411

the

"

duovirus

"

group.

For these

reasons

let

us use a

morphological term for what will be a de-facto morphological classification. Rotavirus has a purely descriptive meaning,4 relates to presently established fact, is unlikely to give rise to subsequent anomalies, and has priority. Regional Virus Laboratory, Ruchill Hospital, Glasgow G20 9NB.

C. R. MADELEY.

PSEUDOMEMBRANOUS COLITIS ASSOCIATED WITH CLINDAMYCIN

SIR,—4 cases of pseudomembranous colitis associated with clindamycin have been described.5 Ultrastructural examination of rectal biopsy specimens from 2 of the

5th months of pregnancy, and one hundred were in the 9th month. A.N.F. was sought by the methods of Roitt and Doniach7 using calf thyroid as substrate, and by Elling’s method,8 using frozen and thawed human granulocytes as substrate. We found low titres of A.N.F. in 4% of pregnant women and 5% of non-pregnant women. Medical Department B and Immunological Laboratory, Meir Hospital, Kfar Saba, Israel.

A. KLAJMAN S. ITAI.

IDIOPATHIC THROMBOCYTOPENIC PURPURA IN THE ELDERLY

SIR,--Idiopathic thrombocytopenic purpura (I.T.P.), even in its chronic form, is generally considered to be a disease of young adults.9 We recently studied an 89-year-old patient with l.T.P. who appears to be the oldest person reported with this disease.

Virus particles in

pseudomembrane of pseudomembranous colitis.

patients revealed the presence of a viral colitis. The viral particles, about 50 nm. diameter, are situated in the pseudomembrane (see accompanying figure), the colonic epithelial cells, and the endothelial cells. A more detailed report of these findings is in preparation. I should like to thank Mr J. H. H. Webster and Mr B. J. Wilken for permission to report these cases. Wessex Neurological Centre, Southampton General Hospital, Shirley, Southampton SO9 4XY.

H. W. STEER.

ANTINUCLEAR FACTOR IN PREGNANT WOMEN et al. SIR,—Polishuk reported binding antinuclear factor (A.N.F.) in 72% of pregnant women and 9-1% of non-pregnant controls. We have examined sera from a hundred and twenty-five pregnant women and one hundred matched non-pregnant women for A.N.F. The women were aged from 19 to 37, twenty-five were in the 3rd and H., Bryden, A. S., Davies, H., Woode, G. N., Bridger J. C., Derrick, J. M. ibid. 1974, ii, 61. 5. Steer, H. W. Lancet, 1974, i, 1176. 6. Polishuk, W. Z., Beyth, Y., Izak, G. Lancet, 1971, ii, 270.

He was admitted to the Veterans Administration Hospital, San Francisco, because of syncope. Four years earlier his platelet-count had been normal. His hsematocrit was 29% and platelets were 4000 per c.mm.; he had scattered petechiae. His medications included meclizine hydrachloride with niacin, indomethacin, and pentaerythrityl tetranitrate. Examination of bone-marrow showed increased megakaryocytes. Scan of liver and spleen revealed no abnormalities. Antibodies to platelets 10. were not found. Prednisone, 100 mg. per day, was administered without response and, after one month, cyclophosphamide was added. Two weeks later his platelets rose to 100,000 per c.mm. The count continued to rise, and the patient was discharged from the hospital with a normal platelet-count. Ten months later, his platelets fell to 100,000 per c.mm. Shortly thereafter, spontaneous massive gastrointestinal bleeding developed; platelets were 2000 per c.mm. Bone-marrow again contained increased numbers of megakaryocytes. Scans of liver and spleen and liver-function tests appeared normal. Treatment with prednisone and cyclophosphamide did not produce an increase in platelets, and splenectomy was performed. The spleen weighed 162 g. and appeared normal microscopically. The patient’s platelet-count never rose, and he died 50 days later with bleeding, infection, liver failure, and coma. Necropsy revealed petechial haemorrhage in the gastrointestinal tract, periportal fibrosis of the liver, and cytomegalovirus inclusions in the lungs, pancreas, liver, and oesophagus. No aetiology for his thrombocytopenia could be detected.

