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HISTIOCYTIC MEDULLARY RETICULOSIS AND ACUTE LYMPHOBLASTIC LEUKAEMIA
818 HISTIOCYTIC MEDULLARY RETICULOSIS AND ACUTE LYMPHOBLASTIC LEUKAEMIA
SIR,-We support the views of Dr Martelli and others (Aug. 21, 446) on the interpretation of histiocytic medullary reticulosis (HMR) in acute lymphoblastic leukaemia (ALL). We have seen a p.
child with ALL who had a haemophagocytic syndrome resembling HMR but who completely recovered on supportive treatment alone.’ Subsequent laboratory data revealed that the episode of HMR was associated with a parainfluenzal infection. HMR complicating ALL has been too readily regarded as a malignant change and it is therefore important to consider the alternative hypothesis that HMR in ALL may represent a reactive process to opportunistic viral infections in immunocompromised hosts.2An exhaustive search for a causal agent by virological and serological studies is mandatory. It is also crucial to recognise this condition as reactive because the use of cytotoxic drugs in these patients may be care and harmful; treatment should include intensive supportive antiviral agents, including, perhaps, interferon.3 M.R.C. Leukaemia Unit, Hammersmith Hospital, London W12 0HS
J. A. LIU YIN D. CATOVSKY
NO INDICATION OF ACTIVE EPSTEIN-BARR VIRUS INFECTION IN TWO FATAL CASES OF HISTIOCYTIC MEDULLARY RETICULOSIS
SIR,-Burkitt’s lymphoma is the leading candidate for a virusinduced human tumour.4There are reports postulating a role for Epstein-Barr virus (EBV) in other lymphoreticular malignancies, such as monocytic leukaemia.5 Moreover, several cases of histiocytic medullary reticulosis (HMR) with positive Paul-Bunnell tests have been recorded.6-8 Also interesting is Purtilo’s suggestion that some fatal cases of infectious mononucleosis may have been misdiagnosed as leukaemia.9 Should the unique histopathology of HMR be included within the spectrum of host responses to EBV 1. Liu Yin JA, Kumaran TO, Marsh GW, Rossiter M,
2.
3.
Catovsky D. Complete recovery of histiocytic medullary reticulosis-like syndrome in a child with acute lymphoblastic leukemia. Cancer (in press). Risdall RJ, McKenna RW, Nesbit ME, Krivit W, Balfour HH, Simmons RL, Brunning RD. Virus associated hemophagocytic syndrome: a benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 1979; 44: 993-1002. Scott GM, Tyrrell DAJ. Interferon: Therapy, fact or fiction for the ’80s? Br Med J 1980; 290: 1558-62.
4. Ziegler JL. Burkitt’s lymphoma N Engl Med 1981; 305: 735-45. J 5. Hehlman R, Walther B, Zöllner N, Wolf H, Deinhardt F. Infectious mononucleosis and acute monocytic leukaemia. Lancet 1980; ii: 652-53. 6. Fowler M. Histiocytic medullary reticulosis in a child. Arch Dis Child 1960; 35:
591-94. 7.
Rosenstock HA, Sandor IM, Hoenecke H. Acute histiocytic medullary reticulosis in
8.
pubescent girl. Tex Med 1969; 65: 56-59. Seligman BR, Rosner F, Fee SL, Kagan MD. Histiocytic medullary reticulosis: Fatal haemorrhage due to massive platelet phagocytosis. Arch Intern Med 1972; 129:
a
109-13.
Immunopathology of infectious mononucleosis. In: Semmers SC, Rosen PP, eds. Pathology annual: Part I. New York. Appleton Century Crofts, 1980: 271.
