Three cases are reported of hypogammaglobulinemic males with recurrent Campylobacter jejuni septicemia and erysipelas-like cellulitis without diarrhoea. In one patient Campylobacter jejuni grew from skin biopsy specimens. The findings in another patient were strongly suggestive of osteomyelitis caused by Campylobacter jejuni. Since the susceptibility of hypogammaglobulinemic patients to infection with Campylobacter jejuni is probably related to a lack of serum bactericidal activity against Campylobacter jejuni due to lack of IgM, two patients in whom previous antimicrobial treatment failed were treated with plasma infusions. This regimen supplemented with imipenem resulted in cure of these relapsing infections. Campylobacter jejuni septicemia must be considered in hypogammaglobulinemic patients who present with periodic fever and cellulitis.
Objective. Azathioprine (AZA) metabolism largely parallels the endogenous purine pathways. To date, thiopurine methyltransferase (TPMT) deficiency has been reported as a cause of AZA‐related bone marrow toxicity in 1 patient with rheumatoid arthritis (RA). We therefore studied purine enzyme activities in 3 patients with RA who experienced AZA‐related bone marrow toxicity.
Methods. Lymphocyte activity of purine nucleoside phosphorylase and 5′‐nucleotidase (5NT) and erythrocyte activity of TPMT, key enzymes in thiopurine catabolism, were measured in 3 RA patients who had experienced AZA‐related bone marrow toxicity and in 16 RA patients without signs of toxicity despite at least 6 months of treatment with AZA.
Results. Two patients with AZA‐related bone marrow toxicity were found to have a TPMT deficiency, 1 partial and 1 total. In the third patient, 5NT activity was found to be well below the lowest level observed in the control subjects.
Conclusion. All 3 patients with severe AZA‐related bone marrow toxicity had abnormal purine enzyme activities. Deficiency of purine enzymes, including TPMT and 5NT, may be a cause of AZA‐related bone marrow toxicity in patients with RA.
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