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BACKGROUND: COVID-19 can induce a systemic inflammatory response with variable clinical manifestations. Similar to various viruses, COVID-19 has been implicated in the pathogenesis of autoimmune diseases. This article highlights the potential for infections including the SARS-CoV-2 virus to induce exacerbations of pre-existing autoimmune diseases or even potentially unmask de novo autoimmune diseases in particular anti-synthetase syndrome (ASSD) in predisposed individuals. Although there are other case reports of ASSD following SARS-CoV-2 infection, here we present the first reported case of a gentleman with a newly diagnosed anti-OJ positive anti-synthetase syndrome following SARS-CoV-2 infection. CASE PRESENTATION: Described is a case of a 70-year-old man presenting to the emergency department with worsening dyspnea in the context of a recent COVID-19 infection. CT-chest revealed changes suggestive of fibrotic lung disease, consistent with usual interstitial pneumonitis (UIP) pattern. Despite recovery from his COVID-19 illness, the patient subsequently developed proximal myopathy with cervical flexion weakness on further assessment with persistently elevated creatinine kinase (CK). Myositis autoantibodies found a strongly positive anti-OJ autoantibody with MRI-STIR and muscle biopsy performed to further confirm the diagnosis. The patient received pulse methylprednisolone 1 g for 3 days with a long oral prednisolone wean and in view of multiple end-organ manifestations, loading immunoglobulin at 2 g/kg administered over two days was given. In addition, he was then commenced and escalated to a full dose of azathioprine given a normal purine metabolism where he remains in clinical remission to this date. At least 267 cases of rheumatic diseases has been associated with SARS-CoV-2 infection as well as COVID-19 vaccination. A literature search on PubMed was made to determine the amount of case reports describing myositis associated with SARS-CoV-2 infection. We found 3 case reports that fit into our inclusion criteria. Further literature searches on diagnostic approach and treatment of ASSD were done. CONCLUSION: Although SARS-CoV-2 infection itself can cause a directly mediated viral myositis, this case report highlights the possibility of developing virus-triggered inflammatory myositis through multiple aforementioned proposed mechanisms. Therefore, further studies are required to explore the relationship and pathophysiology of SARS-CoV-2 infection and the incidence of inflammatory myopathies.
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Ectopic pregnancies (EPs) are potentially fatal if not recognized early. Evidence of an association with chlamydial infection in South East Asia is lacking. This case-control study aims to (i) compare chlamydial infection in women with EP to women who delivered a full-term pregnancy, (ii) investigate classical factors associated with EP, and (iii) investigate rupture status in EP. Seventy-two women with a confirmed diagnosis of EP and sixty-nine who delivered a full-term pregnancy in a tertiary hospital in Malaysia were recruited from November 2019 to January 2022. Demographic and relevant clinical data and intraoperative findings were documented. Blood samples for testing IgG levels of chlamydia were obtained. Women with EP were more likely to have tested positive for chlamydia than those with a full-term delivery (34.7% vs. 13.0%, AOR = 4.18, 95% CI = 1.67-10.48, p = 0.002). The majority did not have the classic risk factors associated with EP. An amount of 52.8% presented with a ruptured EP, with 84.2% of ruptures occurring after six weeks of gestation. An amount of 44.2% had an estimated blood loss of more than 500 cc, with 20% losing more than 1500 cc of blood. The prevalence of prior chlamydial infection in women with EP is significant enough to necessitate a review of early pregnancy care.
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A woman in her 50s with a background of chronic obstructive pulmonary disease secondary to smoking presented with intermittent chest tightness, dyspnoea and vomiting for 4 days. A presumed diagnosis of acute coronary syndrome (ACS) was made based on dynamic ischaemic ECG changes and elevation in high-sensitivity cardiac troponin T levels. She underwent emergent coronary angiography which demonstrated mild coronary artery disease with left ventriculography suggestive of mid-wall variant Takotsubo cardiomyopathy. Thyroid function tests performed to investigate sinus tachycardia were consistent with hyperthyroidism, and her thyroid-stimulating hormone receptor antibody was elevated. A diagnosis of thyroid storm was made in the setting of a newly diagnosed Graves' disease and the patient was subsequently commenced on guideline-based therapy. This case demonstrates that Takotsubo cardiomyopathy, a mimic of ACS, is a possible complication of thyroid storm and therefore hyperthyroidism should be considered in the list of differentials in patients presenting with Takotsubo cardiomyopathy.