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Control systems and the modeling strategies are not only limited to engineering problems. These approaches can be used in the field of bio-mathematics as well and modern studies have promoted this approach to a great extent. The computational modeling and simulation of bone metastasis is painful yet critical after cancer invades the body. This vicious cycle is complex, and several research centers worldwide are devoted to understanding the dynamics and setting up a treatment strategy for this life-threatening behavior of cancer. Cancerous cells activation and the corresponding process of metastasis is reported to boost during the periodic waves of COVID-19, due to the inflammatory nature of the infection associated with SARS-2 and its variants. The bone cells are comprised of two types of cells responsible for bone formation and resorption. The computational framework of such cells, in spatial form, can help the researchers forecast the bone dynamics in a robust manner where the impact of cancer is incorporated into the computational model as a source of perturbation. A series of computational models are presented to explore the complex behavior of bone metastasis with COVID-19 induced infection. The finite difference algorithm is used to simulate the nonlinear computational model. The results obtained are in close agreement with the experimental findings. The computational results can help explore the vicious cycle's fate and help set up control strategies through drug therapies.
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Coronavirus disease 2019 (COVID-19) affects thyroid function. These changes are due to the direct impact of the virus on thyroid cells via angiotensin-convertingenzyme 2 (ACE2) receptors, inflammatory reaction, apoptosis in thyroid follicular cells, suppression of hypothalamus-pituitary-thyroid axis, an increase in activity of adrenocortical axis, and excess cortisol release due to cytokine storm of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Euthyroid sick syndrome (ESS), thyroiditis, clinical and subclinical hypothyroidism, central hypothyroidism, exacerbation of underlying autoimmune thyroid disease, and clinical and subclinical hyperthyroidism can be associated with coronavirus. Adjuvants in coronavirus vaccines induce autoimmune/inflammatory syndrome known as vaccine adjuvants (ASIA) syndrome. Thyroiditis and Graves' disease have been reported to be associated with ASIA syndrome after some coronavirus vaccinations. Some coronavirus medications, such as hydroxychloroquine, monoclonal antibodies, lopinavir/ritonavir, remdesivir, naproxen, anticoagulants, and glucocorticoids can also affect thyroid tests, and correct diagnosis of thyroid disorders will be more difficult. Conclusion: Changes in thyroid tests may be one of the most important manifestations of COVID-19. These changes can be confusing for clinicians and can lead to inappropriate diagnoses and decisions. Prospective studies should be conducted in the future to increase epidemiological and clinical data and optimize the management of thyroid dysfunctions in patients with COVID-19.
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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.
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Thyroid storm is a rare life-threatening condition characterized by severe and exaggerated clinical manifestations of thyrotoxicosis. It can be precipitated by a myriad of acute events and stressors including but not limited to surgery, trauma, or infections. Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily associated with respiratory symptoms, has been reported to be a likely precipitating cause of thyroid storm in a few cases. COVID-19 has been associated with both new-onset thyrotoxicosis and as a flare-up of the disease in remission. Even though the Burch-Wartofsky Point Scale (BWPS) scoring system has been used for years to help diagnose thyroid storms, the relatively low specificity of the score, especially in the setting of viral or bacterial infections, has been challenging for clinicians. Having a low threshold to consider the diagnosis of this life-threatening condition while at the same time meticulously ruling out other potential differential diagnoses is critical for saving lives. In this report, we discuss a case that highlights the importance that clinicians should accord to thyroid storm as one of the differential diagnoses in patients with a history of hyperthyroidism, with a positive test for COVID-19 infection on admission, and presenting with deranged vital signs and change in mentation from baseline.
