A novel common Kell antigen, TOU, and its spatial relationship to other Kell antigens.

A 47-year-old native American (TOU) was admitted to hospital for hip surgery. His serum agglutinated all red blood cells (RBCs) tested except Ko and DTT-treated RBCs and was weakly reactive with RBCs known to have a weak expression of Kell antigens, namely Kmod, McLeod, Kp(a+b-) (KEL:3,-4) and K:-13 (KEL:-13) phenotypes. RBCs from three siblings, a son and a daughter were incompatible with TOU's antibody. TOU's RBCs had the common Kell phenotype: K-k+Kp(a-b+c-)Ku+Js(a-b+)Ul(a-)K:11,-17K:14,-24K:12,13,18,19, 22,-23(KEL:-1,2,-3,4,5,-6,7,-10,11,12,13,14,-17,18,19,-21,22,-23,-24). Since TOU's RBCs were not agglutinated by an unidentified Kell-related antibody (IAN), tests were performed to show that TOU and IAN were mutually compatible. IAN is a Latino female hospitalised for a hysterectomy. The TOU antigen was shown to be located on the Kell glycoprotein by a monoclonal antibody immobilisation of erythrocyte antigen (MAIEA) assay. The unique pattern of reactivity obtained with TOU and IAN antibodies using this assay indicated the TOU epitope to be in an area remote from other Kell antigens, namely K, k, Kpa, Kpb, Kpc, Ku, Jsa, Jsb, U1a, K11, K12, K13, K14, Wka, K18, K19, K22 and K24 (KEL1, KEL2, KEL3, KEL4, KEL5, KEL6, KEL7, KEL11, KEL12, KEL13, KEL14, KEL17, KEL18, KEL4, KEL5, KEL6, KEL7, KEL11, KEL12, KEL13, KEL14, KEL17, KEL18, KEL19, KEL21, KEL22 and KEL24) but close to the low-incidence antigen K23 (KEL23).(ABSTRACT TRUNCATED AT 250 WORDS)

Successful management of paraprotein-associated peripheral polyneuropathies by immunoadsorption of plasma with staphylococcal protein A.

Two patients with paraprotein-associated peripheral polyneuropathy were treated successfully using immunoadsorption of patient's plasma with staphylococcal protein A. Both had previously been treated with immunosuppressive agents or plasma exchange, and were rapidly relapsing at the time of their protein A immunoadsorption therapy. One patient was treated "on-line" with a blood cell separator, and one was treated "off-line." Both responded well to therapy with minimal toxicity. Serum levels of circulating immune complexes were elevated in one patient and remained so during and after therapy. Immunoadsorption with protein A should be investigated as a therapeutic option for patients with paraprotein-associated peripheral polyneuropathy. The therapy is relatively easy to administer, particularly "off-line," and was well tolerated by our patients. More experience, including formal clinical trials, will be required to properly define the indications for, and mechanism of response to, this therapy.