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GROWTH HORMONE IN AFRICAN PYGMIES
596 tion every six years would be required to maintain one’s certification. This is similar in certain ways to the approach of the Royal College of General Practitioners. The similarities between the two systems are further underlined by Dr. Draper’s paper.3 Dr. Draper’s thinking on the details of size and siting of health-service units is much the same as that which is current in New York City’s health services number of people which could be administration, even to the " " served a community-care unit (" ambulaconveniently by tory care unit " in our terms)-namely, 25,000-50,000. One could speculate for a long time on the reasons for these similarities. I think that the most important thing at this time is to recognise that they do exist, so that the benefits of cooperative work and comnarative studies can be realised. STEVEN JONAS. Bedford Health District, Brooklyn, New York 11221.
GROWTH HORMONE IN AFRICAN PYGMIES SIR,-In their letters, Prof. Schreider and Dr. Shee (Jan. 13, p. 92) point out that the mean heights of the pygmies we studied4 were significantly greater than those in previously published figures in the Ituri and Akka pygmies. This discrepancy in mean height is just what one would expect, since we studied the Babinga pygmies of the Central African Republic, north of the Ubangi River. It is well known that the Babinga pygmies are taller than the Ituri or Mbuti pygmy tribes who inhabit the area south of the Ubangi and Congo Rivers (see table). The heights of our relatively small sample HEIGHTS OF PYGMIES
(CM.)
IN VARIOUS STUDIES
of pygmies fit well within the range of previously reported studies of the Babinga.4-6 Furthermore a sampling error, as suggested by Dr. Schreider, is unlikely, since the mean figures obtained in our 22 pygmies are almost identical with those of a sample of 183 Babinga pygmies soon to be published in detail by Cavalli-Sforza et al. The heights of a larger series of 600 Babinga pygmies are at present under analysis and seem to be comparable to those of the smaller samples. The suggestion that the pygmies we studied were Negro/ pygmy hybrids is also unlikely, since all were true forest dwellers and lived in typical pygmy camps. As Prof. Schreider states, any exogamy between pygmy and Negro is one-way, the resultant offspring being absorbed entirely into the Negro 3. 4. 5.
6. 7.
Draper, P. Lancet, 1967, ii, 1406. Rimoin, D. L., Merimee, T. J., Rabinowitz, D., McKusick, V. A., Cavalli-Sforza, L. L. ibid. p. 523. Cavalli-Sforza, L. L., Nezzo, F., Bernini, L., de Jong, W. W. W., Meera-Kahn, P., Siniscalco, M., Nijenhius, L. E., van Loghern, E., Modiano, G., Zonta, L. Studies on African Pygmies. A Pilot Investigation of Babinga Pygmies in the Central African Republic. Unpubl shed. Lalouel, J. Bulletins et Memoires de la Societé d’Anthropologie de Paris; p. 60. Paris, 1949. Gusinde, M. Urwaldmenschen Am Ituri, Vienna, 1948.
We can therefore conclude that our growthhormone studies were performed on a homogeneous group of " " Babinga pygmies whose heights were well within the normal of this tribe. range pygmy Washington University School of Medicine, D. L. RIMOIN. St. Louis, Missouri. T. J. MERIMEE D. RABINOWITZ Johns Hopkins University, V. A. MCKUSICK. Baltimore, Maryland. Istituto di Genetica, L. L. CAVALLI-SFORZA. Universita di Pavia, Italy.
population.
STEROID THERAPY AND HYPEROSMOLAR NON-KETOTIC COMA
SIR,-Boyerand Dr. Kumar (Jan. 6, p. 48) have described patients who were receiving corticosteroids at the time of the diagnosis of hyperosmolar non-ketotic coma. Besides these 5 cases, 4 other similar ones have been described,2-5 in a total of about 120 hitherto reported cases of hyperosmolar nonketotic coma. In order to emphasise the importance of the recognition of this severe complication of corticosteroid therapy we describe here the following 2 cases. Case 1 This
aged 41, who had been treated with prednisone, daily, for 2 years because of systemic lupus erythematosus. She was admitted to this hospital on March 8, 1966, because of increasing dyspnoea, thought to be due to pulmonary hypertension caused by her collagen disease. The daily prednisone dose was increased to 100 mg. After 6 days the dose was lowered to 75 mg., and 2 days later to 50 mg., daily. On March 19, 1966, the patient became tired and thirsty was a
woman,
15 mg.
