Introduction: Viral infections can induce autoimmune diseases in susceptible patients. SARS-CoV-2 has been associated with the development of rheumatic disease, especially small vessel vasculitis and arthritis. Typically, onset occurs days to weeks after the antigenic challenge and in patients with mild COVID-19. We report a case of large vessel vasculitis (LVV) temporally related to SARS-CoV-2 infection. Case description: An otherwise healthy 19-year-old woman presented with fatigue, malaise, and chest and low back pain. The symptoms had begun 5 weeks earlier and 1 month after mild SARS-CoV-2 infection. Serological work-up revealed a marked proinflammatory state and anaemia without signs of infectious or autoimmune disease. Computerized tomography revealed thickening and blurring of the perivascular fat of the descending thoracic and abdominal aorta, progressing along the proximal iliac and renal arteries. Fluorodeoxyglucose positron emission tomography confirmed inflammatory activity. Symptoms and laboratory values normalized after prednisolone treatment. Discussion: Recent SARS-CoV-2 infection may be a trigger for LVV, including Takayasu arteritis, as well as other rheumatic diseases. A prompt and thorough differential diagnosis is essential to exclude aortitis and LVV mimickers. Moreover, physicians should be aware of the potential spectrum of systemic and autoimmune diseases that could be precipitated by SARS-CoV-2 infection. This will allow timely diagnosis and treatment, with significant improvement in prognosis.

Silva Marques et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Type 1 diabetes mellitus (T1DM) and multiple sclerosis (MS) have been described as chronic organ-specific diseases, approached by different medical specialties. However, they share more etiologic and pathologic features than expected between two autoimmune diseases.The authors present the case of a 40-year-old Caucasian male, diagnosed with type 1 diabetes mellitus at age 18, with poor metabolic control in the early years after the diagnosis. Fourteen years after the diagnosis of diabetes, he started complaining of paresthesias in both feet and sexual dysfunction. Months later, he began to have episodes of muscle weakness and decreased strength in the right lower limb, with a relapsingremitting pattern and diplopia. This typical course of the symptoms associated with characteristic findings in brain magnetic resonance imaging, with multiple lesions, with evidence of space and time dissemination, established the diagnosis of multiple sclerosis. The presence of oligoclonal bands in the cerebrospinal fluid analysis sustained this diagnosis. Other alternative etiologies were excluded.People with type 1 diabetes mellitus are at an increased risk for other autoimmune diseases, with autoimmune thyroiditis (AIT), celiac disease, and pernicious anemia being the most common. Other less recognized associations, such as the co-occurrence of type 1 diabetes mellitus and multiple sclerosis, are also more frequent than might be thought, with studies reporting a threefold to fivefold higher prevalence of T1D in patients with MS. The exact mechanism behind this co-occurrence is not fully understood, but environmental factors (viral infections and vitamin D deficiency) and variations in non-human leucocyte antigen (HLA) class II alleles may be implicated. Understanding the similarities in the etiology and pathophysiology of these diseases may help clarify causality and create new strategies for the management of these conditions.

SUMMARY Autoimmune polyglandular syndrome type 2 (APS 2) is defined by the presence of Addison’s disease (AD) associated with autoimmune thyroid disease and/or Type 1 diabetes mellitus (T1DM). It is a rare disease, affecting about 1.4-2 cases/100,000 inhabitants. Its less frequent clinical presentation is the combination of AD, Graves‘ disease, and T1DM. We present the case of a 42-year-old woman with a history of total thyroidectomy due to Graves’ disease, type 2 diabetes mellitus, and hypertension, who sought the ED due to asthenia, dizziness, nausea, and vomiting. She reported having stopped antihypertensive therapy due to hypotension and presented a glycemic record with frequent hypoglycemia. On physical examination, she had cutaneous hyperpigmentation. She had no leukocytosis, anemia, hypoglycemia, hyponatremia or hyperkalemia, and a negative PCR. Serum cortisol <0.5 ug/dl (4,3-22,4), urine free cortisol 9 ug/24h (28-214), ACTH 1384 pg/mL (4,7-48,8), aldosterone and renin in erect position of 0 pg/ml (41-323) and 430.7 uUI/ml (4.4-46.1) respectively. Quantiferon TB was negative; computerized axial tomography of the adrenals showed no infiltrations, hemorrhage, or masses. The 21-hydroxylase antibody assay was positive. B12 vitamin was normal, anti-GAD antibodies were positive, anti-insulin, anti-IA2, and anti-transglutaminase antibodies were all negative. The patient started insulin therapy and treatment for AD with prednisolone and fludrocortisone with good clinical response. This case aims to alert to the need for high clinical suspicion in the diagnosis of AD. Since this is a rare autoimmune disease, it is important to screen for other autoimmune diseases in order to exclude APS.

Whipple's disease (WD) is a rare multisystemic infectious disease caused by Tropheryma whipplei. The pathogenesis of Whipple's disease remains unknown and clinical experience relies solely on various case reports published in the literature. The disease may occur at any age, with most studies describing patients in their fifth decade. Classic WD mainly affects the gastrointestinal tract, but extraintestinal commitment can occur, with the most common manifestations being arthralgias, lymphadenopathy, fever, and neurological symptoms.We present a case of a 69-year-old woman who presented with fever, macular rash, abdominal pain, lymphadenopathy, pleural and pericardial effusion, weight loss, and severely altered mental status over seven days. Initial workup tests only revealed leucopenia, thrombocytopenia, and hyperferritinemia. Since the fever persisted despite antibiotic treatment, an extensive workup was required until the final diagnosis of classic WD through histological examination of duodenal biopsies. Treatment with ceftriaxone was implemented for two weeks, followed by trimethoprim-sulfamethoxazole 160/800mg bid for 12 months. The patient presented full recovery and no recurrence after three years of follow-up.Even though WD was first described more than a century ago, WD is an elusive disease with a wide variety of clinical findings, leading to a still significant delay in diagnosis. WD should be considered in the differential diagnosis of rheumatologic disorders, chronic abdominal pain or diarrhea, neurological manifestations not suggestive of any other specific disease, non-caseating granulomatous diseases, and cases of lymphadenopathies. The authors aim to add additional clinical data and raise awareness for a rare condition that can be lethal if not timely treated. More studies and recommendations are needed concerning screening patients and treatment, with an urgent need to improve the delay in diagnosis.