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GANGRENOUS STOMATITIS IN AIDS
108 PENTAMIDINE SALTS
SIR,-Aerosol-administered pentamidine has proved to be prophylaxis for Pnmmcystis having appreciable systemic toxicity. 1-4 We have been treating seven AID S patients with a first episode of PCP with pentamidine mesylate (’Lomidine’, Specia) given via an
effective and safe as therapy and carirai pneumonia (PCP) without
ultrasonic nebuliser (’Ultraneb 99’, De Vilbiss) at doses of 4 mg/kg for 30-45 min, diluted in physiological saline at 10 mg/ml. The patients have been using the aerosol every 15 days for between 1 and 16 months. The only side-effects have been a dry cough, modest wheeziness, and evidence of bronchospasm, but never to such an extent as to make an interruption of the prophylaxis necessary. The patients have also been treated with zidovudine. Despite the fact that other opportunistic infections have been found among this group there have been no cases of PCP relapse. But this is not the purpose of our letter. A few months ago we inquired about the possibility of buying pentamidine isethionate (’Pentam 300’, LyphoMed), since all our bibliographic references except ones refer to this salt. The cost of importing into Italy a pack containing ten 300 mg vials of pentamidine isethionate was more than$1300 (or about 63 000 lire for 100 mg). Pentamidine mesylate costs us 2000 lire for 100 mg. Worldwide consumption of pentamidine is probably increasing by thousands of vials a day. Why, then, the price difference between the two salts? Should not the area of application of pentamidine mesylate be extended to include prophylaxis for PCP, in view of the fact that it has been suggested6 that the two salts are very similar in efficacy? Controlled comparative studies of the two preparations might yield substantial savings. Department of Infectious and Tropical Diseases, University of Modena, 41100 Modena, Italy
NICOLA MONGIARDO BRUNO DE RIENZO FRANCO SQUADRINI
Montgomery AB, Debs RJ, Luce JM, et al. Aerosolised pentamidine as sole therapy for Pneumocystis carinii pneumonia in patients with acquired immunodeficiency syndrome. Lancet 1987; ii: 480-83. 2. Leoung GS, Montgomery AB, Abrams DA, et al. Aerosol pentamidine for Pneumocystis carinii (PCP) pneumonia: a randomized trial of 439 patients. Programme and abstracts of IV International Conference on AIDS (Stockholm, 1988): 7166. 3. Girard PM, Leprêtre A, Michon C, Camus F, Farinotti R, Coulaud JP. Aerosolized pentamidine (PM) for prophylaxis of pneumocystosis (PCP) in AIDS patients. Programme and abstracts of IV International Conference on AIDS (Stockholm, 1988): 7172. 4. Golden JA, Chemoff D, Hollander H, Feigal D, Conte JE. Prevention of Pneumocystis carinii pneumonia by inhaled pentamidine. Lancet 1989; i: 654-57. 5. Girard PM, Couderc LJ, Farinotti R, et al. Ultrasonic nebulised pentamidine for pneumocystis pneumonia. Lancet 1988; i: 1165. 6. Camus F, de Picciotto C, Leprêtre A, Landman R, Girard PM, Saimot AG. Effets des aerosols prophylactiques de pentamidine sur la fonction respiratoire a moyen terme. Abstracts of V International Conference on AIDS (Montreal, 1989): TB02. 1.
