914
SPIRONOLACTONE AND SERUM-BILE-SALT LEVELS et al.’ suggested that spironolactone might be microsomal enzyme inducer for lowering serum-bilesalt (S.B.S.) concentrations in patients with cirrhosis. They found that spironolactone produced a sharp decrease of s.B.s. in patients with hepatobiliary diseases but did not affect the normal S.B.S. levels of eight controls. We have studied twelve consecutive patients with biopsyproven cirrhosis. Bile-acid concentrations were measured by a radioimmunoassay method using ’1-cholylglycylhistamine as a radioactive label. This assay measures predominantly the conjugated primary bile salts,2 and the normal range is 4"7±2-4 (mean+S.D.). Fasting S.B.S. were measured before and after administration of oral spironolactone 200 mg per day for two weeks. Spironolactone did not lower the s.B.s.--on the contrary it produced a consistent rise in all patients, both as a group (from 211 ±33 to 500±62 limovi, mean±s.E.) and as individuals (see figure). There was no indication that these in-
SIR,-Feher
used
as a
for S.B.S. may have played a role. We are now looking at the effect of spironolactone on s.B.s. in laboratory animals. Sptronolactone has several side-effects and has caused tumours m chronic toxicity studies in rats.3 It should be used with cauuon.
Division of
Gastroenterology,
of Alabama in Birmingham, Birmingham, Alabama 35294, U.S.A.
University
A. R. C. B.
A. MIHAS G. GIBSON E. BURNHAM I. HIRSCHOWITZ
MERALGIA PARÆSTHETICA AND EPSTEIN-BARR VIRUS
SIR,-Infectious mononucleosis has been implicated in a variety of neurological illnesses, including the Guillain-Barré syndrome, Bell’s palsy, transverse myelitis, meningoencephalitis, brachial plexus neuropathy, and mononeuritis multiplex.’ Infectious mononucleosis is due to infection with the Epstein-Barr virus (E.B.V.),2 but infection with this agent does not always result in clinically apparent infectious mononucleosis-indeed, infection may be clinically inapparent in up to 60% of cases.3 Nor does infection with E.B.v. always result in a rise in the heterophile antibody titre.4 When virus-specific serological tests for E.B.v. became widely available, several neurological illnesses were found to be associated with an otherwise inapparent infection with this agent. Grose et al.have suggested that a young adult who has neurological illness without clinical or laboratory evidence for infectious mononucleosis should be suspected of harbouring E.B.v.’1 an acute
We have
three young patients with acute meralgia associated with serological evidence of E.B.v. Inparaesthetica fection. This sensory neuropathy of the lateral femoral cutaneous nerve was described by Bernhardt in 1895. Many factors have been implicated as possibly playing a causative or permissive role: direct trauma to the nerve, pregnancy, pelvic malignancy, entrapment, obesity, ganglion formation, arthritis of the lumbosacral spine, scoliosis, and anomalous nerve course. Our patients (two men aged 19 and 23 and a woman aged 17) had no evidence of the above factors. Serological testing for E.B.v. was done within weeks of the onset of the neuropathy, using the IgM-specific antibody method of Schmitz and Scherer.’ One patient also had a positive heterophile test, but did not otherwise have clinical evidence for infectious mononucleosis. One patient was free of symptoms at the end of 3 months; one continues to have discomfort 2 years later; and one has been lost to follow-up. While
seen
and convalescent serological confirmation of infection temporally related to the development of the neuropathy is lacking, we feel that infection with this virus should be considered in a young patient with otherwise unexplained meralgia paraesthetica. Further studies may show this agent to be responsible for several unexplained mono-neuropathies in young adults. E. WAYNE MASSEY acute
acute E.B.v.
S.B.S. concentrations in fifteen patients with cirrhosis of liver before and 2 weeks after treatment with spironolactone 200 mg
daily.
Department of Neurology, National Naval Medical Center, Bethesda, Maryland 20014, U.S.A.
due to deterioration in liver function since liverremained unchanged. Our findings suggest that spironolactone is not of value in the treatment of raised S.B.S. We cannot explain the discrepancy between our findings and those of the Hungarian group.’ Differences m patient population and assay methods
WM. L. BRANNON, A. B. PLEET
JR
creases were
function
tests
1 Grose, C., Henle, W., Henle, G., Feorino, P. New Engl. J. Med. 1975, 292, 392.
2. Henle, W., Henle, G. in Oncogenesis and Herpesviruses edited by P. M. Biggs, G. de Thé, and L. N. Payne); p. 262. International Agency for Research in Cancer, Lyon, 1972. G. Nathanson, M. Archs Neurol 1972, 26, 353. 3. Silverst in, A. Steinb rg,
4. Evans, A.S Nied rman, J.C
1 Feher, T., Varadi, A., Tanko, A.Lancet,1976i 2 Spenney, J. G., Johnson, B.
J., Hirschowitz, B.I., Mihas, Gastroenterology, 1977, 72, 305.
Drug Bull.
3. F.D.A.
1976, 6, 33.
McCollum, R. W. New Engl. J.Med. 1968, 279, 1 21.
51.
A.A., Gibson, R.
5.Henl,W.Henl,C.Horwitz,C.AHumPath.1974,5 2.