9. Purtilo DT
EVB
IgG, IgM, AND HETEROPHILIC (’MONOTEST’) ANTIBODY TITRES IN TWO NECROPSY CONFIRMED CASES OF HMR
infection in man?10 This hypothesis has been supported by the clinical observations of Dr Martelli and colleagues (Aug. 21, p. 446). We have described three cases ofHMR, 11 in whom no active EBV infection was observed. Two of these patients have now died and we describe here EBV antibody studies in these two necropsy confirmed cases of HMR. The results showed no indication of continuing active EBV infection at the time of presentation (the variation in IgG antibody titres in case 1 was an analytical problem). We conclude that active EBV infection was not involved in these two fatal cases of HMR. Department of Clinical Chemistry, University of Oulu,
J. A. VILPO
SF-90220 Oulu 22, Finland of Internal Medicine
Departments and Virology, University of Turku
J. NIKOSKELAINEN
MALIGNANT MELANOMA AND FLUORESCENT LIGHTING
SiR.—Dr Beral and her colleagues (Aug. 7, p. 290) assert that fluorescent lighting is a contributing factor in malignant melanoma. They may be correct, though the design, analysis, interpretation, and presentation of their study hardly justify this conclusion. Beral et al. state that "the presence of fluorescent lights in the home was not associated with a rise in melanoma risk..."This is vastly more than a minor "inconsistency". If fluorescent light is a risk factor in the office, it should also be a risk factor in the home. Beral et al. should not so discount data that are inconsistent with their conclusion. If there is a risk factor in the office, further research must be done to determine what it is, and questionable results should not be published. If melanoma risk is associated with fluorescent lighting alone and (as one might logically presume) if the intensity of radiation is a factor, then one would expect the head, neck, arms, and trunk (closer to lighting) to have more lesions per unit area than the legs (further from lighting). Beral’s data indicate that the reverse is true, at least for people who have always worked indoors. Beral et al. do not consider other factors known to be associated with cancer, such as cigarette smoke, toxic chemicals (e.g., in the early photocopiers), or radioactive substances present in many common building materials. Such factors are present, with fluorescent lighting, in many offices, and may contribute to malignant melanoma. The hardware used, lighting design, and improvements in safety and quality control over the past twenty years must be taken into consideration when designing studies of the impact of fluorescent lighting in offices. Beral et al. take no account of psychological factors (e.g., personality and recent loss) in cancer. Interviewer and informant beliefs about the effects of fluorescent lighting and possible experimenter-subject effects are ignored. Alternative hypotheses about why the malignant lesions appear on the body are not entertained. Plausible ones (e.g., those involving toxic fumes in the office) are not difficult to generate, and contradict the conclusions of the researchers. Beral et al. state that "More complex statistical techniques than the ones we used are available" to allow for possible breaking of matching control and experimental groups by age and residence, but they felt (my italics) that "their use would be unlikely to affect the results". Their feelings about the statistics are irrelevant. They had three acceptable options: determine that there was no problem with breaking of the matching and use the statistics they used; use the appropriate statistics no matter how difficult; or determine mathematically that the statistics they used were an appropriate
approximation. The study relies entirely their exposure
to
self reporting. Informants recalled lighting over periods ranging up to
on
fluorescent
NP, Davson J. Is histiocytic medullary reticulosis mononucleosis? Lancer 1981, ii: 43.
10. Mallick
11
*Case numbers as in original days after presentation.
s
report.
a
fatal form of infectious
Vilpo JA, Klemi P, Lassila O, Fräki J, Salmi TT. Cytological and functional characterization of three cases of malignant histiocytosis. Cancer 1980; 46: 1795-1801
SIR,-We support the views of Dr Martelli and others (Aug. 21, 446) on the interpretation of histiocytic medullary reticulosis (HMR) in acute lymphoblastic leukaemia (ALL). We have seen a p.
child with ALL who had a haemophagocytic syndrome resembling HMR but who completely recovered on supportive treatment alone.’ Subsequent laboratory data revealed that the episode of HMR was associated with a parainfluenzal infection. HMR complicating ALL has been too readily regarded as a malignant change and it is therefore important to consider the alternative hypothesis that HMR in ALL may represent a reactive process to opportunistic viral infections in immunocompromised hosts.2An exhaustive search for a causal agent by virological and serological studies is mandatory. It is also crucial to recognise this condition as reactive because the use of cytotoxic drugs in these patients may be care and harmful; treatment should include intensive supportive antiviral agents, including, perhaps, interferon.3 M.R.C. Leukaemia Unit, Hammersmith Hospital, London W12 0HS
J. A. LIU YIN D. CATOVSKY
NO INDICATION OF ACTIVE EPSTEIN-BARR VIRUS INFECTION IN TWO FATAL CASES OF HISTIOCYTIC MEDULLARY RETICULOSIS
SIR,-Burkitt’s lymphoma is the leading candidate for a virusinduced human tumour.4There are reports postulating a role for Epstein-Barr virus (EBV) in other lymphoreticular malignancies, such as monocytic leukaemia.5 Moreover, several cases of histiocytic medullary reticulosis (HMR) with positive Paul-Bunnell tests have been recorded.6-8 Also interesting is Purtilo’s suggestion that some fatal cases of infectious mononucleosis may have been misdiagnosed as leukaemia.9 Should the unique histopathology of HMR be included within the spectrum of host responses to EBV 1. Liu Yin JA, Kumaran TO, Marsh GW, Rossiter M,
2.
3.
Catovsky D. Complete recovery of histiocytic medullary reticulosis-like syndrome in a child with acute lymphoblastic leukemia. Cancer (in press). Risdall RJ, McKenna RW, Nesbit ME, Krivit W, Balfour HH, Simmons RL, Brunning RD. Virus associated hemophagocytic syndrome: a benign histiocytic proliferation distinct from malignant histiocytosis. Cancer 1979; 44: 993-1002. Scott GM, Tyrrell DAJ. Interferon: Therapy, fact or fiction for the ’80s? Br Med J 1980; 290: 1558-62.
