Celiac disease affects 1% of the world population; however it is under diagnosed in UAE. The disease has many clinical manifestations, ranging from severe malabsorption to minimally symptomatic or non-symptomatic presentation. Hypocalcaemia is a common finding in celiac disease and could be the only presentation of the disease; however hypercalcemia has been previously reported in patients with celiac disease either due to primary hyperparathyroidism or tertiary hyperparathyroidism due to prolonged hypocalcaemia. A normal calcium level on the other hand in patients with untreated celiac disease who also have primary hyperparathyroidism can be due to interplay of these two conditions and may delay the diagnosis of primary Hyperparathyroidism. We report the very first case from our practice in UAE with untreated celiac disease and normal calcium level at presentation, where a diagnosis of primary hyperparathyroidism was not entertained initially. Patient went on gluten free diet which then caused normalization of intestinal abnormalities and likely calcium absorption manifesting as hypercalcemia on subsequent labs. This led to further work up and finally the diagnosis of Primary hyperparathyroidism due to parathyroid adenoma.
Transglutaminases are a family of Ca2+-dependent enzymes which catalyze post-translational modifications of proteins. The main activity of these enzymes is the cross-linking of glutaminyl residues of a protein/peptide substrate to lysyl residues of a protein/peptide co-substrate. In addition to lysyl residues, other second nucleophilic co-substrates may include monoamines or polyamines (to form mono-or bi-substituted/crosslinked adducts) or -OH groups (to form ester linkages). In absence of co-substrates, the nucleophile may be water, resulting in the net deamidation of the glutaminyl residue. Transglutaminase activity has been suggested to be involved in molecular mechanisms responsible for both physiological and pathological processes. In particular, transglutaminase activity has been shown to be responsible for human autoimmune diseases, and Celiac Disease is just one of them. Interestingly, neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, supranuclear palsy, Huntington’s disease and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. Here we describe the possible molecular mechanisms by which these enzymes could be responsible for such diseases and the possible use of transglutaminase inhibitors for patients with diseases characterized by aberrant transglutaminase activity.
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