Post COVID-19 changes in the structure and function of the thyroid in patients with autoimmune thyroiditis with hypothyroidism

COVID-19 is a severe immunosuppressive disease that can cause changes in the clinical course of autoimmune diseases. Autoimmune thyroiditis (AIT) is no exception. It is relevant to study the features of the clinical course of existing AIT in the post-COVID-19 period. The work aims to study the changes in the structure and function of the thyroid in patients with AIT with subclinical and manifest compensated hypothyroidism who had moderate COVID-19. A total of 123 patients aged 21-49 with AIT with subclinical hypothyroidism - 43 (group 1, 12 of whom had moderate COVID-19) and manifest hypothyroidism in the stage of medical compensation - 80 (group 2, 32 of whom had moderate COVID-19). The duration of AIT ranged from 4 to 13 years. In all cases, upon inclusion in the study and 2 and 6 months after it, changes in the structure of the thyroid gland were studied according to ultrasound data, as well as its functional capacity and the degree of compensation of hypothyroidism according to the thyroid-stimulating hormone indicator. In all patients with AIT, COVID-19 caused the progression of structural changes in the thyroid within one of two variants of the ultrasound picture of thyroiditis - hypoechoic heterogeneous or pseudo micronodular. The hormone-producing function also changed: in 7 out of 12 patients of group 1 of the main subgroup, hypothyroidism changed from subclinical to manifest hypothyroidism in the postoperative period, and in all patients of group 2 of the main subgroup, a further decrease in hormone synthesis was noted. In the post-COVID-19 period, patients with AIT undergo a progression of structural changes in the thyroid gland and a decrease in the synthesis of thyroid hormones.Copyright © 2023 The Authors.

Cool Your Jets Bro

History: Twenty-two year old male basic trainee was brought to the ED after collapsing during a routine ruck march. At mile 8/12, soldier was noted to develop an unsteady gate and had witnessed loss of consciousness. A rectal core temperature was obtained and noted to be >107degreeF. Cooling initiated with ice sheets and EMS was activated. On arrival to the ED, patient demonstrated confusion and persistently elevated core temperatures despite ice sheeting, chilled saline and cold water bladder lavage. Cooling measures were discontinued after patient achieved euthermia in the ED;however, his temperatures subsequently spiked>103degreeF. Given rebound hyperthermia, an endovascular cooling (EVC) device was placed in the right femoral vein and patient was transferred to the ICU. Multiple attempts to place EVC device on standby were unsuccessful with subsequent rebound hyperthermia. Prolonged cooling was required. Physical Exam: VS: HR 121, BP 85/68, RR 22 SpO2 100% RA, Temp 102.4degreeF Gen: young adult male, NAD, shivering, A&Ox2 (person and place only) HEENT: Scleral anicteric, conjunctiva non-injected, moist mucus membranes Neck: Supple, no LAD Chest: CTAB, no wheezes/rales/rhonchi CV: tachycardia, regular rhythm, normal S1, S2 without murmurs, rubs, gallops ABD: NABS, soft/non-distended, no guarding or rebound EXT: No LE edema, tenderness SKIN: blisters with broad erythematous bases on bilateral heels Neuro: CN II-XII grossly intact, 5/5 strength in all extremities. Differential Diagnosis: 216. Septic Shock 217. Hypothalamic Stroke 218. Exertional Heat Stroke (EHS) 219. Neuroleptic Malignant Syndrome 220. Thyroid Storm Test Results: CBC: 18.2>14.5/40.6<167 CMP: 128/3.5 88/1831/2.7<104, AST 264, ALT 80, Ca 8.8 Lactate: 7.1 CK: 11 460 Myoglobin: 18 017 TSH: 3.16 CXR: No acute cardiopulmonary process Blood Cx: negative x2 CSF Cx: Negative COVID/Influenza/EBV: Negative Brain MRI: wnl. Final Diagnosis: Exertional Heat Stroke. Discussion(s): No EVC protocols exist for the management of EHS or rebound/refractory hyperthermia. As a result, the protocol used for this patient was adapted from post-cardiac arrest cooling protocols. It is unclear if this adapted protocol contributed to his delayed cooling and rebound hyperthermia as it was not intended for this patient demographic/ pathophysiology. Furthermore, despite initiating empiric antibiotics upon admission, delayed recognition and tailored therapy for his bilateral ankle cellulitis may have contributed to the difficulty in achieving euthermia. In summary, more research needs to be done to evaluate and develop an EVC protocol for EHS. Outcome(s): Euthermia was achieved and maintained after 36 hours of continuous EVC, at which point it was discontinued. His CK, AST/ALT, creatinine and sodium down-trended after discontinuation of EVC. Patient's antibiotics were transitioned to an oral formulation for treatment of ankle cellulitis and he was prepared for discharge. He was discharged with regular follow-up with the Fort Benning Heat Clinic. Follow-Up: After discharge, patient had regularly scheduled visits with the Fort Benning Heat Clinic. His typical lab markers for exertional heat stroke were regularly monitored. He had continued resolution of his Rhabdomyolysis, acute kidney injury and hyponatremia with typical treatment. Soldier returned to duty after 10 weeks of close monitoring and rehabilitation.