In addition to this patient, we saw a 74-year-old patient and an 81-year-old patient with well-documented I.T.P. The incidental finding of this many elderly patients with I.T.P. (as well as a study 11 in which most of the patients were more than 60 years old, the age distribution being attributed to sample bias)’makes us wonder about the real age distribution of I.T.P. I.T.P. is primarily a diagnosis of exclusion; this is necessary for study of the therapy and immuno-logical basis of the disease, but it makes study of the epidemiology impossible. No reliable laboratory test for Exclusion of cases because there may be I.T.P. exists. another cause of thrombocytopenia will bias the age distribution of the sample if the age distribution of patients with these factors differs from that of all patients with I.T.P. For example, I.T.P. is excluded if the patient has systemic lupus erythematosus. Testing for antinuclear antibodies is part of routine screening for I.T.P., and this antibody is more common among the elderly even after exclusion of patients with collagen-vascular diseases.lE 7.

Roitt, I. M., Doniach, D. in Immunology Techniques. Geneva,

8. 9.

Elling, P. Acta path. microbiol. scand. 1969, 69, Wintrobe, M. M. in Clinical Hematology; p.

1967.

4. Flewett, T.

384. 889.

Philadelphia,

1967. 10. 11. 12.

Howell, E., Perkins, H. A. Transfusion, 1968, 8, 33. Aster, R. H., Keene, W. R. Br. J. Hœmat. 1969, 16, 61. Svec, K. H., Veit, B. C. Arthritis Rheum. 1967, 10, 509.

412 Medication-associated thrombocytopenia

must also be excluded, and the elderly use more medicine than any other age-group.13 Of the five most frequently prescribed drugs for the elderly in 1966,5 three (tolbutamide, chlorothiazide, and hydrochlorothiazide) have been associated with thrombocytopenia. Other diseases associated with thrombocytopenia are also more common among the elderly. Also affecting the age distribution in I.T.P. is the age distribution of the population at risk. Only about 0-5% of the population is 85 years of age or older.5 All these factors bias the age distribution; and this, combined with other factors already mentioned, makes I.T.P. appear, at least, to be rare in the very elderly. Until a definitive diagnostic test is developed, it must be considered that I.T.P. may occur at any age, and that its prevalence may be the same in all age-groups. Therefore, I.T.P. should be considered seriously in differential diagnosis of any patient with thrombocytopenia, irrespective of age. Clinicians must review their concept of I.T.P. and epidemiologists their data.

National Institutes of Health, Bethesda, Maryland 20014, U.S.A. University of California San Francisco, San Francisco, California 94143, U.S.A. 1144 Sonoma Avenue, Santa Rosa, California 95405, U.S.A.

STEROIDS AND

SiR,—Goodall

et

GARY B. WEISS.

JOHN C. KLOCK. HARRY B. RICHARDSON.

GUILLAIN-BARRÉ SYNDROME al.14 reported that corticosteroids have

the clinical course of the Guillain-Barre defined by the criteria of Osler and Sidell. 15 These do not apply to polyneuritis of less acute onset or of a chronic, relapsing nature, which is regarded by some as a form of Guillain-Barre syndrome. We report a case of slowly progressive polyneuritis of Guillain-Barre type which responded unequivocally to treatment with prednino

effect

syndrome

on

as

sone.

An 18-year-old man was well until August, 1973, when hypoaathesia developed in the fingers and toes and was soon followed by mild weakness in the extremities. Generalised weakness progressed slowly with slight fluctuation over the next 7 months until he was barely able to walk, and hypoaesthesia had ascended to the knees and elbows. He noted increasing dyspnrea on exertion and occasional episodes of tachycardia with abrupt onset and cessation. On March 3, 1974, he entered the hospital, where examination revealed pronounced weakness of all muscle groups in the arms and legs, which was greater distally; diminished sensation distal to the knees and elbows; and areflexia. A complete myelogram was normal, and the cerebrospinal fluid contained 252 mg. of protein and no cells. An electromyogram showed evidence of mild, chronic, partial denervation in both proximal and distal muscle groups in the arms and legs. Motor conduction was slowed in median, ulnar, and peroneal nerves, and there were no ascending sensory potentials in median and ulnar nerves. Prednisone, 40 mg. every other day, was begun on March 22, 1974, but the dosage was tapered off to 10 mg. every other day by April 8, 1974, while his weakness progressed to complete loss of movement against gravity. Vital capacity steadily diminished from 45 litres on admission to 3 litres. On April 12, 1974, prednisone 100 mg. every other day was begun, and objective improvement in strength was noted within 2 days. By April 16 vital capacity had increased to 3-75 litres, and the patient was feeding himself. His strength continued to improve steadily, progressing from proximal to distal muscle groups and more rapidly in the arms than in the legs. By May 16 he was able to walk with crutches, and at discharge on June 5 he could walk on Prescription Drugs. The Drug Users: Background Papers. Washington, D.C., 1968. 14. Goodall, J. A. D., Kosmidis, J. C., Geddes, A. M. Lancet, 1974, i,

13. U.S. Task Force

524. 16.

