- Email: [email protected]
A young child with Kawasaki syndrome and AIDS
Although it is true that there is a lower incidence of HIV infection in this age group, failure to consider HIV infection in the elderly as previously reported in two patients from Northern Irelands can have serious medical repercussions. Michael McBride Department of Genitourinary Medicine, Royal Victoria Hospital, Belfast BT12 6BA,
1 2
3 4 5
reply
SiR-With respect to the known diurnal variation in CD4 counts, all blood samples were collected between 09.30 and 11.00 and analysed within 2-3 h. Only one blood sample was taken for each person, irrespective of age, and HIV status was not assessed since individuals’ permission had not been sought. The information with respect to the seroprevalence of HIV infection in Northern Ireland was obtained during 1995 from the Department of Health and Social Services (personal communication, Dr E Mitchell) and is correct for cases of HIV positivity first diagnosed in Northern Ireland and registered with the Public Health Laboratory Service AIDS centre at Communicable Disease Surveillance Centre, UK.’I The occurrence of CD4 lymphopenia was an unexpected finding as part of a continuing study of ageing.2 Although normal sexual activity presumably contributes to healthy ageing and longevity, the study of sexual activity in older people was not the remit of this study. However, all individuals were apparently well and were interviewed by the research nurse who took a personal medical history. There was no known history of drug abuse or homosexuality. Although we are aware of documented cases of HIV positivity and AIDS in older people in a few case studies both in Europe and the USA, there is much stronger evidence that undernutrition or malnutrition is common in older people and is associated with changes in the immune system.3 Protein-calorie malnutrition is often assessed by measurement of the total lymphocyte count, when lower values are suggestive of malnutrition and have been related to increased mortality and morbidity.4 What has not been described previously is an association between one of the lymphocyte subsets, in this case CD4 count, and nutritional markers of malnutrition. CD4 lymphopenia is being increasingly described in several situations in which it is not clear that HIV infection should either be assumed or treated,4 and this raises important ethical issues that should be considered further in a much broader medical context. In the meantime, we think that prophylactic treatment of apparently well 80 or 90-yearold people (not patients as suggested) with co-trimoxazole against possible Pneumocystis carinii pneumonia or other opportunistic infection may well be harmful. The Committee on Safety of Medicines has clear recommendations limiting its prescription, and has special
warnings for its use in elderly age groupS.5 Further, it seems highly improbable that HIV infection could be the cause of 18 cases of CD4 lymphopenia in those 912
no cases were
detected in
*/ M Rea, H D Alexander, TC M Morris *Department of Geriatric Medicine, Queen’s University of Belfast, UK; and Department of Haematology, Belfast City Hospital
Belfast BT9
our
7BL,
UK
Rea IM, Alexander HD, Crockard AD, Morris TCM. CD4 lymphopenia in very elderly people. Lancet 1996; 347: 328-29. Malone JL, Simms TE, Gray GC, et al. Sources of variability in repeated T-helper lymphocyte counts from human immunodeficiency virus type 1-infected patients: total lymphocyte counts fluctuations and diurnal cycle are important. J Acquir Immune Defic Syndr Hum Retrovir 1990; 3: 144-51. Rogstad K, Bignell CJ. Sex and the elderly. BMJ 1989; 299: 1279. Benn KC, Thompson NL. Social and psychological functioning of the ageing male homosexual. Br J Psychiatry 1980; 137: 361-70. McBride MO, Maw RD, Dinsmore WW, Horner T, Nelson JK, Finnegan OC. Acquired immunodeficiency in the elderly. R Soc Med 1992; 85: 240-41.
