- Email: [email protected]
Tuberculosis following immunosuppressive treatment after exposure to toxic smoke
the Epstein-Barr virus," and to carcinoma of the conjunctiva to the human squamous-cell There was, however, no evidence that HIV papillomavirus.5 infection was associated with a large increase in the risk of two other cancers known to be caused by infectionscervical cancer (none of 23 cases was HIV seropositive) and liver cancer (1 of 35 cases was HIV seropositive). The numbers reported here are small, but further study of malignant diseases in people with AIDS may help to clarify the role of infectious agents and the immune system in the aetiology of cancer.
Hodgkin lymphoma
Dr Ngilimana has refugee status in Belgium, Ms Sindikubwabo is in France, and the whereabouts of Agnes Nganyira is unknown. All three of these authors were formerly at the Universite du Rwanda, Butare, Rwanda.
the search for the cause of retroperitoneal fibrosis should include systematic inquiry into asbestos exposure. *J C Boulard, T Hanslik, L A Baglin
Moulonguet Doleris, J Prinseau,
*Department of Internal Medicine and Nephrology, Hôpital Ambroise Paré, 92104 Boulogne-Billancourt, France; and Université René Descartes-Paris V
Maguire GP, Meggs LG, Addonizio J, Del Guercio LRM. Association of asbestos exposure, retroperitoneal fibrosis, and acute renal failure. NY State J Med 1991; 91: 357-59. 2 Auerbach O, Conston AS, Garfinkel L, Parks VR, Kaslow HD, 1
3
Hammond EC. Presence of asbestos bodies in organs other than the lung. Chest 1980; 77: 133-37. Browne K, Smither WJ. Asbestos-related mesothelioma: factors discriminating between pleural and peritoneal sites. Br J Ind Med
1983; 40: 145-52. *R Newton, A
Grulich, V Beral, B Sindikubwabo,
P-J Ngilimana, A Nganyira, D M Parkin *ICRF Cancer Epidemiology Unit, Gibson Building, Radcliffe Infirmary, Oxford OX2 6HE, UK, National Centre in HIV Epidemiology and Clinical Research, Sydney, Australia; and IARC, Lyon, France
1 Beral V. The epidemiology of cancer in AIDS patients. AIDS 1991; 5 (suppl 2): S99-S103. 2 Rwanda HIV Seroprevalence Study Group. Nationwide communitybased serological survey of HIV-1 and other human retrovirus infections in a central African country. Lancet 1989; i: 941-43. 3 Chang Y, Cesarman E, Pessin MS, et al. Identification of herpes-like DNA sequences in AIDS-associated Kaposi’s sarcoma. Science 1994; 266: 1865-69. 4 Luxton JC, Thomas JA, Crawford DH. Aetiology and pathogenesis of Non-Hodgkin lymphoma in AIDS. In: Cancer, HIV and AIDS. Cancer Surv 1991; 10: 103-19. 5 McDonnell JM, Mayr AJ, Martin WJ. DNA of human papillomavirus type 16 in dysplastic and malignant lesions of the conjunctiva and cornea. N Engl J Med 1989; 320: 1442-46.