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Zinc has an important role during infection with the Covid-19 virus, as it regulates the work of the immune system. Zinc deficiency leads to hair loss and graying and affects the functioning of the thyroid hormone. Between 15% and 30% of Covid-19 patients in the hospital suffer from thyroid dysfunction. However, it appears that most of these changes it is limited and that thyroid function in most patients will return to normal once the infection has cleared. Twenty two males and seventy eight females diagnosed with COVID-19 infection during the period from September 1 to December 12, 2020. All patients were suffering from cough, fever, hair loss, loss of smell, sweating, loss of appetite and respiratory discomfort. The age of patient was ranged between 15 to 70 years. 2019-nCoV IgG/IgM COMBO test card was used to diagnose SARS-COV-2 infection. Serum zinc concentration;serum Ferritin levels;TSH;T4 and serum Vitamin D3 were estimated in all patients. The highest rate of infection with the COVID-19 was in females, with a rate of 28.20% within the age group 30-39 years, as well as in males, and a percentage of 36.36% within the same age group. 86 (86%), 74 (74%), 68 (68%) and 18 (18%) patients from a deficiency in TSH, ferritin, Vitamin D3 and zinc levels, respectively. The age group 30-39 years of patients suffered from low levels of zinc, as it was 11 (61.1%), followed by the age group 40-49 years, with a rate of 4 (22.2%). The levels of TSH, ferritin and Vitamin D3 in the age group 30-39 years were 30 (34.8%), 21 (14.28%) and 25 (33.78%), respectively. While the T3 and T4 rates for all patients and for all age groups were within normal levels. In conclusion, COVID-19 patients suffered from zinc deficiency and thyroid dysfunction with significant hair loss in almost all age groups and both sexes.
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Background: COVID-19 disease is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This infectious disease was previously known as Novel Coronavirus-Infected Pneumonia (NCIP) by the WHO, and the virus was dubbed 2019 novel coronavirus (2019-nCoV). Abnormal levels of thyroid hormones alter metabolism, and thyroid hormones are significant determinants of glucose homeostasis, and affect fasting glucose levels by antagonizing insulin action. Aim;The aim of the study is to evaluate of thyroid hormones in diabetic patients who affected with COVID-19. Patients and methods;A total of 120 subjects participated in the present study. patients distributed as follows: Group1(30 patient with COVID-19), Group2 (30 patient with COVID-19 and DM), Group3 (30 patient with DM type2 without COVID-19), Group4 (30 control (apparently healthy subjects)). Their age ranged from 23-70 years old and was investigated for the determination of FBS, HbA1c, CRP, IL-6, T3, T4, and TSH. Results: In our study, there were no significant differences between control and all patients. However, regarding T3, There is a highly significant elevation in T3 concentration of patients with COVID-19 associated with DM, (4.2 ± 0.7ng/ml) as compared with control healthy subjects, (2.3 ± 0.2;P ≤ 0.01). Moreover, there is a significant elevation in the concentration of serum T3 in patients with COVID-19, (3.8 ± 0.4 ng/ml), as compared with control healthy subjects, (2.3 ± 0.2 ng/ml;P≤0.05. Also there is a significant elevation in the concentration of serum T3 of patients with DM type 2 without COVID-19, (3.6 ± 0.4 ng/ml)، as compared with control healthy subjects, (2.3 ± 0.2 ng/ml;P ≤ 0.05). According to T4, there is a highly significant elevation in the concentration of serum T4 of patients with COVID-19 associated with DM, (209.8 ± 34.7 nmol/l) as compared with control healthy subjects, (156.2 ± 11.4;P ≤ 0.01). While, there is no significant elevation in the concentration of serum T4 of patients with COVID-19, (155.6 ± 21.1 nmol/l), as compared with control healthy subjects, (156.2 ± 11.4), but there is a significant elevation in the