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EDITOR
In 1994 McBride reported two cases of a malformed child born to
fathers with thalidomide embryopathy.1 In case 1 the child
had two unaffected brothers, and in case 2 the child had an unaffected
older sibling. McBride suggested that thalidomide might be (the first)
human germ cell mutagen. This contention was countered by several
respondents, but several tabloid newspapers espoused the cause of the
alleged second generation cases of thalidomide embryopathy.
2 3
Subsequent to these exchanges a
comprehensive experimental mutagenicity database was published,
indicating that thalidomide was devoid of mutagenic
activity.4
A major clinical evaluation of the hypothesis presented by
McBride has just been published, and does not support it.5
Stromland et al conducted a retrospective study of the 88 Swedes
recorded with thalidomide embryopathy between 1959 and 1963. Forty six of them were the parents of a total of 86 children, and 34 of the
parents agreed to participate in the study. This allowed reference