Simultaneous Coexistence of Thyrotropin-Prolactin-Secreting Adenoma and Papillary Thyroid Carcinoma.

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.

The profile of autoimmunity in Type 1 diabetes patients.

Background: Type 1 diabetes mellitus (T1DM) is an autoimmune disorder caused by pancreatic ß-cells destruction. Anti-pancreatic antibodies are the witness of ß-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.

RésuméContexte: Le diabète sucré de type 1 est une maladie auto-immune causée par la destruction des cellules bêta pancréatiques. Les anticorps anti-pancréatiques sont les témoins d'une destruction des cellules ß et leur dosage est principalement utilisé pour le diagnostic étiologique. Les patients atteints de diabète de type 1 courent un risque accru de développer d'autres réactions auto-immunes, qui peuvent impliquer d'autres organes, entraînant une maladie auto-immune spécifique à l'organe. Les plus souvent rencontrées sont les maladies thyroïdiennes auto-immunes, suivies des maladies cœliaques et gastriques et d'autres maladies auto-immunes rares. Objectifs: Le but de ce travail est d'étudier la prévalence des marqueurs auto-immunes chez les patients atteints de diabète de type 1. Méthodes: L'étude a été menée au Département d'Endocrinologie de l'Hôpital Militaire Moulay Ismail à Meknès Maroc, de janvier 2016 à décembre 2018. Tous les patients diabétiques de type 1 consultant pendant la période d'étude ont été inclus dans l'étude. Leurs données cliniques et biochimiques ont été recueillies à leur première présentation, composées d'anticorps anti-pancréatiques (anticorps anti acide-glutamique décarboxylase, anticorps anti-tyrosine phosphatase, et les anticorps anti-cellules des îlots de langerhans) et d'autres anticorps spécifiques à certains organes: la thyroïde (anticorps anti-thyroperoxydase, anticorps anti-thyréoglobuline et anticorps anti-récepteur de thyroid stimulating hormon), l'intestin (anticorps anti-transglutaminase IgA), la glande surrénale (anticorps anti-21hydroxylase) et l'estomac (anticorps anti-cellules pariétales gastrique et anticorps anti-facteur intrinsèque). Résultats: 54 patients ont été inclus, avec un âge moyen de 26 ans. Les anticorps anti- acide-glutamique décarboxylase, les anticorps anti-tyrosine phosphatase et les anticorps anti-cellules des îlots de langerhans ont été détectés dans 74%, 22% et 3,7%, respectivement, des 54 patients examinés. La prévalence de l'auto-immunité extrapancréatique était de 45% avec une grande prépondérance parmi les différentes pathologies auto-immunes de ceux des maladies thyroïdiennes et cœliaques. Conclusion: Nos résultats confirment que les patients atteints de diabète de type 1 devraient bénéficier de la recherche de la présence d'autres maladies auto-immunes principalement de la thyroïde et la maladie cœliaque.

Cushing´s syndrome: high aggressiveness of low-grade tumors.

Cushing´s syndrome is caused by prolonged exposition supraphysiological to endogenous or exogenous cortisol. Ectopic production of adrenocorticotropic hormone by lung carcinoid tumors is relatively rare. Most documented cases have been reported individually. This rare neoplasm low grade that may secrete adrenocorticotropin (ACTH) leading to rapid development of hypercortisolism which is the main mode of discovery, can be a real aggressive form. This report shows a high aggressiveness of this endocrine neoplasia, wich was marked on the general, morphological, bone and psychiatric level. The trivialization of clinical signs had caused the delay in diagnosis with irreparable bone consequences.

[Hypokalemic paralysis revealing Sjögren's syndrome associated with auto-immune thyroiditis]. / Quadriparésie hypokaliémique révélant un syndrome de Gougerot-Sjögren associé à une thyroïdite auto-immune.

We report a case of 36-year-old woman, admitted for hypotonic tetraparesis. Laboratory tests revealed severe hypokalaemia, acidosis, hyperchloremia and alkaline urinary pH allowing the diagnosis of distal tubular acidosis. Additional investigations led to the diagnosis of primary Sjögren's syndrome associated with Hashimoto's thyroïditis. The evolution was favorable under potassium citrate alkalinisation, the corticosteroid therapy and hormonal substitution. Based on this observation, the pathogenesis of distal tubular acidosis during auto-immune diseases (Sjögren's syndrome, monoclonal hypergammaglobulinemia, hypothyroidism) was discussed as well as its consequences and management.

Leflunomide-induced toxic epidermal necrolysis in a patient with rheumatoid arthritis.

INTRODUCTION: Leflunomide is an immunomodulating agent with proven efficacy in rheumatoid arthritis. Although its overall safety profile is good, a few cases of toxic epidermal necrolysis have been reported. CASE REPORT: This 36-year-old woman had rheumatoid arthritis that proved refractory to sulfasalazine and methotrexate, which were used successively in combination with symptomatic drugs. Leflunomide was started. A maculopapular rash and a fever developed 2 weeks later. The skin lesions spread rapidly to most of the body, and ulcers of the ocular and oral mucosa appeared. Leflunomide was stopped. Cholestyramine washout and prednisolone (60 mg/day) were given. The skin lesions healed over the next month. Punctate keratitis with keratinization of the cornea led to complete loss of vision. DISCUSSION: The main adverse effects of leflunomide consist of diarrhea, nausea, liver enzyme elevation, hypertension, alopecia, and allergic skin reactions. A few cases of severe skin reactions such as toxic epidermal necrolysis have been reported. They require immediate discontinuation of the drug and a washout procedure to hasten drug elimination from the body. CONCLUSION: Close monitoring for severe skin reactions is in order when using leflunomide.