and vomited several times. She was found to be semiUrine contained 6-1 g. per 100 ml. comatose and dehydrated. of glucose, but no acetone. Blood-glucose was 1130 mg. per 100 ml. She was given within 12 hours 1 litre of isotonic saline solution intravenously, 1 litre of water orally, and a total amount of 120 units of soluble insulin. She improved rapidly and the daily dosage of prednisone was gradually lowered to 15 mg. Within a week insulin treatment could be tapered off, her diabetes remained well controlled by diet, and she was discharged from hospital on April 16. In August, 1966, the daily prednisone dosage was increased This promptly resulted in a clinical picture to 50 mg. resembling the patient’s previous coma, and blood-glucose rose to over 300 mg. per 100 ml. The patient was readmitted, and given large amounts of fluids orally and injections of insulin. Prednisone dosage was lowered to 15 mg. daily. Diabetes was later treated with 16 units of insulin zinc suspension (’ Novo’) daily. In December, 1966, the patient died of fulminant miliary tuberculosis. Necropsy showed nothing abnormal in the pancreas. Case 2 This
was a man, aged 56, who had been found to have myelofibrosis 2 years before. At that time his fasting bloodglucose level was 138 mg. per 100 ml. In July, 1966, severe thrombocytopenia and leucopenia had developed, and treatment with prednisone, 75 mg. daily, had been started. After 5 days the dose had been reduced to 45 mg. daily. After 7 days’ treatment with prednisone he was admitted to this hospital with a 2-day history of tiredness, thirst, polyuria, and vomiting. On admission the patient was dehydrated and semicomatose with clonic twitchings of the left arm. Blood-pressure was 100/65 mm. Hg, pulse 120 per minute, and temperature
Boyer, M. H. J. Am. med. Ass. 1967, 202, 1007. Mach, R. S., de Sousa, R. C. Schweiz. med. Wschr. 1963, 93, 1256. 3. Brocard, H., Akoun, G., Grand, A. Bull. Mém. Soc. méd. Hôp. Paris, 1965, 116, 353. 4. Schwartz, T. B., Apfelbaum, R. I. in Year Book of Endocrinology, 1965-1966 Series (edited by T. B. Schwartz); p. 165. Chicago, 1966. 5. Plauchu, M. M., Palliard, P., Malluret, J., Noel, P., de Montgolfier, R. Lyon méd. 1967, 217, 1921.
1. 2.
GROWTH HORMONE IN AFRICAN PYGMIES SIR,-In their letters, Prof. Schreider and Dr. Shee (Jan. 13, p. 92) point out that the mean heights of the pygmies we studied4 were significantly greater than those in previously published figures in the Ituri and Akka pygmies. This discrepancy in mean height is just what one would expect, since we studied the Babinga pygmies of the Central African Republic, north of the Ubangi River. It is well known that the Babinga pygmies are taller than the Ituri or Mbuti pygmy tribes who inhabit the area south of the Ubangi and Congo Rivers (see table). The heights of our relatively small sample HEIGHTS OF PYGMIES
(CM.)
IN VARIOUS STUDIES
of pygmies fit well within the range of previously reported studies of the Babinga.4-6 Furthermore a sampling error, as suggested by Dr. Schreider, is unlikely, since the mean figures obtained in our 22 pygmies are almost identical with those of a sample of 183 Babinga pygmies soon to be published in detail by Cavalli-Sforza et al. The heights of a larger series of 600 Babinga pygmies are at present under analysis and seem to be comparable to those of the smaller samples. The suggestion that the pygmies we studied were Negro/ pygmy hybrids is also unlikely, since all were true forest dwellers and lived in typical pygmy camps. As Prof. Schreider states, any exogamy between pygmy and Negro is one-way, the resultant offspring being absorbed entirely into the Negro 3. 4. 5.
6. 7.
