黑料网

Celiac Disease; Gluten; Inflammation; Intestinal Absorption; Bone Density; Osteoporosis

Introduction

Accurate diagnosis is made more difficult by the significant degree of variability in the clinical presentation of celiac disease (CD). The autoimmune response in CD mostly affects the intestinal mucosa, but it can also show up as a variety of signs and symptoms that might impact any organ or tissue. Extraintestinal symptoms like low bone mineral density (BMD), decreased bone mass, and increased bone fragility that result in a higher rate of fractures must be taken into account as an indication of an atypical CD presentation [1]. The loss of villous cells in the proximal intestine, where calcium is most actively absorbed, is the primary cause of these bone alternations, which also result in secondary hyperparathyroidism and reduced calcium and vitamin D absorption. Several investigations assessed the condition of the bones in CD patients before and after gluten-free diets. However, because both ancient and new findings are wildly discordant, research concentrating on the incidence of bone derangement in patients with CD is still unclear. A strict, lifelong GFD is currently the only effective treatment for CD [2].

Material and Methods

It is not yet known, however, if GFD alone is sufficient to reverse the changes to the bones or whether certain metabolic bone illnesses are curable. Research on the impact of GFD on bone change in CD has produced conflicting findings. According to several researches, people with CD who follow a GFD had a much lower likelihood of having low BMD. In contrast, the outcomes of additional research revealed that patients with persistent small-intestinal mucosal villous atrophy, despite adherence to a rigid GFD and the absence of had a significant risk of osteoporosis because of symptoms. Patients with CD who also have other bone metabolic issues and bone mineral loss unquestionably need to be managed properly. Early CD treatment may help to reduce the risk of developing cancer, osteoporosis, and other autoimmune illnesses [3]. Given that the majority of bone mass is acquired during the first two decades of life, early CD diagnosis and adherence to a GFD are crucial to ensuring optimal bone metabolism in such situations. Recent clinical trials for several innovative CD therapy modalities are still continuing, however these therapies attempt to reduce the need for a rigid GFD by altering dietary food products, minimise gluten exposure by quick enzymatic breakdown, suppress the synthesis of certain inflammatory mediators, and Small intestinal permeability, also known as immune response regulation. The best method of treating calcium shortage and bone issues in CD patients has not yet been thoroughly studied in humans [4].

CD is a chronic digestive illness that develops in people who are genetically predisposed to it. An immunological response to the gliadin portion of gluten, a protein present in wheat, rye, and barley, is what defines the illness. It is commonly known that CD tends to run in families. The human leukocyte antigen (HLA) genes have a substantial association with this multigane disease. Most of the remaining patients have HLA-DQ8, while 90% to 95% of patients with CD inherit alleles encoding HLA-DQ2. HLA-DQ2 or HLA-DQ8 expression is a required but not sufficient component of CD pathogenesis. Studies on identical twins have revealed that in 25% of the instances examined, one twin did not develop CD [5], confirming the significance of environmental variables in the pathogenesis.

Result

Breastfeeding, when gluten is first consumed, infections, some medicines, and smoking may all play a role in the development of certain diseases. CD was originally believed to very occasionally affect children; however, recent screening tests have shown a significantly greater prevalence of CD than was previously believed. According to reports, the prevalence of CD in Finnish and Italian schoolchildren was 1:99 and 1:106, respectively. In both the United States and the United Kingdom, adult populations, similar prevalence rates have been found. Even though it is less prevalent in most non-Caucasians and is believed to be rare in central Africa and East Asia, this rate makes CD one of the most prevalent diseases, affecting roughly 1% of the global population at any age. In the recent past, more cases are being although more persons with CD are being recognised as a result of widespread serological testing and increasing awareness, the majority of them still go untreated because asymptomatic or atypical presentations are more common [6]. Females predominate over men, adult presentations of CD are more common than juvenile ones, and newly diagnosed CD occurs in patients younger than 60 years of age and in adults.

