January 1992
CORRESPONDENCE
9. Rosenberg JL, Levin B, Wal1 AJ, Kirsner JB. A controlled trial of azathioprine in Crohn’s disease. Am J Dig Dis 1975;20:721-726.
Alcohol and Renal Phosphate
TobJe 1. Serum Inorganic
Phosphate and TmPOJGFR in Controls and Heavy Drinkers Before and After 7 Days ofAbstinente
Controls Serum PO, (mg/mL) TmPO,/GFR (mg/dL)
Active heavy drinkers
Drinkers after 7 days abstinente
3.42 + 0.13
3.02 ? 0.10’
3.15 f 0.07
3.01 + 0.15
2.54+ 0.16b
2.72+ 0.14
NOTE. Mean + SEM. ’ P < 0.02 vs control. b P < 0.05 vs. control. These results suggest that there is some relationship between the degree of renal phosphate losses in alcoholics and the amount of ethanol ingested. The reduced TmPO,/GFR seems reversible after 7 days of alcohol abstinente. A. GARCIA SANCHEZ Cótedra de Reumatologia Department of Medicine J. L. GONZALEZ-CALVIN Gastroenterology Division Department of Medicine M. MUfiOZ-TORRES Endocrinology Division Cátedra de Medicina Interns 1
D. SALVATIERRARIOS Cátedra de Reumatologia Department ofMedicine University Hospita1 of Granada Granada, Spain
Excretion
Dear Sir: We read with interest the paper by Angeli et a1.l who found that a reduced maximum capacity for renal phosphate reabsorption to glomerular filtration rate (TmPO,/GFR) was the major determinant of hypophosphatemia in alcoholics with and without liver disease. We would like to report the results of our study* on 32 male subjects with a drinking habit of more than 40 g ethanol/day for more than 10 years. Nineteen subjects were heavy drinkers (alcohol intake of more than 80 g ethanol/day) and 13 were moderate drinkers (alcohol intake between 40-80 g ethanol/day). None of the subjects had evidente of liver disease on the bases of biochemical and histological data. Patients with altered values of albumin, bilirubin, serum glutamic pyruvic transaminase, or prothombin activity were either excluded from the study or a liver biopsy was performed, and subjects with histological liver cirrhosis or alcoholic hepatitis were excluded. Nineteen healthy control subjects with stated ethanol intake of less than 80 g/week were also studied. Twelve heavy drinkers were studied on two occasions: they were studied once while they were active drinkers and on another occasion 7 days after they abstained from al1 alcohol. Heavy drinkers showed significantly lower serum inorganic phosphate levels than control subjects, and reduced TmPO,/GFRs were also found. A significant increase of both parameters was found after 7 days of abstinente (Table 1). Moderate drinkers had lower serum phosphate levels than controls and reduced TmPO,/GFRs, but these values were not significantly different.
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Angeli P, Gatta A, Caregaro L, Luisetto F, Menon F, Merkel C, Bolognesi M, Ru01 A. Hypophosphatemia and renal tubular disfunction in alcoholics. Gastroenterology 1991;100:502-512. 2. Garcia Sanchez A, Gonzalez-Calvin JL, Muñoz-Torres M, Raya Alvarez E, Ruiz de Almodovar M, Salvatierra Rios D. Bone mass and osteoblastic activity in alcoholic males. Paper for 3rd Congress of the European Society for Biomedical Research on alcoholism and XXI Annual Nordic Meeting on biological Alcohol Research. Oslo, Norway, June 26-29,1991. 1.
Reply. We would like to thank Dr. Sanchez et al. for their comments on our recent paper.’ The authors confirm our observation of a reduced renal tubular reabsorption of phosphate as a cause of hypophosphatemia in patients with heavy alcohol intake and without evidente of alcohol-related liver disease, thus supporting our hypothesis of an alcohol-related renal damage. Moreover, they raise two important remarks: (a) a relationship between renal phosphate losses and the amount of alcohol intake and (b) the reversibility of the alcohol-induced renal tubular dysfunction by short term abstinente from alcohol. Even though, in our opinion, the renal phosphate losses may represent the overt aspect of a wide spectrum of renal injury in alcoholics, we think the first remark is quite important because drinking pattern would probably result as the essential factor in the pathogenesis of renal tubular damage in alcoholics. Nevertheless, the contributory role of other factors such as sex, genetics, and nutrition cannot be underestimated. Studies on a larger population of drinkers would probably succeed in determining a threshold of renal alcohol toxicity considering, as possible, the other pathogenetic factors. As far as the second remark is concerned, since 1984 De Marchi et al. evidenced the reversibility of renal tubular dysfunction, including renal phosphate losses, by short-term abstinente in alcoholics.’ The study of Dr. Sanchez et al. confirms this observation. Moreover, in our preliminary experience, also the brush border damage of renal cells and not only the impairment of renal tubular function seems to be reversible by short-term abstinente from alcohol. PAOLO ANGELI,M.D. ANGEL0 GATTA, M.D. Department of Clinical Medicine University of Padua Padua, Italy 1. Angeli P, Gatta A, Caregaro L, Luisetto G, Menon F, Merkel C, Bolognesi M, Ru01 A. Hypophosphatemia and renal tubular dysfunction in alcoholics: are they related to liver function impairment? Gastroenterology 1991;100:502-512. 2. De Marchi S, Cecchin E, Grimaldi F, Basile A, Tesio F. Reversible tubular function in alcohol abuse. Proc Eur Dyalisis Transplant Assoc Eur Renal Assoc London: Pitman 1984;21:866-874.
