esophagitis include lying on the back during and within 30 minutes after taking the drug, insufficient water when using drugs, the use of large tablets of drugs and / or in a gelatin capsule, as well as the presence of concomitant pathology of the esophagus, characterized by a decrease in pressure in the lower esophageal sphincter [4].

Clinical picture, diagnosis and differential diagnosis

Clinical symptoms of drug-induced esophagitis do not differ from esophagitis of other etiologies [4]. The occurrence of retrosternal pain, odynophagia, dysphagia, nausea and vomiting is noted [4, 7]. Severe cases of drug-induced esophagitis may be accompanied by weight loss and/or gastrointestinal bleeding. The occurrence of these symptoms correlates with the fact and / or time of taking drugs that can cause esophagitis, the time interval ranges from several hours to 10 days. In addition, during the history taking, it is necessary to pay attention to the position of the body in which the patient takes these drugs [4].

Some or other signs of esophageal pathology are found in 99% of patients with drug-induced esophagitis [6]. During endoscopy, various pathological changes can be detected: superficial erythema, mucosal erosion, esophageal ulcers (up to the formation of “kissing” ulcers in 43. 6% of cases [8]), strictures, esophago-respiratory fistulas, esophageal perforation. Lesions of the esophagus are more common in its middle third (in one study, lesions of the middle third of the esophagus amounted to 78.2% [8]), since in this place the esophagus experiences external pressure from the aortic arch and left atrium, although in some cases they can be localized in distal or proximal. Endoscopic examination can detect fragments of drugs [7]. The use of esophagoscopy is especially recommended in cases where the patient does not respond to therapy or the drug cannot be withdrawn [4].

Double-contrast is recommended for esophagography, as single-contrast examination may show normal results. During the procedure, strictures, esophageal ulcers, external compression of the esophagus, and mobility abnormalities are detected [4, 6]. Histological examination of the biopsy of the esophageal mucosa does not reveal the etiology of drug-induced esophagitis. Usually the result is benign ulcers and acute inflammatory changes, however, histological evaluation is necessary for differential diagnosis with infectious pathology and malignant neoplasms of the esophagus [4].

Drug-induced esophagitis must be differentiated from esophagitis of another etiology and other pathology of the esophagus: these are herpetic esophagitis, eosinophilic esophagitis, candidal esophagitis, Crohn’s disease, reflux esophagitis, giant ulcer of the esophagus.

Complications

Complications of drug-induced esophagitis include: gastrointestinal bleeding, esophageal stenosis and stricture, esophageal perforation, intramural esophageal hematoma, mediastinitis, etc. [2].

Treatment

For the treatment of drug-induced esophagitis, it is recommended to stop taking the drug that caused this condition and carry out symptomatic therapy with such drugs [2, 6, 7, 9] as lidocaine (local pain relief), proton pump inhibitors (PPIs) ), h3-receptor antagonists, antacids. Daily intake of PPIs in the morning in most patients can quickly relieve heartburn and cure esophagitis within a few weeks [2, 6]. Patients who do not respond well to a standard single daily dose of PPI should be given PPI twice a day [6]. A number of studies recommend the use of sucralfate in combination with PPIs to create a protective mucosal barrier [10, 11]. It should be noted that special studies on the treatment of exactly drug-induced esophagitis have not been conducted. In severe cases (strictures of the esophagus, bleeding from an ulcer, accumulation of drugs in the affected esophagus, etc.), endoscopic treatment is indicated [4].

Prevention

For the prevention of drug-induced esophagitis, it is recommended not to take drugs at bedtime and in the supine position, and to take one tablet at a time with 200-250 ml of liquid to increase the amplitude and duration of esophageal motility [4 ]. In elderly patients and patients with esophageal dysmotility, it is preferable to take drugs in liquid form, if possible, large gelatin-coated drugs are excluded [4].

Prognosis

The prognosis of patients with timely diagnosed drug-induced esophagitis is usually favorable [2]. As a rule, a week after stopping the drug and starting symptomatic therapy, the esophageal mucosa is restored. Follow-up endoscopy is usually not required [2].