Authors’
over 80 years whereas 15-59 age group.
aged
1 2
3 4 5
Communicable Disease Report 1996; 6: 63. Rea IM, Stewart M, Campbell P, Alexander HD, Crockard AD, Morris TCM. Changes in lymphocyte subsets and interleukin 2 and soluble interleukin 2 receptor in old and very old age. Gerontology 1996; 42: 69-78. Roebothan B, Chandra RK. Relationship between nutritional status and immune function in elderly people. Age Ageing 1994; 23: 49-53. Gibson RS. Principles of nutritional assessment. New York: Oxford University Press, 1990. British National Formulary 1995. London: BMA, 1995.
A young child with Kawasaki AIDS
syndrome and
SiR-The aetiopathogenesis of Kawasaki syndrome and AIDS may be related.’ Three HIV-positive adults who developed Kawasaki syndrome have been reportedand an HIV-1 -positive infant with recurrent Kawasaki syndrome and parvovirus B19 has been described. We report a child with HIV infection who developed Kawasaki syndrome. A 3-year-old boy was found to have perinatal HIV infection after his mother had been diagnosed with AIDS in October, 1994. He was clinically well and had reached all developmental milestones. His haemoglobin was 11-3 g/dL, white cell count 85 X 109/L, total lymphocyte count 07X 109/L, CD4 T lymphocytes 0-2xlO"/L (3%), CD8 T lymphocytes 0-51X10"/L (73%), CD4/CD8 ratio 4%, and he had nonspecific hypergammaglobulinaemia (IgA 5-97 g/L, IgG 23-6 g/L, IgM 2-29 g/L). Enzyme-linked immunosorbent assay, third-generation enzyme immunoassay, and immunoassay fluorescein proved presence of HIV-1-antibodies. Standard assays detected HIV core protein (p24) antigens and showed a gradually increasing titre. Detection of HIV antigens and antibodies confirmed the diagnosis of HIV infection. He was started on prophylactic co-trimoxazole. 2 months later he was admitted with fever up to 39’5°C of 3 days duration, a maculopapular pleomorphic erythematous rash, inflamed oral mucosa, and conjunctivitis. The platelet count was 318X10"/L. Subsequently his lips developed cracks, his fingers and feet desquamated, and his cervical lymph nodes enlarged. The child remained febrile for a further 5 days despite antibiotics. Bacterial, fungal, and viral studies, other than HIV, were negative. A diagnosis of Kawasaki syndrome was made. His fever settled after a single infusion of immunoglobulin 2 g/kg and aspirin 100 mg/kg per day. The rash and the mucosal inflammation gradually resolved. The child was discharged home, 10 days after admission, on aspirin 5 mg/kg daily. 9 months later the aspirin was stopped since the echocardiogram remained normal. However, he developed wasting syndrome with a weight drop from just below the 25th centile to the third centile over 1-year period. He also had repeated episodes of oral thrush, which responded well to nystatin drops. In September, 1995, he had Salmonella typhimurium septicaemia associated with coliform urinary tract infection, but both infections responded well to antibiotics, and imaging of the urinary tract was normal. The child was classified as having CDC stage C3 because of the severe clinical manifestations and profound immunological suppression. Kawasaki syndrome is an acute multisystem vasculitis with immunologically mediated phenomena of unknown aetiology. It was first described in Japan in 19673 but now
world-wide distribution. Kawasaki syndrome is essentially a disease of childhood, and is the main cause of acquired heart disease in this age group in many countries including the United States. The associated mortality, caused by coronary artery disease and myocardial infarction, has led to considerable efforts to establish the aetiology. Raised reverse transcriptase activity, in lymphocyte culture supernatants, has led to speculation that Kawasaki syndrome might be caused by a retrovirus. However, failure to confirm cultures suggested that the a retrovirus in lymphocyte demonstrated was typical of host cells’ activity polymerase DNA-dependent DNA polymerase rather than viral reverse transcriptase. Lin and co-workers,4 on the other hand, reported virus-like particles with reverse transcriptase activity associated with Kawasaki syndrome. They also demonstrated a retrovirus-specific band -in the co-cultivated supernatants obtained from one AIDS and four Kawasaki syndrome patients but not in patients with rubella or in healthy controls.4 A second study speculated that viral tatlike protein might be responsible for raised serum cytokines and CD8 levels in Kawasaki syndrome and HIV infection. This mechanism could also explain similar B cell immunological abnormalities in both conditions.’I In addition, superantigen in Kawasaki syndrome and HIV may activate self-reactive T cells and cause immune-mediated tissue injury. Tissue injury in Kawasaki syndrome is usually self-limiting but is persistent in HIV infection. High-dose immunoglobulin is beneficial in Kawasaki syndrome and HIV infection presumably because it may clear the superantigen residual activity. Physicians should be aware that Kawasaki syndrome may be associated with HIV infection. has
We thank Jacqueline Y 0 Mok for her
help with this
case.
