- Email: [email protected]
MYALGIC ENCEPHALOMYELITIS
154 mg (7.68 mmol) on the 7th day of vitamin supplements. Further investigations are difficult, for the father is an only child and all the grandparents are deceased. Other members of his family are domiciled in Greece, where he was born. In all we have tested 67 healthy volunteers by the 7-day ascorbate test for hyperoxaluria. Of these, 3 have shown the metabolic defect. Since 2 of these subjects were father and son, it seems likely that the defect is inherited. Such people are at risk of urinary-tract stone formation if given regular large doses of vitamin C. It would seem a reasonable precaution to recommend screening for ascorbate-induced hyperoxaluria in all people considering vitamin-C supplementation. Gordon Institute,
Geelong 3216,
MICHAEL BRIGGS
Australia. The protective device in
use.
the catheter is protected from the weight of bedclothes and the patient is free to change position without danger of
ment
direct traction
on
the catheter.
Children’s Hospital,
Ladywood Middleway, Ladywood, Birmingham B16 8ET.
ANN COMLEY
VITAMIN-C-INDUCED HYPEROXALURIA
SIR--The conversion of ascorbic acid to oxalate was described many years ago, 12and 24 hr excretion of urinary oxalate is known to rise slightly but significantly in subjects taking large daily doses of vitamin C.3 In a study to measure oxalate production from ascorbic acid, we encounteredahealthy young man who showed an approximately 10-fold increase in urinary oxalate after a short course of vitamin-C supplements (4 g daily). In an attempt to estimate the population frequency of this metabolic abnormality, we have given 4 g ascorbic acid (1 g four times daily for 7 days to a large group of healthy volunteers. Oxalate was measured in 24 hr urine collections on the day before the vitamin was taken, then again on the 7th day. Each volunteer was given a list of oxalate-rich foods and instructed not to include any in the diet during the trial period. A second young man was found who also showed a large increase in oxalate excretion during vitamin-C supplementation, and we have studied him and other members of his family. was aged 23 and in good health. He was unmarried. Initial 24 urinary oxalate was 43 !tl6 (0-48 mmol), but this rose to 738 mg (8.20 mmol) on the 7th day of vitamin-C supplementation. A third 24 hr collection of urine was made after a further 7 days, during which time no supplementary vitamin C was given. The oxalate output had then dropped to 123 mg (1-37 mmol). A second course of vitamin C was given, and by the 7th day 24 hr urinary oxalate was 695 mg (7-72 mmol). This again fell on withdrawing the supplement for 7 days to
HYPERLIPOPROTEINÆMIA AND PSORIASIS SIR,--Because of a longstanding interest in hyperlipidaemia, one of us (R. K. S.) studied blood-lipids routinely in all dermatological inpatients. It soon became evident that patients with psoriasis tended to have raised cholesterol and/or triglyceride ; levels. McDonald and Calabresi found an increased prevalence of thromboembolic phenomena in psoriatic patients, ’ Since people with hyperlipoproteinaemia are also at greater risk of thromboembolism, it seemed possible that all three entities might be related. Thus, we began a joint study of lipid I levels in consecutive inpatients with and without psoriasis at New York University Medical Center over a one-year period, Our preliminary figures indicate an average increased incidence of random hyperlipidaemia of 18% among psoriatics as opposed to 8% among non-psoriatics. Our study was in prp gress when Puissant et al. reported similar findings. We studied 93 psoriatics and 48 non-psoriatics. The average cholesterol elevations were 10% for psoriatics and 2% for tics, and triglyceride elevations were 12% and 6%. To avoid inclusion of borderline cases the maximum normal triglyceride and cholesterol levels chosen (triglycerides 160 mg/dl, cholesterol 300 mg/d) were slightly higher than the upper-normallimit values at the laboratory performing the studies. We hope this letter will alert clinicians to the possibility of an association between hyperlipoproteinsemia, psoriasis, and thromboembolism and thereby stimulate further investigation. ’
non-psoria
He
hr
151 mg (168 mmol).