GANGRENOUS STOMATITIS IN AIDS
SIR,-Dr Akula and colleagues (April 29, p 955) report severe intraoral lesions of hard and soft tissues in a 30-year-old HIV positive man. They diagnose these lesions as gangrenous stomatitis and recommend aggressive surgery. The symptomatology, laboratory findings, and clinical description of these lesions were consistent with observations we have made in HIV positive men in San Francisco since 1983.1,2 We have now treated more than 25 cases of HIV-associated periodontitis complicated by what we call necrotising stomatitis.1-6 Initially, we used aggressive treatment similar to that described by Akula et al. However, these methods left severe cosmetic and functional deformities and a worsening of the patient’s nutritional state because of compromised mastication from large-scale removal of teeth and periodontal tissues. To establish a rational treatment for these lesions, we evaluated conservative localised debridement and minimal systemic treatment. These necrotising lesions are of periodontal origin. In most cases we have found that the lesions respond quickly and completely to conservative therapy, which includes professional tooth cleaning and appropriate oral hygiene by the patient.3,4The key to effective treatment is complete removal of the putative aetiological agents (supragingival and subgingival plaque and calculus) from the teeth by scaling, root planing, and curettage. Of
equal importance is the maintenance of bacterial plaque at low levels during healing by plaque-control measures. Extensive removal of necrotic bone down to clinically healthy bone does not seem to be required, since the exposed and necrotic bone sequesters in a benign manner when our treatment is used. Sometimes the area of bone that separates is large (1 -5 cm), but the process is surprisingly well tolerated by the patient and rarely requires extraction of teethe In addition, we have found that several adjuncts are of value during treatment and maintenance. For example, subgingival lavage with 10% povidone iodine during the cleaning helps to control bleeding, provides some pain control, and acts as a topical antimicrobial. Furthermore, oral metronidazole 1000 mg daily for four days and twice daily rinses with chlorhexidine mouth rinses minimise the levels of plaque and maintain low levels of intraoral microorganisms during healing. Since intraoral candidiasis is often associated with these necrotising lesions, antifungal treatment may be required, especially when antibiotics are used. However, the importance of the mechanical treatment cannot be overstated. Consequently, after the initial visit and until acceptable healing is achieved, the patient should be seen every few days for evaluation of the effectiveness of mechanical cleaning and for reinforcement of oral hygiene measures. After complete epithelialisation, routine three-month recall is recommended for additional professional cleaning and evaluation of oral hygiene. We agree with Akula and colleagues’ impression that these lesions are due to anaerobic infections and are excellent examples of opportunistic infections taking advantage of the immunocompromised host.3,6 In fact, the acute onset of these lesions is associated with a drop in CD4 cell number below 100/)il.’* Our conservative treatment reduces long-term complications associated with overtreatment, enhances the patient’s quality of life, and does not require admission to hospital. We are concerned that Akula et al did not recommend cover by antifungal drugs, even though Candida albicans was present.
Department of Stomatology (Oral AIDS Center and Division of Peridontology), University of California, San Francisco, California 94143-0650, USA
JAMES R. WINKLER PATRICIA A. MURRAY CHRISTOPH HAMMERLE
1. Winkler JR, Grassi M, Murray PA. Clinical description and etiology of HIVassociated periodontal diseases. In: Perspectives on oral manifestions of AIDS: diagnosis and management of HIV-associated infections. PSG Publishing, 1988. 2. Williams CA, Winkler JR, Grassi M, Murray PA. Necrotizing stomatitis associated with AIDS. IV International Conference on AIDS (Stockholm, 1988). 3. Murray PA, Winkler JR, Sadowski L, et al. The microbiology of HIV-associated gingivitis and periodontal disease. In: Perspectives on oral manifestations of AIDS: diagnosis and management of HIV-associated infections. PSG Publishing, 1988. 4. Grassi M, Williams CA, Winkler JR, Murray PA. Local treatments of HIV-associated periodontal disease. J Dent Res 1988; 66 (suppl): 117A. 5. Winkler JR, Murray PA, Grassi M, Engleman JE, Kornman KS, Holt SC. The microbiology of HIV-associated periodontal lesions. IV International Conference on AIDS (Stockholm, 1988). 6. Winkler JR, Murray PA, Greenspan D, Greenspan JS. Periodontal disease of male homosexuals as related to AIDS virus infection. 2 International Conference on
Acquired Immunodeficiency Syndrome (Pans, 1986).