Asbestos and fibrosis
idiopathic retroperitoneal
SIR-A temporal association between retroperitoneal fibrosis and diffuse pleural thickening has been reported in one patient with a history of asbestos exposure.’ We describe here two men previously exposed to asbestos who had retroperitoneal fibrosis with evidence of pleural involvement. A 51-year-old man, employed for 25 years in road building, was admitted to hospital with acute renal failure. Abdominal echography and magnetic resonance imaging revealed retroperitoneal fibrosis with bilateral ureteral obstruction. The patient refused biopsy. Steroid therapy induced immediate ureteral decompression and renal normalisation. Chest radiographs showed bilateral diaphragmetic calcified pleural plaques typical of asbestos exposure. A 54-year-old man, who was employed for maintenance of the boiler of a thermal power station in the car industry, had been exposed to asbestos for 20 years. He presented with renal failure due to retroperitoneal fibrosis. His chest radiographs showed unilateral chronic pleural thickening. His renal function improved under steroid therapy. In neither patient did we find any of the usual causes of retroperitoneal fibrosis (ie, tumour, retroperitoneal injury, urinary extravasation, abdominal aneurysm, atherosclerosis, abdominal or genitourinary infection, radiation, or medicine
taking). These two cases prompt us to think, like Maguire et al,’1 that asbestos might be a cause of retroperitoneal fibrosis. In necropsies of people exposed to asbestos, numerous asbestos bodies are indeed found in most organs, including retroperitoneal organs.2 Moreover, peritoneal mesothelioma is also associated with asbestos exposure.3 We propose that
Tuberculosis following immunosuppressive treatment after exposure to toxic smoke tuberculosis infection presents clinically malnourished or are immunosuppressed (eg, by drugs or some immunodeficiency disease) and those exposed to a heavy bacterial inoculum. In India more than 600000 people die from tuberculosis every year.’ Poor hygiene and living conditions, subnormal host defence associated with malnutrition or heavy worm infestations, and indiscriminate use of corticosteroids by private practitioners all contribute to this toll. We describe here an outbreak of tuberculosis with an unusual background. On Nov 14, 1994, at 0230 hours, in a poor area of East Delhi, India, people woke up choking on a dense white smoke with pungent odour. More than 1500 people inhaled this toxic smoke, which came from a fire lit by a garbage handler trying to get rid of some chemical waste. The smoke was controlled within 2 hours but 7 people (5 of them children) died and 80 were admitted to hospital with respiratory distress and shock. Cattle died too or were badly affected. Eye witnesses said that the smoke left dark yellowbrown marks on clothes and household surfaces, resulting in serious damage; food was contaminated too. The nature of the smoke remains unknown. In hospital, patients complained of breathlessness and suffocation. They had congestion of nasopharyngeal mucosa and conjunctivae and also dyspnoea. However, none (except those who died) had cyanosis. Chest radiographs and analysis of urine and blood were normal. Patients were treated with heavy doses of corticosteroids and intravenous bronchodilators. However, despite 2 months of such treatment, few patients improved and they continued to complain of breathlessness, weakness, loss of appetite, and a bad taste in the mouth. In more than 200 cases of those exposed, respiratory symptoms got worse and a mild-tomoderate fever developed. In March, 1995, 80 patients selected at random were reexamined. 30 complained of cough, chest pain, and fever, and the clinical findings suggested pulmonary tuberculosis. 20 of these 30 had cough with expectoration, and sputum samples were examined microbiologically. Acid-fast bacilli (+ to ++++) were found in 15 of these 20 suspected cases, 5 in one family (mother and 4 children). Before the gas tragedy only 1 patient was known to have pulmonary tuberculosis. Perhaps she served as a source of infection of her family (children) and neighbours, and the infection may have established itself easily in contacts because they had been on corticosteroids and bronchodilators for 2 months, treatments known to predispose to reactivation of tuberculosis.2 In situations like this, where a whole community is to be treated with
SIR-Mycobacterium in those who
are
1379
immunosuppressive drugs, there is a serious risk of opportunistic infection and reactivation of latent
weight, age, or presence explain the results.
of comorbid conditions could not
tuberculosis infection. *Winona Wall, Liam Martin, Marvin J Fritzler, Steven
Singh, Niti Singh, Syed Kamran Razvi *Department of Laboratory Medicine, All India Institute of Medical Sciences,
Department of Medicine, University of Calgary, 3330 Hospital Alberta, Canada T2N 4N1
New Delhi 110029, India; and Centre for Law and Economics, New Delhi
1
*Sarman
Supreme Courts,
2
1 2
Park JE, Park K. Textbook of preventive and social medicine. 11th ed. Jabalpur: Banarasidas Bhanot, 1986: 164-78. Kumar PJ, Clark ML. Clinical medicine: a textbook for medical students and doctors. 2nd ed. London: ELBS (with Baillière Tindall), 1991: 816-17.
