880 various circulatory diseases fails to support the hypothesis that smoking causes these diseases. If these various findings and arguments are valid we have .to conclude that the risk of death from various circulatory diseases is raised by the use of oral contraceptives-at least among those women who are genetically predisposed to such disorders-but that smoking does not increase the risk. cause
General Infirmary, Leeds LS1 3EX
P. R.
J. BURCH
COMMON CLONAL ORIGIN OF LYMPHOPLASMACYTIC PROLIFERATION AND IMMUNOBLASTIC LYMPHOMA IN INTESTINAL &agr;-CHAIN DISEASE
SIR,-The development of immunoblastic lymphoma in the intestinal form of a-chain disease (a-C.D.) has been morphologically confirmed.’-6 There is also evidence for a common clonal origin for the lymphoplasmacytic proliferation and immunoblastic lymphoma associated with it in two cases of a-C.D.7.8 We have searched for intracellular immunoglobulin in tissue sections from both the benign-appearing lymphoplasmacytic lesions and the immunoblastic lymphomas in three cases with &agr;—C.D., using the peroxidase/antiperoxidase reaction,9,10 as follows : (1) Sections deparaffinised and hydrated with water. (2) Endogenous peroxidase activity blocked with fresh 3% solution of hydrogen peroxide in "tris"-saline buffer for 30 min. (3) Non-specific background staining reduced with normal nonimmune non-conjugated goat serum diluted 1/10 for 10 min. Excess serum removed but not washed off before next stage. (4) Sections treated with monospecific rabbit antisera for 30 min in the following dilutions: 1/40 for anti a, y, and µ, and 1/100 for anti x and &lgr;. All antisera were obtained from Dakopatts A/S Denmark, 1.
Rambaud, J. C., Bognel, C., Prost, A., Bernier, J. J., LeQuintrec, Y., Lambling, A., Danon, F., Hurez, D., Seligmann, M. Digestion, 1968, 1, 321. 2. Rappaport, H., Ramot, B., Hulu, N., Park, J. K. Cancer, 1972, 29, 1502. 3. Rappaport, H. in Maligne Lymphome und Monoklonale Gammophathien (edited by H. Löffler); p. 377. Munich, 1976. 4. Tabbane, S., Tabbane, F., Cammoun, M., Mourall, N. Cancer, 1976, 38, 1989. 5.
Galian, A., Lecestre, M.-J., Scotto, J., Bognel, C., Matuchansky, C., Rambaud, J.-C. ibid. 1977, 39, 2081. 6. Rappaport, H., Pangalis, G. A., Nathwani, B. N. Cold Spring Harbor Symp.
(in the press). 7. Brouet, J. C., Mason, D. Y., Danon, F.,
Preud’homme, J. L., Seligmann, M., Reyes, F., Navab, F., Galian, A., Rene, E., Rambaud, J. C. Lancet, 1977, i, 861. 8. Ramot, B., Levanon, M., Hahn, Y., Lahat, N., Moroz, C. Clin. exp. Immun. 1977, 27, 440. 9. Sternberger, L. A., Hardy, P. H., Jr., Cuculis, J. J., Meyer, H. G. J. Histochem. Cytochem. 1970, 18, 315. 10. Taylor, C. R. Eur. J. Cancer, 1976, 12, 61.
Fig. 2-Immunoblastic lymphoma
in x-C.D.:
immunoperoai-
dase stain.
Many tumour cells positive for a-chains (x 270).
through the Accurate Chemical and Scientific Corporation, Hicksville, N.Y.
(5) Unlabelled
swine anti-rabbit
serum
protein diluted 1/20 for 30
min.
(6) Rabbit peroxidase/antiperoxidase complex diluted 1/100 for 30 min.
(7) Diaminobenzidine reaction
4 min. Wash in tris-saline for 30
min.
(8) Sections counterstained with hæmatoxylin (4 min), eosin (1 s), dehydrated, cleared in xylol and mounted in synthetic medium. The reactions were done in 50 mmol/1 "tris" buffer (pH 7.6) diluted 1/10 with saline. "Tris"-saline was also used for diluting the sera and the washings for 30 min after stages 2, 4, 5, and 6. In all cases a high percentage of plasma cells and plasmacytoid lymphocytes of the morphologically benign-appearing cellular proliferation were specifically and strongly positive for a-chains (fig. 1), while adjacent sections were entirely negative for &ggr;, µ, x and X chains. A similar positivity for a-chains was observed in the neoplastic cells of the immunoblastic lymphomas (fig. 2), while antisera to Y, µ, x and a chains in adjacent sections gave negative results. Our findings further support the concept of the common clonal origin of the lymphoplasmacytic proliferation and the immunoblastic lymphoma in intestinal cx-C.D. In addition, the technique described could be an excellent diagnostic tool for the recognition of a-c.D. in biopsy material, particularly since the identification of the abnormal a chain in serum is sometimes difficult. Department of Anatomic Pathology, City of Hope National Medical Center, Duarte, California 91010, U.S.A.
