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CONGENITAL DISLOCATION OF THE HIP IN BRITTANY
863 units per litre before
treatment to
45-97-2 units per litre
during treatment (p < 0001). We examined the possibility that an abnormally high alkaline phosphatase level could be masked by clofibrate treatment. Three patients with liver disease and constantly elevated serum-alkaline-phosphatase levels were treated with 2 g. clofibrate daily. Alkaline phosphatase decreased from 217, 155, and 134 before to 83, 60, and 57 units per litre, respectively, after 4 weeks of treatment. The mechanism of this reduction is unknown. The addition of serum, obtained from clofibrate-treated patients, to several serum samples, resulted in alkaline phosphatase levels in the mixtures, that closely agreed with the expected values. Therefore, it seems unlikely that clofibrate interferes with the determination of alkaline phosphatase. R. W. B. SCHADE P. N. M. DEMACKER A. VAN ’T LAAR.
Department of Internal Medicine, University of Nijmegen, The Netherlands.
GONADOBLASTOMA IN DYSGENETIC GONADS WITH A Y CHROMOSOME
SIR,-Gonadoblastoma is known to arise in dysgenetic gonads, but, in a review of published reports, Schellhas concluded that a Y chromosome is a prerequisite for gonadal malignancy in gonadal dysgenesis. We feel that the accompanying figure effectively summarises the intricacies of these relations. With rare exceptions, phenotypic males have a Y chromosome, and females do not. Straddling these compartments are circles representing individuals with ambiguous sex characteristics and maldeveloped gonads, including a subgroup with the classic Turner phenotype of short stature, primary amenorrhcea, &c. 60% of all patients with gonadal dysgenesis have the karyotype, 45,X, and are not, as a rule, at risk of gonadal malignancy. Rather, the risk seems confined to patients with a Y chromosome, if not in all cells, at least in some gonadal cells. The probability of malignancy is great, around 25%.
Venn diagram of relation among gonadoblastoma, gonadal dysgenesis, and sex-chromosomal constitution.
For those
treating patients with gonadal dysgenesis, this
information indicates the need
to
search for
a
Y chromo-
cell-line, because of its implications as regards gonadal malignancy. For researchers, the challenge is to understand the pathogenesis. JOHN J. MULVIHILL Epidemiology Branch,
some
National Cancer Institute, Bethesda, Maryland 20014, U.S.A. 1.
Schellhas,
H. F. Obstet.
WANDA M. WADE ROBERT W. MILLER.
Gynec. 1974, 44, 298, 455.
CONGENITAL DISLOCATION OF THE HIP IN BRITTANY
SIR,—Despite a decrease since 1912, the incidence of congenital dislocation of the hip is still high in some rural communities in Brittany.l,2 Clinical and X-ray examination of all newborn infants in Brittany during 1959-60 in a survey organised by the Ministry of Health showed that 752 out of 7916 infants had the disease. Reviewing the data from this survey in relation to month of birth, we found that 15-1% of children with congenital dislocation were born in July, whereas only 2-5% were born in January. This does not accord with results of similar surveys in other countries, where the disease was more commonly found in children born during the winter.33 Plants in Brittany are manganese-deficient as a result of the practice of alkalinising the soil to counteract the natural high acidity.44 Ruminants in the area are liable to develop bone disease as a result of their manganesedeficient diet.5 Restriction of manganese intake in rats results in the birth of offspring with bone defects caused by abnormally low acid-mucopolysaccharide levels in cartilage. 6.7 We suggest that the high incidence of congenital dislocation of the hip in Brittany may be caused by a low maternal manganese intake. Department of Sanitary Environmental Protection, Ministry of Social Services, 4 Voulis Street, Athens 125, Greece.
M. E. XILINAS.
4 Rue Charles
Dickens, Paris, France.