Non-fasting chylomicronaemia in implant patients
3
4
Edworthy
Drive NW
Calgary,
Chait A, Bunzell JD. Chylomicronemia Syndrome. Adv Int Med 1992; 37: 249-73. Martin L. Editorial: silicone breast implants and connective tissue disease: an ongoing controversy. J Rheum 1995; 22: 198-99. Gabnel SE, O’Fallon WM, Kurland LT, Beard CM, Woods JE, Melton LJ. Risk of connective-tissue diseases and other disorders after breast implantation. N Engl J Med 1994; 330: 1697-702. Sanchez-Guerrero J, Karlson EW, Coldi GA, et al. Silicone breast implants (SBI) and connective tissue disease (CTD). Arthritis Rheum 1994; 37: 158-68.
breast
SiR-We assessed serum samples from 1587 women with breast implants and 749 women who underwent other cosmetic surgery to find the relative risk of connective tissue disease in women with breast implants. Sera were collected from patients, stored at -20°C, and subsequently tested for antibodies by indirect immunofluorescence, immuno-
diffusion, and western immunoblotting. During the handling of specimens it was noted that automated pipette equipment became clogged. The sera were then centrifuged in a Beckman J6-B refrigerated
centrifuge at 4°C at 3500 revolutions per min for 10 min. Many of the sera had a layer of opaque, creamy material floating on top. Analysis of this material showed lipid in the form of chylomicrons. A grading scheme was devised to describe the appearance of the sera and then in a blinded fashion all sera were assessed. Lipaemia present in the serum which did not form a fatty layer was described as "normal" lipaemia. Lipaemia which, after centrifugation rose to the top (ie, chylomicrons) was graded as 1, a very thin but distinct layer; 2, a layer up to 1 mm in thickness; 3, a layer about 1-2 mm in thickness; and 4, a very thick layer (pluglike) >2 mm in thickness. A sample of 69 study participants provided fasting blood samples and these were also assessed. Obesity, smoking history, alcohol intake, exercise habits, and comorbid conditions such as diabetes mellitus and hypothyroidism were assessed to determine if these were associated with the serological abnormality. The implant cohort had an increased prevalence of lipaemia (table). No significant difference was found between implant patients who had silicone and those who had saline. Nor was an association found between the duration of implant exposure and lipaemia. Lipaemia was greatly reduced in patients who fasted for 12 hours. Although chylomicrons appear in non-fasting sera in the
general population, under normal conditions, they are cleared rapidly so it is rare to see a thick layer of chylomicrons.’A grading of 3 or more is seldom seen in the normal population (3-2% of our controls). To our knowledge, this is the first time that such an observation has been reported.2 There has been interest in the association of breast implants with cancer and with autoimmune disease, but never with conditions associated with abnormal lipid profiles.34 The history of smoking, alcohol consumption,
Helicobacter pylori seropositivity in myocardial infarction SiR-In 1994, The Lancet published a challenging commentary on Helicobacter pylori and the heart, debating an association between chronic H pylori infection of the stomach and the risk of coronary heart diseaseY We too have observed an increase in the risk of myocardial infarction at younger age for patients with H pylori infection, as judged by the presence of homologous antibodies in the bloodstream. We studied 35 male and 7 female patients admitted to the emergency department of our hospital with myocardial infarction. Coronary arteriography was part of the diagnostic work-up and all 42 patients had more than 70% obstruction of a coronary vessel. We used a commercial ELISA to measure H pylori specific antibodies (table).
Table : H pylori seropositivity among patients and controls (C)
myocardial
infarction
(MI)
The 198 controls were obtained from a cohort of 619 consecutive patients admitted to the same emergency unit during the period Aug 16-30, 1994 (43% of the 619 had a
discharge diagnosis of cardiopulmonary disease). All 7 myocardial infarction patients aged 50-59 had antibodies to H pylori compared with 50% of controls. the association seems less striking (86% vs 67% for men, 71 % vs 52% for women). We plan a large case-control survey to clarify the strength of the association, especially in the younger age group.
However,
at
age 60
or
more
Anna Morgando, Patrizia Sanseverino, Chiara Perotto, Francesca Molino, Valerio Gai, *Antonio Ponzetto Departments of Emergency Medicine, Microbiology, and *Expenmental Gastroenterology, Ospedale Molmette, via Chiabrera 34, 10126 Tunn, Italy 1 2
Glynn JR. Helicobacter pylon and the heart. Lancet 1994; 344: 146. Mendall MA, Goggin PM, Molineaux N, et al. Relation of Helicobacter pylori infection and coronary heart disease. Br Heart J 1994; 71: 437-39.