G. A. PANGALIS H. RAPPAPORT
TRISOMY CLUSTER IN NEW YORK
SIR,—Dr
Warburton and her colleagues (July 23, p. 201) for the cluster of trisomic karyotypes in conceptions that had taken place in the winter of 1976 in New York. Perhaps examination of this finding was restricted totime and place-rather than-widened to the universal phenomenon of seasonality of birth (or of conception) of patients with chromosomal aberrations, congenital malformations, or psychopathology. The months of last menstrual period (L.M.P.) associated with a high rate of trisomy conceptions were also those with a high rate of conceptions leading to spontaneous abortion (i.e., without chromosomal aberrations). In the summer of 1966 an apparent surge in the birth-rate of New York was linked by the lay Press throughout the world with the electricity blackout nine months before. However, Udryl demonstrated that there was no significant difference could find
Fig. 1—&agr;-C.D.: immunoperoxidase stain. Many cells positive for x-chains (arrows) (x270).
1.
no cause
Udry, J. R. Demography, 1970, 7, 325.
881 between the pattern of 1966 and that of the preceding years. Indeed in the U.S.A. conceptions tend to be concentrated in the months from October to January.2 These were the months in which there was clustering of conceptions with trisomic
karyotypes. A seasonal fluctuation in ovulation-rate, at least in women with a temporarily or a chronically unstable hypothalamic/ pituitary/ovarian axis, has been claimed to be responsible for seasonality of conception-rate. 1,4 The apparently simultaneous clustering of disproportionate rates of pathological conceptions with or without chromosomal aberrations4. suggests to us that at the time of the breakthrough from anovulation to ovulation and vice versa, fertilisation of overripe eggs may occur, leading to non-disjunction or otherwise abnormal conceptions. Huize Mana Roepaan, Centre for Observation and Treatment of Mental Retardates, Ottersum (L.), Netherlands
P. H.
Department of Human Genetics, Free University, Amsterdam,
J. H. J. VAN ERKELENS-ZWETS
JONGBLOET
LYMPHOCYTIC LYMPHOMA AFTER IDIOPATHIC HYPERSPLENISM
SIR,-An enlarged spleen is generally secondary to some other condition, but in a few patients no underlying disease is found and in these cases splenectomy usually corrects abnormalities in the blood-count. We have seen a patient who had a lymphocytic lymphoma associated with an immune haemolyticanaemia 6 years after "idiopathic" hyerpsplenism. This 50-year-old woman presented in 1970 with a spleen extending 9 cm below the left ribs. There was no lymphadenopathy and no sign of portal hypertension. The liver was just palpable. She has never been abroad. She had pancytopenia (hemoglobin 12.0g/dl, white blood-cells 2.4x109/1, platelets 55x10/1). The bone-marrow was hyperplastic without evidence of infiltration with malignant cells. Immunoelectrophoresis of serum was normal. No cause for the splenic enlargement was found and the spleen was removed, with liver and retroperitoneal lymph-node biopsy. The liver, spleen, and lymphnodes showed features of reactive hyperplasia only. 4 weeks later the haemoglobin was 14.2g/dl, white blood-cells 10 x 109/1 (69% polymorphs), and platelets 206 x 109/1. Since 1971 she had been on methyldopa for mild essential hypertension. The daily dose was increased in July, 1976, to 1.5 g, when she complained of headaches and fatigue. In December, 1976, she was admitted to hospital with progressive decrease in exercise tolerance, weakness, fatigue, and ankle swelling. She was pale and icteric. Blood-pressure 110/70 mm Hg. Liver palpable 2 cm below the ribs. There were no other abnormal physical signs. Haemoglobin 7-1g/dl, with 11% reticulocytes, white cells 17-2x 109/1 (76% polymorphs), and platelets 440x10/1. Direct Coombs test positive (1/256), due to the binding to red cells of complement only. A non-specific red-cell agglutinin active in saline at room temperature and at 37°C was detected in the serum. Further investigations failed to reveal a cause for the haemolysis. Treatment with methyldopa was discontinued and she was given prednisolone 60 mg/day, but this did not control the haemolytic process. Mean red-cell lifespan was 18 days. Serum-immunoglobulins were below normal. Bipedal lymphangiography demonstrated para-aortic 2 Vital and Health Statistics: Seasonal Variation of Births, United States, 1933-1963, series 21, no. 9. National Center for Health Statistics, Washington, 1966. 3 Jongbloet, P. H. Mental and Physical Handicaps in Connection with Overripeness Ovopathy. Leiden, 1971. 4 Jongbloet, P. H. in Aging Gametes (edited by H. E. Stenfert and N. V. Kroese); p. 300. Basle, 1975. 5. Jongbloet, P. H., van Erkelens-Zwets, J. H. J., Holleman-van der Woude, REAP (Int, J. Res. Exch. Pract. ment. Retard.), 1976, 2, 243.