concentration of serum T4 of patients with DM type 2 only, (181.9 ± 19.7), as compared with control healthy subjects, (156.2 ± 11.4;P ≤ 0.05). TSH in our result shows there are no significant differences in the concentration of serum TSH of patients with COVID-19 associated with DM group and a group of patients of DM without COVID-19 (0.88 ± 0.21), (0.97 ± 0.22) as compared with control healthy subjects (0.84 ± 0.14;P ≤ 0.05). However, there is a significant elevation in the concentration of serum TSH of patients with COVID-19 only, (1.23 ± 0.3), as compared with control healthy subjects, (0.84 ± 0.14;P ≤ 0.05). Regarding FBS and HbA1c, our result presents that there is a significant increase in serum FBS, (P≤ 0.01) in patients with COVID-19 associated with DM, (259.8 ± 90.7) as compared with control subjects, (95.1± 6.7). Also, there is a significant increase in serum FBS, (P≤ 0.01) in patients with COVID-19 associated with DM, (259.8 ± 90.7 mg/dl) as compared with patients with COVID-19 only, (156.4± 40.7 mg/dl). While in HbA1c %, there is significant increase in serum HbA1c %, (P ≤ 0.05) in patients with COVID-19 associated with DM, (9.3 ± 1.7%) as compared with control subjects (1.1 ± 0.6 %). Also, there were significant differences in HbA1c % in patients with COVID-19 associated with DM, and COVID-19 patients as compared with control subjects, (P ≤ 0.01). With regard to Interleukin-6, a highly significant elevation in the concentration of serum IL-6 in patients with COVID-19 associated with DM has been shown, (20.8 ± 7.5 pg/ml) as compared with control healthy subjects, (3.9 ± 0.8;P ≤ 0.01). Moreover, there is a significant elevation in the concentration of serum IL-6 in patients with COVID-19, (14.6 ± 3.5), as compared with control healthy subjects, (3.9 ± 0.8;P ≤ 0.01). However, there is a significant elevation in the concentration of serum IL 6 in patients with DM type 2 without COVID-19, (11.5 ± 0.8), as compared with control healthy subjects, (3.9 ± 0.8;P ≤ 0.05). While CRP has shown a highly significant elevation in its concentration in patients with COVID-19 associated with DM, (53.2 ± 21.6 mg/l) as compared with control healthy subjects, (2.1 ± 0.8;p≤ 0.01). Moreover, there is a significant elevation in the concentration of serum CRP of patients with COVID-19 only, (39.1 ± 10.6), as compared with control healthy subjects, (2.1 ± 0.8;P ≤ 0.01). Also, there is a significant elevation in the concentration of serum CRP of patients with DM type 2 without COVID-19, (4.7 ± 0.9), as compared with control healthy subjects, (2.1 ± 0.8;P ≤ 0.05).
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Background and aims: Approval of a drug therapy for NASH requires a very good safety/tolerability profile and acceptable therapeutic index. MAESTRO-NAFLD-1 (NCT04197479) is a randomized doubleblind (DB) Phase 3 clinical trial of placebo (PBO) versus resmetirom (RES), a once-a-day oral selective thyroid hormone receptor β agonist, in >1100 patients with NAFLD with safety as the primary end point. Method: Enrollment was Dec 2019 to Oct 2020 at 79 US sites. Requirements included 3 metabolic risk factors, fibroscan (FS) ≥5.5 kPa/CAP≥280 dBm, MRI-PDFF≥8%. Randomization was 1:1:1:1 to 3 DB arms, PBO, 80 or 100 mg RES (n = 972) or an 100 mg open label (OL) arm (n = 171). The primary objective was to evaluate the safety and tolerability of 80 or 100 mg RES versus PBO measured by the incidence of adverse events (AEs). Results: At baseline the DB safety population (n = 969) was age 55.9 (11.8);female, 54.4%, white 88.6%;hispanic 34.7%;BMI 35.3 (6.0) type 2 diabetes 49%, hypertension 76.1%, dyslipidemia 87.9%;FS 7.4 (4.7) kPa. Discontinuations (22.5%) did not differ by treatment, most patient decision (pandemic related). DB compliancewas impacted by COVID drug kit delays. AE withdrawals were 80 mg, 2.4%;100 mg, 2.8%;PBO, 1.3%. The primary objective was met. TEAEs were 80 mg, 88.4%;100 mg, 86.1%;PBO, 81.8%. TEAEs ≥grade 3 severity were 80 mg, 7.6%;100 mg, 9.0%;PBO, 9.1%. AEs in excess of PBOwere