4. Ziegler JL. Burkitt’s lymphoma N Engl Med 1981; 305: 735-45. J 5. Hehlman R, Walther B, Zöllner N, Wolf H, Deinhardt F. Infectious mononucleosis and acute monocytic leukaemia. Lancet 1980; ii: 652-53. 6. Fowler M. Histiocytic medullary reticulosis in a child. Arch Dis Child 1960; 35:
591-94. 7.
Rosenstock HA, Sandor IM, Hoenecke H. Acute histiocytic medullary reticulosis in
8.
pubescent girl. Tex Med 1969; 65: 56-59. Seligman BR, Rosner F, Fee SL, Kagan MD. Histiocytic medullary reticulosis: Fatal haemorrhage due to massive platelet phagocytosis. Arch Intern Med 1972; 129:
a
109-13.
Immunopathology of infectious mononucleosis. In: Semmers SC, Rosen PP, eds. Pathology annual: Part I. New York. Appleton Century Crofts, 1980: 271.
9. Purtilo DT
EVB
IgG, IgM, AND HETEROPHILIC (’MONOTEST’) ANTIBODY TITRES IN TWO NECROPSY CONFIRMED CASES OF HMR
infection in man?10 This hypothesis has been supported by the clinical observations of Dr Martelli and colleagues (Aug. 21, p. 446). We have described three cases ofHMR, 11 in whom no active EBV infection was observed. Two of these patients have now died and we describe here EBV antibody studies in these two necropsy confirmed cases of HMR. The results showed no indication of continuing active EBV infection at the time of presentation (the variation in IgG antibody titres in case 1 was an analytical problem). We conclude that active EBV infection was not involved in these two fatal cases of HMR. Department of Clinical Chemistry, University of Oulu,
J. A. VILPO
SF-90220 Oulu 22, Finland of Internal Medicine
Departments and Virology, University of Turku
J. NIKOSKELAINEN
MALIGNANT MELANOMA AND FLUORESCENT LIGHTING
SiR.—Dr Beral and her colleagues (Aug. 7, p. 290) assert that fluorescent lighting is a contributing factor in malignant melanoma. They may be correct, though the design, analysis, interpretation, and presentation of their study hardly justify this conclusion. Beral et al. state that "the presence of fluorescent lights in the home was not associated with a rise in melanoma risk..."This is vastly more than a minor "inconsistency". If fluorescent light is a risk factor in the office, it should also be a risk factor in the home. Beral et al. should not so discount data that are inconsistent with their conclusion. If there is a risk factor in the office, further research must be done to determine what it is, and questionable results should not be published. If melanoma risk is associated with fluorescent lighting alone and (as one might logically presume) if the intensity of radiation is a factor, then one would expect the head, neck, arms, and trunk (closer to lighting) to have more lesions per unit area than the legs (further from lighting). Beral’s data indicate that the reverse is true, at least for people who have always worked indoors. Beral et al. do not consider other factors known to be associated with cancer, such as cigarette smoke, toxic chemicals (e.g., in the early photocopiers), or radioactive substances present in many common building materials. Such factors are present, with fluorescent lighting, in many offices, and may contribute to malignant melanoma. The hardware used, lighting design, and improvements in safety and quality control over the past twenty years must be taken into consideration when designing studies of the impact of fluorescent lighting in offices. Beral et al. take no account of psychological factors (e.g., personality and recent loss) in cancer. Interviewer and informant beliefs about the effects of fluorescent lighting and possible experimenter-subject effects are ignored. Alternative hypotheses about why the malignant lesions appear on the body are not entertained. Plausible ones (e.g., those involving toxic fumes in the office) are not difficult to generate, and contradict the conclusions of the researchers. Beral et al. state that "More complex statistical techniques than the ones we used are available" to allow for possible breaking of matching control and experimental groups by age and residence, but they felt (my italics) that "their use would be unlikely to affect the results". Their feelings about the statistics are irrelevant. They had three acceptable options: determine that there was no problem with breaking of the matching and use the statistics they used; use the appropriate statistics no matter how difficult; or determine mathematically that the statistics they used were an appropriate
approximation. The study relies entirely their exposure
to
self reporting. Informants recalled lighting over periods ranging up to
on
fluorescent
NP, Davson J. Is histiocytic medullary reticulosis mononucleosis? Lancer 1981, ii: 43.
10. Mallick
11
*Case numbers as in original days after presentation.
s
report.
a
fatal form of infectious
Vilpo JA, Klemi P, Lassila O, Fräki J, Salmi TT. Cytological and functional characterization of three cases of malignant histiocytosis. Cancer 1980; 46: 1795-1801