*Saad Mustafa Said Aladhami, William A Arrowsmith, Jim Inglis, M M Madlom Children’s Hospital, Doncaster Royal Infirmary, Doncaster; and *3/2 37 Avenue, Glasgow G4 0PH, UK
detected in the blood 2 months after this second surgery, and then disappeared. We compared these data with histological characteristics of lymph node involvement, and have no evidence of correlation between released melanoma cells and capsule breaking, or the number of involved lymph nodes. Although Eschwege and colleagues’ never found prostate cells shed in the bloodstream following prostatocystectomy in patients with bladder carcinoma, or in those with benign prostatic hyperplasia, it cannot yet be ruled out that any released cells are normal prostatic cells. By contrast, lymph nodes do not normally contain tyrosinase-expressing cells.s Therefore, the cells we detected following lymph node resection can only be released from melanoma metastases. Whether these cells have the potential to develop distant metastases or not is an open question. Longer follow-up of these patients is required to establish the prognostic significance of this dissemination. were
Lipart for expert technical assistance. This work was supported by a grant "Projet Hospitalier de Recherche Clinique 93".
We thank C
*Marc G Denis, Marie-Hélène Tessier, Patrick Lustenberger St
1 Rautonen J, Rautonen N. Tat and Kawasaki disease. Immunol 2
tyrosinase, a key enzyme of melanogenesis expressed by melanocytes.2 Blood samples (10-20 mL) were collected in heparinised tubes. We have described extraction of total RNA from these samples, as well as the nested RT-PCR, elsewhere.3,4 None of 16 patients tested 3 days before surgery had detectable circulating melanocytes in their blood. By contrast, seven were found to have circulating melanocytes 2-4 weeks after node dissection. 1 month later, all patients were again negative, indicating that these released cells had been eliminated by the immune system or that they bound to a target site. Several months after the first resection, one patient developed a regional relapse. Again, lymph nodes were removed. Circulating melanocytes
a
Mungo
*Laboratoire de Biochimie Spécialisée and Unité de Institut de Biologie, 44035 Nantes, France
4
5
Thérapie Cellulaire et Génique,
Today
1
1992; 13: 190-91. Wolf CVH, Wolf JR, Parker JS. Kawasaki’s syndrome in a man with the human immunodeficiency virus. Am J Ophthalmol 1995; 120:
Eschwège P, Dumas F, Blanchet P, et al. Haematogenous dissemination of prostatic cells during radical prostatectomy. Lancet
2
Smith B,
117-18. 3
Brigitte Dréno,
Nigro G, Pisano P, Krzysztofiak A. Recurrent kawasaki associated with co-infection with parvovirus B19 and HIV-1. AIDS 1993; 7: 288-90. Lin CY, Chen IC, Cheng TI, Liu WT, Hwang B, Chiang BN. Viruslike particles with reverse transcriptase activity associated with Kawasaki disease. J Med Virol 1992; 38: 175-82. Kotzin BL. Superantigen and their role in disease. Hosp Pract 1994;
3 4 5
29: 59-63, 68-70.