D. LAGARDE.
ACCIDENTAL INJECTION OF FREUND’S
ADJUVANT SIR,-We report the effects of accidental injection of Freund’s complete adjuvant-a substance widely used in
experimental immunology. A 34-year-old physician was accidentally injected with between 0’1-0-2 ml. of Freund’s complete adjuvant mixed with purified mouse collagen. The needle passed through the foot of a rabbit into his middle finger. Three days later the finger became swollen and the patient experienced pleural pains accompanied by rigors and fever. The fever continued for 2 weeks, and an intermittent pleural friction rub and epididymitis developed. The chest pain and epididymitis subsided over the next 2 months after two small relapses. The patient had been immunised with B.c.G. The erythrocyte sedimentation-rate was 25 mm. (Westergren), and white-blood-cell count was 8000 per c.mm. with a normal differential count. A biopsy specimen taken after 2 weeks at the injection site showed a lipogranuloma with no caseation. Acid-fast bacilli were seen in the material excised, but culture and injections in laboratory animals were negative. Lymphocyte transformation against tuberculin was strongly positive. There was no reaction against collagen, and collagen antibodies were not detected in serial tests.
Injections of Freund’s complete adjuvant (killed tubercle bacilli in mineral oil) are known to produce granulomatous lesions in different animals.8 In rats so-called " adjuvant disease " develops, which resembles Reiter’s disease and rheumatoid arthritis in man and is produced by delayed hypersensitivity.9 However, in other animals, granulomas Damany, P. La Luxation Congénitale de la Hanche (edited by F. Alcan). Paris, 1912. Fèvre, M. Pédiatrie, 1966, 21, 849. Cohen, P. Journal of Interdisciplinary Cycle Research, 1971, 2, 417. Coic, Y. C. R. Séanc. Acad. Agric. Fr. 1960, 46, 287. Résultats obtenus en 1970 sur les carences en oligoelements chez les ruminants en France. Physiopathologie de la Nutrition. Institut National de la Recherche Agronomique, 1970. Hurley, L. S., Everson, G. J. J. Nutr. 1963, 79, 23. Tsai, H-C. C., Everson, G. J. ibid. 1967, 91, 447. Laufer, A., Tal, C., Behar, A. J. Br. J. exp. Path. 1959, 40, 1. Waksman, B. H., Pearson, C. N., Sharp, J. T. J. Immun. 1960, 85, 403.
1. Le
2. 3. 4. 5.
6. 7. 8. 9.
treatment to
45-97-2 units per litre
during treatment (p < 0001). We examined the possibility that an abnormally high alkaline phosphatase level could be masked by clofibrate treatment. Three patients with liver disease and constantly elevated serum-alkaline-phosphatase levels were treated with 2 g. clofibrate daily. Alkaline phosphatase decreased from 217, 155, and 134 before to 83, 60, and 57 units per litre, respectively, after 4 weeks of treatment. The mechanism of this reduction is unknown. The addition of serum, obtained from clofibrate-treated patients, to several serum samples, resulted in alkaline phosphatase levels in the mixtures, that closely agreed with the expected values. Therefore, it seems unlikely that clofibrate interferes with the determination of alkaline phosphatase. R. W. B. SCHADE P. N. M. DEMACKER A. VAN ’T LAAR.
Department of Internal Medicine, University of Nijmegen, The Netherlands.
GONADOBLASTOMA IN DYSGENETIC GONADS WITH A Y CHROMOSOME
SIR,-Gonadoblastoma is known to arise in dysgenetic gonads, but, in a review of published reports, Schellhas concluded that a Y chromosome is a prerequisite for gonadal malignancy in gonadal dysgenesis. We feel that the accompanying figure effectively summarises the intricacies of these relations. With rare exceptions, phenotypic males have a Y chromosome, and females do not. Straddling these compartments are circles representing individuals with ambiguous sex characteristics and maldeveloped gonads, including a subgroup with the classic Turner phenotype of short stature, primary amenorrhcea, &c. 60% of all patients with gonadal dysgenesis have the karyotype, 45,X, and are not, as a rule, at risk of gonadal malignancy. Rather, the risk seems confined to patients with a Y chromosome, if not in all cells, at least in some gonadal cells. The probability of malignancy is great, around 25%.
Venn diagram of relation among gonadoblastoma, gonadal dysgenesis, and sex-chromosomal constitution.
