A 63-year-old black woman presented with a complaint of nail and skin darkening for 5 months. Past medical history included polycythemia vera, hypertension, angina, and hiatal hernia. For several years the patient's medications had included isosorbide dinitrate, iron sulfate, propranolol, and sucralfate. The only recent new medication was hydroxyurea (500 mg to 1.5 g daily), which the patient had started for polycythemia vera 8 months prior to presentation. She now complained of asymptomatic hyperpigmentation of the finger and toenails, which had begun proximally and extended distally over time. She also noted increased pigmentation of her face, neck, arms, and buccal mucosa.Physical examination revealed pigmentary changes in all the nails. Dyschromia varied from blue-grey to brown-black. Three different patterns of pigmentation were noted: transverse and longitudinal bands that alternated with areas of lighter discoloration (Fig. 1) and diffuse hyperpigmentation (Fig. 2). The nail plates and the proximal and lateral nail folds had a normal morphology aside from the color changes. Macular brown pigmentation was present on the patient's face, neck, lower arms, palms, and buccal mucosa (Fig. 3). The patient noted that the pigmentation in all of these areas began after the hydroxyurea was started; those areas of skin and mucosa had previously been normal. Laboratory results were significant for a mild anemia, hemoglobin 11.4 g/dL, and hematocrit 35.2%. The patient refused nail or skin biopsy. The patient also noted increased "hardness" of the nails, which made It difficult for her to cut them.Microscopic observation of sections prepared from nail clippings revealed a keratinized layer with scattered finely granular brownish pigment. Fontana Masson and Schroml's stains for melanin were positive, and Pearl's stain for iron was negative.
We describe the second example of red blood cells (RBCs) with the Lu:–7 phenotype in a 37-year-old Latino female (SA). Her RBCs were nonreactive with anti-Lu7 (Mrs. GA) but were reactive with all other antibodies to high-prevalence antigens tested, including those in the Lutheran blood group system. No Lu:–7 RBCs were available for testing. SA’s serum was nonreactive by the indirect antiglobulin test against (1) recessive and dominant Lu(a–b–) RBCs and (2) trypsin-treated or α-chymotrypsin-treated RBCs of common phenotype. By immunoblotting, eluates containing anti-Lu7 from both Mrs. GA and SA reacted with apparently the same bands in RBC membranes of common phenotype as did human anti-Lub, reacted weakly with Lu(a–b–) RBCs of the dominant type, and were nonreactive with SA’s RBC membranes. These findings raise the Lu7 antigen from its Lutheran-related (para-Lutheran) status to a bona fide member of the Lutheran blood group system. Immunohematology 1996;12:66–68.
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