Circulating micrometastases following oncological surgery SIR-Eschwege and colleagues (Dec 9, p 1506)’ have used a reverse-transcription nested polymerase chain reaction (PCR) with primers derived from the cDNA sequence of prostate-specific membrane antigen to look for prostatic cells in the general circulation of patients undergoing radical prostatectomy. They report that prostatic cells were disseminated during prostate dissection in 12 of 14 patients. Among patients with melanoma presenting with node metastases, 75% will relapse, and the mean time before distant metastases are detected following node resection is about 11months. Thus, detection of circulating melanocytes in peripheral blood might help to select the patients who could benefit from adjuvant therapy after surgery. Therefore, we have looked for melanocytes in the blood of melanoma patients with local or regional lymph node metastases (stage IIIB, M D Anderson). The detection relies on expression of
1995; 346: 1528-30. Selby P, Southgate J,
et
al. Detection of melanoma cells in
peripheral blood by means of reverse transcriptase and polymerase chain reaction. Lancet 1991; 338: 1227-29. Denis MG, Lustenberger P. A simple method of RNA isolation from large blood samples. Methods Mol Cell Biol 1993; 4: 128-30. Denis MG, Lustenberger P. Qualitative low-level internal control for nested RT-PCR. Biotechniques 1995; 19: 906-08. Wang XN, Heller R, Vanvoorhis N, et al. Detection of submicroscopic lymph node metastases with polymerase chain reaction in patients with malignant melanoma. Ann Surg 1994; 220: 768-74.
parasites in the pathogenesis of Chagas’ cardiomyopathy Role of
SiR-Brandariz and colleagues (Nov 18, p 1370),’ showed PCR myocardial Trypanosoma cruzi persistence at necropsy in a patient who had Chagas’ disease. Similar findings have been made in endomyocardial biopsy specimens from patients with Chagas’ cardiomyopathy.2 On the basis of their findings, Brandariz and colleagues concluded that "heart parasitation was a prevalent stimulus for the perpetuation of myocardial inflammation". But is this so? PCR detects DNA sequences, not organisms. The biological significance of these genomes is unclear at the moment. Perhaps they are merely an indicator of previous infection. Similarly, the high serum concentration of crossreacting antibodies in the patient reported by Brandariz may
by
913
1 2
3 4 5
reply
SiR-With respect to the known diurnal variation in CD4 counts, all blood samples were collected between 09.30 and 11.00 and analysed within 2-3 h. Only one blood sample was taken for each person, irrespective of age, and HIV status was not assessed since individuals’ permission had not been sought. The information with respect to the seroprevalence of HIV infection in Northern Ireland was obtained during 1995 from the Department of Health and Social Services (personal communication, Dr E Mitchell) and is correct for cases of HIV positivity first diagnosed in Northern Ireland and registered with the Public Health Laboratory Service AIDS centre at Communicable Disease Surveillance Centre, UK.’I The occurrence of CD4 lymphopenia was an unexpected finding as part of a continuing study of ageing.2 Although normal sexual activity presumably contributes to healthy ageing and longevity, the study of sexual activity in older people was not the remit of this study. However, all individuals were apparently well and were interviewed by the research nurse who took a personal medical history. There was no known history of drug abuse or homosexuality. Although we are aware of documented cases of HIV positivity and AIDS in older people in a few case studies both in Europe and the USA, there is much stronger evidence that undernutrition or malnutrition is common in older people and is associated with changes in the immune system.3 Protein-calorie malnutrition is often assessed by measurement of the total lymphocyte count, when lower values are suggestive of malnutrition and have been related to increased mortality and morbidity.4 What has not been described previously is an association between