Certain drugs associated with the development of drug-induced esophagitis and gastroesophageal reflux disease

Antibiotics. Drug-induced esophagitis can be caused by some antibiotics [6]. After dissolution in saliva, the pH of tetracycline and its derivatives changes to the acid side. There are several reports of the occurrence of severe esophagitis after taking tetracycline with insufficient water and just before bedtime [5, 6]. There are also descriptions of clinical cases of doxycycline-induced esophagitis in patients with malaria [12]. These patients complained of hiccups, and during endoscopy they found erosions and ulcers of the esophagus [6]. In one study, doxycycline-induced esophagitis was found in 24 out of 25 patients [10]. The average age of patients with antibiotic-induced esophagitis is about 30 years [11].

Antiretroviral drugs . Zidovudine, which inhibits human immunodeficiency virus replication, can also cause drug-induced esophagitis, with both multiple and large single ulcers being found [6]. In one study, a patient with a history of zidovudine-induced esophagitis also had episodes of drug use in the supine position and without drinking water [6]. Antiretroviral drugs such as nelfinavir and zalcitabine can also cause drug-induced esophagitis [4].

Glucocorticoids. One study showed the ability of dexamethasone to reduce pressure in the lower esophageal sphincter [13]. In addition, there is evidence that taking prednisolone increases the contact time of hydrochloric acid with the mucosa of the esophagus by more than 2 times and thereby increases the likelihood of esophagitis [5].

NSAIDs . NSAID-induced esophageal injury remains an important public health problem. For example, taking low doses of acetylsalicylic acid can approximately 2-fold increase the likelihood of developing peptic esophagitis [9]. Among the pathogenetic mechanisms for the development of NSAID-induced esophagitis, there is an increase in gastric secretion and a decrease in pH, a direct contact effect of drugs, a decrease in bicarbonate production and a change in the properties of mucus, inhibition of gastric motility and provoking gastroesophageal reflux [9]. There is a high probability of extraesophageal symptoms (cough, choking, morning hoarseness, halitosis, etc.). There are the following risk factors for the occurrence of NSAID-induced lesions of the esophagus [9]: older age, male gender, concomitant use of glucocorticoids, alendronate, low doses of acetylsalicylic acid. Erosive esophagitis is more often found in patients with gastric and duodenal ulcers, as well as in the presence of hiatal hernia [9]. The incidence of esophageal strictures in NSAID-induced esophagitis reaches 40–50% [11]. In one of the retrospective longitudinal controlled studies, it was found that taking NSAIDs increases the risk of GERD by 2. 11 times [5].

Chemotherapeutic drugs. Damage to the esophagus when taking chemotherapeutic drugs is caused mainly by their direct action on the mucous membrane [5]. Cases of esophagitis induced by taking bleomycin, cytarabine, dactinomycin, daunorubicin, fluorouracil, metrotrexate, vincristine are described [7, 14].

Hormones and their derivatives. There is evidence of an increased risk of developing and more severe course of GERD in patients taking conjugated estrogens for a year or more, as well as receiving estrogen therapy alone or progesterone therapy alone [15, 16]. However, when using combined hormone replacement therapy, an increase in the risk of developing GERD was not found [5].

Antiarrhythmic drugs. An association has been established between the occurrence of esophagitis and oral administration of the antiarrhythmic drug quinidine [5, 11]. According to one study, the average age of patients with quinidine-induced esophagitis was 60 years [11].

Anticoagulants. Dabigatran etexilate is an oral anticoagulant that is now increasingly used due to its good tolerability, efficacy, and lack of the need to control the blood coagulation system. However, in the last decade there are more and more reports of side effects from the gastrointestinal tract when taking the drug dabigatran etexilate [17-19]. Y. Toya et al. [20] report the occurrence of dabigatran-induced esophagitis in 20% of study participants, according to endoscopic examination data [20]. There is no study that has identified the prevalence of dabigatran-induced esophagitis, but one retrospective review of 91 case histories of patients treated with dabigatran etexilate noted that 19 (20.9%) patients on upper gastrointestinal endoscopy endoscopic signs of esophagitis were found in the intestinal tract [18, 21].