Cytomegalovirus in AIDS
Infection of the Appendix
Dear Sir: We read with great interest in the July 1991 issue of GASTROENTEROLOGY the single case report by Valerdiz-Casasola and Pardo-Mindan on a case of cytomegalovirus (CMV) infection of the appendix in a patient with the acquired immunodeficiency syndrome (AIDS).’
380
CORRESPONDENCE
However, it appears that a couple of publications in which acute appendicitis was related to CMV infection were missed. In 1984, Blackman et al.* reported a case of ruptured appendix in a 31-year-old homosexual man. Microscopically, CMV inclusions were present in the inflamed appendix and the periappendiceal tissue. Although at the time of the report the patient was not considered to have AIDS, it appears that he probably would have qualified for it at present on the basis of the current recommendations from the CDC3 More recently, in 1999, Lin et al. published what appears to be the first fully documented case of CMV-associated case of acute appendicitis in an AIDS patient.’ The clinical, serological, and microscopic features of their case were comparable with those of the case of Valerdiz-Casasola and Pardo-Mindan. In conclusion, CMV-associated appendicitis in this setting may not be as infrequent as it first appears. Also, the frequent fibrotic and atrophic changes of the vermiform appendix with reduction of the lymphoid tissue that is seen with aging can account for the silent course of CMV infection in the appendix. Routine section of vermiform appendix at autopsy of AIDS patients could provide some pertinent information in this regard. GREGORY Y. LAUWERS, M.D. Department of Pathology Memorial Slaan Kettering Cancer Center 1275 York Avenue New York, New York 10021 Valerdiz-Casasola S, Pardo-Mindan FJ. Cytomegalovirus infection of the appendix in a patient with the acquired immunodeficiency syndrome. Gastroenterology 1991;101:247-249. Blackman E, Vimadalal S, Nash G. Significante of gastrointestina1 cytomegalovirus infection in homosexual males. Am J Gastroenterol 1984;79:935-940. Revision of the CDC surveillance definition for acquired immunodeficiency syndrome. MMWR 1987:36:3-9. Lin J, Bleiweiss IJ, Mendelson MH, Szabo S, Schwartz IS.
GASTROENTEROLOGY Vol. 102, No. 1
Cytomegalovirus-associated appendicitis in a patient with the acquired immunodeficiency syndrome. Am J Medicine 1990;89:377-379. Reply. We appreciate the comments of Dr. Lauwers regarding our articlel about CMV-associated appendicitis. We apologize for not citing two other cases of CMV-associated appendicitis previously reported by Blackman et al.’ and by Lin et a1.,3respectively. Our case is characteristic because CMV-associated appendicitis was the first clinical sign of AIDS. The case reported by Blackman et alZ is very similar to ours, but the diagnosis of AIDS was not confirmed. Lin’s case,3 was published after sending our paper to the editor; CMV-associated appendicitis appeared 1 month after a Pneumocystis carinii pneumonia was diagnosed by broncoscopy. We agree with Dr. Lauwers that CMV-associated appendicitis may be more frequent as it is diagnose& a routine study of appendix in al1 autopsies of patients with AIDS wil1 give the true importante of this entity. However, acute appendicitis, especially due to CMV, is rarely the first clinical sign of AIDS. S.VALERDIZ-CASASOLA F.J.PARDO-MINDAN Clínica Universitaria Facultad de Medicina Universidad de Nevarra 31080 Pamplona, Spain Valerdiz-Casasola S, Pardo-Mindfán FJ. Cytomegalovirus infection of the appendix in a patient with the acquired immunodeficiency syndrome. Gastroenterol 1991;101:247-249. Blackman E, Vimadalal S, Nash G. Significante of gastrointestina1 cytomegalovirus infection in homosexual males. Am J Gastroenterol 1984;79:935-940. Lin J, Bleiweiss IJ, Mendelson MH, Szabo S, Schwartz IS. Cytomegalovirus-associated appendicitis in a patient with the acquired immunodeficiency syndrome. Am J Medicine 1990:89:377-379.