**8. Altered bone metabolism: osteopenia, osteoporosis and CD**

The association of celiac disease with metabolic bone disorders was known even before the origin and treatment of celiac disease was understood. Osteomalacia, a condition characterised by low bone mineral density (BMD), marked deformities and rickets, has frequently been described in the medical literature. This disease preferentially affects children with CD [47], but is rarely part of their routine clinical presentation of CD [48]. The development and availability of the means to measure bone mineral density by non-invasive techniques has confirmed the clear relationship between low BMD and the presence of CD. BMD determination has been routinely used for adult celiac patients since 2005 [49]. Metabolic bone disease remains a significant and very frequent complication of CD determined at the time of diagnosis in children and adults.

The presence of low BMD leads to a deterioration in the quality of life [50], aggravated by its frequent complications, such as the presence of various repeated bone fractures, spontaneously, or after minor trauma. Currently, the finding of a low BMD is the first diagnostic criterion for confirming the presence of osteoporosis, metabolic and skeletal disease defined by lesions at the level of the bone microarchitecture, increased bone fragility and susceptibility to an increased risk of breaks. The WHO has established diagnoses of osteoporosis when bone mass values are less than −2.5 times the standard deviation (SD) of the maximum bone mass (the maximum value of BMD in an adult), and of osteopenia when these values are between −1 and −2.5 SD less than the maximum.

It is estimated that, at the time of diagnosis, one-third of paediatric patients present osteoporosis, and one-third have osteopenia. Only the remaining third of patients with CD have normal BMD [51]. Although more than half the children with CD have low BMD at the time of diagnosis [52], once a GFD has been initiated, most children with CD achieve a normal height and weight for their age, and their rate of bone mineralisation accelerates, in such a way that most of them attain their maximum bone mass when their bones finish growing [48]. The most serious problem arises when CD is diagnosed during adulthood, by which time bone growth is complete and maximum bone mass has been reached. The prevalence of osteoporosis in adult patients with CD is twice that of adults of the same age in the unaffected population [53]. The average prevalence of low BMD in adult CD patients is 40%, compared with 15% in the general adult population. In one series of adult patients with CD, the prevalence of low BMD reached 75% [54]. This low BMD is also characteristic of patients with dermatitis herpetiformis [55].

The first-line treatment for osteoporosis in CD is to establish a permanent GFD. Several studies, of children and adults, have demonstrated its effect on bone density and calcium absorption [56–58]. The greatest gain in bone mass described in these studies has been shown to occur during the first year on the GFD. It leads to an increase of at least 5% in bone mass after 1 year, although this is not enough for the bone mass to become normalised. In clinical practice, the degree of adherence to the GFD also determines the extent of recovery of bone mass, which is generally estimated at around 30% [59]. In addition, the recovery rate is higher in young patients with CD than in adults. This is explained by the fact that 97% of the bone mass accumulates during the first two decades of life, and because complete recovery is difficult for people older than 20 years of age [60].

**9**

patients with CD [73].

individuals with CD [74, 75].

**10. Dermatitis herpetiformis and EC**

*Introductory Chapter: Celiac Disease - An Overview DOI: http://dx.doi.org/10.5772/intechopen.82723*

**9. Thyroid diseases and CD**

higher than in healthy controls [66–69].

In addition to the GFD, an adequate supply of calcium and vitamin D should be ensured, since they are critical factors for the acquisition and maintenance of good bone mass. Adult patients with untreated CD typically experience a decrease of 45% in the level of intestinal absorption of calcium that is followed by a 52% improvement 6 months after beginning the GFD. Serum vitamin D levels at diagnosis are very low in most adult patients. The intake of 1200-1500/day (suppress daily and long-term) calcium and 400 U of vitamin D is recommended, administered in exactly the same

way as it is in cases of osteoporosis that are not associated with CD [61].

It is well known that CD is present in a higher proportion of patients with autoimmune-based thyroid diseases (e.g., Graves' disease and Hashimoto's thyroiditis), with a prevalence of 2–7% [62–65]. Similar observations have been made in celiac patients, whereby their serological signs of autoimmune thyroid disease were present in up to 26% of cases. Thyroid dysfunction was detected in up to 10% of the cases of CD and it was estimated that the risk of disease was at least three times

It has been reported that patients with CD who follow a GFD could develop thyroid problems of an autoimmune nature. In contrast, other studies have described declining anti-thyroid antibody titres after a period of 2–3 years on the GFD [70, 71]. These different results could have arisen because patients had been on their GFD for different lengths of time. The authors prospectively evaluated the presence of thyroid autoimmunity in children and adolescents with CD who had adopted a GFD. After 2 years on the diet, a 7% increase in thyroid autoimmunity was observed, based on levels of l-thyroxine in the CD patients. Thyroid autoimmunity did not appear to be more frequent in paediatric patients and adolescents with CD who followed a GFD than in control groups. Since their clinical development does not seem to affect growth, the authors concluded that a long-term programme screening for thyroid disease might not be necessary for all patients with CD who follow a GFD, but may be

advisable for those for whom there is a suspicion of thyroid disease [72].