Draper, P. Lancet, 1967, ii, 1406. Rimoin, D. L., Merimee, T. J., Rabinowitz, D., McKusick, V. A., Cavalli-Sforza, L. L. ibid. p. 523. Cavalli-Sforza, L. L., Nezzo, F., Bernini, L., de Jong, W. W. W., Meera-Kahn, P., Siniscalco, M., Nijenhius, L. E., van Loghern, E., Modiano, G., Zonta, L. Studies on African Pygmies. A Pilot Investigation of Babinga Pygmies in the Central African Republic. Unpubl shed. Lalouel, J. Bulletins et Memoires de la Societé d’Anthropologie de Paris; p. 60. Paris, 1949. Gusinde, M. Urwaldmenschen Am Ituri, Vienna, 1948.
We can therefore conclude that our growthhormone studies were performed on a homogeneous group of " " Babinga pygmies whose heights were well within the normal of this tribe. range pygmy Washington University School of Medicine, D. L. RIMOIN. St. Louis, Missouri. T. J. MERIMEE D. RABINOWITZ Johns Hopkins University, V. A. MCKUSICK. Baltimore, Maryland. Istituto di Genetica, L. L. CAVALLI-SFORZA. Universita di Pavia, Italy.
population.
STEROID THERAPY AND HYPEROSMOLAR NON-KETOTIC COMA
SIR,-Boyerand Dr. Kumar (Jan. 6, p. 48) have described patients who were receiving corticosteroids at the time of the diagnosis of hyperosmolar non-ketotic coma. Besides these 5 cases, 4 other similar ones have been described,2-5 in a total of about 120 hitherto reported cases of hyperosmolar nonketotic coma. In order to emphasise the importance of the recognition of this severe complication of corticosteroid therapy we describe here the following 2 cases. Case 1 This
aged 41, who had been treated with prednisone, daily, for 2 years because of systemic lupus erythematosus. She was admitted to this hospital on March 8, 1966, because of increasing dyspnoea, thought to be due to pulmonary hypertension caused by her collagen disease. The daily prednisone dose was increased to 100 mg. After 6 days the dose was lowered to 75 mg., and 2 days later to 50 mg., daily. On March 19, 1966, the patient became tired and thirsty was a
woman,
15 mg.
and vomited several times. She was found to be semiUrine contained 6-1 g. per 100 ml. comatose and dehydrated. of glucose, but no acetone. Blood-glucose was 1130 mg. per 100 ml. She was given within 12 hours 1 litre of isotonic saline solution intravenously, 1 litre of water orally, and a total amount of 120 units of soluble insulin. She improved rapidly and the daily dosage of prednisone was gradually lowered to 15 mg. Within a week insulin treatment could be tapered off, her diabetes remained well controlled by diet, and she was discharged from hospital on April 16. In August, 1966, the daily prednisone dosage was increased This promptly resulted in a clinical picture to 50 mg. resembling the patient’s previous coma, and blood-glucose rose to over 300 mg. per 100 ml. The patient was readmitted, and given large amounts of fluids orally and injections of insulin. Prednisone dosage was lowered to 15 mg. daily. Diabetes was later treated with 16 units of insulin zinc suspension (’ Novo’) daily. In December, 1966, the patient died of fulminant miliary tuberculosis. Necropsy showed nothing abnormal in the pancreas. Case 2 This
was a man, aged 56, who had been found to have myelofibrosis 2 years before. At that time his fasting bloodglucose level was 138 mg. per 100 ml. In July, 1966, severe thrombocytopenia and leucopenia had developed, and treatment with prednisone, 75 mg. daily, had been started. After 5 days the dose had been reduced to 45 mg. daily. After 7 days’ treatment with prednisone he was admitted to this hospital with a 2-day history of tiredness, thirst, polyuria, and vomiting. On admission the patient was dehydrated and semicomatose with clonic twitchings of the left arm. Blood-pressure was 100/65 mm. Hg, pulse 120 per minute, and temperature
Boyer, M. H. J. Am. med. Ass. 1967, 202, 1007. Mach, R. S., de Sousa, R. C. Schweiz. med. Wschr. 1963, 93, 1256. 3. Brocard, H., Akoun, G., Grand, A. Bull. Mém. Soc. méd. Hôp. Paris, 1965, 116, 353. 4. Schwartz, T. B., Apfelbaum, R. I. in Year Book of Endocrinology, 1965-1966 Series (edited by T. B. Schwartz); p. 165. Chicago, 1966. 5. Plauchu, M. M., Palliard, P., Malluret, J., Noel, P., de Montgolfier, R. Lyon méd. 1967, 217, 1921.
1. 2.