Creatine Phosphokinase Measurements in Febrile Children To the Editor.\p=m-\Thepresence of creatine phosphokinase (CPK) in high concentration in serum indicates muscle damage from a variety of causes,1.2
including anoxia, exercise,3 parenteral injections,4 surgery,5 trauma, and acute myositis.6 To our knowledge, there is no published information on the question of whether fever itself causes
serum.
elevated levels of CPK in Forty-eight febrile children
as outpatients were studied for this condition. The CPK level was measured with a kit (CPK Activated UV-System), with normal values being up to 50 units/L. Consecutively appearing children admitted to the casualty ward between March and June 1977 with an axillary temperature greater than 38 \s=deg\Cwere studied. In addition to CPK, throat swabs for bacterial culture, pernasal swabs for viral cultures, ESR, hemoglobin level, and WBC and differential cell counts were investigated. The average age of the 39 of the 48 children whose ages were recorded was 3.25 years, with a range of eight months to 11 years. Their tempera¬ tures ranged from 38.0 °C to 40.4 °C, with an average of 39.4 °C. The clinical findings in 37 children were confined to the upper respirato¬ ry tract and included pharyngitis, otitis media, tonsillitis, rhinorrhoea, and cough. Three had vomited, two had febrile convulsions, one had herpetic stomatitis, one had septic arthritis, and two had a flu-like illness. Three had no obvious sign of
presenting
infection.
No pathogens grew from cultures of the throat and nasopharynx in 34 of 48 children. Lancefield group A /?-hemolytic streptococci were isolated from one child. The following viruses were isolated from the remaining 13 chil¬ dren: adenovirus 2, 3, 4, or 7, 6; herpes simplex, 1; echovirus 14, 1; respiratory
syncytial virus, 1; parainfluenza 1, 4. The ESR (Westergren method) was obtained from 45 children, with the norm being up to 20 mm/hr. Values
from six children of 22, 28, 43, 51, and 116 mm/hr were greater than the normal range. The child with the value of 116 mm/hr had septic arthritis.
In 29 children, the WBC count was elevated, being more than 10,000/cu mm. mm
The range was 4,000 to 38,000/cu and the average was 13,500/cu
mm.
All of the children except two had CPK values that fell within the normal range. One boy, aged 8 years, who complained of myalgia and from whom adenovirus 7 was isolated, had a CPK level of 116 units/L. The other value just above normal was 65 units/ L in a 6-year-old child with headache and sore throat from whom no orga¬ nisms were isolated. The distribution of CPK values in the remaining 46 children were as follows: 0 to 10 units/L, 3; 11 to 20 units/L, 15; 21 to 30 units/L, 22; 31 to 40 units/L, 0; 41 to 50 units/L, 6. This study shows that, in children, fever itself is not responsible for an elevation in CPK level. The children studied represented a nonselected sample of patients presenting to a large outpatient department. In the one case where a severe elevation of the CPK level occurred, there was
myalgia. Although myalgia was not a complaint of the other patients, many were too young to give a history. Jayne Henly Antony, MD Royal Alexandra Hospital for Children Bridge Road Camperdown, Australia
1. Munsat T: Creatine phosphokinase alterations in neuromuscular diseases. Isr J Med Sci
13:93-97, 1977.
2. Munsat TL, Baloh R, Pearson CM, et al: Serum enzyme alterations in neuromuscular disorders. JAMA 226:1536-1543, 1973. 3. Vejjajiva A, Teasdale GM: Serum creatine kinase and physical exercise. Br Med J 1:1653\x=req-\
1654, 1965.
4. Armstrong B, Lloyd BL, Balazs NDH: Changes in plasma enzyme concentrations following intramuscular injections and gastros-$
copy. Aust NZ J Med 6:548-551, 1976. 5. Klein MS, Shell WE, Sobel BE: Serum
crea-
tine phosphokinase (CPK) isoenzymes after intramuscular injections, surgery and myocardial infarction. Cardiovasc Res 7:412-418, 1973. 6. McKinlay IA, Mitchell I: Transient acute myosites in childhood. Arch Dis Child 51:135-137, 1976.
