- Email: [email protected]
Reply from Dr Campbell
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LETTERS TO THE EDITOR
significant part of the clinical profile of tuberculosis. Likewise, such patients constituted a sizeable proportion of patients diagnosed by bronchial sampling in the series of both Ip et al. [l] and Sarker et al. [3] and are mainly responsible for the higher yield in these studies. In contrast, tuberculosis would be an unlikely diagnosis of similar clinical features in countries with a low prevalence rate. This difference in clinical perspective is responsible for the difference in yields when studies from high [ 1,3], and low prevalence areas [4] are compared. In the light of the above, and in consideration of manpower and material constraints in developing countries where the prevalence rates are highest, can routine sampling by FOB of, say, 100 patients to identify 3-5 tuberculosis patients be justified? It would be more cost effective if, instead of sampling all patients, clinical situations as described above are identified and bronchoscopic sampling be used selectively, even in countries with high prevalence rates. This is especially so when many of these patients may be diagnosed by sputum culture. Clinical Research Centre V. Pate1 Chest Institute University of Delhi Delhi-110 007. India
Kaushal Pant Rajesh Bhagat
References Ip M, Chau PY, So SY, Lam WK. The value of routine bronchial aspirate culture at fibreoptic bronchoscopy for the diagnosis of tuberculosis. Tube&e 1989; 70: 281-285. Chawla R, Pant K, Jaggi OP, Chandrashekhar S, Thukral SS. Fibreoptic bronchoscopy in smear-negative pulmonary tuberculosis. Eur Respir J 1988; 1: 804-806. Sarkar SK, Sharma TN, Purohit SD, Gupta PR. The diagnostic value of routine culture of bronchial washings in tuberculosis. Br J Dis Chest 1982; 76: 358-360. Russell MD, Torrington KG, Tenholder MF. A ten year experience with fibreoptic bronchoscopy for mycobacterial isolation-impact of the Bactec system. Am Rev Respir Dis 1986; 133: 1069-1071.
Management of jaundice occurring during antituberculosis chemotherapy
In ‘Any Questions’ (Tubercle 1990; 71: 149) Dr Ian Campbell was asked: ‘How should a patient be managed who is being treated for sputum positive pulmonary tuberculosis with rifampicin,
isoniazid and pyrazinamide and becomes jaundiced in the third week of chemotherapy?’ One course of action involves stopping all three drugs, then trying to ‘establish which of the three drugs is the cause of the problem’. This advice follows Dr. Campbell’s remark that ‘. , . it would be important to identify whether rifampicin or isoniazid or the combination of rifampicin and isoniazid were the cause of the problem before proceeding with modified chemotherapy for an appropriate duration’. (Dr Campbell assumes a fully sensitive organism.) Unlike Dr Campbell I am not a tuberculosis expert, but I respectfully question his assertions. He suggests that the patient first be challenged with rifampicin, the most likely culprit. But would not the patient be better served by not provoking jaundice, i.e., by beginning with a drug or combination that is least likely rather than most likely to cause jaundice, although this approach might be scientifically less satisfying? 17 Main Street Sayville, NY 11782, USA
Robert Carlen
Reply from Dr Campbell
I thank Dr Carlen for his interest and his comment. Once placed in the position of having to stop all three drugs, my aim in managing the smear-positive patient would be to re-establish effective chemotherapy as soon as possible and, ideally, I would like this to be with rifampicin and isoniazid so that the duration of chemotherapy would be short. Although likely, it is not inevitable that jaundice will recur on reintroduction of rifampicin and/or isoniazid. Against this background, challenging first with the most likely culprit, rifampicin, is logical. If pyrazinamide is to blame or if the situation is one where the jaundice is simply not going to recur when rifampicin and isoniazid are reintroduced, it will not matter whether one challenges first with rifampicin or with isoniazid. If rifampicin is to blame and the situation is one where the reaction is going to recur on its reintroduction, then challenging first with isoniazid will not avoid the reaction: it will simply delay both the jaundice and the resumption of effective chemotherapy (which in this instance would be with isoniazid and ethambutol for 18 months). If, however, the physician has strong feelings
73
LETTERS TO THE EDITOR
about reducing the probability of jaundice recurring and is not particularly concerned about short course as opposed to 18 months of therapy, then there is clearly merit in starting the challenge with isoniazid. If that challenge is negative, ethambutol can immediately be added to the isoniazid and the regimen continued for 18 months. I would find it scientifically more satisfying to challenge first with isoniazid, then with pyrazinamide, then with rifampicin but, taking into account the factors discussed above, I personally would choose to challenge first with rifampicin in the knowledge that the probability of harming the patient is low and is outweighed by the potential benefit of the scheme of management. Sully Hospital Sully, Penarth South Glamorgan,
Ian Campbell CF6 2YA,
References I. Pateron D, Naveau S, Brivet F, Bedossa P, Poynard T,
Chaput JC. Acute tuberculosis pancreatitis in a patient with acquired immunodeficiency syndrome. Gasferoenter01 Clin Biol 1990; 14: S&83. 2. Ezratty A, Gumaste V. Rose E, Sachar DB. TiscorniaWasserman P. Pancreatic tuberculosis: a frequently fatal but potentially curable disease. J C/in Gastroenterol 1990; 12: 74-77.