Discussion

Although in severe cases, the lesion can spread to the ileum and colon, CD primarily affects the mucosa of the proximal small intestine, with damage gradually getting worse toward the distal small intestine. The age of the patient, the severity and length of the disease and the existence of extra-intestinal symptoms all have a role in how CD presents clinically. Patients range from being asymptomatic to having severe symptoms. According to one study [7], patients with significant CD have frank malabsorption symptoms that are frequently accompanied by symptoms of autoimmune disorders. In addition to diarrhoea, abdominal distension, vomiting, constipation, weight loss, weakness, short stature, flatus, muscular wasting, and hypotonia, general irritability and dissatisfaction are seen in children, just as they are in adolescents and adults [8]. Low vitamin D levels, poor bone growth, and increased Children and adolescents with untreated CD usually have poor BMD and bone resorption indicators. However, gastrointestinal (GI) symptoms are either nonexistent or mild in minimal CD. Instead, patients may experience unrelated symptoms like dyspepsia, bloating and abdominal pain, and mild or sporadic altered bowel habits without malabsorption mimicking irritable bowel syndrome, cryptic hypertransaminasemia, unexplained anaemia, isolated fatigue, infertility, peripheral and central neurologic disorders, osteoporosis, short stature, dental enamel defects, or dermatitis herpetiformis. The silent form of CD is apparently asymptomatic but is characterised by minor intestinal mucosal abnormalities and in most cases by positive serology. Most of these people are relatives of CD patients or people from the general population who have been confirmed to have antiendomysial antibodies [9].

Conclusion

Studies showing that substantial intestine damage may exist without any symptoms in first-degree relatives of CD patients as well as other risk groups (such as people with other autoimmune illnesses) have been conducted. Type 1 diabetes, autoimmune thyroiditis, and morphea are just a few examples of the autoimmune and immune-mediated disorders that are frequently described in conjunction with CD. Additionally, individuals with Down, Turner, or Williams syndromes also have a higher risk of developing CD. Sensitive and specific serological markers, like anti-endomysial and anti-transglutaminase antibodies, are utilised in serological tests as a first round of non-invasive CD screening [10]. Although test findings that are positive may be helpful in making a diagnosis, an upper GI tract biopsy is necessary since only the histologic proof of compatible intestinal mucosal lesions may provide a conclusive diagnosis. The presence of distinctive alterations, such as intraepithelial lymphocytosis, crypt hyperplasia, and varying degrees of diminished villous height, as well as clinical and histologic improvement after gluten withdrawal, are required for the diagnosis. The disease's pathophysiology might be anything from infiltrative lesions with flat mucosa and enhanced intraepithelial lymphocytes with normal architecture. The elimination of gluten from the diet is the cornerstone of CD management. It is generally agreed that with a GFD, it is necessary to avoid wheat, barley, and rye because their prolamines gliadin, hordein, and secalin—are the primary causes of CD. Clinical improvement normally becomes apparent after a few weeks of ceasing gluten consumption, but complete histologic cure of the enteropathy may not occur for up to two years. Some individuals, however, don't seem to be responding to a GFD. A clinical diagnosis of non-responsive celiac disease (NRCD) is made when signs, symptoms, and/or test abnormalities typical of an active CD continue to exist despite following a GFD for at least 6 months. Refractory celiac disease (RCD), the most severe form of NRCD, can be compounded by high rates of morbidity and mortality and has a poor prognosis because severe malabsorption, malnutrition, and the growth of enteropathyassociated T-cell lymphoma or ulcerative jejunitis.

1. Young PC, Chen F (2021) . Annu Rev Control 51: 488-499.

, ,

2. Slater HC, Okell LC, Ghani AC (2017) Elimination. Trends Parasitol 33: 175-184.

, ,

3. Van Niekerk DD, Penkler GP, Du Toit F, Snoep JL (2016) . FEBS J 283: 634–646.

, ,

4. Xu B, Cai J, He D, Chowell G, Xu B (2020) . J Theor Biol 486:1100-1170.

, ,

5. Pitts N, Zero D, Marsh P (2017) .Nat Rev Dis Primers. 3:17030.

, ,

6. Khurshid Z, Naseem M, Sheikh Z, Najeeb S, Shahab S, et al. (2016) .Saudi Pharm J. 24: 515–524.

, ,

7. Tenovuo J, Lumikari M, Soukka T (1991) .Proc Finn Dent Soc. 87:197–208.

,

8. Khurshid Z, Haq JA, Khan R, Altaf M, Najeeb S, et al. (2016) .JPDA. 25: 171.

,

9. Pedersen AML, Belstrøm D (2019) .J Dent. 80: 3–12.

, ,

10. Touger-Decker R, Van Loveren C (2003) . Am J Clin Nutr. 78: 881–892.

, ,