In its structure, dabigatran etexilate contains tartaric acid, which, when released in the esophagus, damages the mucous membrane. Dabigatran-induced esophagitis can either manifest itself with typical symptoms (retrosternal pain, odynophagia, dysphagia, etc.) or be asymptomatic [17, 18]. The asymptomatic course of dabigatran-induced esophagitis may go unnoticed for a long time in patients who do not undergo endoscopy [21]. Most often, patients with esophagitis associated with taking the drug dabigatran etexilate took it during ventricular fibrillation at a dose of 110 mg 2 times a day [19]. Usually, discontinuation of this drug in combination with PPI therapy for 1 week is sufficient to relieve the symptoms of dabigatran-induced esophagitis [18].

Calcium channel blockers. According to one study, the use of calcium channel blockers for 6 years induced the development of GERD in 16.5% of patients [22]. More often, manifestation or exacerbation of GERD occurs when taking nifedipine (21.5%), amlodipine (23.8%) and felodipine (21.5%) [5].

Nitrates. Nitrates reduce pressure in the lower esophageal sphincter, and can also have a direct damaging effect on the mucosa of the esophagus, inducing the development of GERD and esophagitis [5]. There are results from a double-blind, placebo-controlled study showing that isosorbide dinitrate significantly reduces pressure in the esophageal sphincter [23]. Even foods high in nitrates can increase the risk of GERD by 3 times [5].

Adenosinergic drugs. There are data from randomized controlled trials proving the induction of GERD and increased reflux by theophylline drugs due to a decrease in pressure in the lower esophageal sphincter [5, 24].

Anticholinergic drugs. Emepronium bromide is an anticholinergic drug used to reduce the frequency of urination. More often it is prescribed to women, in connection with this, women predominate among patients with esophagitis induced by taking emepronium bromide [11]. However, there is a report of the occurrence of esophagitis in children taking this drug [25].

Antihyperglycemic drugs. There is evidence of the ability of the hypoglycemic drug glimepiride to cause damage to the esophagus, but the mechanism of its occurrence remains unknown [2, 5].

Bisphosphonates. Alendronate, a selective osteoclast inhibitor, prevents bone resorption and is used to prevent and treat postmenopausal osteoporosis. However, the daily use of alendronate at a dose of 40 mg increases the incidence of complications from the gastrointestinal tract due to the direct effect on the mucous membrane [6]. There is a description of a clinical case of the development of alendronate-induced esophagitis in a patient with postmenopausal osteoporosis while taking alendronate for three months at a dose of 10 mg/day [3].

Another bisphosphonate, risedronate, is less toxic. In a pooled study of 9 clinical trials, which included more than 10,000 patients, there was no statistically significant difference between the incidence of esophageal side effects in patients taking risedronate and patients taking placebo [11].

Antidepressants. Long-term use of tricyclic antidepressants can induce the development of GERD due to their anticholinergic action, which causes a decrease in pressure in the lower esophageal sphincter. The highest risk of developing GERD is observed in patients taking amitriptyline. In addition, the occurrence of lesions of the esophagus correlates with the use of dotypine, lofepramine, clomipramine [5].

Anxiolytics. In one study, approximately 30% of patients treated with alprazolam experienced GERD manifestations predominantly at night due to the inhibitory effect of the drug on the central nervous system [5].

Benzodiazepines. There is evidence that benzodiazepine drugs reduce pressure in the lower esophageal sphincter, increasing the duration of reflux in both healthy people and patients with GERD [5]. For example, the appointment of diazepam at a dose of 5 mg / day reduces the level of pressure in the lower esophageal sphincter by 18.9%, and at a dose of 10 mg/day — by 37.8% [5].

Antiepileptic drugs . A clinical case report of esophageal ulceration resulting from the use of phenytoin in an elderly patient has been published [26].