For those
treating patients with gonadal dysgenesis, this
information indicates the need
to
search for
a
Y chromo-
cell-line, because of its implications as regards gonadal malignancy. For researchers, the challenge is to understand the pathogenesis. JOHN J. MULVIHILL Epidemiology Branch,
some
National Cancer Institute, Bethesda, Maryland 20014, U.S.A. 1.
Schellhas,
H. F. Obstet.
WANDA M. WADE ROBERT W. MILLER.
Gynec. 1974, 44, 298, 455.
CONGENITAL DISLOCATION OF THE HIP IN BRITTANY
SIR,—Despite a decrease since 1912, the incidence of congenital dislocation of the hip is still high in some rural communities in Brittany.l,2 Clinical and X-ray examination of all newborn infants in Brittany during 1959-60 in a survey organised by the Ministry of Health showed that 752 out of 7916 infants had the disease. Reviewing the data from this survey in relation to month of birth, we found that 15-1% of children with congenital dislocation were born in July, whereas only 2-5% were born in January. This does not accord with results of similar surveys in other countries, where the disease was more commonly found in children born during the winter.33 Plants in Brittany are manganese-deficient as a result of the practice of alkalinising the soil to counteract the natural high acidity.44 Ruminants in the area are liable to develop bone disease as a result of their manganesedeficient diet.5 Restriction of manganese intake in rats results in the birth of offspring with bone defects caused by abnormally low acid-mucopolysaccharide levels in cartilage. 6.7 We suggest that the high incidence of congenital dislocation of the hip in Brittany may be caused by a low maternal manganese intake. Department of Sanitary Environmental Protection, Ministry of Social Services, 4 Voulis Street, Athens 125, Greece.
M. E. XILINAS.
4 Rue Charles
Dickens, Paris, France.
D. LAGARDE.
ACCIDENTAL INJECTION OF FREUND’S
ADJUVANT SIR,-We report the effects of accidental injection of Freund’s complete adjuvant-a substance widely used in
experimental immunology. A 34-year-old physician was accidentally injected with between 0’1-0-2 ml. of Freund’s complete adjuvant mixed with purified mouse collagen. The needle passed through the foot of a rabbit into his middle finger. Three days later the finger became swollen and the patient experienced pleural pains accompanied by rigors and fever. The fever continued for 2 weeks, and an intermittent pleural friction rub and epididymitis developed. The chest pain and epididymitis subsided over the next 2 months after two small relapses. The patient had been immunised with B.c.G. The erythrocyte sedimentation-rate was 25 mm. (Westergren), and white-blood-cell count was 8000 per c.mm. with a normal differential count. A biopsy specimen taken after 2 weeks at the injection site showed a lipogranuloma with no caseation. Acid-fast bacilli were seen in the material excised, but culture and injections in laboratory animals were negative. Lymphocyte transformation against tuberculin was strongly positive. There was no reaction against collagen, and collagen antibodies were not detected in serial tests.
Injections of Freund’s complete adjuvant (killed tubercle bacilli in mineral oil) are known to produce granulomatous lesions in different animals.8 In rats so-called " adjuvant disease " develops, which resembles Reiter’s disease and rheumatoid arthritis in man and is produced by delayed hypersensitivity.9 However, in other animals, granulomas Damany, P. La Luxation Congénitale de la Hanche (edited by F. Alcan). Paris, 1912. Fèvre, M. Pédiatrie, 1966, 21, 849. Cohen, P. Journal of Interdisciplinary Cycle Research, 1971, 2, 417. Coic, Y. C. R. Séanc. Acad. Agric. Fr. 1960, 46, 287. Résultats obtenus en 1970 sur les carences en oligoelements chez les ruminants en France. Physiopathologie de la Nutrition. Institut National de la Recherche Agronomique, 1970. Hurley, L. S., Everson, G. J. J. Nutr. 1963, 79, 23. Tsai, H-C. C., Everson, G. J. ibid. 1967, 91, 447. Laufer, A., Tal, C., Behar, A. J. Br. J. exp. Path. 1959, 40, 1. Waksman, B. H., Pearson, C. N., Sharp, J. T. J. Immun. 1960, 85, 403.
1. Le
2. 3. 4. 5.
6. 7. 8. 9.