We report the seventh case of Mulvihill-Smith progeria-like syndrome in a 5-year-old boy with a thin, pinched face, failure to thrive, and cutaneous pigmented nevi. The patient's motor and intellectual development were normal. His immune function tests demonstrate evidence of lymphopenia with no selective loss of a major subpopulation, low immunoglobulin (Ig)G2 and IgG4 subclasses, and an absent in vitro proliferative response to pokeweed mitogen. Chromosomal mitomycin and radiation sensitivity were normal. The skin fibroblast growth in culture was slow, and the fibroblasts appeared morphologically different from normal controls in their size and large number of inclusions. In addition, primary cilia, which normally issue from the centrosome, were absent-a new finding in fibroblasts in this disorder. It remains to be seen if the relative absence of centrosomal cilia in cultured fibroblasts in early passages is a consistent finding in this progeria syndrome.

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The presentation of Hodgkin's disease and acute infectious mononucleosis (glandular fever) due to Epstein-Barr virus, have similar seasonal features with the peak incidence around March. The extent of seasonal variation is also similar. Seasonality of Hodgkin's disease is most obvious and also significant in adult age groups below the age of 40. Amongst those over 40 years, seasonality was no longer present in the 40-59 but returned over age 60. Seasonal similarity does not prove a relationship. However two speculations are made on possible mechanisms. Firstly glandular fever may accelerate presentation in young adults, destined to present with HD. Secondly the Epstein-Barr virus may have an inherent seasonal behaviour whether causing acute infectious mononucleosis or when latent and playing a role in the aetiology of Hodgkin's disease.

SUMMARYLinkage studies on two families segregating for antithrombin III deficiency confirm the linkage between AT3 and the Duffy blood group. The maximum lod score including two published families is +4.2 at recombination fractions around 0.1. Two patients with deletions of 1q have 1/2 levels of antithrombin III suggesting that the AT3 locus lies in bands 1 q22 → 1q25.