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OSTEOPOROSIS IN SOUTH AFRICA
431 OSTEOPOROSIS IN SOUTH AFRICA
SIR,-Dr Aitken (Jan. 26, p. 213) asks several pertinent about my Dec. 22/29 paper on osteoporosis in South
questions Africa.
communities in the bone density survey were were among the longest settled and most stable suburban populations in Johannesburg. Although there were differences in family size, income, and housing, both groups are considered to be representative of a healthy, active, working population in a large industrial city. (2) Aitken gained the impression that "20% of the people selected for radiography were not examined." This is not so.
(1) The
two
selected precisely because they
Following accepted epidemiological practice, a complete census study areas was carried out and at least 80% of the total census population finally agreed to come into the survey. A participation rate of 80% is generally regarded as excellent and is certainly statistically valid in random surveys. Everyone selected on this basis was examined in the definitive study. (3) The terms "Caucasoid" and "Negroid" were used synonymously with "Caucasian" (White) and "Negro" (Black). There was no doubt whatever about the ethnic origins
a single major incident. If this is so, it follows that the slower the rate of bone turnover the more likely is it that sufficient microlesions will accumulate in the trabecular lattice to lead to complete fracture. Slowing of bone turnover may have a varity of causes, including subclinical vitamin D deficiency, which are amenable to treatment. In the light of this hypothesis the "logical conclusion" which Aitken draws from my paper is absurd.
Department of Orthopaedic Surgery, Medical School,
University of the Witwatersrand, Johannesburg 2001, South Africa
L. SOLOMON
of the
of the two communities, and neither group included any individual of "mixed" parentage. (4) Health services for the two communities in Johannesburg are today equally good, and it is inconceivable that several hundred femoral neck fractures are going undetected every year in the Black community. (5) Dr Aitken points out that my findings differ from those in previous post-mortem and radiological studies which have shown that Blacks have greater bone density than Whites. The sources he cites bear closer examination:
(a) Trotter et a].’,estimated bone density in skeletons collected over period of "50 or more years", furthermore, they state that "the subjects had died mostly of natural causes and only rarely from accidental death when in a state of good health", and they warn that "generalisations to the living population can be made only with recognition of possible bias." Even if this is discounted, their study on bone density covered only 20 skeletons of each race and sex, and significant differences between Blacks and Whites were found in the vertebrar, upper limb bones, and tibia, but not in the femur. (b) Garn et aJ.3 examined differential sexual dimorphism in bone diameters but presented no statistical comparison of bone density a
between the two ethnic groups. (c) Moldawer’s study’ was based entirely on fracture rates in the two ethnic groups and-as in my own study-they found a much lower fracture rate in Blacks. There was no other measurement of bone density.
Though these (and other) studies are repeatedly quoted in support of the notion that bone density is significantly greater in Blacks than in Whites, none of them fulfil the epidemiological criteria of a true random population survey. It was precisely because of this shortcoming that our own study was set up.
Finally, Aitken questions my conclusion that "osteoporotic fractures" are due to a combination of osteoporosis and some other (qualitative) factor. I had in mind the possibility that this factor might be a critical difference in the rate of bone turnover. It is quite possible that individuals with identical bone mass may have different turnover rates. Freeman et al.5 have presented good evidence that femoral neck fracture results from cumulative fatigue of trabecular bone rather than 1. Trotter M, Broman G, Peterson RR. Densities of bone of white and negro skeletons. J Bone Jt Surg 1960; 42A: 50-58. 2. Trotter M, Hixon BB. Sequential changes in weight, density and percentage ash weight of human skeletons from an early fetal period through old age.
Anat Rec 1974; 179: 1-18. 3. Garn SM, Nagy JM, Sandusky ST. Differential sexual dimorphism in bone diameters of subjects of European and African ancestry. Am JPhys Anthropol 1972, 37: 127-30. 4. Moldawer M, Zimmerman SJ, Collins LC. Incidence of osteoporosis in elderly whites and elderly negroes. JAMA 1965; 194: 859-62. 5. Freeman MA, Todd RC, Pirie CJ. The role of fatigue in the pathogenesis of senile femoral neck fractures. J Bone Jt Surg 1974, 56B: 698.