6. Bernha dt, M. Neurol. Cbl. 1895, i p.24
7. Schmitz, H., Schererf i M. Arch. ges. Visusforsch. 1972, 37, 3 2.
SPIRONOLACTONE AND SERUM-BILE-SALT LEVELS et al.’ suggested that spironolactone might be microsomal enzyme inducer for lowering serum-bilesalt (S.B.S.) concentrations in patients with cirrhosis. They found that spironolactone produced a sharp decrease of s.B.s. in patients with hepatobiliary diseases but did not affect the normal S.B.S. levels of eight controls. We have studied twelve consecutive patients with biopsyproven cirrhosis. Bile-acid concentrations were measured by a radioimmunoassay method using ’1-cholylglycylhistamine as a radioactive label. This assay measures predominantly the conjugated primary bile salts,2 and the normal range is 4"7±2-4 (mean+S.D.). Fasting S.B.S. were measured before and after administration of oral spironolactone 200 mg per day for two weeks. Spironolactone did not lower the s.B.s.--on the contrary it produced a consistent rise in all patients, both as a group (from 211 ±33 to 500±62 limovi, mean±s.E.) and as individuals (see figure). There was no indication that these in-
SIR,-Feher
used
as a
for S.B.S. may have played a role. We are now looking at the effect of spironolactone on s.B.s. in laboratory animals. Sptronolactone has several side-effects and has caused tumours m chronic toxicity studies in rats.3 It should be used with cauuon.
Division of
Gastroenterology,
of Alabama in Birmingham, Birmingham, Alabama 35294, U.S.A.
University
A. R. C. B.
A. MIHAS G. GIBSON E. BURNHAM I. HIRSCHOWITZ
MERALGIA PARÆSTHETICA AND EPSTEIN-BARR VIRUS
SIR,-Infectious mononucleosis has been implicated in a variety of neurological illnesses, including the Guillain-Barré syndrome, Bell’s palsy, transverse myelitis, meningoencephalitis, brachial plexus neuropathy, and mononeuritis multiplex.’ Infectious mononucleosis is due to infection with the Epstein-Barr virus (E.B.V.),2 but infection with this agent does not always result in clinically apparent infectious mononucleosis-indeed, infection may be clinically inapparent in up to 60% of cases.3 Nor does infection with E.B.v. always result in a rise in the heterophile antibody titre.4 When virus-specific serological tests for E.B.v. became widely available, several neurological illnesses were found to be associated with an otherwise inapparent infection with this agent. Grose et al.have suggested that a young adult who has neurological illness without clinical or laboratory evidence for infectious mononucleosis should be suspected of harbouring E.B.v.’1 an acute
We have
three young patients with acute meralgia associated with serological evidence of E.B.v. Inparaesthetica fection. This sensory neuropathy of the lateral femoral cutaneous nerve was described by Bernhardt in 1895. Many factors have been implicated as possibly playing a causative or permissive role: direct trauma to the nerve, pregnancy, pelvic malignancy, entrapment, obesity, ganglion formation, arthritis of the lumbosacral spine, scoliosis, and anomalous nerve course. Our patients (two men aged 19 and 23 and a woman aged 17) had no evidence of the above factors. Serological testing for E.B.v. was done within weeks of the onset of the neuropathy, using the IgM-specific antibody method of Schmitz and Scherer.’ One patient also had a positive heterophile test, but did not otherwise have clinical evidence for infectious mononucleosis. One patient was free of symptoms at the end of 3 months; one continues to have discomfort 2 years later; and one has been lost to follow-up. While
seen
and convalescent serological confirmation of infection temporally related to the development of the neuropathy is lacking, we feel that infection with this virus should be considered in a young patient with otherwise unexplained meralgia paraesthetica. Further studies may show this agent to be responsible for several unexplained mono-neuropathies in young adults. E. WAYNE MASSEY acute
acute E.B.v.
S.B.S. concentrations in fifteen patients with cirrhosis of liver before and 2 weeks after treatment with spironolactone 200 mg
daily.
Department of Neurology, National Naval Medical Center, Bethesda, Maryland 20014, U.S.A.
due to deterioration in liver function since liverremained unchanged. Our findings suggest that spironolactone is not of value in the treatment of raised S.B.S. We cannot explain the discrepancy between our findings and those of the Hungarian group.’ Differences m patient population and assay methods
WM. L. BRANNON, A. B. PLEET
JR
creases were
function
tests
1 Grose, C., Henle, W., Henle, G., Feorino, P. New Engl. J. Med. 1975, 292, 392.
2. Henle, W., Henle, G. in Oncogenesis and Herpesviruses edited by P. M. Biggs, G. de Thé, and L. N. Payne); p. 262. International Agency for Research in Cancer, Lyon, 1972. G. Nathanson, M. Archs Neurol 1972, 26, 353. 3. Silverst in, A. Steinb rg,
4. Evans, A.S Nied rman, J.C
1 Feher, T., Varadi, A., Tanko, A.Lancet,1976i 2 Spenney, J. G., Johnson, B.
J., Hirschowitz, B.I., Mihas, Gastroenterology, 1977, 72, 305.
Drug Bull.
3. F.D.A.
1976, 6, 33.
McCollum, R. W. New Engl. J.Med. 1968, 279, 1 21.
51.
A.A., Gibson, R.
5.Henl,W.Henl,C.Horwitz,C.AHumPath.1974,5 2.
6. Bernha dt, M. Neurol. Cbl. 1895, i p.24
7. Schmitz, H., Schererf i M. Arch. ges. Visusforsch. 1972, 37, 3 2.
