1047
We have recently reported a similar result in a large number of infants weighing less than 1500 g with 25 jlgjml of vancomycin hyperalimentation fluid,’ as recommended by Schwartz et al.4 However, vancomycin serum concentrations in our patients were at a mean of 2 jlgjml and, therefore, never approached therapeutic concentrations. There were no adverse reactions to vancomycin in our study group. We did not see the emergence of vancomycinresistant organisms during our study period with a much stricter surveillance system. Further research is needed to complete our understanding of the epidemiology of CONS bacteraemia in low-birthweight infants. Caution should be used in treating infants indiscriminately with therapeutic doses of antibiotics on the basis of such small patient numbers. Section of Neonatal Medicine, Department of Pediatrics, Albany Medical College, Albany, New York 12208, USA
MICHAEL J. HORGAN
Section of Pediatric Infectious Disease, Department of Pediatrics, Albany Medical College
MARILYN A. KACICA
Department of Epidemiology, Albany
RICHARD A. VENEZIA
1. Leonard MB, Koren G, Stevenson DK, Prober CG. Vancomycin pharmacokinetics in very low birth weight neonates. Pediatr Infect Dis J 1989; 8: 282-86. 2. Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant, 3rd ed. Philadelphia: WB Saunders, 1990: 1049. 3. Kacica MA, Horgan MJ, Venezia RA, Yocum D, Ochoa L, Lepow M. Prevention of gram positive (G+) bacteremia with low dose vancomycin (VA) infusion. Pediatr Res 1992; 31: 278. 4. Schwartz C, Henrickerson KJ, Roghman K, Powell K. Prevention of bacteremia attributed to luminal colonization of tunneled central venous catheters with vancomycin susceptible organisms. Clin Oncol 1990; 8: 1591-97.
*** This letter has been shown to Dr Moller, whose reply to it and previous correspondence follows.-ED. L. SIR,-We appreciate the concerns of Dr Horgan and your other correspondents (Sept 19, p 728; Oct 17, p 975) about our study of prophylactic vancomycin in very-low-birthweight (VLBW) infants. However, we would make further comments. We do not consider that 10 mg/kg daily is a recommended therapeutic dose for vancomycin treatment in VLBW infants, 15-20 mg/kg daily is the recommendation even in infants below 1000 g. 1-3 We were surprised to achieve quite substantial serum concentrations arguing in favour of the use of this low-dose vancomycin even in proven septicaemia with coagulase-negative staphylococci. In 65 patients on vancomycin, peak concentrations averaged 17 g/ml (SD 6-5) and trough values 4-9 ug/ml (2-4). The dose regimen as introduced by Schwartz et al4 with 25 fig/mi of intravenous fluids did not achieve bactericidal concentrations and only increased the interval between catheter insertion and sepsis, while not alleviating septic episodes. 2 of our patients in the treatment group underwent evaluation for sepsis. Even if regarded as true septic episodes their results would not alter the difference from our control group. All specimens for blood cultures (0-5 ml) were diluted in 20 ml of blood culture media (Bactec, Becton and Dickinson), diluting vancomycin concentrations to below the minimum inhibitory concentration (MIC). In our control group, the observation time was terminated in 8 patients because of proven septicaemia (6 CONS, 2 gram-negative), in 5 because of suspected septicaemia, and in all the 7 other patients because intravenous (iv) access ended. By contrast, in 14 patients in the treatment group, vancomycin was discontinued because of the termination of iv access. The time of total parenteral nutrition did not differ between the two groups. No patient showed signs of sepsis more than once. We are aware of the risk of inducible resistance of enterococci to vancomycin and the possible dissemination of resistance to other groups of gram-positive organisms. There are of course some doubts about the magnitude of this risk because there has not been an increase in staphylococcal resistance to vancomycin in three decades.s Since in Germany VLBW-infants are kept on double or triple antibiotic treatment in 98-8% of cases for a median of 19 days6 our
regimen