REACTIVATION OF HEPATITIS B IN AIDS
SIR,-Dr Maeland and Professor Mosley and their colleagues , (May 13, p 1083) discuss our report on reactivation of hepatitis B in three patients with AIDS. They suggest reinfection by a virus of a different HBsAg subtype as being responsible for the clinical and serological findings. This is not the case. We have now subtyped with monoclonal antibodies HBsAg and anti-HBs of our patient 2. HBsAg and anti-HBs, both before and after reactivation, were of the same subtype (ad). Although stored serum is not available for our patients 1 and 3, it is unlikely that they had acquired new HBV infections, since anti-HBs disappeared from serum four months and one month, respectively, before reappearance of HBsAg. Furthermore in our patients we observed overt clinical hepatitis (with alanine aminotransferase [ALT] peaks between 898 and 2490 U/1), which is characteristic of reactivation,’ whereas new infections with different HBV subtypes are not usually associated with a clinical illness.3 Indeed our patients are the only cases of clinical hepatitis in HIV-infected subjects reported, since
SIR,-Aerosol-administered pentamidine has proved to be prophylaxis for Pnmmcystis having appreciable systemic toxicity. 1-4 We have been treating seven AID S patients with a first episode of PCP with pentamidine mesylate (’Lomidine’, Specia) given via an
effective and safe as therapy and carirai pneumonia (PCP) without
ultrasonic nebuliser (’Ultraneb 99’, De Vilbiss) at doses of 4 mg/kg for 30-45 min, diluted in physiological saline at 10 mg/ml. The patients have been using the aerosol every 15 days for between 1 and 16 months. The only side-effects have been a dry cough, modest wheeziness, and evidence of bronchospasm, but never to such an extent as to make an interruption of the prophylaxis necessary. The patients have also been treated with zidovudine. Despite the fact that other opportunistic infections have been found among this group there have been no cases of PCP relapse. But this is not the purpose of our letter. A few months ago we inquired about the possibility of buying pentamidine isethionate (’Pentam 300’, LyphoMed), since all our bibliographic references except ones refer to this salt. The cost of importing into Italy a pack containing ten 300 mg vials of pentamidine isethionate was more than$1300 (or about 63 000 lire for 100 mg). Pentamidine mesylate costs us 2000 lire for 100 mg. Worldwide consumption of pentamidine is probably increasing by thousands of vials a day. Why, then, the price difference between the two salts? Should not the area of application of pentamidine mesylate be extended to include prophylaxis for PCP, in view of the fact that it has been suggested6 that the two salts are very similar in efficacy? Controlled comparative studies of the two preparations might yield substantial savings. Department of Infectious and Tropical Diseases, University of Modena, 41100 Modena, Italy
NICOLA MONGIARDO BRUNO DE RIENZO FRANCO SQUADRINI
Montgomery AB, Debs RJ, Luce JM, et al. Aerosolised pentamidine as sole therapy for Pneumocystis carinii pneumonia in patients with acquired immunodeficiency syndrome. Lancet 1987; ii: 480-83. 2. Leoung GS, Montgomery AB, Abrams DA, et al. Aerosol pentamidine for Pneumocystis carinii (PCP) pneumonia: a randomized trial of 439 patients. Programme and abstracts of IV International Conference on AIDS (Stockholm, 1988): 7166. 3. Girard PM, Leprêtre A, Michon C, Camus F, Farinotti R, Coulaud JP. Aerosolized pentamidine (PM) for prophylaxis of pneumocystosis (PCP) in AIDS patients. Programme and abstracts of IV International Conference on AIDS (Stockholm, 1988): 7172. 4. Golden JA, Chemoff D, Hollander H, Feigal D, Conte JE. Prevention of Pneumocystis carinii pneumonia by inhaled pentamidine. Lancet 1989; i: 654-57. 5. Girard PM, Couderc LJ, Farinotti R, et al. Ultrasonic nebulised pentamidine for pneumocystis pneumonia. Lancet 1988; i: 1165. 6. Camus F, de Picciotto C, Leprêtre A, Landman R, Girard PM, Saimot AG. Effets des aerosols prophylactiques de pentamidine sur la fonction respiratoire a moyen terme. Abstracts of V International Conference on AIDS (Montreal, 1989): TB02. 1.