CORRECTION
Table:
1380
Lipaemia counts and percentages
Invasive pneumococcal infections in children--In this letter by Booy and colleagues (May 13, p 1245) a line was inadvertently omitted from the fourth and fifth sentence of the second paragraph. These sentences should have read: "That outbreak also arose in the context of Hib elimination by a vaccine programme, and so provides another possible example of upsurge in pneumococcal disease after Hib control. Were the pneumococcal isolates in the Tampere region typed?".
.
Hodgkin lymphoma
Dr Ngilimana has refugee status in Belgium, Ms Sindikubwabo is in France, and the whereabouts of Agnes Nganyira is unknown. All three of these authors were formerly at the Universite du Rwanda, Butare, Rwanda.
the search for the cause of retroperitoneal fibrosis should include systematic inquiry into asbestos exposure. *J C Boulard, T Hanslik, L A Baglin
Moulonguet Doleris, J Prinseau,
*Department of Internal Medicine and Nephrology, Hôpital Ambroise Paré, 92104 Boulogne-Billancourt, France; and Université René Descartes-Paris V
Maguire GP, Meggs LG, Addonizio J, Del Guercio LRM. Association of asbestos exposure, retroperitoneal fibrosis, and acute renal failure. NY State J Med 1991; 91: 357-59. 2 Auerbach O, Conston AS, Garfinkel L, Parks VR, Kaslow HD, 1
3
Hammond EC. Presence of asbestos bodies in organs other than the lung. Chest 1980; 77: 133-37. Browne K, Smither WJ. Asbestos-related mesothelioma: factors discriminating between pleural and peritoneal sites. Br J Ind Med
1983; 40: 145-52. *R Newton, A
Grulich, V Beral, B Sindikubwabo,
P-J Ngilimana, A Nganyira, D M Parkin *ICRF Cancer Epidemiology Unit, Gibson Building, Radcliffe Infirmary, Oxford OX2 6HE, UK, National Centre in HIV Epidemiology and Clinical Research, Sydney, Australia; and IARC, Lyon, France
1 Beral V. The epidemiology of cancer in AIDS patients. AIDS 1991; 5 (suppl 2): S99-S103. 2 Rwanda HIV Seroprevalence Study Group. Nationwide communitybased serological survey of HIV-1 and other human retrovirus infections in a central African country. Lancet 1989; i: 941-43. 3 Chang Y, Cesarman E, Pessin MS, et al. Identification of herpes-like DNA sequences in AIDS-associated Kaposi’s sarcoma. Science 1994; 266: 1865-69. 4 Luxton JC, Thomas JA, Crawford DH. Aetiology and pathogenesis of Non-Hodgkin lymphoma in AIDS. In: Cancer, HIV and AIDS. Cancer Surv 1991; 10: 103-19. 5 McDonnell JM, Mayr AJ, Martin WJ. DNA of human papillomavirus type 16 in dysplastic and malignant lesions of the conjunctiva and cornea. N Engl J Med 1989; 320: 1442-46.
Asbestos and fibrosis
idiopathic retroperitoneal
SIR-A temporal association between retroperitoneal fibrosis and diffuse pleural thickening has been reported in one patient with a history of asbestos exposure.’ We describe here two men previously exposed to asbestos who had retroperitoneal fibrosis with evidence of pleural involvement. A 51-year-old man, employed for 25 years in road building, was admitted to hospital with acute renal failure. Abdominal echography and magnetic resonance imaging revealed retroperitoneal fibrosis with bilateral ureteral obstruction. The patient refused biopsy. Steroid therapy induced immediate ureteral decompression and renal normalisation. Chest radiographs showed bilateral diaphragmetic calcified pleural plaques typical of asbestos exposure. A 54-year-old man, who was employed for maintenance of the boiler of a thermal power station in the car industry, had been exposed to asbestos for 20 years. He presented with renal failure due to retroperitoneal fibrosis. His chest radiographs showed unilateral chronic pleural thickening. His renal function improved under steroid therapy. In neither patient did we find any of the usual causes of retroperitoneal fibrosis (ie, tumour, retroperitoneal injury, urinary extravasation, abdominal aneurysm, atherosclerosis, abdominal or genitourinary infection, radiation, or medicine
taking). These two cases prompt us to think, like Maguire et al,’1 that asbestos might be a cause of retroperitoneal fibrosis. In necropsies of people exposed to asbestos, numerous asbestos bodies are indeed found in most organs, including retroperitoneal organs.2 Moreover, peritoneal mesothelioma is also associated with asbestos exposure.3 We propose that