grade 1–2 AEs of diarrhea (80 mg, 23.5%;100 mg, 31.2%;PBO, 13.8%) and nausea (80 mg, 11.9%;100 mg, 18.2%;PBO, 7.9%), in the first few weeks. ALT increases ≥3XULN were 80 mg, 0.61%;100 mg, 0.31%;PBO,1.6%. Therewere no changes in bodyweight or HR. BP decreased by 2–3 mmHg in the RES arms. Key 2o end points were met (Table). Comparative mean reduction in FS VCTE was not significant;a responder analysis of FS and MRE showed significant reductions with RES treatment. Conclusion: RES achieved the primary safety end point in this 52- week Phase 3 NAFLD clinical trial that identified patients by metabolic risk and non-invasive imaging. Key 2o end points were met including LDL-C, ApoB, triglycerides, MRI-PDFF, FS (CAP).(Table Presented) 1MRE combined RES groups.
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Tissue hypoxia is one of the main pathophysiologic mechanisms in sepsis and particularly in COVID-19. Microvascular dysfunction, endothelialitis and alterations in red blood cell hemorheology are all implicated in severe COVID-19 hypoxia and multiorgan dysfunction. Tissue hypoxia results in tissue injury and remodeling with re-emergence of fetal programming via hypoxia-inducible factor-1α (HIF-1a)-dependent and -independent pathways. In this context, thyroid hormone (TH), a critical regulator of organ maturation, may be of relevance in preventing fetal-like hypoxia-induced remodeling in COVID-19 sepsis. Acute triiodothyronine (T3) treatment can prevent cardiac remodeling and improve recovery of function in clinical settings of hypoxic injury as acute myocardial infarction and by-pass cardiac surgery. Furthermore, T3 administration prevents tissue hypoxia in experimental sepsis. On the basis of this evidence, the use of T3 treatment was proposed for ICU (Intensive Care Unit) COVID-19 patients (Thy-Support, NCT04348513). The rationale for T3 therapy in severe COVID-19 and preliminary experimental and clinical evidence are discussed in this review.
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COVID-19 Drug Treatment , Sepsis , Humans , Hypoxia/metabolism , Thyroid Hormones/metabolism , Thyroid Hormones/therapeutic use , Triiodothyronine/therapeutic useABSTRACT
Introduction: Biotin is a vitamin-B supplement and is sold over-the-counter alone or in combination with other vitamins and minerals to improve skin, nail, and hair health. Exogenous biotin intake is becoming a common cause of apparent abnormal thyroid function tests in endocrine practice. We present a case report. Case Description: A 55-year-old lady was referred to endocrinology clinic for low TSH but normal fT4. The only symptom she had was abnormal smell of ‘smoke’. She had no ongoing symptoms of thyrotoxicosis or hypothyroidism apart from hair thinning. She had COVID-19 infection with pyrexia and constitutional symptoms a year ago. There was no other past medical or family history of note. On direct questioning, she admitted taking biotin 300ug every day in preceding six months for hair loss. Examination revealed euthyroidism and no goitre. TFTs prior to commencing biotin were normal. Further TFTs confirmed low TSH but normal fT4 and fT3 and thyroid receptor antibody was negative. TFTs off biotin for three days were normal and she was reassured. Discussion: There is no in vivo relationship between biotin and thyroid hormones, but high dose biotin affects thyroid function test in vitro when assessed with immunoassays using streptavidin-biotin immobilizing system. Apparently low TSH with or without raised T4 suggests thyrotoxicosis or thyroxine over-replacement. All patients presenting with such abnormal thyroid function tests should be questioned about biotin intake along with iodine as many multivitamins contain high dose biotin and patients are often unaware. This can avoid unnecessary investigations, patient anxiety, and healthcare costs. American Thyroid Association advises stopping biotin two days before thyroid function test. Patients can continue to take biotin except temporarily before thyroid blood tests.