Hepatotoxicity From Marijuana Gummies

Introduction: We report a case of drug-induced liver injury (DILI) induced by cannabis gummies containing Corydalis Rhizome. Case Description/Methods: A 37-year-old female presented to her primary care clinic with recurrent fevers, night sweats, and myalgias for 7 weeks accompanied by eye redness, brain fog, headache, nausea, and abdominal pain. She denied rashes, tick-bites, cough, dyspnea, chest pain, joint swelling, or genitourinary symptoms. Past medical history was notable for IBS, migraines, and anxiety. She reported edible marijuana use four times a week, rare alcohol use, and denied tobacco use. She denied a family history of liver disease. Physical exam was notable for tachycardia to 110 and scleral injection with the remainder of vitals and exam unremarkable. Initial labs were notable for AST 61, ALT 44 and CRP of 12. CBC, BMP, urinalysis, ESR, blood cultures, blood smear for parasite screen, tests for Lyme disease, Babesia, Tularemia, Anaplasma, Ehrlichia, Rickettsia, EBV, HIV, RPR, ANA, CMV, parvovirus B19, and chest x-ray were all negative. The patient was referred to infectious disease with further testing for West Nile, Leptospira, lymphocytic choriomeningitis virus, and COVID-19 returning negative. Repeat LFTs showed worsening transaminitis with ALT 979 and AST 712, alkaline phosphatase 88, total bilirubin 0.7, and albumin 4.9. Hepatitis workup including hepatitis A, B, and C, HSV, EBV, VZV serologies, AMA, ASMA, antiLKM Ab, acetaminophen level, INR, iron panel, CPK, TSH, and abdominal ultrasound were all normal. It was later discovered that her marijuana gummies contained Corydalis rhizome extract known to be hepatotoxic. Cessation of this drug was strongly advised. She was discharged with hepatology follow-up and underwent a liver biopsy showing patchy periportal and lobular inflammation with extension across the limiting plate, hepatocyte injury and apoptosis, and increased lipofuscin for age compatible with mild to moderate hepatitis. She had complete recovery after cessation of Corydalis-containing gummies. (Figure) Discussion: Our patient consumed '1906 Midnight', an American cannabis brand containing Corydalis rhizopus 100 mg, advertised to improve sleep, pain, and have a liver protective effect. A Korean systematic review on herbal-induced liver injury reported that Corydalis was the 3rd most frequent causative herb, with 36 cases. Although there are several personal accounts on social networking sites and other websites, there are no American-based publications reported on DILI from Corydalis. (Table Presented).

A Case of Primary Biliary Cirrhosis With New Onset Hyperthyroidism and Supratherapeutic INR

Introduction: Hyperthyroidism is known to increase catabolism of vitamin-K-dependent clotting factors (II, VII, IX, X) and increase the response of vitamin K antagonists, usually warfarin. Primary biliary cirrhosis (PBC) has been associated with thyroid dysfunction (TD), especially with autoimmune thyroid disease. In the below case, a patient with known PBC on warfarin is found to have severely elevated INR related to new-onset hyperthyroidism with clinical consequences of hemorrhage including upper GI bleed. Case Description/Methods: A 64-year-old female with PBC and antiphospholipid antibody syndrome on warfarin was admitted for hemorrhagic epiglottitis requiring emergency intubation and supratherapeutic INR. Her PBC was diagnosed as stage II on biopsy 23 years ago and has remained clinically stable on ursodiol therapy. On presentation, the patient was tachycardic, tachypneic, and had O2 saturations <90% on HFNC prior to intubation. Physical exam significant for larger goiter with diffuse upper airway swelling. She was admitted and found to have COVID-19 infection, INR .16.0 and PT>200.0 (limit of lab), WBC of 22.8, and lactate of 2.5. LFTs WNL aside from albumin of 2.0. TSH was <0.0017 (limit of lab) and free T4 of 3.4, free T3 of 5.3. TSH receptor antibody (TRAB) and thyroid stimulating immunoglobulin (TSI) levels were normal. Her last TSH was normal a year ago. CTA chest found a 5.7cm heterogeneous, partially calcified superior mediastinal mass consistent with multinodular thyroid goiter. Patient was initially given prothrombin complex concentrate and vitamin K with correction of INR over the following few days. She was extubated and started on methimazole. During the hospital course, she was found to have coffee ground emesis for which an EGD was done with findings of non-bleeding gastric ulcer (Forrest Class IIc) and LA Grade D esophagitis with adherent clot and bleeding for which hemostatic spray was applied. Patient was discharged a few days later following resumption of warfarin and on pantoprazole and methimazole. Discussion(s): The above case demonstrates a rare case of PBC and new-onset hyperthyroidism due to multinodular thyroid goiter causing significantly elevated INR in the setting of warfarin use with hospital course complicated by GI bleed. PBC is associated with TD - hyperthyroidism, hypothyroidism, and thyroid cancer. Hyperthyroidism is less commonly associated with PBC compared to other TDs but should be considered especially with a finding of elevated INR.

