4) Response to treatment. Patients who responded to treatment invariably became mauve factor or kp factor negative. However, there were many patients who no longer excreted this factor but who had not recovered. I have not examined whether these patients might have responded to longer treatment. In my recent report (6) on chronic patients it is evident that many chronic patients need five to seven years of treatment. Perhaps some of the negative excretors after having been positive might have fallen into this group. Patients who were well and were kp free were followed for months or years. If they became positive at any time they also became clinically ill within a matter of weeks or months.
Generally, the presence of kp is associated with clinical conditions characterized by a high degree of perceptual disorganization. These are chiefly the schizophrenic patients, but also includes a substantial proportion of other psychiatric diseases also characterized by perceptual changes. Unfortunately psychiatrists do not search their patients’ mental state adequately and miss many of these changes. They can be readily detected using perceptual tests such as the HOD test. (7) In other words, the presence of kp correlates strongly with high scores on these perceptual tests. Perhaps Dr. Kraus’s detailed report will arouse interest in this test, sadly neglected for so many years.
In 1960 I examined a seven year old boy who had been diagnosed retarded and preparations were being made to send him to a special school. His parents were very concerned and asked me whether I would examine him. For over a year he had difficulty in school, could not read, and avoided going to school as much as he could, often staying away from home all day but not at school. His mother, a teacher, had been spending a lot of time giving him special instruction without improvement. He was also developing behavioral problems at home. I examined him early in 1960 and could not locate any particular problem, perhaps because I had not had much experience treating children. I then had his urine analyzed for mauve factor, kp, and to my surprise found a large amount. I called his father, a friend of mine, and said in jest “You are in luck, your son has schizophrenia.” He answered, “Why does that make me so lucky?” I then told him I was kidding him, and added seriously he was certainly not schizophrenic, but since he had the same biochemical factor in his urine we had found in schizophrenics, and since they had responded well to vitamin therapy, this suggested that his son might respond in a similarly beneficial way.
I started him on niacinamide 1 gram after each meal. In the fall his father asked me would I like to know what had happened to his son. He then told me that two months after his son had started on the vitamin he had begun to read, that he had spent a few months reading voraciously and that he was no longer concerned about his behaviour. His son was normal and remained well. He took his niacinamide regularly until he was about 14. One day he asked his mother why he was taking the pills. She brought him to see me and I explained why I thought he should remain on the vitamin until at least age 18 at which time he could determine how well he could do without it. He is still well, happily married with children, and is fully employed in a responsible job.
This illustrates the use of the kp urine test for pyrolleuria, and the use of niacinamide in large doses to treat this condition successfully. I did not use vitamin B6 nor zinc in 1960. Pyridoxine is essential for the conversion of tryptophan to nicotinamide adenine dinucleotide, the vitamin B3 coenzyme. With a deficiency of pyridoxine, the synthesis of NAD in the body is reduced. A pyridoxine deficiency will produce a form of pellagra not distinguishable clinically from the pellagra caused by a deficiency of vitamin B3.