VLBW-infants such as immunoglobulins have not been proven effective,’ so we think that our regimen in the group of VLBWinfants with a high frequency of CONS-sepsis is an alternative to no prevention. Close microbiological monitoring of the MIC for CONS and enterococci is obligatory, as are further dose finding studies. Paediatric Clinic, Medical School,
University of Lubeck, D-2400 Lübeck, Germany
JENS MÖLLER
1. Schaad UB, McCracken GH, Nelson JD Clinical pharmacology and efficacy of vancomycin in pediatric patients. J Pediatr 1980; 96: 119-26. 2. Lisby-Sutch SM, Nahata MC. Dosage guidelines for the use of vancomycin based on its pharmacokinetics in infants. Eur J Clin Pharmacol 1988; 35: 637-42. 3. Leonard MB, Koren G, Stevenson BK, Prober CG. Vancomycin pharmacokinetics in very low birth weight infants. Pediatr Inf Dis 1989; 8: 282-86. 4. Schwartz C, Henrickson KJ, Roghmann K, Powell K. Prevention of bacteremia attributed to luminal colonization of tunneled central venous catheters with vancomycin-susceptible organisms. J Clin Oncol 1990; 8: 1591-97. 5. Watanakunakorn C. In-vitro induction of resistance in coagulase-negative staphylococci to vancomycin and teicoplanin. J Antimicrob Chemother 1988; 22: 321-24. 6. Gortner L, Bernsau U, Brand M, Hellwegge HH, Hieronimi G, Jorch G. Drug utilization in very premature infants in neonatal intensive care units. Dev Pharmacol
Ther 1991; 17: 167-71. LE, Stoll BJ, Keusser TJ, et al. Intravenous immune globulin therapy for early-onset sepsis in premature neonates. J Pediatr 1992; 121: 434-43.
7. Weisman
Prevalence of
specific antibodies to Chlamydia pneumoniae (TWAR) in Swedish orienteers SiR,--6 Swedish elite orienteers have died suddenly during competition or training during the past three years.1 At necropsy, degenerative changes with a small lymphocytic infiltration were found in the myocardium of the last four cases. The last case had high IgG and IgM antibodies to Chlamydia pneumoniae in a blood specimen taken 1 month before death. A 463 basepair fragment specific for C pneumoniae was found in tissues from the lung and heart septum by polymerase chain reaction. We have investigated a total of 268 male and 94 female orienteers living in Stockholm. Specimens were taken during a relay in 1990. We studied the prevalence of specific IgG, IgM, and IgA antibodies to C pneumoniae with microimmunofluorescence (MIF). The results were corrected for possible interference from antibodies against C trachomatis and compared with results from all new blood donors (173 male and 112 female) at the Gavie Central Hospital during 1990. Gävle is situated where all six sudden death cases occurred, about 175 km north of Stockholm. Specific IgG antibodies, inverted titres of 64 or more, to C pneumoniae were detected in 52-78% of the male orienteers and male blood donors, depending on age. Female blood donors over 39 were less exposed to C pneumoniae, whereas female orienteers of the same age had almost the same rate of exposure as the males (table). Orienteers with specific antibodies to C pneumoniae had a higher geometric mean titre (GMT) than blood donors (table), which might signify more recent exposure among orienteers. This is further supported by the finding of IgM antibodies in 7 male (2-6%) and 2 female (31%) orienteers but in only 1 (0-6%) male blood donor. IgA antibodies, which may be indicative of chronic infection/ were found in 22% of male and 14% of female orienteers RATE OF EXPOSURE TO CHLAMYDIA PNEUMONIAE IN HEALTHY BLOOD DONORS AND IN ORIENTEERS
with
not seem too
a single drug therapy for a median of 7 days does aggressive. Other means to fight septic infections in
*Individuals with inverted
specific IgG
titre
against C pneumoniae of ;;,64
1048
and in 13% and 4% of the male and female blood
donors,
Our results indicate that the male orienteers were not more to C pneumoniae than healthy blood donors, but the difference usually seen in antibody prevalence between the sexes3 was almost eliminated at ages over 40 among orienteers. We have no explantion for the observed difference in prevalence of IgA antibodies between female orienteers and blood donors.