Familial Occurrence of
Entrapment
Neuropathies To the Editor.\p=m-\Weread with interest the letter by E. W. Massey, MD,1 in the March 1978 issue of the Archives, which pointed out the familial occur-
Downloaded From: http://archneur.jamanetwork.com/ by a Oakland University User on 06/06/2015
of meralgia paraesthetica. It that other entrapment neuropathies, such as carpal tunnel syndrome, can also be familial. We recently reviewed the case of a 53-year-old woman complaining of nocturnal numbness and tingling in the hands. Both carpel tunnels were decompressed surgically, and the symptoms were alleviated. At operation, the median nerves were seen to be constricted under thickened transverse carpal ligaments. Later it was discovered that the patient's father had similar bilateral signs with weakness and wasting of the abductor pollicis brevis muscles. At operation, the same constrictions as in the daughter's case were found. Ultrastructural examination of the ligaments showed collagenous connective tissue without any evidence of amyloid. The reports of Rukavina et al2 and Malhoudji et al,3 describing cases of Swiss and German families with familial carpal syndrome, are well known. In these cases, pathologic studies showed extensive visceral amyloidosis and local amyloid in the rence
seems
carpal ligaments. Surgical decompres¬ sion has led to relief of the carpal tunnel syndrome in almost all cases. In 1975, Danta4 reported the cases of four patients from the same family. As in our two patients, at operation
both median nerves were found to be constricted beneath thickened trans¬ verse carpal ligaments that did not show any local amyloid infiltration. It appears that while carpal tunnel syndrome among related family mem¬ bers is possible, the incidence of this syndrome has not been precisely defined in the literature. J. M. Vallat, MD Department of Neurology
J. Dunoyer, MD Department of Orthopedics
University Hospital Limoges, France
1.
Massey
EW: Familial
occurrence
of meral-
gia paraesthetica. Arch Neurol 35:182, 1978. 2. Rukavina JG, Block WD, Jackson CE, et al: Primary systemic amyloidosis. Medicine 35:239\x=req-\ 334, 1956. 3. Malhoudji M, Teasdall RD, Adamkiewicz JJ: The genetic amyloidosis with particular references to hereditary neuropathy amyloidosis type II. Medicine 48:1-37, 1939. 4. Danta G: Familial carpal tunnel syndrome with onset in childhood. J Neurol Neurosurg Psychiatry 38:350-355, 1971.
including anoxia, exercise,3 parenteral injections,4 surgery,5 trauma, and acute myositis.6 To our knowledge, there is no published information on the question of whether fever itself causes
serum.
elevated levels of CPK in Forty-eight febrile children
as outpatients were studied for this condition. The CPK level was measured with a kit (CPK Activated UV-System), with normal values being up to 50 units/L. Consecutively appearing children admitted to the casualty ward between March and June 1977 with an axillary temperature greater than 38 \s=deg\Cwere studied. In addition to CPK, throat swabs for bacterial culture, pernasal swabs for viral cultures, ESR, hemoglobin level, and WBC and differential cell counts were investigated. The average age of the 39 of the 48 children whose ages were recorded was 3.25 years, with a range of eight months to 11 years. Their tempera¬ tures ranged from 38.0 °C to 40.4 °C, with an average of 39.4 °C. The clinical findings in 37 children were confined to the upper respirato¬ ry tract and included pharyngitis, otitis media, tonsillitis, rhinorrhoea, and cough. Three had vomited, two had febrile convulsions, one had herpetic stomatitis, one had septic arthritis, and two had a flu-like illness. Three had no obvious sign of
presenting
infection.
No pathogens grew from cultures of the throat and nasopharynx in 34 of 48 children. Lancefield group A /?-hemolytic streptococci were isolated from one child. The following viruses were isolated from the remaining 13 chil¬ dren: adenovirus 2, 3, 4, or 7, 6; herpes simplex, 1; echovirus 14, 1; respiratory
syncytial virus, 1; parainfluenza 1, 4. The ESR (Westergren method) was obtained from 45 children, with the norm being up to 20 mm/hr. Values
from six children of 22, 28, 43, 51, and 116 mm/hr were greater than the normal range. The child with the value of 116 mm/hr had septic arthritis.
In 29 children, the WBC count was elevated, being more than 10,000/cu mm. mm
The range was 4,000 to 38,000/cu and the average was 13,500/cu
mm.
