Alcohol abuse effects people of all ethnicities, genders, and socioeconomic statuses and can silently cause serious issues in the human body. Mainstream alcohol consumption is common throughout the world due to easy access, low cost and the variety of beverage choices available. In the United States alone, it is estimated that 1 out of 10 people are categorized into consuming at-risk quantities of alcohol. The overall cost is billions of healthcare dollars spent and premature death.1 Although, reducing alcoholism is a top priority across the board, the treatment and management of this disease is very complex and difficult to control. Treatment plans must be individualized with a multi-faceted approach focusing on pharmaceutical detoxification protocols involving withdrawal symptoms, mental health, potential relapse, and more importantly metabolic and organ health for optimal outcomes.123
During detoxification, it is crucial for clinicians to use all tools and resources at their disposal especially when dealing with liver-associated abuse. Checking metabolic panels and blood plasma levels are an easy way to understand the disease-state associated with alcohol abuse. One common area of concern is ammonia levels in the blood. According to Liu et al, ammonia is a common byproduct within the blood and relatively safe in low numbers (>50 µmol/L). Ammonia is produced by the gastrointestinal tract, muscles and kidneys and catabolized by the liver before elimination as urea.2,4 However, with chronic alcohol abuse the hepatic system loses the ability to act as a filter breaking down these toxins within the body. It is essential that pharmaceuticals be used used to help lower potential risks associated with excessive ammonia levels in the blood.
Primary Hyperammonemia can lead to acute encephalopathy causing seizures, coma or death. Another issue that arises with hyperammonemia is that is can cause a massive production of the amino acid glutamine within the brain effecting the central nervous system’s ability to control and fire neurons appropriately. This can lead to a secondary or chronic neurodegenerative condition effecting the central nervous system, such as Parkinson’s or Alzheimer’s.2 Pharmaceutical intervention is one of the best ways to approach the reduction of ammonia to avoid these conditions. There are many drugs that counter hyperammonemia but no gold standard or thorough algorithm that delineates the most appropriate care has been set. Understanding pharmaceutical options and literature available will assist in determining the best approach to reducing blood plasma levels providing better outcomes.
Research suggests that Lactulose or Rifaximin are the most studied and widely used antibiotics to reduce hyperammonemia to date.2,4,5 There are many differences between the two drugs such as the mechanism of action, side effects and consumer reports. Lactulose is usually the first line choice and is broken down into lactic acid which helps with the production of normal flora of the of the gastrointestinal track while reducing pathogenic bacteria. The osmotic pressure within the colon is increased drawing out the ammonia before it can be absorbed by the body.2 While, Rifaximin has been shown to bind to bacterial DNA causing a cascade effect eliminating the steps needed for transcription of pathogenic bacteria in the human gut.2,5 Lactulose is generally cheaper and has far less adverse side effects than Rifaximin. The elimination of ammonia from these drugs usually comes from excrement from soft stool or diarrhea so clinical education on what to expect and nutritional advise is very important, so all parties are on the same page.
In conclusion, hyperammonemia is a condition where excess ammonia in the blood is caused by the malfunctioning ability of the liver to filtrate toxic waste. Hyperammonemia is common among chronic alcohol abusers. Liver disease associated from alcohol abuse is generally unremarkable.2 This can be difficult for clinicians to diagnose, treat and manage since not all chronic abusers present to detoxification for help. Usually when manifestations of the liver disease are present it signifies that the patient’s body is starting to fail. The clinician is now up against the clock in providing appropriate care. Therefore, it is vital for all clinicians to get a through history to better understand the patient’s current status before it is too late. Finally, when dealing with chronic alcohol abuse whether in clinic or a detoxification facility the management of each person should be on an individualized approach with a multi-faceted protocol including pharmaceutical intervention, mental health, dietary and social support for optical outcomes.