It is well known that in celiac disease, malabsorption of calcium leads to secondary hyperparathyroidism as a response to hypocalcemia, and that secondary hyperparathyroidism is probably also due to concomitant vitamin D deficiency [1]. In patients with celiac disease, bone loss and derangement are extremely frequent, and there are recent data that show in celiac disease the release of proinflammatory cytokines activating osteoclasts may contribute to osteopenia and osteoporosis. Although the risk of fractures in celiac disease patients seems only slightly increased, it remains a clinical concern. Furthermore, osteomalacia in celiac patients is sometimes seen even if its exact prevalence remains unknown. A possible association between primary hyperparathyroidism and celiac disease has been reported recently [2, 3]. Here, we describe and discuss two cases of patients who simultaneously had both clinical conditions. Patient A: A 45-year-old woman hospitalized for severe osteomalacia, with inability to walk, history of nephrolithiasis, and iron-deficiency anemia unresponsive to oral iron therapy, was diagnosed with celiac disease which was confirmed by characteristic histologic changes on duodenal biopsy. At the time of her diagnosis, laboratory findings were as follows: hemoglobin 8.5 g/dL with mean corpuscular volume (MCV) 66 fl (83–97); serum calcium 2.38 mmol/L (2.1–2.55); phosphorus 0.53 mmol/L (0.87–1.45); parathyroid hormone (PTH) 478 pg/mL (11–64); 25-hydroxyvitamin D 3 ng/mL (9–38); ferritin 2 ng/mL (12–200); vitamin B12 168 pg/mL (211–911). The patient was started on a gluten-free diet, calcitriol 0.75 lg, calcium lactate-gluconate/calcium carbonate 2,000 mg daily and parenteral administration of iron and vitamin B12. With the start of the therapy, there was a marked improvement in the overall clinical picture with normalization of blood counts, and after 9 months, a return to the normal range of levels of antigliadin antibodies IgA—from 359.6 ng/mL to 5.5 ng/mL (0–5.9)—and antiendomysial antibodies IgA—positive from 1:2,560 to 1:5 (\1:5). However, despite correction of vitamin D deficiency (25-hydoxyvitamin D increased to 31 ng/mL), PTH levels remained high, 393 pg/mL, with evidence of hypercalcemia, 2.7 mmol/L and persistence of hypophosphatemia, 0.47 mmol/L. Her therapy was stopped (at that time calcitriol 0.25 lg, calcium lactate-gluconate/calcium carbonate 500 mg daily) and an ultrasound examination of the neck was performed with evidence of a hypoechoic oval structure, 1.8 cm in diameter, near the left lower pole of a normal thyroid gland, which suggested the possibility of an enlarged parathyroid gland. The patient underwent a technetium-99 m-labeled sestamibi scintigraphy that revealed a focus of activity consistent with a single left inferior parathyroid adenoma. The excision of the left parathyroid gland was carried out by an endocrine surgeon and then the histopathological examination showed a parathyroid adenoma. Thereafter, the patient experienced a progressive increase in bone mass density (with normal serum levels related to osteo-calcium metabolism), and she is now leading a normal life albeit with gluten-free diet. Patient B: A 42-year-old woman was examined for evaluation of a syndrome characterized by generalized weakness, anxiety and depression, and iron deficiency anemia unresponsive to oral iron therapy. By clinical S. C. Wu S. Caravita M. B. Secchi (&) Azienda Ospedaliera Istituti Clinici di Perfezionamento, U.O.C. Medicina Interna, Ospedale Bassini, via Massimo Gorki 50, 20092 Cinisello Balsamo, Milan, Italy e-mail: beatrice.secchi@fastwebnet.it