Cases That Test Your Skills

When a patient with chronic alcohol use abruptly stops drinking

Current Psychiatry. 2023 April;22(4):42-46,48 | doi: 10.12788/cp.0349

References

1. Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br J Addict. 1989;84(11):1353-1357.

2. Trevisan LA, Boutros N, Petrakis IL, et al. Complications of alcohol withdrawal: pathophysiological insights. Alcohol Health Res World. 1998;22(1):61-66.

3. Holleck JL, Merchant N, Gunderson CG. Symptom-triggered therapy for alcohol withdrawal syndrome: a systematic review and meta-analysis of randomized controlled trials. J Gen Intern Med. 2019;34(6):1018-1024.

4. Clapp P, Bhave SV, Hoffman PL. How adaptation of the brain to alcohol leads to dependence: a pharmacological perspective. Alcohol Res Health. 2008;31(4):310-339.

5. Burnette EM, Nieto SJ, Grodin EN, et al. Novel agents for the pharmacological treatment of alcohol use disorder. Drugs. 2022;82(3):251-274.

6. Selim R, Zhou Y, Rupp LB, et al. Availability of PEth testing is associated with reduced eligibility for liver transplant among patients with alcohol-related liver disease. Clin Transplant. 2022;36(5):e14595.

7. Ulwelling W, Smith K. The PEth blood test in the security environment: what it is; why it is important; and interpretative guidelines. J Forensic Sci. 2018;63(6):1634-1640.

8. Botros M, Sikaris KA. The de ritis ratio: the test of time. Clin Biochem Rev. 2013;34(3):117-130.

9. Ballard HS. The hematological complications of alcoholism. Alcohol Health Res World. 1997;21(1):42-52.

10. Kaferle J, Strzoda CE. Evaluation of macrocytosis. Am Fam Physician. 2009;79(3):203-208.

11. Martin PR, Singleton CK, Hiller-Sturmhöfel S. The role of thiamine deficiency in alcoholic brain disease. Alcohol Res Health. 2003;27(2):134-142.

12. Palmer BF, Clegg DJ. Electrolyte disturbances in patients with chronic alcohol-use disorder. N Engl J Med. 2017;377(14):1368-1377.

13. Silczuk A, Habrat B. Alcohol-induced thrombocytopenia: current review. Alcohol. 2020;86:9-16. doi:10.1016/j.alcohol.2020.02.166

14. Pettinati HM, Rabinowitz AR. New pharmacotherapies for treating the neurobiology of alcohol and drug addiction. Psychiatry (Edgmont). 2006;3(5):14-16.

15. Anton RF, Latham P, Voronin K, et al. Efficacy of gabapentin for the treatment of alcohol use disorder in patients with alcohol withdrawal symptoms: a randomized clinical trial. JAMA Intern Med. 2020;180(5):728-736.

16. Chockalingam L, Burnham EL, Jolley SE. Medication prescribing for alcohol use disorders during alcohol-related encounters in a Colorado regional healthcare system. Alcoholism Clin Exp Res. 2022;46(6):1094-1102.

17. Mintz CM, Hartz SM, Fisher SL, et al. A cascade of care for alcohol use disorder: using 2015-2019 National Survey on Drug Use and Health data to identify gaps in past 12-month care. Alcohol Clin Exp Res. 2021;45(6):1276-1286.

18. Esser MB, Leung G, Sherk A, et al. Estimated deaths attributable to excessive alcohol use among US adults aged 20 to 64 years, 2015 to 2019. JAMA Netw Open. 2022;5(11):e2239485. doi:10.1001/jamanet workopen.2022.39485

19. The Community Guide. CPSTF Findings for Excessive Alcohol Consumption. Updated June 27, 2022. Accessed December 1, 2022. https://www.thecommunityguide.org/pages/task-force-findings-excessive-alcohol-consumption.html

20. The Community Guide. Alcohol Excessive Consumption: Privatization of Retail Alcohol Sales. Updated June 27, 2022. Accessed December 1, 2022. https://www.thecommunityguide.org/findings/alcohol-excessive-consumption-privatization-retail-alcohol-sales.html

21. The Community Guide. What is the CPSTF? Updated June 27, 2022. Accessed December 1, 2022. https://www.thecommunityguide.org/pages/what-is-the-cpstf.html

The author’s observations

Though regular clinical assessment of PEth varies, it is considered to have high sensitivity and specificity to detect alcohol use.⁶ When ethanol is present, the phospholipase D enzyme acts upon phosphatidylcholine, forming a direct biomarker, PEth, on the surface of the red blood cell.^6,7 PEth’s half-life ranges from 4.5 to 12 days,⁶ and it can be detected in blood for 3 to 4 weeks after alcohol ingestion.^6,7A PEth value <20 ng/mL indicates light or no alcohol consumption; 20 to 199 ng/mL indicates significant consumption; and >200 ng/mL indicates heavy consumption.⁷ Since Mr. G has a history of chronic alcohol use, his PEth level is expected to be >200 ng/mL.

AST/ALT and MCV are indirect biomarkers, meaning the tests are not alcohol-specific and the role of alcohol is instead observed by the damage to the body with excessive use over time.⁷ The expected AST:ALT ratio is 2:1. This is related to 3 mechanisms. The first is a decrease in ALT usually relative to B6 deficiency in individuals with alcohol use disorder (AUD). Another mechanism is related to alcohol’s propensity to affect mitochondria, which is a source for AST. Additionally, AST is also found in higher proportions in the kidneys, heart, and muscles.⁸

An MCV <100 fL would be within the normal range (80 to 100 fL) for red blood cells. While the reasons for an enlarged red blood cell (or macrocyte) are extensive, alcohol can be a factor once other causes are excluded. Additional laboratory tests and a peripheral blood smear test can help in this investigation.Alcohol disrupts the complete maturation of red blood cells.^9,10 If the cause of the macrocyte is alcohol-related and alcohol use is terminated, those enlarged cells can resolve in an average of 3 months.⁹

Vitamin B1 levels >200 nmol/L would be within normal range (74 to 222 nmol/L). Mr. G’s chronic alcohol use would likely cause him to be vitamin B1–deficient. The deficiency is usually related to diet, malabsorption, and the cells’ impaired ability to utilize vitamin B1. A consequence of vitamin B1 deficiency is Wernicke-Korsakoff syndrome.¹¹

Due to his chronic alcohol use, Mr. G’s magnesium stores most likely would be below normal range (1.7 to 2.2 mg/dL). Acting as a diuretic, alcohol depletes magnesium and other electrolytes. The intracellular shift that occurs to balance the deficit causes the body to use its normal stores of magnesium, which leads to further magnesium depletion. Other common causes include nutritional deficiency and decreased gastrointestinal absorption.¹² The bleeding the physician suspected was a result of drinking likely occurred through direct and indirect mechanisms that affect platelets.^9,13 Platelets can show improvement 1 week after drinking cessation. Some evidence suggests the risk of seizure or DTs increases significantly with a platelet count <119,000 µL per unit of blood.¹³

Continue to: TREATMENT Pharmacotherapy for alcohol use disorder