Correspondence
Clinical Problem-Solving: We Blew It
N Engl J Med 1995; 333:520-521August 24, 1995
- Article
To the Editor:
Dr. Kreisberg (April 6 issue)1 makes the ex-cellent clinical point that deciphering liver conditions is difficult in patients with AIDS. I am a little skeptical about viewing trimethoprim–sulfamethoxazole as the sole problem in the case presented. According to the case history, the patient consumed alcohol regularly, albeit in amounts that were apparently modest. The ratio of aspartate aminotransferase to alanine aminotransferase was more than 3:1, a finding that is common in patients with alcoholic hepatitis rather than drug-induced hepatitis. Admittedly, the levels are higher than those that alcoholic hepatitis typically causes. Therefore, I would hypothesize that there was a synergy between alcohol and the drug.
1 ReferencesA. Sidney Barritt, III, M.D.
Veterans Affairs Medical Center, Salem, VA 241531
Kreisberg R . We blew it. N Engl J Med 1995;332:945-949
Full Text | Web of Science | Medline
To the Editor:
We were struck by the lack of attention to the 34-year-old patient's alcohol intake. Alcohol is used by more Americans than any other drug; twice as many people use alcohol as tobacco.1 One of the largest surveys on substance use found that the lifetime prevalence of alcohol-related disorders was 13.5 percent; the lifetime prevalence for men was 23.8 percent, and the prevalence was highest among persons between the ages of 18 and 45 years.2
People who abuse alcohol may rationalize their drinking and minimize the quantity when reporting their intake. Many grossly inebriated patients insist that they have had only “a couple of drinks.” The article states that this patient “consumed two to three alcoholic drinks daily.” Were these drinks half glasses of wine or full tumblers of vodka? The patient had a disease (human immunodeficiency virus infection) known to be worsened by alcohol,3 had had hepatitis B, and had taken hepatotoxic drugs (zidovudine and didanosine), yet he continued to drink. Histologic evidence of fatty changes and cholestasis, as reported in this case, can be seen in alcoholic liver disease.4 We would be interested in the author's comments about the role of alcohol in the pathogenesis of this patient's liver disease.
4 ReferencesBonnie D. Gifford, M.D.
Riverside Methodist Hospitals, Columbus, OH 43214Anne Garrett, M.D.
Lawrence Hofmann, B.S.
Ohio State University College of Medicine, Columbus, OH 432101
Lowinson JH, Ruiz P, Millman RB, Langrod JG, eds. Substance abuse: a comprehensive textbook. 2nd ed. Baltimore: Williams & Wilkins, 1992.
2
Robins LN, Regier DA. Psychiatric disorders in America: the epidemiologic catchment area study. New York: Free Press, 1991.
3
Fong IW ,Read S ,Wainberg MA ,Chia WK ,Major C . Alcoholism and rapid progression to AIDS after seroconversion. Clin Infect Dis 1994;19:337-338
CrossRef | Web of Science | Medline4
Trinchet JC ,Gerhardt MF ,Balkau B ,Munz C ,Poupon RE . Serum bile acids and cholestasis in alcoholic hepatitis: relationship with usual liver tests and histological features. J Hepatol 1994;21:235-240
CrossRef | Web of Science | Medline
To the Editor:
Dr. Kreisberg points out the potential dangers of herbal preparations, although they were irrelevant to the patient's condition. Poison-control data reveal a remarkably low incidence of adverse events associated with herbal medication among the 3 percent of the U.S. population that uses them, whereas the toxicity of conventional drugs makes a large contribution to morbidity, mortality, and the total cost of health care. Although the toxicity of herb constituents such as the pyrolizidine alkaloids, aristolochic acid, and phorbol esters needs to be recognized and guarded against, the relative safety of plant medicines is hard to dispute. . . .
We also “blow it” when we use the red herring of herbal medication to divert attention from the deficits of conventional medicine. It was complacent confidence in conventional treatment that resulted in the missed diagnosis in the first place.
Carlo Calabrese, N.D., M.P.H.
Margaret Frederick, M.A., M.P.H.
Bastyr University, Seattle, WA 98105-3753Author/Editor Response
Dr. Kreisberg replies:
To the Editor: The suggestion that we may have underestimated the role of alcohol is well taken. The “lack of attention” to alcohol in the clinical case was a reflection of my interpretation of the information in the medical record, which indicated that the patient had ceased alcohol consumption nine months before signs of his liver illness appeared. I cannot prove that alcohol did not contribute to the liver disease; however, I think it is unlikely that the patient would have trivialized his use of alcohol since he seemed open about other personal issues. Nonetheless, the point that Gifford et al. make about being more precise in quantifying alcohol intake is appropriate.
Dr. Barritt raises the issue of the characteristic ratio of aspartate aminotransferase to alanine aminotransferase (>2) in patients with alcoholic hepatitis. The relatively low levels of both aspartate aminotransferase and alanine aminotransferase in alcoholic hepatitis are attributed to low levels of pyridoxal 5-phosphate, which is necessary for the activation of both enzymes and is depleted in alc0holics.1 Although a pyridoxine deficiency might account for the relatively low levels of the two enzymes in this patient, it does not explain the selective increase of aspartate aminotransferase over alanine aminotransferase. However, alcohol-induced mitochondrial damage would result in a preferential increase in aspartate aminotransferase (Zimmerman H: personal communication). Certainly, in this patient, there was no impairment in the generation of higher levels of both enzymes, supporting the suggestion that his liver disease reflected a synergy between a drug and alcohol. A similar observation has been made with acetaminophen-induced liver damage (Zimmerman H: personal communication).
1 ReferencesRobert Kreisberg, M.D.
Baptist Health System, Birmingham, AL 35213