All of the children except two had CPK values that fell within the normal range. One boy, aged 8 years, who complained of myalgia and from whom adenovirus 7 was isolated, had a CPK level of 116 units/L. The other value just above normal was 65 units/ L in a 6-year-old child with headache and sore throat from whom no orga¬ nisms were isolated. The distribution of CPK values in the remaining 46 children were as follows: 0 to 10 units/L, 3; 11 to 20 units/L, 15; 21 to 30 units/L, 22; 31 to 40 units/L, 0; 41 to 50 units/L, 6. This study shows that, in children, fever itself is not responsible for an elevation in CPK level. The children studied represented a nonselected sample of patients presenting to a large outpatient department. In the one case where a severe elevation of the CPK level occurred, there was
myalgia. Although myalgia was not a complaint of the other patients, many were too young to give a history. Jayne Henly Antony, MD Royal Alexandra Hospital for Children Bridge Road Camperdown, Australia
1. Munsat T: Creatine phosphokinase alterations in neuromuscular diseases. Isr J Med Sci
13:93-97, 1977.
2. Munsat TL, Baloh R, Pearson CM, et al: Serum enzyme alterations in neuromuscular disorders. JAMA 226:1536-1543, 1973. 3. Vejjajiva A, Teasdale GM: Serum creatine kinase and physical exercise. Br Med J 1:1653\x=req-\
1654, 1965.
4. Armstrong B, Lloyd BL, Balazs NDH: Changes in plasma enzyme concentrations following intramuscular injections and gastros-$
copy. Aust NZ J Med 6:548-551, 1976. 5. Klein MS, Shell WE, Sobel BE: Serum
crea-
tine phosphokinase (CPK) isoenzymes after intramuscular injections, surgery and myocardial infarction. Cardiovasc Res 7:412-418, 1973. 6. McKinlay IA, Mitchell I: Transient acute myosites in childhood. Arch Dis Child 51:135-137, 1976.
Familial Occurrence of
Entrapment
Neuropathies To the Editor.\p=m-\Weread with interest the letter by E. W. Massey, MD,1 in the March 1978 issue of the Archives, which pointed out the familial occur-
Downloaded From: http://archneur.jamanetwork.com/ by a Oakland University User on 06/06/2015
of meralgia paraesthetica. It that other entrapment neuropathies, such as carpal tunnel syndrome, can also be familial. We recently reviewed the case of a 53-year-old woman complaining of nocturnal numbness and tingling in the hands. Both carpel tunnels were decompressed surgically, and the symptoms were alleviated. At operation, the median nerves were seen to be constricted under thickened transverse carpal ligaments. Later it was discovered that the patient's father had similar bilateral signs with weakness and wasting of the abductor pollicis brevis muscles. At operation, the same constrictions as in the daughter's case were found. Ultrastructural examination of the ligaments showed collagenous connective tissue without any evidence of amyloid. The reports of Rukavina et al2 and Malhoudji et al,3 describing cases of Swiss and German families with familial carpal syndrome, are well known. In these cases, pathologic studies showed extensive visceral amyloidosis and local amyloid in the rence
seems
carpal ligaments. Surgical decompres¬ sion has led to relief of the carpal tunnel syndrome in almost all cases. In 1975, Danta4 reported the cases of four patients from the same family. As in our two patients, at operation
both median nerves were found to be constricted beneath thickened trans¬ verse carpal ligaments that did not show any local amyloid infiltration. It appears that while carpal tunnel syndrome among related family mem¬ bers is possible, the incidence of this syndrome has not been precisely defined in the literature. J. M. Vallat, MD Department of Neurology
J. Dunoyer, MD Department of Orthopedics
University Hospital Limoges, France
1.
Massey
EW: Familial
occurrence
of meral-
gia paraesthetica. Arch Neurol 35:182, 1978. 2. Rukavina JG, Block WD, Jackson CE, et al: Primary systemic amyloidosis. Medicine 35:239\x=req-\ 334, 1956. 3. Malhoudji M, Teasdall RD, Adamkiewicz JJ: The genetic amyloidosis with particular references to hereditary neuropathy amyloidosis type II. Medicine 48:1-37, 1939. 4. Danta G: Familial carpal tunnel syndrome with onset in childhood. J Neurol Neurosurg Psychiatry 38:350-355, 1971.