Mild Androgen Insensitivity Syndrome presenting in male with infertility and sexual difficulties

Androgen insensitivity syndrome has a wide spectrum of presentations. It results from a mutation in androgen receptor (AR) gene. It ranges from mild androgen insensitivity syndrome (MAIS) which is the mildest form to complete androgen insensitivity syndrome (CAIS). In case of MAIS, the abnormality that can be observed appears to be male infertility and sexual difficulties including premature ejaculation and erectile dysfunction. In this case report, we discuss a case of MAIS in a 37-year-old male who presented with infertility, premature ejaculation, and secondary erectile dysfunction.Copyright © 2023, Ibn Sina Trust. All rights reserved.

Subacute Thyroiditis Following Vaccination with COVID-19 mRNA Vaccine

Introduction: Subacute thyroiditis is a self-limiting post-viral inflammatory disorder occurring in 3 phases (hyper-, hypo-, and euthyroidism) Post-vaccine thyroiditis has also been reported, but is rare. Case Description: A 36-year-old Emirati female presented to our clinic with generalized fatigue, mild to moderate vague neck pain, intermittent palpitations, and loss of appetite 2 weeks after receiving her first dose of Pfizer-BioNTech mRNA vaccine against COVID-19. Clinical examination findings and laboratory test results were consistent with subacute thyroiditis. Patient is a mother of 5 healthy children, youngest is breast-fed infant (11 months old). There was no history suggestive of postpartum thyroiditis and no family history of thyroid dysfunction. Physical examination at initial visit showed mild tachycardia, and a normal blood pressure. She weighed 66 kg. Thyroid function tests revealed a suppressed TSH of 0.011 muIU/mL, high Free T4 of >100 pmol/l), and Free T3 FT3 of 29.6 pmol/L. Both TSH receptor antibodies, and Thyroid antibodies (TPO) were negative. Thyroid scintigraphy showed decreased uptake in both lobes. Thyroid ultrasound showed hypoechoic heterogeneous echotexture of the thyroid gland with vascular conglomerate and micro-calcification, along with normal sized reactive lymph nodes at sternal angle. Symptoms aggravated through the next week;patient dropped 3kg of her body weight and her palpitations increased, with a recorded resting heart rate between 120-130 beats/min. TSH decreased to 0.001muIU/mL while FT4 remained high, with an improvement to 90 pmol/L. Subsequently, the patient started to regain weight. Palpitations improved within a month. She developed a biochemically hypothyroid picture followed by clinical and biochemical euthyroidism after one more month. Second dose of the vaccine was uneventful. Last evaluation was 10 months later;TSH, FT3 and FT4 were all in normal range, acute-phase reactants were completely normal and in complete remission. Discussion(s): The exact mechanism for post-vaccination subacute thyroiditis remains unknown, vaccine adjuvants may induce diverse autoimmune and inflammatory reaction. Subacute thyroiditis has rarely been reported with other COVID-19 vaccines contains no Polyethylene glycol (PEG). A possible cross-reactivity between thyroid cell antigens and spike protein of the coronavirus produced by mRNA vaccines might be responsible. Further research is needed to investigate the incidence of subacute thyroiditis in COVID-19 pandemic days.Copyright © 2023

Thyroiditis Post COVID-19 mRNA Booster Dose Vaccination

Introduction: SARS-CoV-2 vaccines have been associated with thyroid dysfunction including thyroiditis and Graves' disease. We report a patient who developed thyrotoxicosis secondary to thyroiditis after COVID-19 mRNA booster dose vaccination. Case Description: A 74-year-old man with no known personal or family history of thyroid disorders went to his primary care physician with symptoms of palpitations. Of note, he had the first booster (third dose) of the Pfizer/BioNTech vaccine about 1 week before. He did not recall any similar symptoms after the first two doses of the same vaccine. There were no other symptoms of thyrotoxicosis such as hand tremors, weight loss or mood change. There was no family history of thyroid disorders. He was not on any medications such as amiodarone and was not taking any herbal supplements. He did not have any symptoms of upper respiratory tract infection. There was no neck pain. Physical examination was unremarkable with no goiter or thyroid eye manifestations. Thyroid function: free T4 elevated at 46.7 pmol/L (11.5-22.7) and TSH suppressed at 0.01 mIU/L (0.5-4.5). Thyroid stimulating immunoglobulin was positive at 200% (50-179). He was initially started on carbimazole 15mg daily. However, the patient became rapidly hypothyroid despite dose reduction and subsequent discontinuation of carbimazole with free T4 of 8 pmol/L and TSH of 36.4 mIU/L. An ultrasound of the thyroid gland showed vascularity with no discrete nodules. No thyroid uptake scan was done. The diagnosis was revised to thyroiditis post vaccination. Hypothyroidism persisted despite discontinuation of carbimazole before recovery 8 months later. Patient was well and did not require any thyroxine supplementation. Discussion(s): It is postulated that COVID-19 vaccines triggered thyroiditis via an autoimmune inflammatory syndrome caused by the vaccine adjuvants. A high index of suspicion is necessary and a thyroid uptake scan may be useful in making the diagnosis. Thyroiditis is a self-limiting condition and recognising it is important as no specific thyroid treatment is necessary in most patients. Patients should not be deterred from subsequent vaccination as COVID-19 infection has higher mortality risk than thyroiditis.Copyright © 2023

Thyroid Eye Disease Following COVID-19 Infection in a Patient with a History of Graves' Disease