exposed
Departments of Clinical Microbiology and Infectious Diseases, Gavle Central Hospital, S-801 87 Gavle, Sweden; and Departments of Infectious Diseases and Clinical Immunology,
Huddinge University Hospital, Stockholm
Therefore, measurements of cardiac TnT in the medical management and monitoring of endurance athletes, especially during periods of extraordinary unremitting exercise or when athletes present with obscure symptoms. JOHANNES MAIR THOMAS WOHLFARTER ARNOLD KOLLER Departments of Medical Chemistry and Biochemistry, Internal Medicine, MARKUS MAYR and Sportsmedicine, ERIKA ARTNER-DWORZAK of Innsbruck, University BERND PUSCHENDORF A-6020 Innsbruck, Austria
one
marathon
may be
respectively.
HÅKAN GNARPE JUDY GNARPE BO SUNDELÖF ROLF GUSTAFSON ANN GARDULF
-
1. Editorial. Troponin T and myocardial damage. Lancet 1991; 338: 23-24 2. Apple FS, Rogers MA, Sherman WM, Costill DL, Hagermann C, Ivy JL. Profile of creatine
3. 1. Wesslén L, Påhlson C, Friman G, Fohlman J, Lindquist O, Johansson C. Myocarditis
caused by Chlamydia pneumoniae (TWAR) and sudden unexpected death in a Swedish elite orienteer. Lancet 1992; 340: 427. 2. Saikku P, Leinonen M, Tenkanen L, et al. Chronic Chlamydia pneumomae infection as a risk factor for coronary heart disease in the Helsinki Heart Study. Ann Intern Med 1992; 116: 273-78. 3. Grayston JT, Wang SP, Kuo CC, Campbell LA Current knowledge of chlamydia TWAR, an important cause of pneumonias and other acute respiratory diseaes. Eur J Clin Microbiol Infect Dis 1989; 8: 191-202
Serum cardiac troponin T after extraordinary endurance exercise SiR,—Dr Rowe’s hypothesis (Sept 19, p 712) on the pathophysiological mechanisms of myocardial injury in unremitting endurance exercise prompts us to report cardiac troponin T (TnT) concentrations in athletes before and after extraordinary endurance exercise. Rowe suggests that coronary vasospasm secondary to high catecholamine concentrations and other mechanisms causes focal necrosis, which leads to focal fibrosis of the myocardium. Cardiac TnT measurements are very sensitive and specific for the detection of myocardial darnage1 and may be the only non-invasive method to demonstrate minimal myocardial injury after endurance exercise. Creatine kinase isoenzyme MB is less suitable for this purpose because of its well established, substantial release from skeletal muscles of endurance-trained athletes after exercise.2 We investigated 20 male runners (aged 25-55 years, mean 42) who took part in the 1990 Berlinmarathon and 8 male participants (aged 25-48, mean 35) of the 1991 Otztal Radmarathon, which is a 230 km bicycle race in the Tyrol, including four mountain passes (total difference of altitude about 5000 m). Although all 28 athletes were amateur sportsmen, they can be regarded as elite endurancetrained athletes because they were able to finish their races in times equivalent to that standard. Blood samples were obtained 2 days before marathon, after finishing, and 2 days later in runners, and the day before the race, after finishing, and 1, 2, 3, 5, and 8 days thereafter in bicyclists. We measured cardiac TnT with an enzyme-immunometric one-step sandwich assay (Boehringer
Mannheim).3 All 28 athletes completed their races without evidence of myocardial ischaemia or extraordinary exhaustion during and after the competition. In all 28, cardiac TnT baseline concentrations were normal (mean [SD], runners 0 18 [0.14] µg/1; bicyclists 0.16 [0.06] jJ.g/1). These findings demonstrate that endurance training alone does not lead to an enhanced breakdown of myocardial muscle fibres. In runners and bicyclists, cardiac TnT did not increase significantly over baseline after competition. In all but one sample cardiac TnT concentrations were normal. The one abnormal result was in a 51-year-old apparently healthy marathon runner who had a TnT concentration of 10 µg/litre 2 days after competition. The mechanisms outlined by Rowe might cause focal myocardial necrosis during extraordinary endurance exercise even in the absence of coronary atherosclerosis and ventricular hypertrophy. However, in this 51-year-old man we cannot with certainty exclude silent myocardial ischaemia on the basis of coronary atherosclerosis. A single extraordinary endurance exercise does not usually lead to an increase in cardiac TnT serum concentrations. However, there is a potential cardiac risk, as indicated by the slight increase of TnT in
runner.
