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DELAYED HYPERSENSITIVITY IN TOXIC AGRANULOCYTOSIS
386 in 1 case, and again the affected side was the left.13 As seen in the table in the trisomy-18 syndrome phocomelia or aplasia of the radius are almost always unilateral in contrast to thalidomide embryopathy where the limb defects are always bilateral. At present I have no explanation for this asymmetry, which might well be due to chance alone. The left limbs are also more severely affected than the right limbs in thalidomide embryopathy. This difference, however, is not so distinct as that in the trisomy-18 syndrome. I am indebted to Dr. R. A. Pfeiffer and Dr. M. L. Voorhess for their suggestions. This study was supported in part by research grant AM-02504, National Institute of Arthritis and Metabolic Diseases, United States Public Health Service. Genetic and Endocrine Unit, Department of Pediatrics, State University of New York, Upstate Medical Center, TADASHI KAJII. Syracuse, New York 13210, U.S.A.
CHROMOSOMES IN TESTICULAR TUMOURS SIR,-In their letter (Jan. 28, p. 216) Dr. Fischer and Dr. Golob describe the chromosomes in a case of seminoma and discuss a remarkable similarity between the marker chromosomes in it and in the case I have described.14 I have now examined 9 cases in all of tumour histologically classified as seminoma. 8 of the 9 show marker chromosomes longer than any chromosome of the normal complement: most of these are dicentric or have a secondary constriction. 4 cases contain an acrocentric longer than normal D-group chromosomes. The case of Dr. Fischer and Dr. Golob indeed confirms that these types of marker chromosomes often occur in seminomas. I am now, however, calculating the relative length and centromeric index of these abnormal chromosomes by the method of Lejeune and Berger,15 and I find that these values are not identical for the markers of different tumours. What is evident is that there seems to be an end-to-end attraction or association between chromosomes in this sort of tumour. Whether such associations are confined to particular chromosomes is at the moment impossible to say; the methods of analysis at our disposal are limited. So it is important to make the most of them and compare abnormal chromosomes by their measurements as well as by their superficial morphology. Department of Clinical Research, The Royal Marsden Hospital and The Institute of Cancer Research, Fulham Road, London S.W.3.
SIR,-In 1965 we stated that a thorough comparison between primary and secondary brain tumours had never been made, and we stressed the need for such a study. Dr. Barnett and Dr. Millac 16 have attempted to establish valid criteria for this differential diagnosis. Unfortunately, their series of secondary tumours was fairly small, containing only 27 patients with metastatic brain tumours. In our series 17 of 104 patients with metastatic lesions of the brain, 48 had choked discs on admission, and 28 patients had had epileptic seizures, mostly focal. Therefore we cannot support the idea that a history of fits and papillaedema favours the diagnosis of a primary brain tumour. It is doubtful whether this differentiation could be made on purely neurological signs, without complementary investigations such as chest radiograph
erythrocyte-sedimentation
glioma
two years we at necropsy.
have
seen at
least 3
cases
of multilocular
J. H. M. University Hospital of Groningen, The Netherlands.
VAN
ECK
K. G. Go E. J. EBELS.
DELAYED HYPERSENSITIVITY IN TOXIC AGRANULOCYTOSIS a 43-year-old woman patient, blood-group I (0) negative, with aminopyrine (’Pyramidon’) agranulocytosis, we have observed in the acute stage a significant decrease of delayed hypersensitivity, together with active antibody-synthesis as shown by high antistreptolysin 0 titres and hypergammaglobulinasmia (X); ultracentrifugation of
SIR,-In
Rh
serum showed an increase of 7S and 19S components. On the other hand, the Mantoux test, done on the 5th day of the illness, was negative, though the patient had 5 years before spent a long period in hospital for lung tuberculosis; the test became strongly positive 20 days later, when haematological and clinical remission, which had begun on the 7th day, was complete. Skin-graft from Mantoux-negative group-II (A) Rh-positive male donor, carried out on the 8th day, remained intact for 15 days on the criteria indicated by Rapaport et al.,’ although in our experience and that of others rejection usually occurs within 6-8 days. In the acute stage there were less than 400 white blood-cells per c.mm. (large lymphocytes 80%, small lymphocytes 20%). Prednisone, 50 mg. daily, was given from the 3rd day, and in a dose of 25 mg. daily from the 5th day until the 9th day, but this drug does not seem to have caused the described results, for administration was begun only 2 days before the finding of the negative tuberculin reaction, and the total dosage was not sufficient to have influenced graft survival. The negative tuberculin skin test could be ascribable to concomitant decrease of lymphocytes (300-400 per c.mm.), most of which were large lymphocytes; nevertheless prolonged survival of the skin-graft, when the hxmatological conditions returned to normal, suggests that either delayed hypersensitivity was not, for some reason, restored immediately, or that it was provoked by other factors. LUIGI BUSCARINI Medical Department, MARIO REGOLISTI Hospital of Fiorenzuola D’Arda, EDMONDO DAMONI. Italy.