Introduction: Autoimmune and inflammatory thyroid diseases have been reported following SARS-CoV-2 infection or vaccination, but thyroid eye disease (TED) post-COVID-19 infection is less common. We describe a case of TED following SAR-CoV-2 infection in a patient with a history of Graves' disease. Case Description: A 59-year-old female with history of Graves' disease status post radioiodine ablation therapy in 2002. She developed post-ablative hypothyroidism which has been stable on levothyroxine 88 mcg daily. In January 2021, the patient's husband and daughter were diagnosed with COVID-19 infection. A few days later, the patient developed an upper respiratory tract infection associated with loss of sense of smell and taste consistent with COVID-19 infection. Three days later, she developed bilateral watery eyes which progressed to eye redness, eyelid fullness, retraction, and pain with eye movement over 1-month duration. Her eye examination was significant for severe periocular soft tissue swelling, lagophthalmos and bilateral exophthalmos. The laboratory workup was consistent with normal TSH 0.388 mIU/L (0.358-3.740 mIU/L) and positive TSI 1.01 (0.0-0.55). The patient was referred to an Ophthalmologist for evaluation of TED. He noted bilateral exophthalmos, no restrictive ocular dysmotility or compressive optic neuropathy (clinical activity score 4/7 points). CT scan of orbit showed findings compatible with thyroid orbitopathy. Based on clinical activity score of 4, treatment with Teprotumumab was recommended pending insurance approval. Discussion(s): Many cases of new-onset Graves' hyperthyroidism have been reported after COVID-19, with only a few associated with TED. Our patient has been in remission for 20 years before she developed COVID-19 infection with occurence of TED.This suggests that COVID-19 infection may have played a role. SARS-CoV-2 may act through several mechanisms, including breakdown of central and peripheral tolerance, molecular mimicry between viral and self-antigens, stimulation of inflammasome with release of type I interferon. In our patient, treatment with Teprotumumab was indicated due to Graves' orbitopathy clinical activity score greater than or equal to 3. In conclusion, it is very uncommon for TED to present after COVID-19 infection. Our case reinforces the speculative hypothesis that SARS-CoV-2 virus could have triggered an autoimmune response against eye antigens. There is a need for increased awareness about the link between COVID-19 and autoimmunity to help better define the management of patients.Copyright © 2023

Silent Thyroiditis as a Complication of Severe Acute Respiratory Syndrome Coronavirus 2 Vaccine

Introduction: Silent autoimmune thyroiditis, a type of chronic autoimmune thyroiditis, as an adverse effect of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination is infrequently reported in the literature. We hereby describe a case of silent thyroiditis followed by Grave's orbitopathy after vaccination against SARS-CoV2. Case Description: An 84-year-old male presented to clinic with a 10-pound weight loss with no other symptoms of hyperthyroidism, no personal history of thyroid illnesses, or recent viral infections. He had normal thyroid function 3 months prior to presentation. He had received 3 doses of SARS-CoV2 Pfizer-BioNTech vaccine with the last dose 5 months prior to presentation. Thyroid exam was normal. Laboratory testing revealed thyroid stimulating hormone (TSH) level of 0.005 IU/ml (0.45-4.5 IU/ml), total T4 14.4 g/dl (4.5-12.1 g/dl), and total T3 1.22 nmol/l (0.6-1.81 nmol/l). Thyroid Ultrasound revealed a heterogeneous atrophic thyroid gland with no nodules or hypervascularity. He was started on Methimazole by primary care provider. Four months later, he was seen in the Endocrinology clinic and reported no hyperthyroidism symptoms. His TSH level at that time was 65.9 IU/ml, free T4 0.47 ng/dl (normal: 0.82-1.77 ng/dl), total T3 level 75 ng/dl (normal: 71-180 ng/dl), thyroid stimulating immunoglobulin 2.05 IU/l (0-0.55 IU/L), thyrotropin receptor antibody level 2.8 (0-1.75). Methimazole was discontinued. At 6 months after initial presentation laboratory testing showed TSH 5.010 IU/ml, free T4 1.2 ng/dl, thyroid peroxidase antibody of 148 IU/ml (normal 0-34 IU/ml), thyroglobulin antibody 131.6 IU/ml (normal 0.0-0.9 IU/ml). He was diagnosed with silent autoimmune thyroiditis. A few weeks later, the patient presented to an ophthalmologist with bilateral eye bulging and impaired vision. He was diagnosed with acute Graves' orbitopathy and started on pulse-dose of intravenous Methylprednisolone 250 mg twice daily and urgently referred to a tertiary ophthalmology center for teprotumumab infusion. His thyroid function tests were normal at that time on no thyroid medications. Discussion(s): The underlying mechanisms of thyroid impairment following SARS-CoV2 vaccination are not completely understood. There is a role of molecular mimicry between SARS-CoV2 antigens and thyroid antigens that may help to hasten the emergence of autoimmunity in vulnerable individuals. Our patient developed multiple thyroid-related antibodies following vaccination. Silent painless thyroiditis is a self-limiting condition, characterized by temporary thyrotoxicosis, followed by a brief period of hypothyroidism and then a complete return to normal thyroid function. A radioactive iodine uptake scan can help differentiate between the different causes of thyrotoxicosis in the acute thyrotoxic phase. Development of severe Graves orbitopathy following silent autoimmune thyroiditis after SARS COV2 vaccination has not been previously reported.Copyright © 2023