one of the lymphocyte subsets, in this case CD4 count, and nutritional markers of malnutrition. CD4 lymphopenia is being increasingly described in several situations in which it is not clear that HIV infection should either be assumed or treated,4 and this raises important ethical issues that should be considered further in a much broader medical context. In the meantime, we think that prophylactic treatment of apparently well 80 or 90-yearold people (not patients as suggested) with co-trimoxazole against possible Pneumocystis carinii pneumonia or other opportunistic infection may well be harmful. The Committee on Safety of Medicines has clear recommendations limiting its prescription, and has special
warnings for its use in elderly age groupS.5 Further, it seems highly improbable that HIV infection could be the cause of 18 cases of CD4 lymphopenia in those 912
no cases were
detected in
*/ M Rea, H D Alexander, TC M Morris *Department of Geriatric Medicine, Queen’s University of Belfast, UK; and Department of Haematology, Belfast City Hospital
Belfast BT9
our
7BL,
UK
Rea IM, Alexander HD, Crockard AD, Morris TCM. CD4 lymphopenia in very elderly people. Lancet 1996; 347: 328-29. Malone JL, Simms TE, Gray GC, et al. Sources of variability in repeated T-helper lymphocyte counts from human immunodeficiency virus type 1-infected patients: total lymphocyte counts fluctuations and diurnal cycle are important. J Acquir Immune Defic Syndr Hum Retrovir 1990; 3: 144-51. Rogstad K, Bignell CJ. Sex and the elderly. BMJ 1989; 299: 1279. Benn KC, Thompson NL. Social and psychological functioning of the ageing male homosexual. Br J Psychiatry 1980; 137: 361-70. McBride MO, Maw RD, Dinsmore WW, Horner T, Nelson JK, Finnegan OC. Acquired immunodeficiency in the elderly. R Soc Med 1992; 85: 240-41.
Authors’
over 80 years whereas 15-59 age group.
aged
1 2
3 4 5
Communicable Disease Report 1996; 6: 63. Rea IM, Stewart M, Campbell P, Alexander HD, Crockard AD, Morris TCM. Changes in lymphocyte subsets and interleukin 2 and soluble interleukin 2 receptor in old and very old age. Gerontology 1996; 42: 69-78. Roebothan B, Chandra RK. Relationship between nutritional status and immune function in elderly people. Age Ageing 1994; 23: 49-53. Gibson RS. Principles of nutritional assessment. New York: Oxford University Press, 1990. British National Formulary 1995. London: BMA, 1995.
A young child with Kawasaki AIDS
syndrome and
SiR-The aetiopathogenesis of Kawasaki syndrome and AIDS may be related.’ Three HIV-positive adults who developed Kawasaki syndrome have been reportedand an HIV-1 -positive infant with recurrent Kawasaki syndrome and parvovirus B19 has been described. We report a child with HIV infection who developed Kawasaki syndrome. A 3-year-old boy was found to have perinatal HIV infection after his mother had been diagnosed with AIDS in October, 1994. He was clinically well and had reached all developmental milestones. His haemoglobin was 11-3 g/dL, white cell count 85 X 109/L, total lymphocyte count 07X 109/L, CD4 T lymphocytes 0-2xlO"/L (3%), CD8 T lymphocytes 0-51X10"/L (73%), CD4/CD8 ratio 4%, and he had nonspecific hypergammaglobulinaemia (IgA 5-97 g/L, IgG 23-6 g/L, IgM 2-29 g/L). Enzyme-linked immunosorbent assay, third-generation enzyme immunoassay, and immunoassay fluorescein proved presence of HIV-1-antibodies. Standard assays detected HIV core protein (p24) antigens and showed a gradually increasing titre. Detection of HIV antigens and antibodies confirmed the diagnosis of HIV infection. He was started on prophylactic co-trimoxazole. 2 months later he was admitted with fever up to 39’5°C of 3 days duration, a maculopapular pleomorphic erythematous rash, inflamed oral mucosa, and conjunctivitis. The platelet count was 318X10"/L. Subsequently his lips developed cracks, his fingers and feet desquamated, and his cervical lymph nodes enlarged. The child remained febrile for a further 5 days despite antibiotics. Bacterial, fungal, and viral studies, other than HIV, were negative. A diagnosis of Kawasaki syndrome was made. His fever settled after a single infusion of immunoglobulin 2 g/kg and aspirin 100 mg/kg per day. The rash and the mucosal inflammation gradually resolved. The child was discharged home, 10 days after admission, on aspirin 5 mg/kg daily. 