lymph-node enlargement. Liver scan showed even uptake throughout. At laparotomy grossly enlarged para-aortic lymph-nodes were found, and biopsy revealed diffuse replacement by a poorly differentiated lymphocytic lymphoma. Haemolysis persisted and was difficult to control despite treatment of the lymphoma with chemotherapy. Two of the ten patients with primary hypersplenism described by Dacie et al.I subsequently had lymphoma. Our patient resembles one of theirs both in the interval between presentation and development of lymphoma (6 years and 4 i years, respectively) and in the fact that the autoimmune hsemolytic ansemia was a’ major feature of both patients. Autoimmune haemolysis in our patient was at first thought to be related to treatment with methyldopa, but continuation of haemolysis several months after withdrawal of the drug and particularly the serological finding of a "complement only" pattern would essentially rule this out.2 We cannot say whether non-tropical idiopathic hypersplenism is a pre-lymphoma or merely an abnormal immune response to endogenous or exogenous stimuli, as suggested by Dacie et al. Long and Aisenberg3 suggested that idiopathic splenomegaly is a benign inflammatory lesion; none of their ten patients had had lymphoma after 1-8 years of follow-up. Skarin et al.4 described eleven patients with primary lymphosarcoma, eight of whom had hypersplenism, but our patient does not resemble those in Skarin’s series either histologically or clinically. Further study is required to elucidate criteria for predicting which patients with idiopathic splenomegaly are likely to develop lymphoma subsequently. Department of Haematology, University Hospital of Wales
S. A. D. AL-ISMAIL D. P. BENTLEY J. A. WHITTAKER
and Welsh National School of Medicine, Cardiff CF4 4XW
ROLE OF ANTIBIOTICS IN INFLAMMATORY DISC LESIONS IN CHILDREN
SIR,-None would question the use of antibiotics where a bacterial aetiology is clear or the clinical and laboratory evidence is strongly suggestive-e.g., early haematogenous osteomyelitis in children. Where such evidence is lacking, the routine use of antibiotics, some of which may have harmful side-effects, should be challenged. Inflammation of the intervertebral discs in young children ("discitis") falls into this category: it is an important, but uncommon, condition which runs a benign, self-limiting course and frequently poses diagnostic difficulties. We have reviewed thirty-five cases of inflammatory disc lesions treated at the Royal Alexandra Hospital for Children over the years 1960-75. The average age at onset was 2 years and 11 months for the twenty girls and fifteen boys in the series. The variable mode of presentation is well-recognised, and most of the children were admitted to wards other than orthopaedic. A battery of investigations was done in the search for an infectious aetiology, and, as in previous reports, positive results were notably absent. The one common positive finding was a raised erythrocyte-sedimentation rate (E.S.R.) which averaged 48 mm in the 1st hour (Westergren) with a range of 25-80. Seventeen children had mild leucocytosis. Management differed considerably according to the specialty under which the children were admitted. Immobilisation was either by bed rest or abduction frame. Antibiotics (many and various) did not accelerate the disappearance of symptoms and signs or the return of the E.s.R. to normal (see table). The same held true when the data for bed rest and frame immobilisation were compared, irrespective of whether or not antibiotics had been given. -
1. 2. 3. 4. 5.
Dacie, J. V., and others. Br. J. Hœmat. 1969, 17, 317. Brown, E. B. Progr. Hœmat. 1973, 3, 45. Long, J. C., Aisenberg, A. C. Cancer, 1973, 33, 1054. Skarin, A. T. Archs intern. Med. 1971, 127, 259. Menelaus, M. J. Bone Jt Surg. 1964, 46B, 16.