3. Cho KC, Lucak SL. Delany HM, Morehouse HT, Jennings TA. CT appearance in tuberculous pancreatic abscess. J Comput Assist Tomogr 1990; 14: 152-154. 4. Berson BD, Mend&on DS, Janus CL. Tuberculous abscess of the pancreas in AIDS: CT findings. MI Sinai M Med 1989; 56: 297-299. 5. Tetzeli JP, Pisegna JR, Barkin JS. Tuberculous pancreatic abscess as a manifestation of AIDS. Am J Gastroenterol 1989; 84: 581-582. 6. Meinke AK. Pancreatic tuberculous abscess. Corm Med 1989; 53: 139-141.
UK
Tuberculous pancreatitis and AIDS I would like to comment on the case report by Knowles et al (Tubercle 1990; 71: 65-68) of tuberculous pancreatitis occurring in the course of miliary and meningeal tuberculosis in a 26-yearold Haitian woman who had been in Canada for 2.5 years. No mention was made of her HIV status. She had generalised lymphadenopathy and a depressed CD4/CDS T-cell ratio, either of which could have been due to tuberculosis alone. My experience in Zimbabwe, and published reports, indicate that miliary disease and the presence of intrathoracic lymphadenopathy in adults with tuberculosis are both very suggestive of the co-existence of HIV infection. The patient had oesophageal candidiasis which is also highly suggestive of HIV infection. Although, as the authors point out, tuberculous pancreatitis was a rare complication in the past, I have recently seen six case reports of this condition in patients with HIV infection [l-6]. I therefore think it highly probable that this woman had AIDS. Department of Medicine Stan Houston University of Alberta 2E4.11 WC Mackenzie Health Sciences Centre Edmonton, Alberta, Canada
Bad news from North Lebanon Tuberculosis has not been a common disease in recent times in the north of Lebanon, but there have been fears of an epidemic in view of the long period of civil war and disruption of health services within the region [l]. No survey of the disease has been reported, but skin test surveys of children living in the districts of Akkar and Zgharta were carried out between 1980 and 1984 [2, 31. The evidence then suggested that there were no more than isolated cases of the disease. The situation has now changed dramatically. A survey in progress (September to October 1990) shows that the number of cases has increased tenfold since the early 1980s. A clinic in Tripoli seeing 25-35 cases annually at the beginning of the decade, saw 325 cases in 1989, and the same pattern is recorded throughout the region. About 80% of diagnosed cases are in adults and 20% in children. Drugs are in short supply and the majority of patients remain untreated. A skin test survey has just been completed in some of the villages in Akkar that were surveyed previously. In 1980-1984, 3.8% of children aged 7-11 were tuberculin positive, compared with 11% now: 8.1% of older children were positive in 198&1984 and 20% are positive now. There was no evidence of an increase in tuberculin positivity over the years of the earlier study, so the change has occurred since 1984. Plans are being made to vaccinate the 300-
LETTERS TO THE EDITOR
significant part of the clinical profile of tuberculosis. Likewise, such patients constituted a sizeable proportion of patients diagnosed by bronchial sampling in the series of both Ip et al. [l] and Sarker et al. [3] and are mainly responsible for the higher yield in these studies. In contrast, tuberculosis would be an unlikely diagnosis of similar clinical features in countries with a low prevalence rate. This difference in clinical perspective is responsible for the difference in yields when studies from high [ 1,3], and low prevalence areas [4] are compared. In the light of the above, and in consideration of manpower and material constraints in developing countries where the prevalence rates are highest, can routine sampling by FOB of, say, 100 patients to identify 3-5 tuberculosis patients be justified? It would be more cost effective if, instead of sampling all patients, clinical situations as described above are identified and bronchoscopic sampling be used selectively, even in countries with high prevalence rates. This is especially so when many of these patients may be diagnosed by sputum culture. Clinical Research Centre V. Pate1 Chest Institute University of Delhi Delhi-110 007. India
Kaushal Pant Rajesh Bhagat