helpful
kinase
isoenzymes
m
skeletal muscles of marathon
runners.
Clin Chem
1984; 30: 413-16. Katus HA, Looser S, Hallermayer K, et al. Development and m vitro characterization of a new immunoassay of cardiac troponin T. Clin Chem 1992; 38: 386-93.
Lover’s
arm
SIR,-Deep-vein thrombosis of the arm is infrequent (reported are 1-2% of all deep-vein thrombosis1,2). Patients are usually classified into two distinct groups-those with spontaneouus and those with secondary thrombosis. We have seen a patient with an unusual secondary thrombosis. A 23-year-old woman woke up at 0400 h with a painful right arm. 5 h later she had a swollen, cyanotic, and painful arm and paraesthesia in her fingers. Ultrasonography confirmed our clinical suspicion of thrombosis of the right subclavian and brachial vein. She was given heparin and coumarin for eight months and took Mercilon rather than Marvelon as contraceptive agent (containing 20 pg and 30 jlg of ethinyloestradiol, respectively). We did not find other risk factors or laboratory abnormalities (protein C and S, antithrombin III, fibrinogen, activated partial thromboplastin time, prothrombin time, thrombin time, and clotting factor II) and the family history was negative. She was thrombosis free for 30 months, after which she presented with signs of thrombosis which had again occurred in the morning. This time the left arm was affected. The diagnosis was established by venography. All laboratory tests were normal and she had no risk factors. After a estimates
second conversation with a female member of staff we discovered that our patient’s habit was to lie with her arm under her partner’s head, which rested on her shoulder before falling asleep. After the first thrombotic episode she thought that compression on her right arm might be harmful and from that time on her partner slept on her left arm with his head in the same position as before. Although this sleeping habit cannot with certainty be attributed to be the cause of thrombosis, we believe that a triggering influence is highly probable. This seems analogous to the so called "paralysie des amoureux",3 in which the radial nerve is damaged by outside pressure on the upper arm instead of the vein. We feel that physicians should be aware of this possibility in young adults with axillary vein thrombosis. Departments of Clinical Epidemiology and Haematology, University Hospital Leiden, PO Box 9600, 2300 RC Leiden, Netherlands
T. KOSTER H. H. VAN BOVEN S. S. G. E. VAN BOOM E. BRIËT
1. Prescott SM, Tikoff G. Deep venous thrombosis of the upper extremity a reappraisal. Circulation 1979; 59: 350-55. 2. Horattas MC, Wright DJ, Fenton AH, et al. Changing concepts of deep venous thrombosis of the upper extremity: report of a series and review of the literature.
Surgery 1988; 104: 561-67. 3 Downie A. Peripheral nerve compression syndromes. In: Matthews WB, Glaser GH, eds. Recent advances m clinical neurology, no 3. Edinburgh: Churchill Livingstone, 1982. 47-66
CORRECTION Mortality and morbidity after high-titre measles vaccine in Mexico. -In this letter by Dr J. L. Diaz-Ortega and colleagues (Oct 10, p 924), reference 3 was wrongly included throughout and should be deleted. Reference 4 then becomes reference 3. In addition the plaque-forming units in the table were expressed as log10.