These findings suggest some type of enzyme-induction mechanism which shows high sensitivity to excess ascorbic acid in affected individuals. Since the rise in oxalate after large doses of vitamin C is small in most subjects,3 it is likely that enzymes of the ascorbate-oxalate pathways are normally of low induci-
bility. Several relatives of our second subject have also now comtests for ascorbic-acid-induced hyperoxaluria. We have examined both parents, the subject’s brother (aged 16), two sisters (aged 18 and 31), and the elder sister’s daughter (aged 11). These members of the family were all in good health, except the father, who is a maturity-onset diabetic. Results for urinary oxalate following the 7-day test with 4 g daily vitamin C were normal for the brother and all female
pleted
members of the
hr
urinary
family.
The father,
oxalate of 32 mg
however, had
(036 mmol), which
an
initial 24
rose to
1. Burns, J. J., Burch, H. B., King, C. G. J. biol. Chem. 1951, 191, 501. 2. Hellman, L., Burns, J. J. ibid. 1958, 230, 923. 3. Lamden, M. P., Chrystowski, G. A. Proc. Soc. exp. Biol. Med. 1954, 190. 4. Briggs, M. H., Garcia-Webb, P., Davies, P. Lancet, 1973, ii, 201.
691
85,
DENNIS M. BRUSTEIN RICHARD K. SCHER* ROBERT AUERBACH
Department of Dermatology, New York University School of Medicine. *Communications should be addressed
to
R. K.
S., 193 Broadway, Amityville
New York 11701.
MYALGIC ENCEPHALOMYELITIS Dr CELIA WOOKEY (51 Lake View, Edgware, Middlesex 75A) writes: "I and some fellow doctor sufferers of myal-
HAS
would like to form a group to further research into this unusual illness and to provide help for those affected. We believe that the disease is not hysterical but 0 organic entity, but, because of the protean nature of the clinIcal picture, diagnosis is difficult. We would like to establish criteria for diagnosis (e.g., the typical history in chronic relapsing cases and a preceding sore throat or attack of diarrhrea and vomiting in acute ones). There is no definitive diagnostic test. and the cause of the illness is unknown. The classical descnf tion is Acheson’s.3 Our impression is that myalgic encepho myelitis often goes unrecognised unless it erupts in an out, break at an institution, but sporadic cases do occur. We secl help from general practitioners and from hospital consultant and would be pleased to hear from anyone interested in tJu!
gic encephalomyelitis
project." 1. McDonald, C. J., Calabresi, P. Archs Derm. 1973, 107, 2. Puissant, A., Duperrat, B., Pfahl, F., Rouffy, J. Skin
6, 26. 3. Acheson, E. D.
Am. J
Med. 1959,
26, 569.
918. Allergy News, 1975
Geelong 3216,
MICHAEL BRIGGS
Australia. The protective device in
use.
the catheter is protected from the weight of bedclothes and the patient is free to change position without danger of
ment
direct traction
on
the catheter.
Children’s Hospital,
Ladywood Middleway, Ladywood, Birmingham B16 8ET.
ANN COMLEY
VITAMIN-C-INDUCED HYPEROXALURIA
SIR--The conversion of ascorbic acid to oxalate was described many years ago, 12and 24 hr excretion of urinary oxalate is known to rise slightly but significantly in subjects taking large daily doses of vitamin C.3 In a study to measure oxalate production from ascorbic acid, we encounteredahealthy young man who showed an approximately 10-fold increase in urinary oxalate after a short course of vitamin-C supplements (4 g daily). In an attempt to estimate the population frequency of this metabolic abnormality, we have given 4 g ascorbic acid (1 g four times daily for 7 days to a large group of healthy volunteers. Oxalate was measured in 24 hr urine collections on the day before the vitamin was taken, then again on the 7th day. Each volunteer was given a list of oxalate-rich foods and instructed not to include any in the diet during the trial period. A second young man was found who also showed a large increase in oxalate excretion during vitamin-C supplementation, and we have studied him and other members of his family. was aged 23 and in good health. He was unmarried. Initial 24 urinary oxalate was 43 !tl6 (0-48 mmol), but this rose to 738 mg (8.20 mmol) on the 7th day of vitamin-C supplementation. A third 24 hr collection of urine was made after a further 7 days, during which time no supplementary vitamin C was given. The oxalate output had then dropped to 123 mg (1-37 mmol). A second course of vitamin C was given, and by the 7th day 24 hr urinary oxalate was 695 mg (7-72 mmol). This again fell on withdrawing the supplement for 7 days to