TREATMENT OF GONORRHŒA CAUSED BY
&bgr;-LACTAMASE PRODUCING STRAIN OF NEISSERIA GONORRHÆA WITH CEFOTAXIME
SIR,-Cefotaxime, a new cephalosporin undergoing clinical trials in gonorrhoea,’ has excellent in vitro activity against Neisseria gonorrhaeae, including penicillin-resistant strains.2 We describe its successful use in a patient with acute gonorrhoea caused by a p-lactamase producing strain of N. gonorrhaeae. We believe this to be the first such report. A 22-year-old female was seen in the clinic for sexually transmitted diseases in September, 1979, with a complaint of mild dysuria of a few days’ duration. She had recently taken penicillin V for a dental infection. Acute gonorrhoea was suspected, and this was confirmed by isolation of N. gonorrhaeae from a cervical swab. She was given intramuscular kanamycin (2 g) but subsequently became reinfected by her regular boyfriend who had been given inadequate treatment for acute urethritis whilst in Bangkok. At this stage a 7-day course of oral tetracycline (1g/day) and 7 days of oral erythromycin (1 g/day) were prescribed. Subsequently cervical and urethral swabs yielded a p-lactamase producing strain of N. gonorrhwv. The patient was therefore given intramuscular cefotaxime (2 g) in 1% lignocaine, the dose being divided between each buttock. She was seen at 3, 5, and 49 days after treatment when both clinical and bacteriological examinations showed no evidence of gonorrhoea. Her boyfriend, who had not responded to intramuscular penicillin (4 megaunits ’Bicillin’) and oral probenecid (1 g), was treated with intramuscular spectinomycin (2 g) and remained both symptom-free and culture-negative on follow-up for a similar length of time. The strain of N. gonorrhaeae isolated produced p4actamase (phenol red3 and chromogenic cephalosporin4 tests). It had an MIC to penicillin of 100 mg/l. It was also resistant to tetracycline (MIC>2 mg/1) in common with other Far East strains,5 but disc sensitivity testing showed it to be susceptible to kanamycin, erythromycin, and spectinomycin. These findings were confirmed by the V.D. Reference Laboratory at the London Hospital. The MIC of cefotaxime for this strain was 0.015S mg/1 by the agar incorporation method using 5% lysed horse blood in D.S.T. agar (Oxoid). Although further evaluation is necessary, this report suggests that cefotaxime may prove a useful alternative to spec1. Hubrechts JM, Vanhoof R, Denolf R, Ghosen V, Foulon N, Butzler JP. Treatment of uncomplicated gonorrhea with cefotaxime. Proceedings of the 11th International Congress of Chemotherapy and 19th Interscience Conference on Antimicrobial Agents and Chemotherapy, Boston, 1979. 2. Murray PR, Christman JL, Medoff G. In vitro action of HR 756, a new cephalosporin against Neisseria gonorrhœœ. Antimicrob Ag Chemother
1979; 15: 452-54. 3. Escamilla J. Susceptibility of H. influenzœ to ampicillin as determined by use of a modified one minute Beta-Lactamase Test. Antimicrob Ag Chemother
1976; 9: 196-98. Morris A, Kirby SM, Shingler AH. Novel method for detection of beta-lactamases by using a chromogenic cephalosporin sub-
4. O’Callaghan CH,
strate. Antimicrob Ag Chemother 1972; 1: 283-88. Thornsberry C, Schalla W, et al. Evidence of two distinct of penicillin-producing N. gonorrhœœ. Lancet 1977; ii: 993-95.
5. Perine PL,
types
SIR,-Dr Aitken (Jan. 26, p. 213) asks several pertinent about my Dec. 22/29 paper on osteoporosis in South
questions Africa.
communities in the bone density survey were were among the longest settled and most stable suburban populations in Johannesburg. Although there were differences in family size, income, and housing, both groups are considered to be representative of a healthy, active, working population in a large industrial city. (2) Aitken gained the impression that "20% of the people selected for radiography were not examined." This is not so.
(1) The
two
selected precisely because they
Following accepted epidemiological practice, a complete census study areas was carried out and at least 80% of the total census population finally agreed to come into the survey. A participation rate of 80% is generally regarded as excellent and is certainly statistically valid in random surveys. Everyone selected on this basis was examined in the definitive study. (3) The terms "Caucasoid" and "Negroid" were used synonymously with "Caucasian" (White) and "Negro" (Black). There was no doubt whatever about the ethnic origins
a single major incident. If this is so, it follows that the slower the rate of bone turnover the more likely is it that sufficient microlesions will accumulate in the trabecular lattice to lead to complete fracture. Slowing of bone turnover may have a varity of causes, including subclinical vitamin D deficiency, which are amenable to treatment. In the light of this hypothesis the "logical conclusion" which Aitken draws from my paper is absurd.
Department of Orthopaedic Surgery, Medical School,
University of the Witwatersrand, Johannesburg 2001, South Africa
L. SOLOMON
of the
of the two communities, and neither group included any individual of "mixed" parentage. (4) Health services for the two communities in Johannesburg are today equally good, and it is inconceivable that several hundred femoral neck fractures are going undetected every year in the Black community. (5) Dr Aitken points out that my findings differ from those in previous post-mortem and radiological studies which have shown that Blacks have greater bone density than Whites. The sources he cites bear closer examination:
(a) Trotter et a].’,estimated bone density in skeletons collected over period of "50 or more years", furthermore, they state that "the subjects had died mostly of natural causes and only rarely from accidental death when in a state of good health", and they warn that "generalisations to the living population can be made only with recognition of possible bias." Even if this is discounted, their study on bone density covered only 20 skeletons of each race and sex, and significant differences between Blacks and Whites were found in the vertebrar, upper limb bones, and tibia, but not in the femur. (b) Garn et aJ.3 examined differential sexual dimorphism in bone diameters but presented no statistical comparison of bone density a
between the two ethnic groups. (c) Moldawer’s study’ was based entirely on fracture rates in the two ethnic groups and-as in my own study-they found a much lower fracture rate in Blacks. There was no other measurement of bone density.