We have recently reported a similar result in a large number of infants weighing less than 1500 g with 25 jlgjml of vancomycin hyperalimentation fluid,’ as recommended by Schwartz et al.4 However, vancomycin serum concentrations in our patients were at a mean of 2 jlgjml and, therefore, never approached therapeutic concentrations. There were no adverse reactions to vancomycin in our study group. We did not see the emergence of vancomycinresistant organisms during our study period with a much stricter surveillance system. Further research is needed to complete our understanding of the epidemiology of CONS bacteraemia in low-birthweight infants. Caution should be used in treating infants indiscriminately with therapeutic doses of antibiotics on the basis of such small patient numbers. Section of Neonatal Medicine, Department of Pediatrics, Albany Medical College, Albany, New York 12208, USA
MICHAEL J. HORGAN
Section of Pediatric Infectious Disease, Department of Pediatrics, Albany Medical College
MARILYN A. KACICA
Department of Epidemiology, Albany
RICHARD A. VENEZIA
1. Leonard MB, Koren G, Stevenson DK, Prober CG. Vancomycin pharmacokinetics in very low birth weight neonates. Pediatr Infect Dis J 1989; 8: 282-86. 2. Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant, 3rd ed. Philadelphia: WB Saunders, 1990: 1049. 3. Kacica MA, Horgan MJ, Venezia RA, Yocum D, Ochoa L, Lepow M. Prevention of gram positive (G+) bacteremia with low dose vancomycin (VA) infusion. Pediatr Res 1992; 31: 278. 4. Schwartz C, Henrickerson KJ, Roghman K, Powell K. Prevention of bacteremia attributed to luminal colonization of tunneled central venous catheters with vancomycin susceptible organisms. Clin Oncol 1990; 8: 1591-97.
*** This letter has been shown to Dr Moller, whose reply to it and previous correspondence follows.-ED. L. SIR,-We appreciate the concerns of Dr Horgan and your other correspondents (Sept 19, p 728; Oct 17, p 975) about our study of prophylactic vancomycin in very-low-birthweight (VLBW) infants. However, we would make further comments. We do not consider that 10 mg/kg daily is a recommended therapeutic dose for vancomycin treatment in VLBW infants, 15-20 mg/kg daily is the recommendation even in infants below 1000 g. 1-3 We were surprised to achieve quite substantial serum concentrations arguing in favour of the use of this low-dose vancomycin even in proven septicaemia with coagulase-negative staphylococci. In 65 patients on vancomycin, peak concentrations averaged 17 g/ml (SD 6-5) and trough values 4-9 ug/ml (2-4). The dose regimen as introduced by Schwartz et al4 with 25 fig/mi of intravenous fluids did not achieve bactericidal concentrations and only increased the interval between catheter insertion and sepsis, while not alleviating septic episodes. 2 of our patients in the treatment group underwent evaluation for sepsis. Even if regarded as true septic episodes their results would not alter the difference from our control group. All specimens for blood cultures (0-5 ml) were diluted in 20 ml of blood culture media (Bactec, Becton and Dickinson), diluting vancomycin concentrations to below the minimum inhibitory concentration (MIC). In our control group, the observation time was terminated in 8 patients because of proven septicaemia (6 CONS, 2 gram-negative), in 5 because of suspected septicaemia, and in all the 7 other patients because intravenous (iv) access ended. By contrast, in 14 patients in the treatment group, vancomycin was discontinued because of the termination of iv access. The time of total parenteral nutrition did not differ between the two groups. No patient showed signs of sepsis more than once. We are aware of the risk of inducible resistance of enterococci to vancomycin and the possible dissemination of resistance to other groups of gram-positive organisms. There are of course some doubts about the magnitude of this risk because there has not been an increase in staphylococcal resistance to vancomycin in three decades.s Since in Germany VLBW-infants are kept on double or triple antibiotic treatment in 98-8% of cases for a median of 19 days6 our
regimen