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Introduction: Hashimoto's encephalopathy (HE) manifests itself with neuro-psychiatric disorders, which can reach coma;HE usually occurs in euthyroid, being less frequent states of thyroid dysfunction. We present the case of a patient with HE and severe hypothyroidism. Case Description: A 71-year-old woman;history of rheumatoid arthritis, hypertension and cerebral infarction without sequelae. The family referred a 3-week history of illness characterized by disorientation and "jerking" movements, she progressed to drowsiness with left hemiparesis, focal epileptic seizures and myoclonus. The brain CT showed atrophy and left frontal malacia;diagnosed status epilepticus and cerebral infarction, indicating phenytoin. During hospitalization she was added valproic acid and levetiracetam, without improvement. Brain MRI showed cerebral atrophy and periventricular leukoaraiosis. The study of the CSF: hyperproteinorraquia;EEG: diffuse slowing and periodic lateralized discharges in the right hemisphere. They request an endocrinology evaluation for TSH: > 75uIU/ml, Free T4: 0.31ng/dl, we expand with Anti-TPO > 1000 and Anti-thyroglobulin > 3000, and we indicate treatment for severe hypothyroidism with levothyroxine for nasogastric tube and intravenous hydrocortisone for 5 days and with minimal recovery from sensory disorder. After the withdrawal of hydrocortisone, she developed drowsiness and intensified myoclonus despite an improvement in the blood concentration of thyroid hormones. Having excluded infectious, metabolic and paraneoplastic etiology of encephalopathy, with the presence of elevated antithyroid antibodies in blood and CSF, the diagnosis of Hashimoto's encephalopathy was raised, receiving methylprednisolone (1 g/day for 5 days), then human immunoglobulin (25g for 5 days) Faced with poor response, she received 5 sessions of plasmapheresis with favorable clinical and paraclinical evolution. After overcoming hospital infection by COVID-19, she was discharged at 3 months. In the follow-up, cognitive deterioration, partial dependence, without epileptic seizures or myoclonus were reported. Discussion: HE is rare, with variable clinical presentation. HE has a good response to corticosteroids, although it sometimes requires other interventions. The alteration of thyroid function itself can be confusing at the time of diagnosis. Severe hypothyroidism can present neurological complications such as seizures, dementia, or psychosis;but it differs from HE in that manifestations improve when thyroxine is replaced.
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Introduction: Coronavirus disease 2019 (COVID-19) infection has led to multiple endocrinopathies. We present a case of panhypopituitarism induced by COVID -19 infection. Case Description: 76 yo male with history of type 2 diabetes, hypertension, and 1.5 cm stable, nonfunctioning, pituitary macroadenoma diagnosed in 2017 had multiple admissions for altered mental status and hyponatremia following COVID-19 infection in April 2020. Workup revealed low free T4 0.60 ng/dL (0.8-1.8), low random cortisol 1.8 mcg/dL(2.9-19.4), high prolactin 33.5 ng/mL (2-18), low total testosterone < 10 ng/dl (175-781), SHBG 32.7 nmol/L (13.3-89.5), and low gonadotropins. While hospitalized, he was diagnosed with pan-hypopituitarism and started on glucocorticoids and levothyroxine. Repeat MRI pituitary done after discharge, documented stability of the macroadenoma without hemorrhage. To date, the patient remains on glucocorticoid replacement and thyroid hormone replacement in stable state. Discussion: Hypopituitarism from any etiology has an incidence of 4.2 per 100,000. Hormone replacement therapy remains the mainstay of treatment. This case represents a patient who had unexplained recurrent hyponatremia after COVID-19 infection and later diagnosed with pan-hypopituitarism. Given the continued pandemic, more endocrinopathies related to the COVID-19 infection have been reported. We have data for other viral infections, such as SARS and Dengue, documenting pituitary dysfunction. Review of literature documents SARS infection leading to post infectious hypophysitis with resulting secondary hypocortisolism and hypothyroidism. The cause was thought to be virus binding to pituitary angiotensin-converting enzyme 2 (ACE2) receptors. There is also data supporting COVID-19 infection leading to pituitary apoplexy and hypophysitis, though the number of cases reported is limited. The pathophysiology is thought to be the COVID 19 virus binding to pituitary ACE2 receptors for which it has a 10-20-fold higher affinity. Furthermore, the hypothalamus also expresses ACE2 receptors making it a target for the virus. The binding leads to cellular destruction and autoimmune collateral damage. Hypothalamic pituitary dysfunction could be due to direct effect of virus. The virus can also lead to reversible hypophysitis.