General Infirmary, Leeds LS1 3EX
P. R.
J. BURCH
COMMON CLONAL ORIGIN OF LYMPHOPLASMACYTIC PROLIFERATION AND IMMUNOBLASTIC LYMPHOMA IN INTESTINAL &agr;-CHAIN DISEASE
SIR,-The development of immunoblastic lymphoma in the intestinal form of a-chain disease (a-C.D.) has been morphologically confirmed.’-6 There is also evidence for a common clonal origin for the lymphoplasmacytic proliferation and immunoblastic lymphoma associated with it in two cases of a-C.D.7.8 We have searched for intracellular immunoglobulin in tissue sections from both the benign-appearing lymphoplasmacytic lesions and the immunoblastic lymphomas in three cases with &agr;—C.D., using the peroxidase/antiperoxidase reaction,9,10 as follows : (1) Sections deparaffinised and hydrated with water. (2) Endogenous peroxidase activity blocked with fresh 3% solution of hydrogen peroxide in "tris"-saline buffer for 30 min. (3) Non-specific background staining reduced with normal nonimmune non-conjugated goat serum diluted 1/10 for 10 min. Excess serum removed but not washed off before next stage. (4) Sections treated with monospecific rabbit antisera for 30 min in the following dilutions: 1/40 for anti a, y, and µ, and 1/100 for anti x and &lgr;. All antisera were obtained from Dakopatts A/S Denmark, 1.
Rambaud, J. C., Bognel, C., Prost, A., Bernier, J. J., LeQuintrec, Y., Lambling, A., Danon, F., Hurez, D., Seligmann, M. Digestion, 1968, 1, 321. 2. Rappaport, H., Ramot, B., Hulu, N., Park, J. K. Cancer, 1972, 29, 1502. 3. Rappaport, H. in Maligne Lymphome und Monoklonale Gammophathien (edited by H. Löffler); p. 377. Munich, 1976. 4. Tabbane, S., Tabbane, F., Cammoun, M., Mourall, N. Cancer, 1976, 38, 1989. 5.
Galian, A., Lecestre, M.-J., Scotto, J., Bognel, C., Matuchansky, C., Rambaud, J.-C. ibid. 1977, 39, 2081. 6. Rappaport, H., Pangalis, G. A., Nathwani, B. N. Cold Spring Harbor Symp.
(in the press). 7. Brouet, J. C., Mason, D. Y., Danon, F.,
Preud’homme, J. L., Seligmann, M., Reyes, F., Navab, F., Galian, A., Rene, E., Rambaud, J. C. Lancet, 1977, i, 861. 8. Ramot, B., Levanon, M., Hahn, Y., Lahat, N., Moroz, C. Clin. exp. Immun. 1977, 27, 440. 9. Sternberger, L. A., Hardy, P. H., Jr., Cuculis, J. J., Meyer, H. G. J. Histochem. Cytochem. 1970, 18, 315. 10. Taylor, C. R. Eur. J. Cancer, 1976, 12, 61.
Fig. 2-Immunoblastic lymphoma
in x-C.D.:
immunoperoai-
dase stain.
Many tumour cells positive for a-chains (x 270).
through the Accurate Chemical and Scientific Corporation, Hicksville, N.Y.
(5) Unlabelled
swine anti-rabbit
serum
protein diluted 1/20 for 30
min.
(6) Rabbit peroxidase/antiperoxidase complex diluted 1/100 for 30 min.
(7) Diaminobenzidine reaction
4 min. Wash in tris-saline for 30
min.
(8) Sections counterstained with hæmatoxylin (4 min), eosin (1 s), dehydrated, cleared in xylol and mounted in synthetic medium. The reactions were done in 50 mmol/1 "tris" buffer (pH 7.6) diluted 1/10 with saline. "Tris"-saline was also used for diluting the sera and the washings for 30 min after stages 2, 4, 5, and 6. In all cases a high percentage of plasma cells and plasmacytoid lymphocytes of the morphologically benign-appearing cellular proliferation were specifically and strongly positive for a-chains (fig. 1), while adjacent sections were entirely negative for &ggr;, µ, x and X chains. A similar positivity for a-chains was observed in the neoplastic cells of the immunoblastic lymphomas (fig. 2), while antisera to Y, µ, x and a chains in adjacent sections gave negative results. Our findings further support the concept of the common clonal origin of the lymphoplasmacytic proliferation and the immunoblastic lymphoma in intestinal cx-C.D. In addition, the technique described could be an excellent diagnostic tool for the recognition of a-c.D. in biopsy material, particularly since the identification of the abnormal a chain in serum is sometimes difficult. Department of Anatomic Pathology, City of Hope National Medical Center, Duarte, California 91010, U.S.A.