MARY MARTINEAU.
PRIMARY AND METASTATIC BRAIN TUMOURS
and
the past
rate.
We feel that demonstration of multiple lesions by angiography, air studies, or (as in our series) isotope studies, does not warrant a definite diagnosis of metastatic tumour, for in 13. Weichsel, M. E., Luzzatti, L. J. Pediat. 1965, 67, 324. 14. Martineau, M. Lancet, 1966, i, 839. 15. Lejeune, J., Berger, R. C.r. Acad. Sci., Paris, 1966, 262, 1885. 16. Barnett, A., Millac, P. Lancet, 1966, ii, 1344. 17. Van Eck, J. H. M., Go, K. G., Ebels, E. J. Folia psychiat. neurol. neurochir. neerl. 1965, 68, 443.
ASPIRIN AND PLATELET STICKINESS SiR,—The finding that a fairly small dose of acetylsalicylic acid prolongs the Duke bleeding-time in some normal individuals and often strikingly in patients with the Minot/von Willebrand syndrome has introduced a new facet into hsemostasis which will undoubtedly elicit various explanations. Dr. Morris (Feb. 4, p. 279) suggests that the action of acetylsalicylic acid is related to platelet function or to a platelet-aggregating factor causing decreasing platelet stickiness. Such an explanation is not in accord with the observation of Cronberg et al. who found that in von Willebrand’s disease there appeared to be " no defect in platelet adhesiveness to glass or any abnormal reaction to A.D.P. or collagen ". Since the bleeding-time is normal in patients with severe coagulation defects and is sometimes drastically prolonged when no coagulation or platelet abnormality is demonstrable, a factor independent of both coagulation and platelets is suggested as a determinant of a normal bleeding-time. The observation that sodium salicylate does not prolong the Duke bleeding-time is a clue which implicates the acetyl linkage. My explanation3 is that in normal subjects the Duke bleedingtime measures the haemostatic response to a standardised Rapaport, F. T., Lawrence, H. S., Thomas, L., Converse, J. M., Tillet, W. S., Mulholland, H. H. J. clin. Invest. 1962, 41, 2166. 2. Cronberg, S., Nilsson, I. M., Silwer, J. Acta med. scand. 1966, 180, 43. 3. Quick, A. J. Am. J. clin. Path. (in the press). 1.
CHROMOSOMES IN TESTICULAR TUMOURS SIR,-In their letter (Jan. 28, p. 216) Dr. Fischer and Dr. Golob describe the chromosomes in a case of seminoma and discuss a remarkable similarity between the marker chromosomes in it and in the case I have described.14 I have now examined 9 cases in all of tumour histologically classified as seminoma. 8 of the 9 show marker chromosomes longer than any chromosome of the normal complement: most of these are dicentric or have a secondary constriction. 4 cases contain an acrocentric longer than normal D-group chromosomes. The case of Dr. Fischer and Dr. Golob indeed confirms that these types of marker chromosomes often occur in seminomas. I am now, however, calculating the relative length and centromeric index of these abnormal chromosomes by the method of Lejeune and Berger,15 and I find that these values are not identical for the markers of different tumours. What is evident is that there seems to be an end-to-end attraction or association between chromosomes in this sort of tumour. Whether such associations are confined to particular chromosomes is at the moment impossible to say; the methods of analysis at our disposal are limited. So it is important to make the most of them and compare abnormal chromosomes by their measurements as well as by their superficial morphology. Department of Clinical Research, The Royal Marsden Hospital and The Institute of Cancer Research, Fulham Road, London S.W.3.