New-Onset Thyroid Eye Disease After COVID-19 Infection in Patient with Graves' Disease Post-Radioactive Iodine Treatment

Introduction: Coronavirus disease 2019 (COVID-19) has been associated with dysregulation of the immune system and abnormal thyroid function. The aim of this novel case report is to inform physicians of the possibility that COVID-19 infection may precipitate thyroid eye disease (TED) in patients with Graves' Disease (GD) even after treatment with radioactive iodine (RAI). Case Description: In this report, we describe a patient with GD treated with RAI who developed TED after COVID-19 infection. The patient was initially diagnosed with GD in 2018. A thyroid uptake scan (I-123) was consistent with GD with moderately elevated uptake. She was initially managed with methimazole and atenolol and was eventually treated with RAI (16.32 millicurie I-131) in February 2021. She had post-ablative hypothyroidism managed with levothyroxine. The patient contracted COVID-19 in January 2022. In February 2022, the patient started experiencing eye irritation, dryness, protrusion of eyes, eyelid swelling, and visual disturbances. Thyroid stimulating hormone (TSH) receptor auto-antibodies (7.33 IU/L, normal < /=1.00 IU/L) and thyroid stimulating immunoglobulin (4.30 IU/L, normal < /=1.00 IU/L) were elevated. TSH was normal (2.180 mIU/L, normal 0.270 - 4.200 mIU/L) on levothyroxine 125 mcg daily. She was later diagnosed with TED. Discussion(s): GD is an autoimmune thyroid disorder related to the presence of TSH receptor-stimulating antibodies and is often associated with ocular symptoms. Activation of an autoimmune response during COVID-19 infection, may induce onset or relapse of GD. A study using the national health insurance service database in South Korea noted an increase in the incidence of subacute thyroiditis in 2020 in association with the COVID-19 pandemic. TED is usually seen in patients with GD. Radioactive iodine is widely used in the treatment of GD and has been associated with development or worsening of TED. There are published cases of TED occurring in patients with GD after receiving COVID-19 vaccine. It is thought that the inflammatory syndrome induced by the adjuvants could induce molecular mimicry, which could trigger TED. In most cases this adverse effect was transient, lasting a few months after treatment. There have been case reports of TED occurring after 3 to 21 days of COVID-19 vaccination in patients with controlled GD. Symptoms improved in 4-8 months. Development of TED in patients with GD who have been treated with RAI typically occurs soon after RAI therapy. For TED to occur in a GD patient 11 months after receiving RAI therapy is unusual. COVID-19 infection appears to have been the trigger for this patient's eye disease. This is highly unusual and has not been published to our knowledge.Copyright © 2023

Thyroid Adverse Events after SARS-CoV-2 Vaccination

Introduction: Subacute thyroiditis and autoimmune thyroiditis are known complications of COVID-19 infection. With the development of SARS-CoV-2 vaccine, new cases of thyroiditis following vaccination have been reported. In accordance, we report on a series of patients who present with hyperthyroidism, elevated TSH receptor activating antibodies, concerning for activation of Graves disease after receiving SARS-Cov-2 messenger RNA (mRNA) vaccine. This association underpins the possible immune modulation affecting the presentation of autoimmune thyroiditis post vaccination. Case Description: We describe four patients who present with symptoms of hyperthyroidism after receiving SARS-CoV-2 mRNA vaccine. All were females, median age 49 (range 44-59). Two patients presented with de novo hyperthyroidism 25-29 days following SARS-CoV-2 mRNA vaccine. Two patients have previously had diagnosed Graves disease in remission for longer than 3 years and presented after 40-60 days after receiving SARS-CoV-2 mRNA vaccine. All four patients had TSH receptor antibodies positive (range 6.21-11.87IU/L) Discussion: Although vaccines are one of the most successful medical advances clarifying associated conditions and risks is of interest to practicing physicians. It is not known if these 4 cases of Graves disease were diagnosed coincidentally following SARS-CoV-2 vaccine and association between this vaccine and autoimmune manifestations remains to be further investigated. This report adds information to current knowledge and understanding of autoimmune manifestations following SARS-CoV-2 vaccine.Copyright © 2023

Nanopore single-molecule analysis of biomarkers: Providing possible clues to disease diagnosis

Biomarker detection has attracted increasing interest in recent years due to the minimally or non-invasive sampling process. Single entity analysis of biomarkers is expected to provide real-time and accurate biological information for early disease diagnosis and prognosis, which is critical to the effective disease treatment and is also important in personalized medicine. As an innovative single entity analysis method, nanopore sensing is a pioneering single-molecule detection technique that is widely used in analytical bioanalytical fields. In this review, we overview the recent progress of nanopore biomarker detection as new approaches to disease diagnosis. In highlighted studies, nanopore was focusing on detecting biomarkers of different categories of communicable and noncommunicable diseases, such as pandemic COVID-19, AIDS, cancers, neurologic diseases, etc. Various sensitive and selective nanopore detecting strategies for different types of biomarkers are summarized. In addition, the challenges, opportunities, and direction for future development of nanopore-based biomarker sensors are also discussed.Copyright © 2023 Elsevier B.V.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) complicating myocarditis