References Ip M, Chau PY, So SY, Lam WK. The value of routine bronchial aspirate culture at fibreoptic bronchoscopy for the diagnosis of tuberculosis. Tube&e 1989; 70: 281-285. Chawla R, Pant K, Jaggi OP, Chandrashekhar S, Thukral SS. Fibreoptic bronchoscopy in smear-negative pulmonary tuberculosis. Eur Respir J 1988; 1: 804-806. Sarkar SK, Sharma TN, Purohit SD, Gupta PR. The diagnostic value of routine culture of bronchial washings in tuberculosis. Br J Dis Chest 1982; 76: 358-360. Russell MD, Torrington KG, Tenholder MF. A ten year experience with fibreoptic bronchoscopy for mycobacterial isolation-impact of the Bactec system. Am Rev Respir Dis 1986; 133: 1069-1071.
Management of jaundice occurring during antituberculosis chemotherapy
In ‘Any Questions’ (Tubercle 1990; 71: 149) Dr Ian Campbell was asked: ‘How should a patient be managed who is being treated for sputum positive pulmonary tuberculosis with rifampicin,
isoniazid and pyrazinamide and becomes jaundiced in the third week of chemotherapy?’ One course of action involves stopping all three drugs, then trying to ‘establish which of the three drugs is the cause of the problem’. This advice follows Dr. Campbell’s remark that ‘. , . it would be important to identify whether rifampicin or isoniazid or the combination of rifampicin and isoniazid were the cause of the problem before proceeding with modified chemotherapy for an appropriate duration’. (Dr Campbell assumes a fully sensitive organism.) Unlike Dr Campbell I am not a tuberculosis expert, but I respectfully question his assertions. He suggests that the patient first be challenged with rifampicin, the most likely culprit. But would not the patient be better served by not provoking jaundice, i.e., by beginning with a drug or combination that is least likely rather than most likely to cause jaundice, although this approach might be scientifically less satisfying? 17 Main Street Sayville, NY 11782, USA
Robert Carlen
Reply from Dr Campbell
I thank Dr Carlen for his interest and his comment. Once placed in the position of having to stop all three drugs, my aim in managing the smear-positive patient would be to re-establish effective chemotherapy as soon as possible and, ideally, I would like this to be with rifampicin and isoniazid so that the duration of chemotherapy would be short. Although likely, it is not inevitable that jaundice will recur on reintroduction of rifampicin and/or isoniazid. Against this background, challenging first with the most likely culprit, rifampicin, is logical. If pyrazinamide is to blame or if the situation is one where the jaundice is simply not going to recur when rifampicin and isoniazid are reintroduced, it will not matter whether one challenges first with rifampicin or with isoniazid. If rifampicin is to blame and the situation is one where the reaction is going to recur on its reintroduction, then challenging first with isoniazid will not avoid the reaction: it will simply delay both the jaundice and the resumption of effective chemotherapy (which in this instance would be with isoniazid and ethambutol for 18 months). If, however, the physician has strong feelings
73
LETTERS TO THE EDITOR
about reducing the probability of jaundice recurring and is not particularly concerned about short course as opposed to 18 months of therapy, then there is clearly merit in starting the challenge with isoniazid. If that challenge is negative, ethambutol can immediately be added to the isoniazid and the regimen continued for 18 months. I would find it scientifically more satisfying to challenge first with isoniazid, then with pyrazinamide, then with rifampicin but, taking into account the factors discussed above, I personally would choose to challenge first with rifampicin in the knowledge that the probability of harming the patient is low and is outweighed by the potential benefit of the scheme of management. Sully Hospital Sully, Penarth South Glamorgan,
Ian Campbell CF6 2YA,
References I. Pateron D, Naveau S, Brivet F, Bedossa P, Poynard T,
Chaput JC. Acute tuberculosis pancreatitis in a patient with acquired immunodeficiency syndrome. Gasferoenter01 Clin Biol 1990; 14: S&83. 2. Ezratty A, Gumaste V. Rose E, Sachar DB. TiscorniaWasserman P. Pancreatic tuberculosis: a frequently fatal but potentially curable disease. J C/in Gastroenterol 1990; 12: 74-77.