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Eosinophilic pancarditis (EP) is a rare, often unrecognized condition caused by endomyocardial infiltration of eosinophil granulocytes (referred as eosinophilic myocarditis, EM) associated with pericardial involvement. EM has a variable clinical presentation, ranging from asymptomatic cases to acute cardiogenic shock requiring mechanical circulatory support (MCS) or chronic restrictive cardiomyopathy at high risk of progression to dilated cardiomyopathy (DCM). EP is associated with high in‐hospital mortality, particularly when associated to endomyocardial thrombosis, coronary arteries vasculitis or severe left ventricular systolic dysfunction. To date, there is a lack of consensus about the optimal diagnostic algorithm and clinical management of patients with biopsy‐proven EP. The differential diagnosis includes hypersensitivity myocarditis, eosinophil granulomatosis with polyangiitis (EGPA), hypereosinophilic syndrome, parasitic infections, pregnancy‐related hypereosinophilia, malignancies, drug overdose (particularly clozapine) and Omenn syndrome (OMIM 603554). To our knowledge, we report the first case of pancarditis associated to eosinophilic granulomatosis with polyangiitis (EGPA) with negative anti‐neutrophil cytoplasmic antibodies (ANCA). Treatment with steroids and azathioprine was promptly started. Six months later, the patient developed a relapse: treatment with subcutaneous mepolizumab was added on the top of standard therapy, with prompt disease activity remission. This case highlights the role of a multimodality approach for the diagnosis of cardiac involvement associated to systemic immune disorders.
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Introduction: Phosphorus is an essential component of many macromolecules found in bone, lipid membranes, and DNA. It circulates in serum as phosphate. Phosphate level is mainly determined by kidney function. Other factors such as 1, 25 vitamin D3, thyroid hormone and low phosphorous intake can increase renal absorption of phosphate. Hyperphosphatemia presents when serum phosphate is above 4.5 mg/dl (1.45 mmol/L). The phosphate target for hemodialysis (HD) patients is 5.5 mg/dl (1.77 mmol/L) or less. Serum phosphate is commonly measured through the colorimetric method and can also be measured isotopically. Depending on the method used to measure the serum phosphate, many factors have been reported to produce falsely elevated levels. Methods: 52-year-old female with past medical history of end stage renal disease on HD, heart failure with severely reduced ejection fraction secondary to ischemic cardiomyopathy status post left ventricular assist device (LVAD), type 2 diabetes, hypertension, upper gastrointestinal bleeding, anemia, was admitted at a rehabilitation center after a hospital stay due to COVID-19 infection and E. faecium bacteremia secondary to a drive-line infection of the LVAD which was treated with daptomycin. On admission, the patient was found to have a phosphorus level of 6.3 mg/dl, PTH 265 pg/mL, corrected calcium 10 mg/dl, and hemoglobin 9.1 g/dL. Results: Patient was started on oral Sevelamer tablets 800 mg every 8 hours and underwent regular full HD sessions. However, the hyperphosphatemia persisted. Sevelamer was increased to 1600 mg every 8 hours, and she was maintained on a strict low phosphorous renal diet. Four days later while on the new regimen, the phosphorous increased to 12.2 mg/dl. She remained asymptomatic. Hemolysis and hyperbilirubinemia were excluded. A serum protein electrophoresis revealed a monoclonal