VLBW-infants such as immunoglobulins have not been proven effective,’ so we think that our regimen in the group of VLBWinfants with a high frequency of CONS-sepsis is an alternative to no prevention. Close microbiological monitoring of the MIC for CONS and enterococci is obligatory, as are further dose finding studies. Paediatric Clinic, Medical School,
University of Lubeck, D-2400 Lübeck, Germany
JENS MÖLLER
1. Schaad UB, McCracken GH, Nelson JD Clinical pharmacology and efficacy of vancomycin in pediatric patients. J Pediatr 1980; 96: 119-26. 2. Lisby-Sutch SM, Nahata MC. Dosage guidelines for the use of vancomycin based on its pharmacokinetics in infants. Eur J Clin Pharmacol 1988; 35: 637-42. 3. Leonard MB, Koren G, Stevenson BK, Prober CG. Vancomycin pharmacokinetics in very low birth weight infants. Pediatr Inf Dis 1989; 8: 282-86. 4. Schwartz C, Henrickson KJ, Roghmann K, Powell K. Prevention of bacteremia attributed to luminal colonization of tunneled central venous catheters with vancomycin-susceptible organisms. J Clin Oncol 1990; 8: 1591-97. 5. Watanakunakorn C. In-vitro induction of resistance in coagulase-negative staphylococci to vancomycin and teicoplanin. J Antimicrob Chemother 1988; 22: 321-24. 6. Gortner L, Bernsau U, Brand M, Hellwegge HH, Hieronimi G, Jorch G. Drug utilization in very premature infants in neonatal intensive care units. Dev Pharmacol
Ther 1991; 17: 167-71. LE, Stoll BJ, Keusser TJ, et al. Intravenous immune globulin therapy for early-onset sepsis in premature neonates. J Pediatr 1992; 121: 434-43.
7. Weisman
Prevalence of
specific antibodies to Chlamydia pneumoniae (TWAR) in Swedish orienteers SiR,--6 Swedish elite orienteers have died suddenly during competition or training during the past three years.1 At necropsy, degenerative changes with a small lymphocytic infiltration were found in the myocardium of the last four cases. The last case had high IgG and IgM antibodies to Chlamydia pneumoniae in a blood specimen taken 1 month before death. A 463 basepair fragment specific for C pneumoniae was found in tissues from the lung and heart septum by polymerase chain reaction. We have investigated a total of 268 male and 94 female orienteers living in Stockholm. Specimens were taken during a relay in 1990. We studied the prevalence of specific IgG, IgM, and IgA antibodies to C pneumoniae with microimmunofluorescence (MIF). The results were corrected for possible interference from antibodies against C trachomatis and compared with results from all new blood donors (173 male and 112 female) at the Gavie Central Hospital during 1990. Gävle is situated where all six sudden death cases occurred, about 175 km north of Stockholm. Specific IgG antibodies, inverted titres of 64 or more, to C pneumoniae were detected in 52-78% of the male orienteers and male blood donors, depending on age. Female blood donors over 39 were less exposed to C pneumoniae, whereas female orienteers of the same age had almost the same rate of exposure as the males (table). Orienteers with specific antibodies to C pneumoniae had a higher geometric mean titre (GMT) than blood donors (table), which might signify more recent exposure among orienteers. This is further supported by the finding of IgM antibodies in 7 male (2-6%) and 2 female (31%) orienteers but in only 1 (0-6%) male blood donor. IgA antibodies, which may be indicative of chronic infection/ were found in 22% of male and 14% of female orienteers RATE OF EXPOSURE TO CHLAMYDIA PNEUMONIAE IN HEALTHY BLOOD DONORS AND IN ORIENTEERS
with
not seem too
a single drug therapy for a median of 7 days does aggressive. Other means to fight septic infections in
*Individuals with inverted
specific IgG
titre
against C pneumoniae of ;;,64
1048
and in 13% and 4% of the male and female blood
donors,
Our results indicate that the male orienteers were not more to C pneumoniae than healthy blood donors, but the difference usually seen in antibody prevalence between the sexes3 was almost eliminated at ages over 40 among orienteers. We have no explantion for the observed difference in prevalence of IgA antibodies between female orienteers and blood donors.