Myocarditis can lead to myocardial infarction in the absence of coronary artery obstruction. We report a case of probable myocarditis, complicated by myocardial infarction with non-obstructive coronary arteries. A 19-year-old man presented with chest pain typical of myocarditis. He was a smoker but was otherwise well. Electrocardiogram revealed diffuse ST-elevation and echocardiography revealed a thin, akinetic apex. Troponin-T levels on admission were raised leading to an initial diagnosis of myocarditis being made. However, late gadolinium enhancement study on cardiac magnetic resonance imaging demonstrated transmural enhancement typical of ischaemia. Coronary angiogram was normal, leading to a likely diagnosis of myocardial infarction with non-obstructive coronary arteries. It is important to highlight that coronary assessment remains important when working up for myocarditis, as myocardial infarction with non-obstructive coronary arteries can often complicate myocarditis in cases of normal angiography. Another important lesson was on how cardiac magnetic resonance imaging provided vital evidence to support underlying ischaemia despite normal coronary angiogram, leading to a diagnosis of myocardial infarction with non-obstructive coronary arteries. Myocardial infarction with non-obstructive coronary arteries remains a broad 'umbrella' term and cardiac magnetic resonance imaging, as well as more invasive coronary imaging techniques during angiography, can further assist in its diagnosis. Our case provides a reminder that myocardial infarction with non-obstructive coronary arteries, although increasingly recognised, remains under-diagnosed and can often overlap with peri-myocarditis, highlighting the need to employ multi-modality imaging in guiding management.Copyright © The Author(s) 2021.

Thyroid dysfunction reflects severity of COVID-19 pneumonia in hospitalized patients

Introduction: Coronavirus disease 2019 COVID-19 is clearly the pandemic of the new millennium. COVID-19 determines multi organ dysfunction including the inflammatory immune responses of thyroid gland. Objective(s): To determine whether the involvement of the thyroid gland by COVID-19 manifests as thyroid hormonal changes and development of thyroid disorders. Method(s): We studied prospectively 60 patients with COVID-19 pneumonia,without previous known history of thyroid disease nor pre-existing endocrine disorders, hospitalized between May and July 2021, and we performed serum thyroid hormonal analysis within the first 24 hours after admission, including TSH, Free T3, Free T4 and their antithyroglobulin antibodies (Anti-TG and Anti-TPO), and correlate them with clinical and laboratory data. Result(s): Samples were collected from 60 patients (31 males, 51.7%). 32 out of 60 (53.3%) showed significantly lower values of TSH (0,29 +- 0,07 mIU/mL) with decreased Free T3 serum levels (2,07 +- 0,131 pmol/L) and the thyroid autoantibodies (both Anti-TG and Anti-TPO) were positive. These 32 patients (27 males) demonstrated moderate to critical illness and they needed high oxygen flow. The other 28 patients with no evidence of thyroid abnormalities showed mild to moderate COVID-19 pneumonia and none needed high oxygen flows. Conclusion(s): In our study, 32/60 (53.3%) patients with moderate to severe COPVID-19 pneumonia were diagnosed with thyroid abnormalities. Thus, the development and the progression of respiratory failure due to SARS-COV-2 may affect the thyroid function.

Relationship between thyroid function tests and mortality in severe Covid-19 pneumonia cases admitted to the intensive care unit Severe COVID-19 and thyroid function tests

Aim: In severe COVID-19 infection, most organs are affected, including the thyroid gland. A decrease in thyroid functions can be seen in relation to the severity of the disease. We aimed to retrospectively analyze the relationship between thyroid function tests and mortality in patients admitted to the intensive care unit (ICU) with severe COVID-19 pneumonia. Material(s) and Method(s): The study was performed retrospectively on 46 adult patients admitted to the intensive care unit with severe COVID-19 pneumonia. Demographic, clinical, laboratory data were recorded. Patients were grouped into two according to mortality. Laboratory data were compared between groups. Additionally, the correlation of free triiodothyronine (fT3), free thyroxine (fT4), and thyrotropin (TSH) with infection parameters was investigated. Result(s): At the time of ICU admission, fT3 levels below the normal range were present in 91.3%, fT4 levels were below normal in 39.13%, and TSH levels were below normal in 52.17% of the study patients. There was a positive correlation between fT4 and CRP (r=0.315, p<0.05), while there were no significant correlations between other parameters. TSH, fT3, or fT4 did not differ between patients with and without mortality. Partial arterial oxygen pressure/fraction of inspired oxygen was lower in patients with mortality (p=0.015). Discussion(s): Low thyroid hormone levels and TSH are common occurrences in patients admitted to the ICU with severe COVID-19 pneumonia. No relationship could be shown between low thyroid function test levels and mortality in patients with severe COVID-19 pneumonia.Copyright © 2022, Derman Medical Publishing. All rights reserved.

