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Clinical parameters characterizing the efficacy and safety of favipiravir were examined in a multicenter, non-interventional (before-and-after study design) trial in 264 patients with mild COVID-19. It is shown that on the background of 14-day therapy with favipiravir body temperature normalized, blood oxygen saturation improved, and the frequency of tachycardia detection reduced by 16% (p < 0.0001). A statistically significant decrease by 91,3% (p 0.0001) in the frequency of SARS-nCoV-2 RNA detection in the nasopharyngeal mucosa discharge was revealed. A decrease in the concentration of ferritin (by 69% compared to initial values), blood glucose (by 21%), creatinine (by 10%), C-reactive protein (by 36%) (p 0.0001), and D-dimer by 61% (p = 0.016) was noted. The results of the SF-36 health survey questionnaire revealed a significant (p 0.05) improvement in the quality of life in terms of physical functioning (by 35%), and role functioning associated with physical and emotional state by 107% and 160%, respectively. Analysis of the COV19-QoL questionnaire revealed a decrease by 24% in negative perception of the disease (p < 0,01). Among the identified adverse events, elevated level of ALT (in 39.47% of patients), hyperuricemia (in 28.95% of patients), and elevated AST (in 23.68% of patients) prevailed. All the adverse events occurred with mild or moderate severity. There were no lethal outcomes in the studied sample of patients. The analysis showed a satisfactory level of the tolerability of the treatment.Copyright © 2023 Izdatel'stvo Meditsina. All rights reserved.
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Clinical parameters characterizing the efficacy and safety of favipiravir were examined in a multicenter, non-interventional (before-and-after study design) trial in 264 patients with mild COVID-19. It is shown that on the background of 14-day therapy with favipiravir body temperature normalized, blood oxygen saturation improved, and the frequency of tachycardia detection reduced by 16% (p < 0.0001). A statistically significant decrease by 91,3% (p 0.0001) in the frequency of SARS-nCoV-2 RNA detection in the nasopharyngeal mucosa discharge was revealed. A decrease in the concentration of ferritin (by 69% compared to initial values), blood glucose (by 21%), creatinine (by 10%), C-reactive protein (by 36%) (p 0.0001), and D-dimer by 61% (p = 0.016) was noted. The results of the SF-36 health survey questionnaire revealed a significant (p 0.05) improvement in the quality of life in terms of physical functioning (by 35%), and role functioning associated with physical and emotional state by 107% and 160%, respectively. Analysis of the COV19-QoL questionnaire revealed a decrease by 24% in negative perception of the disease (p < 0,01). Among the identified adverse events, elevated level of ALT (in 39.47% of patients), hyperuricemia (in 28.95% of patients), and elevated AST (in 23.68% of patients) prevailed. All the adverse events occurred with mild or moderate severity. There were no lethal outcomes in the studied sample of patients. The analysis showed a satisfactory level of the tolerability of the treatment.Copyright © 2023 Izdatel'stvo Meditsina. All rights reserved.
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COVID-19 disease is caused by the new coronavirus SARS-CoV-2. The disease first appeared in China in 2019 and quickly spread throughout the world. It primarily affects the respiratory tract, manifested by fever, cough and the devel-opment of dyspnoea, but the symptoms and complications can affect any organ system. Neurological symptoms include headaches, muscle and joint pain, taste and smell disorders. Complications include inflammatory diseases of the central nervous system, ataxia, peripheral nerve and muscle diseases, worsening of extra-pyramidal diseases, and neuropsychiatric disorders. This paper presents a case report of a 62-year-old man with cere bellar syndrome, ataxia, intentional tremor and hypermetria when dealing with COVID-19 disease.Copyright © 2021 Neuroendocrinology Letters.
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Objective To explore the occurrence and influencing factors of serum uric acid elevation in patients with coronavirus disease 2019 (COVID-19) treated with favipiravir. Methods Medical records of patients with COVID-19 who were hospitalized in Beijing Ditan Hospital between June 1, 2020 and June 30, 2021 and treated with the 5- or 10-day regimen of favipiravir were collected and retrospectively analyzed. After favipiravir withdrawal, if the elevation in serum uric acid was >=30% of baseline level, it was defined as serum uric acid elevation. Then patients were divided into serum uric acid elevation group and non-serum uric acid elevation group. The clinical characteristics such as gender, age, body mass index, comorbidities, smoking and drinking behavior, COVID-19 grade, favipiravir regimen, and serum uric acid level and renal function before treatment in patients between the 2 groups were compared. Influencing factors of favipiravir-associated serum uric acid elevation was analyzed using multivariate logistic regression method. Results A total of 179 patients were included in the analysis, including 104 (58.1%) males and 75 (41.9%) females, aged from 19 to 70 years with a median age of 43 years. The level of serum uric acid in 179 patients after favipiravir treatment was significantly higher than before [(451+/-119) mumol/L vs. (332+/-94) mumol/L, P<0.001]. The change rate of serum uric acid from baseline level ranged from -57.1% to 157.8% with the median of 38.6%. The elevation in serum uric acid of >= 30% of baseline level occurred in 108 (60.3%) patients. The incidences of serum uric acid elevation in patients treated with 5-day and 10-day regi- mens of favipiravir were 46.8% (36/77) and 70.6% (72/102), respectively, and the difference between them was significant (P=0.001). Multivariate logistic regression analysis showed that body mass index 24.0 to <28.0 kg/m2 (OR=3.109, 95%CI: 1.209-7.994, P=0.019) and 10-day regimen of favipiravir (OR=3.017, 95%CI: 1.526-5.964, P=0.001) were independent risk factors for favipiravir-associated serum uric acid elevation. Conclusions More than half of COVID-19 patients treated with favipiravir can develop serum uric acid elevation. Overweight and 10-day regimen of favipiravir are independent risk factors for serum uric acid elevation in patients.Copyright © 2022 Adverse Drug Reactions Journal.
