Search

Objective: It is widely believed that Clostridium difficile (C. difficile)-associated diarrhea is a more severe disease in the elderly than in the young, associated with increased morbidity and mortality. These beliefs are largely anecdotal, and there are few data supporting them., Methods: We conducted an evaluation in an urban, tertiary care hospital of 89 inpatients in whom C. difficile-associated diarrhea was identified. These patients were evaluated prospectively, and the group was divided by age into those < 60 yr of age (younger) and those > or = 60 yr (elderly)., Results: There was no difference in mortality or morbidity in elderly individuals with C. difficile-associated diarrhea when compared with younger persons similarly infected. The response to standard treatment was similar in both groups. Older patients were more likely to have an elevated white blood cell count in association with C. difficile-associated diarrhea (60% vs 26%, p < 0.05), and were more likely to have acquired their infection in the hospital (89% vs 50%, p < 0.0001)., Conclusions: In the elderly, C. difficile-associated diarrhea is almost always acquired in institutions, and may not be obvious among patients' other problems. The elderly do not seem to have an increase in C. difficile diarrhea-associated morbidity or mortality. There is no evidence that C. difficile-associated diarrhea is more severe in the elderly than it is in the young.

A beta globin gene from a patient with homozygous beta+ thalassemia has been cloned and completely sequenced. No changes from normal are found in the 200 nucleotides 5' to the cap site, in the 3' untranslated region up to the poly A addition site, in the small intervening sequence (IVS 1), or in the coding sequence except for a third base change in codon 2. The only other differences are in the large intervening sequence (IVS 2). One of these, at a position 16 nucleotides from the 5' end of IVS 2, has been reported previously in normal individuals, and is probably a polymorphism. Four other changes, at positions 74, 81, 666, and 705 are also seen in IVS 2. Abnormal beta globin mRNA precursors detected in the bone marrow cells of this patient, and abnormal beta globin RNA splicing observed when this gene is transcribed in a tissue culture system taken together with these IVS 2 changes, suggest that the beta+ thalassemia phenotype is produced by a decrease in normal beta globin mRNA processing.

Human delta globin is expressed at approximately 1-2% of the level of human beta globin in erythroid cells despite the marked homology between these two globins. To determine the DNA sequences responsible for this effect, delta and beta globin genes and fusion products of these genes constructed in vitro were transfected and expressed in HeLa cells. The results indicate that when the small intervening sequence of the beta gene (beta IVS 1) is replaced by delta IVS 1, expression of the chimeric gene is the same as that of the normal beta globin gene. By contrast, when the large intervening sequence of the beta gene (beta IVS 2) is replaced by delta IVS 2, expression of the chimeric gene is markedly reduced. These results suggest that there are signals within IVS 2 of the delta and beta genes which affect their relative expression.