G. A. PANGALIS H. RAPPAPORT
TRISOMY CLUSTER IN NEW YORK
SIR,—Dr
Warburton and her colleagues (July 23, p. 201) for the cluster of trisomic karyotypes in conceptions that had taken place in the winter of 1976 in New York. Perhaps examination of this finding was restricted totime and place-rather than-widened to the universal phenomenon of seasonality of birth (or of conception) of patients with chromosomal aberrations, congenital malformations, or psychopathology. The months of last menstrual period (L.M.P.) associated with a high rate of trisomy conceptions were also those with a high rate of conceptions leading to spontaneous abortion (i.e., without chromosomal aberrations). In the summer of 1966 an apparent surge in the birth-rate of New York was linked by the lay Press throughout the world with the electricity blackout nine months before. However, Udryl demonstrated that there was no significant difference could find
Fig. 1—&agr;-C.D.: immunoperoxidase stain. Many cells positive for x-chains (arrows) (x270).
1.
no cause
Udry, J. R. Demography, 1970, 7, 325.
881 between the pattern of 1966 and that of the preceding years. Indeed in the U.S.A. conceptions tend to be concentrated in the months from October to January.2 These were the months in which there was clustering of conceptions with trisomic
karyotypes. A seasonal fluctuation in ovulation-rate, at least in women with a temporarily or a chronically unstable hypothalamic/ pituitary/ovarian axis, has been claimed to be responsible for seasonality of conception-rate. 1,4 The apparently simultaneous clustering of disproportionate rates of pathological conceptions with or without chromosomal aberrations4. suggests to us that at the time of the breakthrough from anovulation to ovulation and vice versa, fertilisation of overripe eggs may occur, leading to non-disjunction or otherwise abnormal conceptions. Huize Mana Roepaan, Centre for Observation and Treatment of Mental Retardates, Ottersum (L.), Netherlands
P. H.
Department of Human Genetics, Free University, Amsterdam,
J. H. J. VAN ERKELENS-ZWETS
JONGBLOET
LYMPHOCYTIC LYMPHOMA AFTER IDIOPATHIC HYPERSPLENISM
SIR,-An enlarged spleen is generally secondary to some other condition, but in a few patients no underlying disease is found and in these cases splenectomy usually corrects abnormalities in the blood-count. We have seen a patient who had a lymphocytic lymphoma associated with an immune haemolyticanaemia 6 years after "idiopathic" hyerpsplenism. This 50-year-old woman presented in 1970 with a spleen extending 9 cm below the left ribs. There was no lymphadenopathy and no sign of portal hypertension. The liver was just palpable. She has never been abroad. She had pancytopenia (hemoglobin 12.0g/dl, white blood-cells 2.4x109/1, platelets 55x10/1). The bone-marrow was hyperplastic without evidence of infiltration with malignant cells. Immunoelectrophoresis of serum was normal. No cause for the splenic enlargement was found and the spleen was removed, with liver and retroperitoneal lymph-node biopsy. The liver, spleen, and lymphnodes showed features of reactive hyperplasia only. 4 weeks later the haemoglobin was 14.2g/dl, white blood-cells 10 x 109/1 (69% polymorphs), and platelets 206 x 109/1. Since 1971 she had been on methyldopa for mild essential hypertension. The daily dose was increased in July, 1976, to 1.5 g, when she complained of headaches and fatigue. In December, 1976, she was admitted to hospital with progressive decrease in exercise tolerance, weakness, fatigue, and ankle swelling. She was pale and icteric. Blood-pressure 110/70 mm Hg. Liver palpable 2 cm below the ribs. There were no other abnormal physical signs. Haemoglobin 7-1g/dl, with 11% reticulocytes, white cells 17-2x 109/1 (76% polymorphs), and platelets 440x10/1. Direct Coombs test positive (1/256), due to the binding to red cells of complement only. A non-specific red-cell agglutinin active in saline at room temperature and at 37°C was detected in the serum. Further investigations failed to reveal a cause for the haemolysis. Treatment with methyldopa was discontinued and she was given prednisolone 60 mg/day, but this did not control the haemolytic process. Mean red-cell lifespan was 18 days. Serum-immunoglobulins were below normal. Bipedal lymphangiography demonstrated para-aortic 2 Vital and Health Statistics: Seasonal Variation of Births, United States, 1933-1963, series 21, no. 9. National Center for Health Statistics, Washington, 1966. 3 Jongbloet, P. H. Mental and Physical Handicaps in Connection with Overripeness Ovopathy. Leiden, 1971. 4 Jongbloet, P. H. in Aging Gametes (edited by H. E. Stenfert and N. V. Kroese); p. 300. Basle, 1975. 5. Jongbloet, P. H., van Erkelens-Zwets, J. H. J., Holleman-van der Woude, REAP (Int, J. Res. Exch. Pract. ment. Retard.), 1976, 2, 243.