Osler, L. D., Sidell, A. D. New Engl. J. Med. 1960, 262, 964.

without assistance. The dose of prednisone was tapered off from May 12 and had fallen to 20 mg. every other day by midJuly, when an increase in weakness was noted. 2 weeks later the patient was barely able to walk with crutches, but increasing the prednisone dose to 100 mg. every other day resulted in slow increase in strength to his former level. He is now maintained on 100 mg. every other day and is able to walk a quarter of a mile with a cane.

Except for the slow, progressive onset, this case has all the clinical and laboratory features of the Guillain-Barré syndrome. Several of the diagnostic criteria of Osler and Sidell are lacking, but these have been criticised by some workers 16-18as being too restrictive in view of the variability of sensory findings, bladder symptoms, and clinical course reported in many series, including that of Guillain.6 There can be little doubt that the course of our patient’s disease was affected by prednisone. After a 7-month progression to almost total paralysis, recovery began within 2 days of starting high-dose therapy. Relapse coincided with tapering off the prednisone and was reversed by increasing the dose. This response is similar to that reported by others in treatment of slowly progressive 20,21 A trial of high-dose and recurrent 22,23 polyneuritis. corticosteroid treatment in these two categories of polyneuritis therefore seems justifiable. Division of Neurology, Dartmouth-Hitchcock Medical Center, R. L. SULLIVAN Hanover, New Hampshire 03755, A. G. REEVES. U.S.A.

NATURAL ŒSTROGENS AND ANTITHROMBIN-III LEVELS SiR,-The association of low serum-antithrombin-iii levels with the administration of oestrogens in the form of combination oral contraceptives was first noted by von Kaulla and von KauUa.24 Since then, several reports have confirmed this observation. 25-28 Antithrombin ill is believed to be the main antithrombin in plasma and serum. Egeberg 29 linked antithrombin-ni levels with thrombosis in a family with a hereditary thrombotic diathesis and very low antithrombin-ni levels. A similar family has been reported by others.30 The fall in antithrombin-ni activity during oestrogen therapy may therefore be relevant to the association between these drugs and thrombosis. To our knowledge antithrombin-ni levels in patients taking " natural" cestrogens have not been reported. Antithrombin-m levels were estimated by the method of von Kaulla and von Kaulla 24 in five groups of subjects. Nineteen healthy young White women receiving no medication and twenty healthy young White women on combination type oral contraceptives were studied. Various commercial preparations were used, but the cestrogen Wiederholt, W. C., Mulder, D. W., Lambert, E. H. Proc. Staff meet. Mayo Clin. 1964, 39, 427. 17. Marshall, J. Brain, 1963, 86, 55. 18. McFarland, H. R., Heller, G. L. Archs Neurol. 1966, 14, 196. 19. Guillain, G. Archs Neurol. Psychiat., Chicago, 1936, 36, 975. 20. Hinman, R. C., Magee, K. R. Ann. intern. Med. 1967, 67, 1007. 21. DeVivo, D. C., Engel, W. K. J. Neurol. Neurosurg. Psychiat. 1970, 33, 62. 22. Austin, J. H. Brain, 1958, 81, 157. 23. Thomas, P. K., Lascelles, R. G., Hallpike, J. F., Hewer, R. L. ibid. 1969, 92, 589. 24. von Kaulla, E., von Kaulla, K. N. Am. J. clin. Path. 1967, 48, 69. 25. Fagerhol, M. K., Abildgaard, U. Scand. J. Hœmat. 1970, 7, 10. 26. Fagerhol, M. K., Abildgaard, U., Bergsjo, P., Jacobsen, J. H. Lancet, 1970, i, 1175. 27. Howie, P. W., Mallinson, A. C., Prentice, C. R. M., Horne, C. H. W., McNicol, G. P. ibid. 1970, ii, 1329. 28. von Kaulla, E., Droegemeuller, W., Aoki, N., von Kaulla, K. N. Am. J. Obstet. Gynec. 1971, 109, 868. 29. Egeberg, O. Thromb. Diath. Hœmorrh. 1965, 13, 516. 30. van der Meer, J., Stoepman-van Dalen, E. A., Jensen, J. M. S. J. clin. Path. 1973, 26, 532. 16.

Letter: Idiopathic thrombocytopenic purpura in the elderly.

411 the " duovirus " group. For these reasons let us use a morphological term for what will be a de-facto morphological classification. Rota...
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