3. Cho KC, Lucak SL. Delany HM, Morehouse HT, Jennings TA. CT appearance in tuberculous pancreatic abscess. J Comput Assist Tomogr 1990; 14: 152-154. 4. Berson BD, Mend&on DS, Janus CL. Tuberculous abscess of the pancreas in AIDS: CT findings. MI Sinai M Med 1989; 56: 297-299. 5. Tetzeli JP, Pisegna JR, Barkin JS. Tuberculous pancreatic abscess as a manifestation of AIDS. Am J Gastroenterol 1989; 84: 581-582. 6. Meinke AK. Pancreatic tuberculous abscess. Corm Med 1989; 53: 139-141.
UK
Tuberculous pancreatitis and AIDS I would like to comment on the case report by Knowles et al (Tubercle 1990; 71: 65-68) of tuberculous pancreatitis occurring in the course of miliary and meningeal tuberculosis in a 26-yearold Haitian woman who had been in Canada for 2.5 years. No mention was made of her HIV status. She had generalised lymphadenopathy and a depressed CD4/CDS T-cell ratio, either of which could have been due to tuberculosis alone. My experience in Zimbabwe, and published reports, indicate that miliary disease and the presence of intrathoracic lymphadenopathy in adults with tuberculosis are both very suggestive of the co-existence of HIV infection. The patient had oesophageal candidiasis which is also highly suggestive of HIV infection. Although, as the authors point out, tuberculous pancreatitis was a rare complication in the past, I have recently seen six case reports of this condition in patients with HIV infection [l-6]. I therefore think it highly probable that this woman had AIDS. Department of Medicine Stan Houston University of Alberta 2E4.11 WC Mackenzie Health Sciences Centre Edmonton, Alberta, Canada
Bad news from North Lebanon Tuberculosis has not been a common disease in recent times in the north of Lebanon, but there have been fears of an epidemic in view of the long period of civil war and disruption of health services within the region [l]. No survey of the disease has been reported, but skin test surveys of children living in the districts of Akkar and Zgharta were carried out between 1980 and 1984 [2, 31. The evidence then suggested that there were no more than isolated cases of the disease. The situation has now changed dramatically. A survey in progress (September to October 1990) shows that the number of cases has increased tenfold since the early 1980s. A clinic in Tripoli seeing 25-35 cases annually at the beginning of the decade, saw 325 cases in 1989, and the same pattern is recorded throughout the region. About 80% of diagnosed cases are in adults and 20% in children. Drugs are in short supply and the majority of patients remain untreated. A skin test survey has just been completed in some of the villages in Akkar that were surveyed previously. In 1980-1984, 3.8% of children aged 7-11 were tuberculin positive, compared with 11% now: 8.1% of older children were positive in 198&1984 and 20% are positive now. There was no evidence of an increase in tuberculin positivity over the years of the earlier study, so the change has occurred since 1984. Plans are being made to vaccinate the 300-