This study investigated the clonal nature of cold agglutinin disease in a series of nine patients, which included the benign or idiopathic form as well as cases with an underlying lymphoma. Surface marker phenotyping and karyotypic analysis were performed on peripheral blood lymphocytes. An increased proportion of B cells was found in four cases and in three of these patients a monoclonal B cell population was identified with a mu, kappa phenotype. In the same three cases, as well as an additional patient, an aberrant karyotype was demonstrated. The cytogenetic abnormality present in all four cases included trisomy 3; two patients also had a trisomy 12. One of these four patients had a well-differentiated lymphoma and underwent a splenectomy. Splenic lymphocytes were transformed with Epstein-Barr virus and cultured en masse. Eight clones were established producing the same cold agglutinin with identical specificity as that present in the patient's plasma. Five of these clones were studied cytogenetically, and all had the same abnormal karyotype (51,XX,+3,+9,+12,+13,+18) found in peripheral blood and splenic lymphocytes. Thus, in this case, the cold reactive autoantibody was produced by the chromosomally abnormal, neoplastic clone of lymphocytes. Our findings support the view that cold agglutinin disease represents a spectrum of clonal disorders.
M ethods of closure of the amputated finger stump are legion. Certain levels of amputation, however, demand preservation of length for optimum function. The visor flap provides this, together with sensation, padding and scars that avoid volar pressure points. The design of the flap follows the principles of three-dimensional rather than plane geomery. PRINCIPLES OF FLAP DESIGN The visor flap is a bipedicled flap based on the dorsal branches of the volar digital neurovascular bundles (Figure 1). Transverse amputations of the distal, middle and distal proximal phalanges are most suitable for this technique. Figure 2 illustrates the design of the dorsal flap. The volar/dorsal diameter of the amputation site is measured (A-B). To achieve adequate coverage, a similar area of dorsal skin and subcuta-neous tissue must be obtained (A-C), therefore, A-B is equal to A-C. The extent of the lateral incisions are to the mid axial line (D). The pivot point, D, restricts the volar transposition of this bipedicled flap because C-D is shorter than A-C. Therefore, a back cut (Figure 3) is made so that AD 1 is equal to C-D 1. The new pivot point of D 1 allows adequate volar transposition of the flap. The back cut must be through dermis only to avoid potential damage to the neurovascular structures in the subcutaneous plane. The dissection is deepened down to but not through the paratenon level. The flap is undermined and transposed distally, and sutured with a nonabsorbable suture. The donor defect is covered with a split thickness skin graft and dressed appropriately: excess skin (dog ears) may be prominent laterally, but these should not be tailored because this may interfere with the neurovascular supply to the flap. Physiotherapy to maintain range of motion is initiated on postoperative day 7. Skin graft maturation and contraction aids in the resolution of the dog ears and acts as a force in drawing the volar scar dorsally, leaving a volar surface free of a potentially prominent and/or painful scar line.
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