HYPERLIPOPROTEINÆMIA AND PSORIASIS SIR,--Because of a longstanding interest in hyperlipidaemia, one of us (R. K. S.) studied blood-lipids routinely in all dermatological inpatients. It soon became evident that patients with psoriasis tended to have raised cholesterol and/or triglyceride ; levels. McDonald and Calabresi found an increased prevalence of thromboembolic phenomena in psoriatic patients, ’ Since people with hyperlipoproteinaemia are also at greater risk of thromboembolism, it seemed possible that all three entities might be related. Thus, we began a joint study of lipid I levels in consecutive inpatients with and without psoriasis at New York University Medical Center over a one-year period, Our preliminary figures indicate an average increased incidence of random hyperlipidaemia of 18% among psoriatics as opposed to 8% among non-psoriatics. Our study was in prp gress when Puissant et al. reported similar findings. We studied 93 psoriatics and 48 non-psoriatics. The average cholesterol elevations were 10% for psoriatics and 2% for tics, and triglyceride elevations were 12% and 6%. To avoid inclusion of borderline cases the maximum normal triglyceride and cholesterol levels chosen (triglycerides 160 mg/dl, cholesterol 300 mg/d) were slightly higher than the upper-normallimit values at the laboratory performing the studies. We hope this letter will alert clinicians to the possibility of an association between hyperlipoproteinsemia, psoriasis, and thromboembolism and thereby stimulate further investigation. ’
non-psoria
He
hr
151 mg (168 mmol).
These findings suggest some type of enzyme-induction mechanism which shows high sensitivity to excess ascorbic acid in affected individuals. Since the rise in oxalate after large doses of vitamin C is small in most subjects,3 it is likely that enzymes of the ascorbate-oxalate pathways are normally of low induci-
bility. Several relatives of our second subject have also now comtests for ascorbic-acid-induced hyperoxaluria. We have examined both parents, the subject’s brother (aged 16), two sisters (aged 18 and 31), and the elder sister’s daughter (aged 11). These members of the family were all in good health, except the father, who is a maturity-onset diabetic. Results for urinary oxalate following the 7-day test with 4 g daily vitamin C were normal for the brother and all female
pleted
members of the
hr
urinary
family.
The father,
oxalate of 32 mg
however, had
(036 mmol), which
an
initial 24
rose to
1. Burns, J. J., Burch, H. B., King, C. G. J. biol. Chem. 1951, 191, 501. 2. Hellman, L., Burns, J. J. ibid. 1958, 230, 923. 3. Lamden, M. P., Chrystowski, G. A. Proc. Soc. exp. Biol. Med. 1954, 190. 4. Briggs, M. H., Garcia-Webb, P., Davies, P. Lancet, 1973, ii, 201.
691
85,
DENNIS M. BRUSTEIN RICHARD K. SCHER* ROBERT AUERBACH
Department of Dermatology, New York University School of Medicine. *Communications should be addressed
to
R. K.
S., 193 Broadway, Amityville
New York 11701.
MYALGIC ENCEPHALOMYELITIS Dr CELIA WOOKEY (51 Lake View, Edgware, Middlesex 75A) writes: "I and some fellow doctor sufferers of myal-
HAS
would like to form a group to further research into this unusual illness and to provide help for those affected. We believe that the disease is not hysterical but 0 organic entity, but, because of the protean nature of the clinIcal picture, diagnosis is difficult. We would like to establish criteria for diagnosis (e.g., the typical history in chronic relapsing cases and a preceding sore throat or attack of diarrhrea and vomiting in acute ones). There is no definitive diagnostic test. and the cause of the illness is unknown. The classical descnf tion is Acheson’s.3 Our impression is that myalgic encepho myelitis often goes unrecognised unless it erupts in an out, break at an institution, but sporadic cases do occur. We secl help from general practitioners and from hospital consultant and would be pleased to hear from anyone interested in tJu!
gic encephalomyelitis
project." 1. McDonald, C. J., Calabresi, P. Archs Derm. 1973, 107, 2. Puissant, A., Duperrat, B., Pfahl, F., Rouffy, J. Skin
6, 26. 3. Acheson, E. D.
Am. J
Med. 1959,
26, 569.
918. Allergy News, 1975