SIR,-In 1965 we stated that a thorough comparison between primary and secondary brain tumours had never been made, and we stressed the need for such a study. Dr. Barnett and Dr. Millac 16 have attempted to establish valid criteria for this differential diagnosis. Unfortunately, their series of secondary tumours was fairly small, containing only 27 patients with metastatic brain tumours. In our series 17 of 104 patients with metastatic lesions of the brain, 48 had choked discs on admission, and 28 patients had had epileptic seizures, mostly focal. Therefore we cannot support the idea that a history of fits and papillaedema favours the diagnosis of a primary brain tumour. It is doubtful whether this differentiation could be made on purely neurological signs, without complementary investigations such as chest radiograph
erythrocyte-sedimentation
glioma
two years we at necropsy.
have
seen at
least 3
cases
of multilocular
J. H. M. University Hospital of Groningen, The Netherlands.
VAN
ECK
K. G. Go E. J. EBELS.
DELAYED HYPERSENSITIVITY IN TOXIC AGRANULOCYTOSIS a 43-year-old woman patient, blood-group I (0) negative, with aminopyrine (’Pyramidon’) agranulocytosis, we have observed in the acute stage a significant decrease of delayed hypersensitivity, together with active antibody-synthesis as shown by high antistreptolysin 0 titres and hypergammaglobulinasmia (X); ultracentrifugation of
SIR,-In
Rh
serum showed an increase of 7S and 19S components. On the other hand, the Mantoux test, done on the 5th day of the illness, was negative, though the patient had 5 years before spent a long period in hospital for lung tuberculosis; the test became strongly positive 20 days later, when haematological and clinical remission, which had begun on the 7th day, was complete. Skin-graft from Mantoux-negative group-II (A) Rh-positive male donor, carried out on the 8th day, remained intact for 15 days on the criteria indicated by Rapaport et al.,’ although in our experience and that of others rejection usually occurs within 6-8 days. In the acute stage there were less than 400 white blood-cells per c.mm. (large lymphocytes 80%, small lymphocytes 20%). Prednisone, 50 mg. daily, was given from the 3rd day, and in a dose of 25 mg. daily from the 5th day until the 9th day, but this drug does not seem to have caused the described results, for administration was begun only 2 days before the finding of the negative tuberculin reaction, and the total dosage was not sufficient to have influenced graft survival. The negative tuberculin skin test could be ascribable to concomitant decrease of lymphocytes (300-400 per c.mm.), most of which were large lymphocytes; nevertheless prolonged survival of the skin-graft, when the hxmatological conditions returned to normal, suggests that either delayed hypersensitivity was not, for some reason, restored immediately, or that it was provoked by other factors. LUIGI BUSCARINI Medical Department, MARIO REGOLISTI Hospital of Fiorenzuola D’Arda, EDMONDO DAMONI. Italy.
MARY MARTINEAU.
PRIMARY AND METASTATIC BRAIN TUMOURS
and
the past
rate.
We feel that demonstration of multiple lesions by angiography, air studies, or (as in our series) isotope studies, does not warrant a definite diagnosis of metastatic tumour, for in 13. Weichsel, M. E., Luzzatti, L. J. Pediat. 1965, 67, 324. 14. Martineau, M. Lancet, 1966, i, 839. 15. Lejeune, J., Berger, R. C.r. Acad. Sci., Paris, 1966, 262, 1885. 16. Barnett, A., Millac, P. Lancet, 1966, ii, 1344. 17. Van Eck, J. H. M., Go, K. G., Ebels, E. J. Folia psychiat. neurol. neurochir. neerl. 1965, 68, 443.
ASPIRIN AND PLATELET STICKINESS SiR,—The finding that a fairly small dose of acetylsalicylic acid prolongs the Duke bleeding-time in some normal individuals and often strikingly in patients with the Minot/von Willebrand syndrome has introduced a new facet into hsemostasis which will undoubtedly elicit various explanations. Dr. Morris (Feb. 4, p. 279) suggests that the action of acetylsalicylic acid is related to platelet function or to a platelet-aggregating factor causing decreasing platelet stickiness. Such an explanation is not in accord with the observation of Cronberg et al. who found that in von Willebrand’s disease there appeared to be " no defect in platelet adhesiveness to glass or any abnormal reaction to A.D.P. or collagen ". Since the bleeding-time is normal in patients with severe coagulation defects and is sometimes drastically prolonged when no coagulation or platelet abnormality is demonstrable, a factor independent of both coagulation and platelets is suggested as a determinant of a normal bleeding-time. The observation that sodium salicylate does not prolong the Duke bleeding-time is a clue which implicates the acetyl linkage. My explanation3 is that in normal subjects the Duke bleedingtime measures the haemostatic response to a standardised Rapaport, F. T., Lawrence, H. S., Thomas, L., Converse, J. M., Tillet, W. S., Mulholland, H. H. J. clin. Invest. 1962, 41, 2166. 2. Cronberg, S., Nilsson, I. M., Silwer, J. Acta med. scand. 1966, 180, 43. 3. Quick, A. J. Am. J. clin. Path. (in the press). 1.