9 months later the aspirin was stopped since the echocardiogram remained normal. However, he developed wasting syndrome with a weight drop from just below the 25th centile to the third centile over 1-year period. He also had repeated episodes of oral thrush, which responded well to nystatin drops. In September, 1995, he had Salmonella typhimurium septicaemia associated with coliform urinary tract infection, but both infections responded well to antibiotics, and imaging of the urinary tract was normal. The child was classified as having CDC stage C3 because of the severe clinical manifestations and profound immunological suppression. Kawasaki syndrome is an acute multisystem vasculitis with immunologically mediated phenomena of unknown aetiology. It was first described in Japan in 19673 but now
world-wide distribution. Kawasaki syndrome is essentially a disease of childhood, and is the main cause of acquired heart disease in this age group in many countries including the United States. The associated mortality, caused by coronary artery disease and myocardial infarction, has led to considerable efforts to establish the aetiology. Raised reverse transcriptase activity, in lymphocyte culture supernatants, has led to speculation that Kawasaki syndrome might be caused by a retrovirus. However, failure to confirm cultures suggested that the a retrovirus in lymphocyte demonstrated was typical of host cells’ activity polymerase DNA-dependent DNA polymerase rather than viral reverse transcriptase. Lin and co-workers,4 on the other hand, reported virus-like particles with reverse transcriptase activity associated with Kawasaki syndrome. They also demonstrated a retrovirus-specific band -in the co-cultivated supernatants obtained from one AIDS and four Kawasaki syndrome patients but not in patients with rubella or in healthy controls.4 A second study speculated that viral tatlike protein might be responsible for raised serum cytokines and CD8 levels in Kawasaki syndrome and HIV infection. This mechanism could also explain similar B cell immunological abnormalities in both conditions.’I In addition, superantigen in Kawasaki syndrome and HIV may activate self-reactive T cells and cause immune-mediated tissue injury. Tissue injury in Kawasaki syndrome is usually self-limiting but is persistent in HIV infection. High-dose immunoglobulin is beneficial in Kawasaki syndrome and HIV infection presumably because it may clear the superantigen residual activity. Physicians should be aware that Kawasaki syndrome may be associated with HIV infection. has
We thank Jacqueline Y 0 Mok for her
help with this
case.
*Saad Mustafa Said Aladhami, William A Arrowsmith, Jim Inglis, M M Madlom Children’s Hospital, Doncaster Royal Infirmary, Doncaster; and *3/2 37 Avenue, Glasgow G4 0PH, UK
detected in the blood 2 months after this second surgery, and then disappeared. We compared these data with histological characteristics of lymph node involvement, and have no evidence of correlation between released melanoma cells and capsule breaking, or the number of involved lymph nodes. Although Eschwege and colleagues’ never found prostate cells shed in the bloodstream following prostatocystectomy in patients with bladder carcinoma, or in those with benign prostatic hyperplasia, it cannot yet be ruled out that any released cells are normal prostatic cells. By contrast, lymph nodes do not normally contain tyrosinase-expressing cells.s Therefore, the cells we detected following lymph node resection can only be released from melanoma metastases. Whether these cells have the potential to develop distant metastases or not is an open question. Longer follow-up of these patients is required to establish the prognostic significance of this dissemination. were
Lipart for expert technical assistance. This work was supported by a grant "Projet Hospitalier de Recherche Clinique 93".