The coexistence of CD and autoimmune thyroid disease has been explained in terms of several mechanisms, such as the genetic predisposition and the association of both diseases with the gene that codes for antigen 4, which is associated with cytotoxic T lymphocytes and which confers susceptibility to thyroid autoimmunity. It has also been shown that the tTG-2 IgA reacts with thyroid tissue and that this association could contribute to the onset and development of thyroid disease in

Dermatitis herpetiformis (DH) was first described in 1885 by the French dermatologist Louis Duhring, and, indeed, is still known as Duhring's disease in some countries. In 1966, Marks et al. identified the presence of histological alterations in the small intestine of these patients that were identical to those observed in

The primary cutaneous lesions appear as erythematous papules, associated with liquid-containing vesicles in different areas of the body, especially those where there is rubbing, where they are distributed symmetrically on the extensor surfaces of the extremities. The vesicles produce a great deal of itching, causing patients to scratch themselves frequently, bursting their blisters, which releases their liquid content,

*Introductory Chapter: Celiac Disease - An Overview DOI: http://dx.doi.org/10.5772/intechopen.82723*

*Celiac Disease - From the Bench to the Clinic*

of diagnosis in children and adults.

between −1 and −2.5 SD less than the maximum.

guidelines recommend carrying out systematic screening for CD, their application in clinical practice, particularly in children, adolescents and young adults, has not yet reached the desired level of performance in many countries of the world [45, 46].

The association of celiac disease with metabolic bone disorders was known even before the origin and treatment of celiac disease was understood. Osteomalacia, a condition characterised by low bone mineral density (BMD), marked deformities and rickets, has frequently been described in the medical literature. This disease preferentially affects children with CD [47], but is rarely part of their routine clinical presentation of CD [48]. The development and availability of the means to measure bone mineral density by non-invasive techniques has confirmed the clear relationship between low BMD and the presence of CD. BMD determination has been routinely used for adult celiac patients since 2005 [49]. Metabolic bone disease remains a significant and very frequent complication of CD determined at the time

The presence of low BMD leads to a deterioration in the quality of life [50], aggravated by its frequent complications, such as the presence of various repeated bone fractures, spontaneously, or after minor trauma. Currently, the finding of a low BMD is the first diagnostic criterion for confirming the presence of osteoporosis, metabolic and skeletal disease defined by lesions at the level of the bone microarchitecture, increased bone fragility and susceptibility to an increased risk of breaks. The WHO has established diagnoses of osteoporosis when bone mass values are less than −2.5 times the standard deviation (SD) of the maximum bone mass (the maximum value of BMD in an adult), and of osteopenia when these values are

It is estimated that, at the time of diagnosis, one-third of paediatric patients present osteoporosis, and one-third have osteopenia. Only the remaining third of patients with CD have normal BMD [51]. Although more than half the children with CD have low BMD at the time of diagnosis [52], once a GFD has been initiated, most children with CD achieve a normal height and weight for their age, and their rate of bone mineralisation accelerates, in such a way that most of them attain their maximum bone mass when their bones finish growing [48]. The most serious problem arises when CD is diagnosed during adulthood, by which time bone growth is complete and maximum bone mass has been reached. The prevalence of osteoporosis in adult patients with CD is twice that of adults of the same age in the unaffected population [53]. The average prevalence of low BMD in adult CD patients is 40%, compared with 15% in the general adult population. In one series of adult patients with CD, the prevalence of low BMD reached 75% [54]. This low

BMD is also characteristic of patients with dermatitis herpetiformis [55].

recovery is difficult for people older than 20 years of age [60].

The first-line treatment for osteoporosis in CD is to establish a permanent GFD. Several studies, of children and adults, have demonstrated its effect on bone density and calcium absorption [56–58]. The greatest gain in bone mass described in these studies has been shown to occur during the first year on the GFD. It leads to an increase of at least 5% in bone mass after 1 year, although this is not enough for the bone mass to become normalised. In clinical practice, the degree of adherence to the GFD also determines the extent of recovery of bone mass, which is generally estimated at around 30% [59]. In addition, the recovery rate is higher in young patients with CD than in adults. This is explained by the fact that 97% of the bone mass accumulates during the first two decades of life, and because complete

**8. Altered bone metabolism: osteopenia, osteoporosis and CD**

**8**

In addition to the GFD, an adequate supply of calcium and vitamin D should be ensured, since they are critical factors for the acquisition and maintenance of good bone mass. Adult patients with untreated CD typically experience a decrease of 45% in the level of intestinal absorption of calcium that is followed by a 52% improvement 6 months after beginning the GFD. Serum vitamin D levels at diagnosis are very low in most adult patients. The intake of 1200-1500/day (suppress daily and long-term) calcium and 400 U of vitamin D is recommended, administered in exactly the same way as it is in cases of osteoporosis that are not associated with CD [61].