GANGRENOUS STOMATITIS IN AIDS
SIR,-Dr Akula and colleagues (April 29, p 955) report severe intraoral lesions of hard and soft tissues in a 30-year-old HIV positive man. They diagnose these lesions as gangrenous stomatitis and recommend aggressive surgery. The symptomatology, laboratory findings, and clinical description of these lesions were consistent with observations we have made in HIV positive men in San Francisco since 1983.1,2 We have now treated more than 25 cases of HIV-associated periodontitis complicated by what we call necrotising stomatitis.1-6 Initially, we used aggressive treatment similar to that described by Akula et al. However, these methods left severe cosmetic and functional deformities and a worsening of the patient’s nutritional state because of compromised mastication from large-scale removal of teeth and periodontal tissues. To establish a rational treatment for these lesions, we evaluated conservative localised debridement and minimal systemic treatment. These necrotising lesions are of periodontal origin. In most cases we have found that the lesions respond quickly and completely to conservative therapy, which includes professional tooth cleaning and appropriate oral hygiene by the patient.3,4The key to effective treatment is complete removal of the putative aetiological agents (supragingival and subgingival plaque and calculus) from the teeth by scaling, root planing, and curettage. Of
equal importance is the maintenance of bacterial plaque at low levels during healing by plaque-control measures. Extensive removal of necrotic bone down to clinically healthy bone does not seem to be required, since the exposed and necrotic bone sequesters in a benign manner when our treatment is used. Sometimes the area of bone that separates is large (1 -5 cm), but the process is surprisingly well tolerated by the patient and rarely requires extraction of teethe In addition, we have found that several adjuncts are of value during treatment and maintenance. For example, subgingival lavage with 10% povidone iodine during the cleaning helps to control bleeding, provides some pain control, and acts as a topical antimicrobial. Furthermore, oral metronidazole 1000 mg daily for four days and twice daily rinses with chlorhexidine mouth rinses minimise the levels of plaque and maintain low levels of intraoral microorganisms during healing. Since intraoral candidiasis is often associated with these necrotising lesions, antifungal treatment may be required, especially when antibiotics are used. However, the importance of the mechanical treatment cannot be overstated. Consequently, after the initial visit and until acceptable healing is achieved, the patient should be seen every few days for evaluation of the effectiveness of mechanical cleaning and for reinforcement of oral hygiene measures. After complete epithelialisation, routine three-month recall is recommended for additional professional cleaning and evaluation of oral hygiene. We agree with Akula and colleagues’ impression that these lesions are due to anaerobic infections and are excellent examples of opportunistic infections taking advantage of the immunocompromised host.3,6 In fact, the acute onset of these lesions is associated with a drop in CD4 cell number below 100/)il.’* Our conservative treatment reduces long-term complications associated with overtreatment, enhances the patient’s quality of life, and does not require admission to hospital. We are concerned that Akula et al did not recommend cover by antifungal drugs, even though Candida albicans was present.
Department of Stomatology (Oral AIDS Center and Division of Peridontology), University of California, San Francisco, California 94143-0650, USA
JAMES R. WINKLER PATRICIA A. MURRAY CHRISTOPH HAMMERLE
1. Winkler JR, Grassi M, Murray PA. Clinical description and etiology of HIVassociated periodontal diseases. In: Perspectives on oral manifestions of AIDS: diagnosis and management of HIV-associated infections. PSG Publishing, 1988. 2. Williams CA, Winkler JR, Grassi M, Murray PA. Necrotizing stomatitis associated with AIDS. IV International Conference on AIDS (Stockholm, 1988). 3. Murray PA, Winkler JR, Sadowski L, et al. The microbiology of HIV-associated gingivitis and periodontal disease. In: Perspectives on oral manifestations of AIDS: diagnosis and management of HIV-associated infections. PSG Publishing, 1988. 4. Grassi M, Williams CA, Winkler JR, Murray PA. Local treatments of HIV-associated periodontal disease. J Dent Res 1988; 66 (suppl): 117A. 5. Winkler JR, Murray PA, Grassi M, Engleman JE, Kornman KS, Holt SC. The microbiology of HIV-associated periodontal lesions. IV International Conference on AIDS (Stockholm, 1988). 6. Winkler JR, Murray PA, Greenspan D, Greenspan JS. Periodontal disease of male homosexuals as related to AIDS virus infection. 2 International Conference on
Acquired Immunodeficiency Syndrome (Pans, 1986).
REACTIVATION OF HEPATITIS B IN AIDS
SIR,-Dr Maeland and Professor Mosley and their colleagues , (May 13, p 1083) discuss our report on reactivation of hepatitis B in three patients with AIDS. They suggest reinfection by a virus of a different HBsAg subtype as being responsible for the clinical and serological findings. This is not the case. We have now subtyped with monoclonal antibodies HBsAg and anti-HBs of our patient 2. HBsAg and anti-HBs, both before and after reactivation, were of the same subtype (ad). Although stored serum is not available for our patients 1 and 3, it is unlikely that they had acquired new HBV infections, since anti-HBs disappeared from serum four months and one month, respectively, before reappearance of HBsAg. Furthermore in our patients we observed overt clinical hepatitis (with alanine aminotransferase [ALT] peaks between 898 and 2490 U/1), which is characteristic of reactivation,’ whereas new infections with different HBV subtypes are not usually associated with a clinical illness.3 Indeed our patients are the only cases of clinical hepatitis in HIV-infected subjects reported, since