DIAGNOSIS, TREATMENT AND COURSE: These investigations indicated atypical celiac disease with malabsorption, anemia and osteoporosis. The patient received nutritional counseling and was put on a gluten-free diet. Supplementary iron, folic acid and vitamin B (12) were prescribed. A bloodtransfusion was given for the symptomatic anemia. The osteoporosis was treated with calcium and vitamin D3. A follow-up examination after four months revealed complete remission of the abnormal clinical and laboratory findings with partial remission of endoscopic and histologic changes (reduced to Marsh stage 2).
CONCLUSION: Because of the lack of gastrointestinal symptoms, the diagnosis of atypical celiac disease is often made only at an advanced stage and advanced age. The disease is often associated with other autoimmune disorders.[Atypical celiac disease in a patient with type 1 diabetes mellitus and Hashimoto's thyreoiditis.]
PMID: 21225554 Jan 20100
CONCLUSION: : In this study, more than half of the patients with diabetes mellitus type 1 had at least one pathologically increased antibody titer apart from diabetes without clinical sign of an additional AIEK. 31% of patients with increased antibodies presented with symptoms of another AIEK (increase by 3.6% within 1 year). Patients with diabetes mellitus type 1 should be screened for other AIEKs. Thyropathy had the greatest prevalence and increased by 3.5% within 1 year's time.
[Prevalence of polyglandular autoimmune syndrome in patients with diabetes mellitus type 1.]
PMID: 19337707 Mar 2009
PMID: 18463048 April 2008
This paper presents a hypothesis of the aetiology of the increasing incidence of type 1 diabetes (T1D). This together with the global increased incidence of celiac disease (CD) and that these increases cannot be explained by genetic factors suggest a common environmental factor for these two diseases. Even though enterovirus (EV) infections are believed to trigger T1D and gluten is the trigger of CD, the increasing intake of gluten containing products all over the world could be the trigger for both diseases directly and indirectly. It has been shown that the duration of exposure to gluten is related to the prevalence of T1D. It has also been shown that T1D patients at onset have an inflammatory reaction in the gut. Hence, early diagnose of CD followed by elimination of dietary gluten will lead to a decreased incidence of T1D.
The most frequent reported CD associated conditions are type 1 diabetes mellitus and autoimmune thyroiditis. Associated autoimmune antibodies are frequent in CD and their first-degree relatives, spanning anti-endocrine, anti-gastrointestinal, anti-nuclear, anti-cytoskeleton and anti-neurological antibodies. More specifically, antibodies against thyroid and the endocrine pancreas, anti-gastric and liver, anti-nuclear constituents, anti-reticulin, actin, smooth muscle, calreticulin, desmin, collagens and bone, anti-brain, ganglioside, neuronal and blood vessel were described in sera of the patients in numerous studies.
There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment.
This paper presents a series of 10 hypotheses on the etiology of type 1 diabetes. We begin with the hypothesis that wheat gluten is one of the elusive environmental triggers in type 1 diabetes.
Both diseases have common immunology and genetic characters. Prevalence of celiac sprue in patients with type I diabetes is several times higher compared to prevalence of this disease in the population. There is the prevalence of celiac sprue 3.6-5.1% in children with type I diabetes mellitus in the Czech Republic, silent form of the disease is the most frequent one. It is necessary to assess (at least once per two years) actively and on regular basis endogenous myosin and/or tissue transglutaminase antibodies in patients with type I diabetes.