Pectin has a promising pharmaceutical uses and is presently
considered as a carrier material in colon-specific drug delivery
systems (for systemic action or a topical treatment of diseases such
as ulcerative colitis, Crohn’s disease, colon carcinomas), as
indicated by the large number of studies published over the last few
years (Table 2). The potential of pectin or its salt as a carrier for
colonic drug delivery was first demonstrated by two studies, i.e.
Ashford et al. (1993) and Rubinstein et al. (1993). The rationale for
this is that pectin and calcium pectinate will be degraded by colonic
pectinolytic enzymes (Englyst et al., 1987), but will retard drug
release in the upper gastrointestinal tract due to its insolubility and
because it is not degraded by gastric or intestinal enzymes (Sandberg
et al., 1983). Rubinstein et al. (1992) demonstrated that
pectin-degrading bacteria, Klebsiella oxytoca, could adhere to
a film casted of low methoxylated pectin. The ability of the bacteria
to adhere to the films, however, was not correlated with their
ability to degrade pectin. When the dissolution of pectin matrix
tablets was analysed with and without K. oxytoca, a significant
retardation in the dissolution rate was observed in the presence of
K. oxytoca, suggesting the formation of a biofilm on the matrix or
sedimentation of insoluble pectin salts.