exposed
Departments of Clinical Microbiology and Infectious Diseases, Gavle Central Hospital, S-801 87 Gavle, Sweden; and Departments of Infectious Diseases and Clinical Immunology,
Huddinge University Hospital, Stockholm
Therefore, measurements of cardiac TnT in the medical management and monitoring of endurance athletes, especially during periods of extraordinary unremitting exercise or when athletes present with obscure symptoms. JOHANNES MAIR THOMAS WOHLFARTER ARNOLD KOLLER Departments of Medical Chemistry and Biochemistry, Internal Medicine, MARKUS MAYR and Sportsmedicine, ERIKA ARTNER-DWORZAK of Innsbruck, University BERND PUSCHENDORF A-6020 Innsbruck, Austria
one
marathon
may be
respectively.
HÅKAN GNARPE JUDY GNARPE BO SUNDELÖF ROLF GUSTAFSON ANN GARDULF
-
1. Editorial. Troponin T and myocardial damage. Lancet 1991; 338: 23-24 2. Apple FS, Rogers MA, Sherman WM, Costill DL, Hagermann C, Ivy JL. Profile of creatine
3. 1. Wesslén L, Påhlson C, Friman G, Fohlman J, Lindquist O, Johansson C. Myocarditis
caused by Chlamydia pneumoniae (TWAR) and sudden unexpected death in a Swedish elite orienteer. Lancet 1992; 340: 427. 2. Saikku P, Leinonen M, Tenkanen L, et al. Chronic Chlamydia pneumomae infection as a risk factor for coronary heart disease in the Helsinki Heart Study. Ann Intern Med 1992; 116: 273-78. 3. Grayston JT, Wang SP, Kuo CC, Campbell LA Current knowledge of chlamydia TWAR, an important cause of pneumonias and other acute respiratory diseaes. Eur J Clin Microbiol Infect Dis 1989; 8: 191-202
Serum cardiac troponin T after extraordinary endurance exercise SiR,—Dr Rowe’s hypothesis (Sept 19, p 712) on the pathophysiological mechanisms of myocardial injury in unremitting endurance exercise prompts us to report cardiac troponin T (TnT) concentrations in athletes before and after extraordinary endurance exercise. Rowe suggests that coronary vasospasm secondary to high catecholamine concentrations and other mechanisms causes focal necrosis, which leads to focal fibrosis of the myocardium. Cardiac TnT measurements are very sensitive and specific for the detection of myocardial darnage1 and may be the only non-invasive method to demonstrate minimal myocardial injury after endurance exercise. Creatine kinase isoenzyme MB is less suitable for this purpose because of its well established, substantial release from skeletal muscles of endurance-trained athletes after exercise.2 We investigated 20 male runners (aged 25-55 years, mean 42) who took part in the 1990 Berlinmarathon and 8 male participants (aged 25-48, mean 35) of the 1991 Otztal Radmarathon, which is a 230 km bicycle race in the Tyrol, including four mountain passes (total difference of altitude about 5000 m). Although all 28 athletes were amateur sportsmen, they can be regarded as elite endurancetrained athletes because they were able to finish their races in times equivalent to that standard. Blood samples were obtained 2 days before marathon, after finishing, and 2 days later in runners, and the day before the race, after finishing, and 1, 2, 3, 5, and 8 days thereafter in bicyclists. We measured cardiac TnT with an enzyme-immunometric one-step sandwich assay (Boehringer
Mannheim).3 All 28 athletes completed their races without evidence of myocardial ischaemia or extraordinary exhaustion during and after the competition. In all 28, cardiac TnT baseline concentrations were normal (mean [SD], runners 0 18 [0.14] µg/1; bicyclists 0.16 [0.06] jJ.g/1). These findings demonstrate that endurance training alone does not lead to an enhanced breakdown of myocardial muscle fibres. In runners and bicyclists, cardiac TnT did not increase significantly over baseline after competition. In all but one sample cardiac TnT concentrations were normal. The one abnormal result was in a 51-year-old apparently healthy marathon runner who had a TnT concentration of 10 µg/litre 2 days after competition. The mechanisms outlined by Rowe might cause focal myocardial necrosis during extraordinary endurance exercise even in the absence of coronary atherosclerosis and ventricular hypertrophy. However, in this 51-year-old man we cannot with certainty exclude silent myocardial ischaemia on the basis of coronary atherosclerosis. A single extraordinary endurance exercise does not usually lead to an increase in cardiac TnT serum concentrations. However, there is a potential cardiac risk, as indicated by the slight increase of TnT in
runner.
