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LETTERS 1075numbers of patients studied. However, if the numbers of patients from various studies are pooled, as shown by Baer et a1 (2), then there is no difference between slow and fast acetylators in SLE patients and control subjects. This finding, of course, is different from that seen in many patients with drug-related lupus.In one particular study from my laboratory (3), we showed a difference in acetylator phenotype between white SLE patients (71% slow acetylators) and black SLE patients (58% slow acetylators). This result reflects the clinical observations in the US, that drug-related lupus occurs more frequently in white subjects than in black subjects.I agree with Sardas and coworkers' other conclusions, and would point out that more and better data in different population groups and different racial groups are needed.

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she has been hospitalized six more times because of pain in the right hypochondrium, vomiting, and fever, but no definite diagnosis could be made. During one hospitalization elsewhere (in 1974) she also had a maculopapular eruption all over the body. In 1974 she underwent drainage of a perianal abscess, and thereafter she was hospitalized for prolonged fever of unknown origin with abdominal pain. A short time after this she was admitted to a psychiatric hospital for depression. In the last month she suffered pain in both hands, and these complaints prevailed during this last entire hospitalization. On examination her general condition was good, blood pressure was 130/80. Her temperature was subfebrile (37-38°C) during many weeks. Occasional expiratory wheezing was heard over both lungs.The main complaint during this hospitalization was pain in both hands accompanied by fever. There were no signs of arthritis, and x-rays of the joints were normal. A complete laboratory examination on admission to the rheumatology department showed no special changes, except for a transient leukopenia (3000/mm3) and thrombocytopenia (60,000/mm3). A connective tissue disorder was suspected, but no definite diagnosis could be made.Later on, during her hospitalization peripheral neuropathy appeared. A thorough checkup ruled out many causes of peripheral neuropathy, including metal poisoning, vitamin deficiency, and diabetes. Repeated neurological examinations disclosed bilateral distal hypoalgesia of the hands (gloves-form, without sharply defined borders). The ulnar nerves on both sides and the greater auricular nerve on the right side seemed to be thickened and were tender on palpation. On the forehead a faint reddish infiltrate was visible; the right earlobe was slightly reddish and swollen, and there was partial alopecia of the eyebrows. I n both legs and forearms there was an inability to discriminate sharp from blunt and changes of temperature or touch. Both optic discs were normal. X-ray of skull and EEG were normal. A skin biopsy of the ear lobule and a nasal smear did not reveal acid-fast bacili. EMG revealed decreased conduction in the right ulnar nerve at the elbow region. Surgical decompression of the right ulnar nerve at this site was performed. During this procedure, a biopsy was done from a minor branch of this nerve, which microscopically showed signs of nerve fiber degenerations (including hydropic degeneration) and groups of acid-fast bacilli.Thus, lepra reaction of Hansen's disease could be diagnosed. After a short course of thalidomide therapy her pain disappeared. Later she was transferred to a

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