lymph-node enlargement. Liver scan showed even uptake throughout. At laparotomy grossly enlarged para-aortic lymph-nodes were found, and biopsy revealed diffuse replacement by a poorly differentiated lymphocytic lymphoma. Haemolysis persisted and was difficult to control despite treatment of the lymphoma with chemotherapy. Two of the ten patients with primary hypersplenism described by Dacie et al.I subsequently had lymphoma. Our patient resembles one of theirs both in the interval between presentation and development of lymphoma (6 years and 4 i years, respectively) and in the fact that the autoimmune hsemolytic ansemia was a’ major feature of both patients. Autoimmune haemolysis in our patient was at first thought to be related to treatment with methyldopa, but continuation of haemolysis several months after withdrawal of the drug and particularly the serological finding of a "complement only" pattern would essentially rule this out.2 We cannot say whether non-tropical idiopathic hypersplenism is a pre-lymphoma or merely an abnormal immune response to endogenous or exogenous stimuli, as suggested by Dacie et al. Long and Aisenberg3 suggested that idiopathic splenomegaly is a benign inflammatory lesion; none of their ten patients had had lymphoma after 1-8 years of follow-up. Skarin et al.4 described eleven patients with primary lymphosarcoma, eight of whom had hypersplenism, but our patient does not resemble those in Skarin’s series either histologically or clinically. Further study is required to elucidate criteria for predicting which patients with idiopathic splenomegaly are likely to develop lymphoma subsequently. Department of Haematology, University Hospital of Wales
S. A. D. AL-ISMAIL D. P. BENTLEY J. A. WHITTAKER
and Welsh National School of Medicine, Cardiff CF4 4XW
ROLE OF ANTIBIOTICS IN INFLAMMATORY DISC LESIONS IN CHILDREN
SIR,-None would question the use of antibiotics where a bacterial aetiology is clear or the clinical and laboratory evidence is strongly suggestive-e.g., early haematogenous osteomyelitis in children. Where such evidence is lacking, the routine use of antibiotics, some of which may have harmful side-effects, should be challenged. Inflammation of the intervertebral discs in young children ("discitis") falls into this category: it is an important, but uncommon, condition which runs a benign, self-limiting course and frequently poses diagnostic difficulties. We have reviewed thirty-five cases of inflammatory disc lesions treated at the Royal Alexandra Hospital for Children over the years 1960-75. The average age at onset was 2 years and 11 months for the twenty girls and fifteen boys in the series. The variable mode of presentation is well-recognised, and most of the children were admitted to wards other than orthopaedic. A battery of investigations was done in the search for an infectious aetiology, and, as in previous reports, positive results were notably absent. The one common positive finding was a raised erythrocyte-sedimentation rate (E.S.R.) which averaged 48 mm in the 1st hour (Westergren) with a range of 25-80. Seventeen children had mild leucocytosis. Management differed considerably according to the specialty under which the children were admitted. Immobilisation was either by bed rest or abduction frame. Antibiotics (many and various) did not accelerate the disappearance of symptoms and signs or the return of the E.s.R. to normal (see table). The same held true when the data for bed rest and frame immobilisation were compared, irrespective of whether or not antibiotics had been given. -
1. 2. 3. 4. 5.
Dacie, J. V., and others. Br. J. Hœmat. 1969, 17, 317. Brown, E. B. Progr. Hœmat. 1973, 3, 45. Long, J. C., Aisenberg, A. C. Cancer, 1973, 33, 1054. Skarin, A. T. Archs intern. Med. 1971, 127, 259. Menelaus, M. J. Bone Jt Surg. 1964, 46B, 16.