Vitamins. Ascorbic acid, due to its damaging effect on the mucous membrane of the esophagus, can cause esophagitis and increase reflux [5, 27].

Macro and microelements. Potassium chloride-associated esophagitis has been reported to be more common in women with rheumatic heart disease [11]. In addition, there is a possibility of developing damage to the esophagus induced by the intake of iron sulfate [11].

Other drugs. In addition to those listed, some other drugs can cause damage to the esophagus, such as pinaverium bromide, tiropramide [2].

Medication-associated lesions of the esophagus remain an urgent problem, as they are accompanied by clinical symptoms that significantly impair the quality of life of patients, and can also cause severe complications. Timely diagnosis, treatment and prevention of drug-induced diseases of the esophagus are important tasks for the practitioner. It is necessary to raise the awareness of general practitioners, therapists, and narrow specialists about the possibility of drug-induced esophagitis, since there is a wide range of drugs that cause it, which are used in various fields of medicine.

The authors declare no conflicts of interest.

The authors declare no conflict of interest .

Gastritis, duodenitis and gastroduodenitis – description, symptoms and treatment / Gastro-hepatocenter EXPERT and dysfunction of the stomach. Chronic inflammation of the mucous membrane of the stomach and duodenum is called chronic gastroduodenitis.

Gastritis and duodenitis are acid-dependent conditions that occur when the balance of defense and aggression factors is disturbed in the mucous membrane of the stomach and duodenum. These aggressive factors include the bacterium Helicobacter pylori.

Chronic gastritis is much more common than other pathologies of the digestive system and is often a disease preceding or accompanying an ulcer or stomach cancer.

Causes of gastritis

The development of gastritis can be triggered by the following reasons:

• Helicobacter pylori bacterium (helicobacter pylori gastritis occurs in most patients)
• damage to the gastric mucosa of an autoimmune nature (self-antibodies)
• toxic damage to the gastric mucosa (by bile thrown into the stomach from the duodenum, alcohol or drugs )
• malnutrition (excessive use of preservatives, fried, spicy, smoked, too hot or cold food)
• smoking and alcohol abuse
• frequent exposure to stress
• rare causes (effects of radiotherapy, allergies, etc.).

Symptoms of gastritis

Superficial gastritis itself does not cause symptoms. All signs of this disease are caused by functional dyspepsia.

Some conditions are observed when chronic gastritis is exacerbated. Symptoms during exacerbation are associated with severe inflammation and the appearance of erosion. Also, a prolonged course of gastritis provokes extensive atrophy of the gastric mucosa. This condition is accompanied by gastrointestinal and non-specific disorders.

Gastrointestinal conditions:

• Feeling of heaviness in the stomach, distension in the epigastric region, aggravated after eating
• Belching
• Nausea and vomiting
• Bad taste in the mouth 57 defecation disorders
• flatulence
• pain and burning in a stomach.

General symptoms:

• severe fatigue and weakness, drowsiness
• hiccups
• weight loss
• pallor
• increased sweating
• other conditions.

Diagnosis of gastritis

The following methods are used in our clinic to diagnose gastritis:

• 7 Abdominal ultrasound
• Helicobacter breath test
• Coprogram
• analysis stool for occult blood
• blood tests, including gastropanel with stimulation
• stool test for Helicobacter antigens and blood test for antibodies to Helicobacter

The required volume and diagnostic methods are determined by a gastroenterologist.

Treatment of gastritis

After the diagnosis of gastritis is confirmed, our gastroenterologist draws up a treatment plan depending on the stage of the disease, the characteristics of its course, and the causes of its development.

In our clinic, exacerbation of chronic gastritis is treated in stages. At the first stage, the doctor prescribes:

• regimen and therapeutic nutrition
• basic drugs, the choice of which depends on the excess or lack of gastric secretions
• additional drugs, the choice of which depends on the degree of inflammation of the gastric mucosa intestines into the stomach
• antibiotics (for helicobacteriosis)
• iron preparations (for anemia).