Is The Co-administration of Metformin and Clomiphene Superior to Induce Ovulation in Infertile Patients with Poly Cystic Ovary Syndrome and Confirmed Insulin-resistance: A Double Blind Randomized Clinical Trial

Objective: This study aimed to compare the effects of clomiphene citrate (CC) combined with metformin or placebo on infertile patients with poly cystic ovary syndrome (PCOS) and insulin resistance (IR). Material(s) and Method(s): We included 151 infertile women with PCOS and IR in a university hospital from November 2015 to April 2022 in this prospective, double-blind, randomized, placebo-controlled trial. Patients were randomized into two groups;group A: received CC plus metformin (n = 76) and group B: received CC plus placebo (n = 75). The ovulation rate was the main outcome measure. Clinical pregnancy, ongoing pregnancy, live birth and abortion rates were secondary outcome measures. Result(s): There was no remarkable difference in ovulation rate in two groups. Moreover, no significant changes were observed in clinical pregnancy, ongoing pregnancy, live birth and abortion rates between two groups. A larger proportion of women in group A suffered from side effects of metformin (9.3% versus 1.4%;p=0.064), although this was not significant. Conclusion(s): In IR infertile women with PCOS, metformin pre-treatment did not increase the ovulation, clinical pregnancy and live birth rates in patients on clomiphene citrate.Copyright © 2023 Tehran University of Medical Sciences.

A case of subacute thyroiditis after influenza vaccination

A 40-year-old Japanese woman presented to the outpatient clinic with fever and palpitations 2 days after receiving the influenza vaccine (Influenza HA Vaccine 'KMB') following the second dose of coronavirus disease 2019 (COVID-19) vaccine (COVID-19 vaccine Moderna intramuscular injection). At the first visit, the patient presented with a swollen thyroid gland with mild tenderness, and she was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free T3: 5.42 pg/mL;free T4: 2.34 ng/dL;and thyroid-stimulating hormone (TSH): <0.01 muIU/mL), a high C-reactive protein level (5.77 mg/dL), a negative TSH receptor antibody, and characteristic ultrasound findings. The patient's human leukocyte antigen types were A2, A11, B35, B51, DR4, and DR1403. Prednisolone (15 mg/day) was given as an initial dose, after which the fever subsided, and the dose was tapered and discontinued after 6 weeks. The patient was thought to have developed SAT due to influenza vaccination. SAT after influenza vaccination may be overlooked. For patients with SAT, it is necessary to obtain information regarding their vaccination history.Copyright © 2023 The authors.

Long COVID: Rapid Evidence Review

Postacute sequelae of COVID-19, also known as long COVID, affects approximately 10% to 30% of the hundreds of millions of people who have had acute COVID-19. The Centers for Disease Control and Prevention defines long COVID as the presence of new, returning, or ongoing symptoms associated with acute COVID-19 that persist beyond 28 days. The diagnosis of long COVID can be based on a previous clinical diagnosis of COVID-19 and does not require a prior positive polymerase chain reaction or antigen test result to confirm infection. Patients with long COVID report a broad range of symptoms, including abdominal pain, anosmia, chest pain, cognitive impairment (brain fog), dizziness, dyspnea, fatigue, headache, insomnia, mood changes, palpitations, paresthesias, and postexertional malaise. The presentation is variable, and symptoms can fluctuate or persist and relapse and remit. The diagnostic approach is to differentiate long COVID from acute sequelae of COVID-19, previous comorbidities, unmasking of preexisting health conditions, reinfections, new acute concerns, and complications of prolonged illness, hospitalization, or isolation. Many presenting symptoms of long COVID are commonly seen in a primary care practice, and management can be improved by using established treatment paradigms and supportive care. Although several medications have been suggested for the treatment of fatigue related to long COVID, the evidence for their use is currently lacking. Holistic treatment strategies for long COVID include discussion of pacing and energy conservation;individualized, symptom-guided, phased return to activity programs;maintaining adequate hydration and a healthy diet;and treatment of underlying medical conditions.Copyright © 2022 American Academy of Family Physicians.

Unusual case of Obesity and Hypoventilation in Childhood

Objectives Childhood obesity can be monogenic or polygenic in etiology and is associated with significant morbidities. Rapid-onset obesity with hypoventilation, hypothalamic dysfunction, and autonomic dysregulation, and neural crest tumor (ROHHHAD[NET]) syndrome, is a rare autonomic and respiratory pediatric disorder presenting with rapid weight gain in early childhood, hypothalamic-pituitary dysfunction, central hypoventilation, and an association with neural crest tumors. Methods A 6-year-old Asian girl with abnormal weight gain since the age of 3 years, presented to the pediatrician's office due to pulse oximeter readings in the 60s at home. Parents were monitoring saturations at home as a way of screening for COVID-19 infection. The pediatrician confirmed hypoxemia and transferred the patient to the Children's Medical Center emergency department on oxygen via EMS. She had occasional snoring and nighttime cough, but no history of respiratory distress, or signs of infection. There was no hyperphagia, neonatal hypoglycemia, or developmental or behavioral concerns. On examination her body weight was 30 kg (+1.56 SD) and height was 113 cm (-1.46 SD) with a body mass index (BMI) of 23.4 kg/m2 (+2.33 SD). No acanthosis nigricans, cushingoid features, or respiratory distress were noted on examination. In the intensive care unit, she was diagnosed with central hypoventilation requiring mechanical ventilation. Her laboratory work-up revealed central hypothyroidism (low Free T4 of 0.64 ng/dl, TSH 1.553 microIU/L). Other anterior pituitary hormones were normal (adrenocorticotropic hormone, 16.3 pg/mL;cortisol, 10.7 mug/dL;prolactin, 9.95 ng/ml;Insulin-like growth factor-1, 83 ng/mL;and IGF binding protein 3, 3.02 mg/L). Genetic investigations revealed no known mutations in the PHOX2B gene, making a diagnosis of central hypoventilation syndrome unlikely. Results Rapid onset weight gain around 3 years of age, central hypoventilation, and anterior pituitary hormone deficiency in our patient with negative PHOX2B is consistent with a clinical diagnosis of ROHHHAD[NET]. Our patient was started on levothyroxine;received tracheostomy for mechanical ventilation;and gastrostomy for pharyngeal dysphagia. She is doing well, goes to school, and is tolerating trials off the ventilator during the day. Conclusions ROHHAD is an important differential to consider for any child with rapid and early obesity and hypoventilation as early diagnosis is critical in improving the clinical management and the prognosis.