Tuberculosis following immunosuppressive treatment after exposure to toxic smoke tuberculosis infection presents clinically malnourished or are immunosuppressed (eg, by drugs or some immunodeficiency disease) and those exposed to a heavy bacterial inoculum. In India more than 600000 people die from tuberculosis every year.’ Poor hygiene and living conditions, subnormal host defence associated with malnutrition or heavy worm infestations, and indiscriminate use of corticosteroids by private practitioners all contribute to this toll. We describe here an outbreak of tuberculosis with an unusual background. On Nov 14, 1994, at 0230 hours, in a poor area of East Delhi, India, people woke up choking on a dense white smoke with pungent odour. More than 1500 people inhaled this toxic smoke, which came from a fire lit by a garbage handler trying to get rid of some chemical waste. The smoke was controlled within 2 hours but 7 people (5 of them children) died and 80 were admitted to hospital with respiratory distress and shock. Cattle died too or were badly affected. Eye witnesses said that the smoke left dark yellowbrown marks on clothes and household surfaces, resulting in serious damage; food was contaminated too. The nature of the smoke remains unknown. In hospital, patients complained of breathlessness and suffocation. They had congestion of nasopharyngeal mucosa and conjunctivae and also dyspnoea. However, none (except those who died) had cyanosis. Chest radiographs and analysis of urine and blood were normal. Patients were treated with heavy doses of corticosteroids and intravenous bronchodilators. However, despite 2 months of such treatment, few patients improved and they continued to complain of breathlessness, weakness, loss of appetite, and a bad taste in the mouth. In more than 200 cases of those exposed, respiratory symptoms got worse and a mild-tomoderate fever developed. In March, 1995, 80 patients selected at random were reexamined. 30 complained of cough, chest pain, and fever, and the clinical findings suggested pulmonary tuberculosis. 20 of these 30 had cough with expectoration, and sputum samples were examined microbiologically. Acid-fast bacilli (+ to ++++) were found in 15 of these 20 suspected cases, 5 in one family (mother and 4 children). Before the gas tragedy only 1 patient was known to have pulmonary tuberculosis. Perhaps she served as a source of infection of her family (children) and neighbours, and the infection may have established itself easily in contacts because they had been on corticosteroids and bronchodilators for 2 months, treatments known to predispose to reactivation of tuberculosis.2 In situations like this, where a whole community is to be treated with
SIR-Mycobacterium in those who
are
1379
immunosuppressive drugs, there is a serious risk of opportunistic infection and reactivation of latent
weight, age, or presence explain the results.
of comorbid conditions could not
tuberculosis infection. *Winona Wall, Liam Martin, Marvin J Fritzler, Steven
Singh, Niti Singh, Syed Kamran Razvi *Department of Laboratory Medicine, All India Institute of Medical Sciences,
Department of Medicine, University of Calgary, 3330 Hospital Alberta, Canada T2N 4N1
New Delhi 110029, India; and Centre for Law and Economics, New Delhi
1
*Sarman
Supreme Courts,
2
1 2
Park JE, Park K. Textbook of preventive and social medicine. 11th ed. Jabalpur: Banarasidas Bhanot, 1986: 164-78. Kumar PJ, Clark ML. Clinical medicine: a textbook for medical students and doctors. 2nd ed. London: ELBS (with Baillière Tindall), 1991: 816-17.
Non-fasting chylomicronaemia in implant patients
3
4
Edworthy
Drive NW
Calgary,
Chait A, Bunzell JD. Chylomicronemia Syndrome. Adv Int Med 1992; 37: 249-73. Martin L. Editorial: silicone breast implants and connective tissue disease: an ongoing controversy. J Rheum 1995; 22: 198-99. Gabnel SE, O’Fallon WM, Kurland LT, Beard CM, Woods JE, Melton LJ. Risk of connective-tissue diseases and other disorders after breast implantation. N Engl J Med 1994; 330: 1697-702. Sanchez-Guerrero J, Karlson EW, Coldi GA, et al. Silicone breast implants (SBI) and connective tissue disease (CTD). Arthritis Rheum 1994; 37: 158-68.