At the second stage, the effectiveness of the treatment is evaluated:

1. If drug therapy reduces the activity of the disease and improves the patient’s well-being, then the doctor decides to expand the diet and reduce the dose and frequency of medication. In cases where the treatment is not effective enough, the doctor adjusts the therapy plan.
2. If therapy against Helicobacteriosis was carried out, then a control breath test is performed one month after the end of treatment. In the event of a negative test result, if the patient feels well, further preventive visits to the doctor are arranged. If Helicobacter is still present in the patient’s body, repeated antibiotic therapy is prescribed, or its sensitivity to them is detected by seeding the bacteria.

Prognosis for gastritis

Prolonged Helicobacter pylori gastritis without adequate treatment causes atrophy of the gastric mucosa. Chronic atrophic gastritis increases the likelihood of stomach cancer.

Timely treatment of chronic gastritis and Helicobacter pylori infection with further regular visits to the gastroenterologist for prevention reduces the likelihood of developing stomach cancer to a minimum.

Prevention and advice

To avoid the development of gastritis, as well as the recurrence of the disease, the following recommendations will help:

• proper and regular nutrition (you should eat five times a day, not hot, mechanically processed food)
• smoking cessation lining of the stomach (if possible).

Diet for gastritis in the acute stage

1. Diet “Table No. 1” is indicated for people with gastritis with high acidity. It implies the rejection of food that contributes to any irritation of the gastric mucosa. You should eat six times a day mashed food of medium temperature, boiled or steamed. Drink a glass of milk or cream at night
2. Diet “Table №2” is prescribed for patients with gastritis with low acidity. Such a diet implies the rejection of food that contributes to mechanical irritation of the gastric mucosa. At the same time, nutrition should stimulate the activity of its secret. The patient eats dishes of various degrees of thermal and mechanical processing and foods rich in fiber. Excluded are foods that are difficult to digest, as well as any irritants of the gastric mucosa (too cold or hot food, spicy dishes, etc.).

Doctors treating the disease

Zinovieva Evgenia Nikolaevna

Chief Physician, gastroenterologist, hepatologist, PhD, associate professor

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Andrey Kharitonov

Gastroenterologist, Ph. D. Ph.D.

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Sokolova Ksenia Sergeevna

Gastroenterologist, hepatologist, therapist

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Pakhomova Inna Grigorievna

Gastroenterologist, hepatologist of the highest category, Candidate of Medical Sciences, Associate Professor

5 Therapist of the highest category, gastroenterologist, hepatologist

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Silishchev Roman Sergeevich

Endoscopist

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Dubossarsky Yuri Sergeevich

Endoscopist0005

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Savelyeva Karolina Anatolyevna

Endocrinologist-nutritionist, Ph.D.

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Clinical cases

Gastritis due to stress

Patient E., 40 years old, applied to the EXPERT gastro-hepatocenter with complaints of pain in the stomach area that occurs immediately after eating, disappears during fasting.

From the anamnesis it is known that the patient eats irregularly, recently there have been many stressful situations. After a comprehensive examination in the center, including EGD with a test for Helicobacter and histological examination of the gastric mucosa, the diagnosis was made: chronic gastritis of a high degree of activity, the HP test was negative. Patient E., 40 years old, applied to the EXPERT gastrohepatocenter complaints of pain in the stomach that occurs immediately after eating, disappearing during fasting.

From the anamnesis it is known that the patient eats irregularly, recently there have been many stressful situations. After a comprehensive examination at the center, including FGDS with a test for Helicobacter pylori and histological examination of the gastric mucosa, the diagnosis was made: chronic gastritis of a high degree of activity, HP test was negative.

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Helicobacter Pylori bacteria and gastritis

Patient G., 23 years old, came to the EXPERT center in 2010 with complaints of aching pain 1.5 hours after eating and at night, passing after eating. When studying the anamnesis, it turned out that the patient’s diet was irregular, often fast food, the young man was fond of tourism, where food often takes place in unsanitary conditions.