678 A.E., and may enhance absorption of this essential ment in normal human neonates.
Department of Nutrition, Agricultural Experimental Station,
College of Agricultural and Environmental Sciences, Sciences,
University of California, Davis, California 95616, U.S.A.
LUCILLE S. HURLEY BO LÖNNERDAL ANNA G. STANISLOWSKI
POLYARTERITIS NODOSA AND HAIRY-CELL LEUKÆMIA
SIR,-Classic polyarteritis nodosa is
a systemic necrotising affecting medium and small muscular arteries. The aetiology is usually unknown, though some cases seem to be related to hepatitis-B-virus infection.’ The host factors which allow virus-antibody complexes to persist in the circulation and deposit in vessel wallsl,2 are poorly defined. The occurrence of vasculitis in patients with chronic lymphoproliferative neoplasms3 such as chronic lymphatic leukaemia, Hodgkin’s disease, and multiple myeloma may provide insight into this problem since immunological abnormalities and recurrent infections are common to all. Patients with hairy-cell leukaemia are very susceptible to infection4’ and are reported to have serum factors which impair monocyte function.6 For this reason, we believe that the coincidence of hairy-cell leuksemia and polyarteritis nodosa in the patient described in this report may have pathogenetic implications. A 36-year-old man presented with an indolent septic ulcer on the right index finger in April, 1976. He was pale and had moderate splenomegaly. He had pancytopenia with typical hairy-cells accounting for 4% of the total white-cell count. Splenectomy was done in July, 1976, after which he had bacterial pneumonia and herpes labialis. Several minor skin and oropharyngeal infections occurred after discharge from hospi-
2 months the patient had severe rest pain. He was admitted to hospital where he was noted to be normotensive with weak pulsations in the right dorsalis pedis and posterior tibial arteries. The ankle-occlusion pressure was 140 mm Hg on the left and 95 mm Hg on the right. The rest of the physical examination was normal apart from mild axillary and inguinal lympha-
denopathy. The Hb was 10.8 g/dl, w.B.c. 4x 109/1 (4% hairy-cells), and platelets 400x 109/1. Bone-marrow and lymph-node histology revealed extensive hairy-cell infiltration. Renal and liver function tests were normal and neither HBs antigen nor antibody were detected. Serum-IgG was raised at 38.0 g/1 but tests for rheumatoid factor, antinuclear antibody, and cryoglobulins were negative. Total serum complement (CHsa) and the early complement components were low, suggesting activation of the classical pathway. Circulating immune complexes were detected (Clq binding assay). Arteriography showed numerous microaneurysms 2-5 mm in diameter in the inferior mesenteric circulation and in the arteries of both legs (see figure). Since both polyarteritis nodosa and hairy-cell leukaemia are a chance association is highly unlikely. The susceptibility of patients with hairy-cell leuksemia to infection is largely due to neutropenia, but may also result from a profound monocytopenia and impaired monocyte function.4 The monocyte-macrophage system has a central role in the clearance of immune complexes, and any factor interfering with function of this system could result in the prolonged circulation and deposition of these complexes. Although current reviews’5 do not comment on the occurrence of vasculitic disorders in hairy-cell leukaemia, the frequent use of corticosteroids and immunosuppressive drugs may modify the nature and expression of a concurrent vasculitis. We believe this to be the first report of an association between the two conditions. More detailed studies of other patients with hairy-cell leukaemia are in progress.
tal. 1977 the patient had several episodes of arthritis of both knees which responded to short courses of prednisone. In March, 1978, intermittent claudication of the right leg developed. The claudication distance rapidly decreased and within
Gocke, D. J., Hsu, K., Morgan, C., Bombardieri, S., Lockshin, M., Christian, C. L. Lancet, 1970, ii, 1149. 2. Gerber, M. A., Brodin, A., Steinberg, D., Vernance, S., Yang, C. H., Paronetto, F. New Engl. J. Med. 1972, 286, 14. 3. Fauci, A. S., Haynes, B. F., Katz, P. Ann intern. Med. 1978, 89, 660 4 Golomb, H. M., Catovsky, D., Golde, D.W. ibid. 1978, 89, 677. 5. Turner, A., Kjeldsberg, C. R. Medicine, 1978, 57, 478. 6. Kjeldsberg, C. R. Ann, intern Med. 1978, 88, 268.
Royal Postgraduate Medical School, London W12
G. R. V. HUGHES K. B. ELKON R. SPILLER D. CATOVSKY
YERSINIA ENTEROCOLITICA AND THYROID DISEASES IN SPAIN
SIR,-Studies in Denmark’2 and the U.S.A.3 have revealed high incidence of anti Yersinia enterocolitica (Y.E.) antibodies in several thyroid diseases. In Denmark, the prevalence of a
anti-Y.E. antibodies in the normal population is higher than it is in U.S.A.; nevertheless the incidence of antibodies to Y.E. serotype 3 is similar in patients of both countries with thyroid diseases. We have looked for anti-Y.E. antibodies serotypes 3 and 9, in sera of 154 patients with a variety of thyroid diseases and in 44 controls. Agglutination was done in a microtitre system
(Dynatech Corporation, Cambridge, Massachusetts) using as antigen strains supplied by Dr Sten Winblad (Lund University, Mahno, Sweden). In positive cases, seroagglutination to brucella was tested by the same method to see if there was a crossreaction. Titres of 1/8 or greater were considered significant (see table). The frequency of anti-Y.E. antibodies was similar in control individuals and in patients with thyroid diseases; positive cases were serotype 9 except in 1 control and in 1 patient with multinodular goitre. In positive cases with Graves’ disease, there was no relation to functional status; none of the positive cases 1. 2.
in arteries of both
Bech, K., Larsen, J. H., Hansen, J. M. Lancet, 1974, ii, 951. Bech, K., Nerup, J., Larsen, J. H. Acta endocr. 1977, 84, 87. 3. Shenkman, L., Bottone, E. J. Ann. intern. Med. 1976, 85, 735.