Though these (and other) studies are repeatedly quoted in support of the notion that bone density is significantly greater in Blacks than in Whites, none of them fulfil the epidemiological criteria of a true random population survey. It was precisely because of this shortcoming that our own study was set up.
Finally, Aitken questions my conclusion that "osteoporotic fractures" are due to a combination of osteoporosis and some other (qualitative) factor. I had in mind the possibility that this factor might be a critical difference in the rate of bone turnover. It is quite possible that individuals with identical bone mass may have different turnover rates. Freeman et al.5 have presented good evidence that femoral neck fracture results from cumulative fatigue of trabecular bone rather than 1. Trotter M, Broman G, Peterson RR. Densities of bone of white and negro skeletons. J Bone Jt Surg 1960; 42A: 50-58. 2. Trotter M, Hixon BB. Sequential changes in weight, density and percentage ash weight of human skeletons from an early fetal period through old age.
Anat Rec 1974; 179: 1-18. 3. Garn SM, Nagy JM, Sandusky ST. Differential sexual dimorphism in bone diameters of subjects of European and African ancestry. Am JPhys Anthropol 1972, 37: 127-30. 4. Moldawer M, Zimmerman SJ, Collins LC. Incidence of osteoporosis in elderly whites and elderly negroes. JAMA 1965; 194: 859-62. 5. Freeman MA, Todd RC, Pirie CJ. The role of fatigue in the pathogenesis of senile femoral neck fractures. J Bone Jt Surg 1974, 56B: 698.
TREATMENT OF GONORRHŒA CAUSED BY
&bgr;-LACTAMASE PRODUCING STRAIN OF NEISSERIA GONORRHÆA WITH CEFOTAXIME
SIR,-Cefotaxime, a new cephalosporin undergoing clinical trials in gonorrhoea,’ has excellent in vitro activity against Neisseria gonorrhaeae, including penicillin-resistant strains.2 We describe its successful use in a patient with acute gonorrhoea caused by a p-lactamase producing strain of N. gonorrhaeae. We believe this to be the first such report. A 22-year-old female was seen in the clinic for sexually transmitted diseases in September, 1979, with a complaint of mild dysuria of a few days’ duration. She had recently taken penicillin V for a dental infection. Acute gonorrhoea was suspected, and this was confirmed by isolation of N. gonorrhaeae from a cervical swab. She was given intramuscular kanamycin (2 g) but subsequently became reinfected by her regular boyfriend who had been given inadequate treatment for acute urethritis whilst in Bangkok. At this stage a 7-day course of oral tetracycline (1g/day) and 7 days of oral erythromycin (1 g/day) were prescribed. Subsequently cervical and urethral swabs yielded a p-lactamase producing strain of N. gonorrhwv. The patient was therefore given intramuscular cefotaxime (2 g) in 1% lignocaine, the dose being divided between each buttock. She was seen at 3, 5, and 49 days after treatment when both clinical and bacteriological examinations showed no evidence of gonorrhoea. Her boyfriend, who had not responded to intramuscular penicillin (4 megaunits ’Bicillin’) and oral probenecid (1 g), was treated with intramuscular spectinomycin (2 g) and remained both symptom-free and culture-negative on follow-up for a similar length of time. The strain of N. gonorrhaeae isolated produced p4actamase (phenol red3 and chromogenic cephalosporin4 tests). It had an MIC to penicillin of 100 mg/l. It was also resistant to tetracycline (MIC>2 mg/1) in common with other Far East strains,5 but disc sensitivity testing showed it to be susceptible to kanamycin, erythromycin, and spectinomycin. These findings were confirmed by the V.D. Reference Laboratory at the London Hospital. The MIC of cefotaxime for this strain was 0.015S mg/1 by the agar incorporation method using 5% lysed horse blood in D.S.T. agar (Oxoid). Although further evaluation is necessary, this report suggests that cefotaxime may prove a useful alternative to spec1. Hubrechts JM, Vanhoof R, Denolf R, Ghosen V, Foulon N, Butzler JP. Treatment of uncomplicated gonorrhea with cefotaxime. Proceedings of the 11th International Congress of Chemotherapy and 19th Interscience Conference on Antimicrobial Agents and Chemotherapy, Boston, 1979. 2. Murray PR, Christman JL, Medoff G. In vitro action of HR 756, a new cephalosporin against Neisseria gonorrhœœ. Antimicrob Ag Chemother
1979; 15: 452-54. 3. Escamilla J. Susceptibility of H. influenzœ to ampicillin as determined by use of a modified one minute Beta-Lactamase Test. Antimicrob Ag Chemother
1976; 9: 196-98. Morris A, Kirby SM, Shingler AH. Novel method for detection of beta-lactamases by using a chromogenic cephalosporin sub-
4. O’Callaghan CH,
strate. Antimicrob Ag Chemother 1972; 1: 283-88. Thornsberry C, Schalla W, et al. Evidence of two distinct of penicillin-producing N. gonorrhœœ. Lancet 1977; ii: 993-95.
5. Perine PL,
types