IDIOPATHIC TROPONEMIA AFTER TRANSCAROTID ARTERY REVASCULARIZATION

SESSION TITLE: Etiologies of Cardiovascular Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Troponin level (Tnl) is usually used as confirmation of acute myocardial infarction (AMI) and is a sensitive marker. It is usually increased within 2-3 hours after AMI. In most cases, increased in Tnl is associated with symptomatic chest pain, cardiac ischemia, chronic coronary syndromes, etc. It can also be elevated in other conditions without cardiac injuries, like critical illness: COVID infection, septic shock, acute stroke and burns. CASE PRESENTATION: A 72 y/o man with history of b/l internal carotid artery (ICA) stenosis (70% in R-ICA and 80-90% in L-ICA) underwent elective left trans-carotid artery revascularization (TCAR). He was transferred to ICU after an uneventful procedure, for monitoring. His history was significant for HTN, HLD, Meniere's disease, gout, prior CVA of L-frontal lacunar and R-PICA (posterior inferior cerebellar artery). Postop vitals: BP 114/60 mmHg, HR 65, RR 16, O2 sat 98%. Tnl increased to 1.95 and then declined (normal 0 - 0.4 ng/ml). He was AAOx4, and asymptomatic. Post-op serial EKGs: normal sinus rhythm with no ST/T wave changes. Echo: EF 60%, normal biventricular size and function. LDL <70, A1C 5.9, normal TSH, no CPK elevation. Other labs: normal, No new neurological deficits. He was continued on ASA, clopidogrel, metoprolol, amlodipine and lisinopril. His hospital stay was uneventful, and he was discharged on post-op day 3. DISCUSSION: Cardiac troponin complex has its distinct subunits according to their functions: highly conserved Ca2+ binding subunit (cTnC);actomyosin ATPase inhibitory subunit and tropomyosin binding subunit. They play the pivotal role in regulating myocardial muscle contraction and relaxation and demonstrate as sensitive biomarkers for the myocardial injuries. Interestingly, there are many other causes that lead to increased cardiac troponin level without remarkable myocardial injuries or ischemia. Elevated Tnl after TCAR procedure can also be due to its surgical complication of a chance of hypoperfusion during the procedure. Our patient's surgery was uneventful. In one randomized controlled trial, it is stated that the risk of having CVA and AMI is higher in carotid endarterectomy compared to revascularization in patients with carotid artery stenosis. Our patient did not have any post-op complication, and only had an idiopathic elevation of troponin. CONCLUSIONS: The role of Tnl plays an important role in confirmation of myocardial infarction or ischemia but it can be idiopathic. Unpublished data from our institution revealed no increase in troponin s/p TCAR after uneventful procedures. This is the first reported case presenting with elevated troponin level without any pertinent positive findings (EKG changes/symptoms). Maybe in uneventful TCAR procedure troponin should not be ordered? Reference #1: Defilippi, C.R., Tocchi, M., Parmar, R.J., Rosanio, S., Abreo, G., Potter, M.A., Runge, M.S., & Uretsky, B.F. (2000). Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes. Journal of the American College of Cardiology, 35 7, 1827-34. Reference #2: Gordon AM, Homsher E, Regnier M. Regulation of contraction in striated muscle. Physiol Rev. 2000 Apr;80(2):853-924. doi: 10.1152/physrev.2000.80.2.853. PMID: 10747208. Reference #3: Brott, T.G., Hobson, R.W., Howard, G., Roubin, G.S., Clark, W.M., Brooks, W., Mackey, A., Hill, M.D., Leimgruber, P.P., Sheffet, A.J., Howard, V.J., Moore, W.S., Voeks, J., Hopkins, L.N., Cutlip, D.E., Cohen, D.J., Popma, J.J., Ferguson, R.D., Cohen, S.N., Blackshear, J.L., Silver, F.L., Mohr, J.P., Lal, B.K., & Meschia, J.F. (2010). Stenting versus endarterectomy for treatment of carotid-artery stenosis. The New England journal of medicine, 363 1, 11-23. DISCLOSURES: No relevant relationships by Moses Bachan No relevant relationships by Zin Min Htet No relevant relationships by Z nobia Khan No relevant relationships by Zin Oo