spike in the gamma region with gamma % of 38.5 (normal range 11-20), gamma globulin 3.0 g/dL (normal range 0.6 – 1.6 g/dL), and quantification of the abnormal protein of 0.41 g/dL (5.3% total). Serum immunofixation showed a probable IgG Lambda monoclonal band. A serum free light chain assay demonstrated a Kappa light chain free serum of 548.9 mg/L (normal range 3.3 – 19.4 mg/L) and Lambda light chain free serum 549.7 mg/L (normal range 5.7 – 26.3 mg/L). Patient was diagnosed with a monoclonal gammopathy, and the elevated phosphorus deemed to be pseudohyperphosphatemia secondary to paraproteinemia. Conclusions: Colorimetric assay with phosphomolybdate ultraviolet (UV) is commonly used for measurement of serum phosphate. The ammonium molybdate reacts with the phosphate to form a cloudy complex, UV absorbance is measured at a specific wavelength. Several factors have been reported to cause falsely high phosphate such as hyperlipidemia, hyperbilirubinemia, hemolysis, liposomal amphotericin B, recombinant tissue plasminogen activator, heparin sulfate, and gammopathies. The paraproteinemia present in monoclonal gammopathies creates a cloudier sample which increases the absorbance of UV light leading to spurious elevation of serum phosphate. Although hyperphosphatemia is a common finding in dialysis patients, the presence of persisting or worsening hyperphosphatemia in a compliant patient taking phosphorous binders and adhering to a low phosphorus diet should raise concern for pseudohyperphosphatemia. No conflict of interest
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Nowadays, emerging evidence has shown adverse pregnancy outcomes, including preterm birth, preeclampsia, cesarean, and perinatal death, occurring in pregnant women after getting infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), but the underlying mechanisms remain elusive. Thyroid hormone disturbance has been unveiled consistently in various studies. As commonly known, thyroid hormone is vital for promoting pregnancy and optimal fetal growth and development. Even mild thyroid dysfunction can cause adverse pregnancy outcomes. We explored and summarized possible mechanisms of thyroid hormone abnormality in pregnant women after coronavirus disease 2019 (COVID-19) infection and made a scientific thypothesis that adverse pregnancy outcomes can be the result of thyroid hormone disorder during COVID-19. In which case, we accentuate the importance of thyroid hormone surveillance for COVID-19-infected pregnant women.
Subject(s)
COVID-19 , Criminals , Pregnancy Complications, Infectious , Premature Birth , Female , Humans , Infant, Newborn , Infectious Disease Transmission, Vertical , Pregnancy , Pregnancy Outcome , SARS-CoV-2 , Thyroid Gland , Thyroid HormonesABSTRACT
Sepsis and septic shock result in impaired microcirculation and red blood cell rheology which lead to tissue hypoxia and multi-organ failure. Early administration of triiodothyronine prevents tissue hypoxia in experimental sepsis. In this context, a clinical trial was initiated to test the efficacy of acute triiodothyronine administration to combat tissue hypoxia in critically ill COVID19 patients. Here, we provide preliminary data from interim analysis of this study showing a novel acute effect of triiodothyronine on erythrocyte sedimentation rate which may have an important therapeutic impact on red blood cell rheology and tissue hypoxia in sepsis and particular in COVID19 critical illness.Trial registration: ClinicalTrials.gov, NCT04348513. Registered 16 April 2020, https://clinicaltrials.gov/ct2/show/NCT04348513.