breast
SiR-We assessed serum samples from 1587 women with breast implants and 749 women who underwent other cosmetic surgery to find the relative risk of connective tissue disease in women with breast implants. Sera were collected from patients, stored at -20°C, and subsequently tested for antibodies by indirect immunofluorescence, immuno-
diffusion, and western immunoblotting. During the handling of specimens it was noted that automated pipette equipment became clogged. The sera were then centrifuged in a Beckman J6-B refrigerated
centrifuge at 4°C at 3500 revolutions per min for 10 min. Many of the sera had a layer of opaque, creamy material floating on top. Analysis of this material showed lipid in the form of chylomicrons. A grading scheme was devised to describe the appearance of the sera and then in a blinded fashion all sera were assessed. Lipaemia present in the serum which did not form a fatty layer was described as "normal" lipaemia. Lipaemia which, after centrifugation rose to the top (ie, chylomicrons) was graded as 1, a very thin but distinct layer; 2, a layer up to 1 mm in thickness; 3, a layer about 1-2 mm in thickness; and 4, a very thick layer (pluglike) >2 mm in thickness. A sample of 69 study participants provided fasting blood samples and these were also assessed. Obesity, smoking history, alcohol intake, exercise habits, and comorbid conditions such as diabetes mellitus and hypothyroidism were assessed to determine if these were associated with the serological abnormality. The implant cohort had an increased prevalence of lipaemia (table). No significant difference was found between implant patients who had silicone and those who had saline. Nor was an association found between the duration of implant exposure and lipaemia. Lipaemia was greatly reduced in patients who fasted for 12 hours. Although chylomicrons appear in non-fasting sera in the
general population, under normal conditions, they are cleared rapidly so it is rare to see a thick layer of chylomicrons.’A grading of 3 or more is seldom seen in the normal population (3-2% of our controls). To our knowledge, this is the first time that such an observation has been reported.2 There has been interest in the association of breast implants with cancer and with autoimmune disease, but never with conditions associated with abnormal lipid profiles.34 The history of smoking, alcohol consumption,
Helicobacter pylori seropositivity in myocardial infarction SiR-In 1994, The Lancet published a challenging commentary on Helicobacter pylori and the heart, debating an association between chronic H pylori infection of the stomach and the risk of coronary heart diseaseY We too have observed an increase in the risk of myocardial infarction at younger age for patients with H pylori infection, as judged by the presence of homologous antibodies in the bloodstream. We studied 35 male and 7 female patients admitted to the emergency department of our hospital with myocardial infarction. Coronary arteriography was part of the diagnostic work-up and all 42 patients had more than 70% obstruction of a coronary vessel. We used a commercial ELISA to measure H pylori specific antibodies (table).
Table : H pylori seropositivity among patients and controls (C)
myocardial
infarction
(MI)
The 198 controls were obtained from a cohort of 619 consecutive patients admitted to the same emergency unit during the period Aug 16-30, 1994 (43% of the 619 had a
discharge diagnosis of cardiopulmonary disease). All 7 myocardial infarction patients aged 50-59 had antibodies to H pylori compared with 50% of controls. the association seems less striking (86% vs 67% for men, 71 % vs 52% for women). We plan a large case-control survey to clarify the strength of the association, especially in the younger age group.
However,
at
age 60
or
more
Anna Morgando, Patrizia Sanseverino, Chiara Perotto, Francesca Molino, Valerio Gai, *Antonio Ponzetto Departments of Emergency Medicine, Microbiology, and *Expenmental Gastroenterology, Ospedale Molmette, via Chiabrera 34, 10126 Tunn, Italy 1 2
Glynn JR. Helicobacter pylon and the heart. Lancet 1994; 344: 146. Mendall MA, Goggin PM, Molineaux N, et al. Relation of Helicobacter pylori infection and coronary heart disease. Br Heart J 1994; 71: 437-39.
CORRECTION
Table:
1380
Lipaemia counts and percentages
Invasive pneumococcal infections in children--In this letter by Booy and colleagues (May 13, p 1245) a line was inadvertently omitted from the fourth and fifth sentence of the second paragraph. These sentences should have read: "That outbreak also arose in the context of Hib elimination by a vaccine programme, and so provides another possible example of upsurge in pneumococcal disease after Hib control. Were the pneumococcal isolates in the Tampere region typed?".
.