Background: Type 1 diabetes mellitus (T1DM) is an autoimmune disorder caused by pancreatic β-cells destruction. Anti-pancreatic antibodies are the witness of β-cell destruction and their dosage is mainly used for etiological diagnosis. Patients with T1DM are at increased risk of developing other autoimmune reactions, which may involve other organs, resulting in organ specific autoimmune disease. The most frequently encountered are autoimmune thyroid disease, followed by celiac and gastric disease and other rare autoimmune diseases. Objectives: The purpose of this study is to investigate the prevalence of autoimmune markers in patients with T1DM. Methods: The study was conducted at the Department of Endocrinology of the Military Hospital Moulay Ismail in Meknes Morocco, from January 2016 to December 2018. All Type 1 diabetes patients consulting during the study period were included in the study. Their clinical and biochemical data were collected at their first presentation, made up of anti-pancreatic antibodies (glutamic acid decarboxylase [GAD] antibody, tyrosine phosphatase antibody, and islet cell antibody) and other organ-specific antibodies: the thyroid (antithyroid peroxidase antibody, antithyroglobulin antibody, and antithyroid-stimulating hormone receptor antibody), the intestine (IgA antitissue transglutaminase antibody), the adrenal gland (anti-21 hydroxylase antibody), and the stomach (antigastric parietal cell antibody and anti-intrinsic factor antibody). Results: Fifty-four patients were included, with an average age of 26 years. GAD, tyrosine phosphatase, and islet cell antibodies were detected in 74%, 22%, and 3.7%, respectively, of the 54 patients examined. The prevalence of extrapancreatic autoimmunity was 45% with a large preponderance among different immunities of those from thyroid and celiac diseases (CDs). Conclusion: Our results confirm that patients with Type 1 diabetes should be investigated for the presence of autoimmune diseases mainly from thyroid and CDs.

Background. The thyrotropin-secreting adenomas are very rare and even more rare when they simultaneously coexist with thyroid carcinoma. So far, only sixteen cases have been reported in the literature. Here, we present a unique case of successful management of a concurrent case of thyrotropin-prolactinoma with papillary thyroid carcinoma. Case Presentation. A 50-year-old Moroccan woman underwent a total thyroidectomy and complementary totalization by iratherapy for papillary thyroid carcinoma, who presented persistence of an inappropriate secretion of the thyroid-stimulating hormone (TSH > 4 mUI/L) despite of levothyroxine suppressive therapy (300 μg/d). After eliminating noncompliance, interfering medicines, and thyroid malabsorption, a pituitary adenoma (12 mm) was documented at magnetic resonance imaging. The patient has had transsphenoidal pituitary adenomectomy with histology confirming a thyrotropin-prolactin-secreting adenoma. After surgery and lanreotide treatment failures, we noted a complete response (TSH < 0.5) with cabergoline treatment (3 mg/week). Conclusion. The unusual association of thyroid adenocarcinoma and TSHoma enriches the hypothesis of a potential link between thyrotropic hypersecretion and thyroid carcinogenesis. Our case also illustrates the difficulty of monitoring thyroid carcinoma in nonremission of a TSHoma.

We related the case of medullary thyroid carcinoma, revealed by multiple inaugural pharyngolaryngeal metastases, requiring the use of a rescue tracheotomy. Their histopathology confirmed by laryngeal biopsy performed during a panendoscopy of the upper aerodigestive tract. Following the exclusion of remote metastases by positron emission tomography scan, a mutation of the RET protooncogene was investigated, allowing the family nature of the carcinoma to be excluded. The patient received an external radiotherapy with a palliative aim in front of the inextricable character of the tumor. Therapeutic modalities of this rare form of pharyngolaryngeal localization of medullary thyroid carcinoma are discussed.

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