We thank C
*Marc G Denis, Marie-Hélène Tessier, Patrick Lustenberger St
1 Rautonen J, Rautonen N. Tat and Kawasaki disease. Immunol 2
tyrosinase, a key enzyme of melanogenesis expressed by melanocytes.2 Blood samples (10-20 mL) were collected in heparinised tubes. We have described extraction of total RNA from these samples, as well as the nested RT-PCR, elsewhere.3,4 None of 16 patients tested 3 days before surgery had detectable circulating melanocytes in their blood. By contrast, seven were found to have circulating melanocytes 2-4 weeks after node dissection. 1 month later, all patients were again negative, indicating that these released cells had been eliminated by the immune system or that they bound to a target site. Several months after the first resection, one patient developed a regional relapse. Again, lymph nodes were removed. Circulating melanocytes
a
Mungo
*Laboratoire de Biochimie Spécialisée and Unité de Institut de Biologie, 44035 Nantes, France
4
5
Thérapie Cellulaire et Génique,
Today
1
1992; 13: 190-91. Wolf CVH, Wolf JR, Parker JS. Kawasaki’s syndrome in a man with the human immunodeficiency virus. Am J Ophthalmol 1995; 120:
Eschwège P, Dumas F, Blanchet P, et al. Haematogenous dissemination of prostatic cells during radical prostatectomy. Lancet
2
Smith B,
117-18. 3
Brigitte Dréno,
Nigro G, Pisano P, Krzysztofiak A. Recurrent kawasaki associated with co-infection with parvovirus B19 and HIV-1. AIDS 1993; 7: 288-90. Lin CY, Chen IC, Cheng TI, Liu WT, Hwang B, Chiang BN. Viruslike particles with reverse transcriptase activity associated with Kawasaki disease. J Med Virol 1992; 38: 175-82. Kotzin BL. Superantigen and their role in disease. Hosp Pract 1994;
3 4 5
29: 59-63, 68-70.
Circulating micrometastases following oncological surgery SIR-Eschwege and colleagues (Dec 9, p 1506)’ have used a reverse-transcription nested polymerase chain reaction (PCR) with primers derived from the cDNA sequence of prostate-specific membrane antigen to look for prostatic cells in the general circulation of patients undergoing radical prostatectomy. They report that prostatic cells were disseminated during prostate dissection in 12 of 14 patients. Among patients with melanoma presenting with node metastases, 75% will relapse, and the mean time before distant metastases are detected following node resection is about 11months. Thus, detection of circulating melanocytes in peripheral blood might help to select the patients who could benefit from adjuvant therapy after surgery. Therefore, we have looked for melanocytes in the blood of melanoma patients with local or regional lymph node metastases (stage IIIB, M D Anderson). The detection relies on expression of
1995; 346: 1528-30. Selby P, Southgate J,
et
al. Detection of melanoma cells in
peripheral blood by means of reverse transcriptase and polymerase chain reaction. Lancet 1991; 338: 1227-29. Denis MG, Lustenberger P. A simple method of RNA isolation from large blood samples. Methods Mol Cell Biol 1993; 4: 128-30. Denis MG, Lustenberger P. Qualitative low-level internal control for nested RT-PCR. Biotechniques 1995; 19: 906-08. Wang XN, Heller R, Vanvoorhis N, et al. Detection of submicroscopic lymph node metastases with polymerase chain reaction in patients with malignant melanoma. Ann Surg 1994; 220: 768-74.
parasites in the pathogenesis of Chagas’ cardiomyopathy Role of
SiR-Brandariz and colleagues (Nov 18, p 1370),’ showed PCR myocardial Trypanosoma cruzi persistence at necropsy in a patient who had Chagas’ disease. Similar findings have been made in endomyocardial biopsy specimens from patients with Chagas’ cardiomyopathy.2 On the basis of their findings, Brandariz and colleagues concluded that "heart parasitation was a prevalent stimulus for the perpetuation of myocardial inflammation". But is this so? PCR detects DNA sequences, not organisms. The biological significance of these genomes is unclear at the moment. Perhaps they are merely an indicator of previous infection. Similarly, the high serum concentration of crossreacting antibodies in the patient reported by Brandariz may
by
913