helpful
kinase
isoenzymes
m
skeletal muscles of marathon
runners.
Clin Chem
1984; 30: 413-16. Katus HA, Looser S, Hallermayer K, et al. Development and m vitro characterization of a new immunoassay of cardiac troponin T. Clin Chem 1992; 38: 386-93.
Lover’s
arm
SIR,-Deep-vein thrombosis of the arm is infrequent (reported are 1-2% of all deep-vein thrombosis1,2). Patients are usually classified into two distinct groups-those with spontaneouus and those with secondary thrombosis. We have seen a patient with an unusual secondary thrombosis. A 23-year-old woman woke up at 0400 h with a painful right arm. 5 h later she had a swollen, cyanotic, and painful arm and paraesthesia in her fingers. Ultrasonography confirmed our clinical suspicion of thrombosis of the right subclavian and brachial vein. She was given heparin and coumarin for eight months and took Mercilon rather than Marvelon as contraceptive agent (containing 20 pg and 30 jlg of ethinyloestradiol, respectively). We did not find other risk factors or laboratory abnormalities (protein C and S, antithrombin III, fibrinogen, activated partial thromboplastin time, prothrombin time, thrombin time, and clotting factor II) and the family history was negative. She was thrombosis free for 30 months, after which she presented with signs of thrombosis which had again occurred in the morning. This time the left arm was affected. The diagnosis was established by venography. All laboratory tests were normal and she had no risk factors. After a estimates
second conversation with a female member of staff we discovered that our patient’s habit was to lie with her arm under her partner’s head, which rested on her shoulder before falling asleep. After the first thrombotic episode she thought that compression on her right arm might be harmful and from that time on her partner slept on her left arm with his head in the same position as before. Although this sleeping habit cannot with certainty be attributed to be the cause of thrombosis, we believe that a triggering influence is highly probable. This seems analogous to the so called "paralysie des amoureux",3 in which the radial nerve is damaged by outside pressure on the upper arm instead of the vein. We feel that physicians should be aware of this possibility in young adults with axillary vein thrombosis. Departments of Clinical Epidemiology and Haematology, University Hospital Leiden, PO Box 9600, 2300 RC Leiden, Netherlands
T. KOSTER H. H. VAN BOVEN S. S. G. E. VAN BOOM E. BRIËT
1. Prescott SM, Tikoff G. Deep venous thrombosis of the upper extremity a reappraisal. Circulation 1979; 59: 350-55. 2. Horattas MC, Wright DJ, Fenton AH, et al. Changing concepts of deep venous thrombosis of the upper extremity: report of a series and review of the literature.
Surgery 1988; 104: 561-67. 3 Downie A. Peripheral nerve compression syndromes. In: Matthews WB, Glaser GH, eds. Recent advances m clinical neurology, no 3. Edinburgh: Churchill Livingstone, 1982. 47-66
CORRECTION Mortality and morbidity after high-titre measles vaccine in Mexico. -In this letter by Dr J. L. Diaz-Ortega and colleagues (Oct 10, p 924), reference 3 was wrongly included throughout and should be deleted. Reference 4 then becomes reference 3. In addition the plaque-forming units in the table were expressed as log10.