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The purpose: to study the association of hyperuricemia and renal dysfunction in convalescents of new coronavirus infection. Materials and methods: The study included 234 people who had a new coronavirus infection COVID-19 and were observed two months after convalescence. The mean age was 54.10±12.88 years. Three groups of patients were formed according to the anamnesis according to the severity of the new coronavirus infection: mild (n=108), moderate (n=112), and severe (n=14). In patients, BMI, creatinine, and uric acid levels were determined. Statistical processing of the obtained results was performed using the SPSS software package. Results: the average level of GFR was 80.34±16.66 ml/min/1.73 m2. In patients with a mild course of coronavirus infection, the average GFR was 82.52±15.78 ml/min/1.73 m2, with a moderate course – 78.33±17.69 ml/min/1.73 m2, with a severe course – 79.71±13.38 ml/min/1.73 m2. А decrease in GFR below 90 ml/min/1.73 m2 occurred in 69.3% of cases. Significant differences were obtained between the 1st and 2nd groups (p=0.046). Hyperuricemia was registered in 33.8% of cases. Moreover, in patients with a severe course of coronavirus infection, hyperuricemia was more common than in those with a mild course (64.3% vs 26.4%, p=0.0001) and those with a moderate course (64.3% vs 31.8%, p=0.002). Decreased GFR in patients with a mild form of COVID-19 is associated with the presence of hyperglycemia. In addition, an increase in BMI by 1 kg/m2 leads to a 10% reduction in the risk of developing renal dysfunction. In patients who had moderate COVID-19, a decrease in GFR was associated only with hyperuricemia. Conclusion: hyperuricemia is observed in 33.8% of patients 2 months after a new coronavirus infection. A decrease in GFR of less than 60 ml/min/1.73 m2 was observed in 10% of patients. Hyperuricemia is directly related to the severity of COVID-19 infection. The causal relationship between hyperuricemia in patients after COVID-19 and impaired renal function requires further research. © 2022 Authors. All rights reserved.
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Background: Currently, the present world is facing a new deadly challenge from a pandemic disease called COVID-19, which is caused by a coronavirus named SARS-CoV-2. To date, no drug or vaccine can treat COVID-19 completely, but some drugs have been used primarily, and they are in different stages of clinical trials. This review article discussed and compared those drugs which are running ahead in COVID-19 treatments. Method(s): We have explored PUBMED, SCOPUS, WEB OF SCIENCE, as well as press releases of WHO, NIH and FDA for articles related to COVID-19 and reviewed them. Result(s): Drugs like favipiravir, remdesivir, lopinavir/ritonavir, hydroxychloroquine, azithromycin, ivermectin, corticosteroids and interferons have been found effective to some extent, and partially approved by FDA and WHO to treat COVID-19 at different levels. However, some of these drugs have been disapproved later, although clinical trials are going on. In parallel, plasma therapy has been found fruitful to some extent too, and a number of vaccine trials are going on. Conclusion(s): This review article discussed the epidemiologic and mechanistic characteristics of SARS-CoV-2, and how drugs could act on this virus with the comparative discussion on progress and drawbacks of major drugs used till date, which might be beneficial for choosing therapies against COVID-19 in different countries.Copyright © 2022 Bentham Science Publishers.
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Introduction: Complement-mediated thrombotic microangiopathy (CM-TMA) is a rare disease characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia and organ injury. The absence of hemolysis and thrombocytopenia is rare. We present a case of kidney limited CM-TMA successfully treated with eculizumab. Method(s): A 36 year-old man with poorly controlled hypertension, obesity, CKD (baseline creatinine (sCr) 2,6mg/dL, albuminuria 150mg/g), hyperlipidemia, obstructive sleep apnea, hyperuricemia, SARS-CoV-2 infection 3 months earlier, and family history of CKD of unknown etiology (father started kidney replacement therapy (KRT) at young age) presented to the ER with high blood pressure and right hemiplegy. Head CT scan showed left thalamo-capsular hemorrhage. Oftalmologic exam was normal. Laboratory findings were: hemoglobin (Hb) 12.5g/dL, elevated white cell count (17.900/uL), platelet count 214.000/uL, sCr 4.3mg/dL, lactate dehydrogenase (LDH) 303U/L. Urine dipstick revealed protein+ and Hb++. Chest X-ray showed signs of pneumonia. The patient was admitted in ICU and mechanically ventilated. After 3 weeks, renal function recovered to its baseline (sCr 1.5mg/dL, no proteinuria) without KRT, and the patient was transferred to the medical ward. Several infectious complications prolonged hospital stay. After 3 months, a new mild SARS-CoV-2 infection was detected. At this time: Hb 9.9g/dL, platelets 220.000/uL, sCr 2.2mg/dL. Six days later the patient showed Hb 9.5 g/dL, without reticulocytosis, platelets 195.000/uL, sCr 6.3mg/dL, LDH 348U/L, normal haptoglobin, no schizocytes on blood smear. After 3 days, the patient was anuric and sCr increased to 10mg/dL, prompting KRT. Kidney ultrasound showed no abnormalities. Autoimmunity study was negative, normal C3/C4, no monoclonal gammopathy, and negative viral serologies. Kidney biopsy (KB) was performed as the etiology of AKI remained unclear. Light microscopy revealed thickned glomerular capillary walls with subendothelial expansion forming double contouring, arteriolar intimal expansion and fibrin thrombi occluding the vascular lumina. Scarse C3 deposition was observed in capillary walls. Since the morphological features were consistent with TMA, secondary causes were excluded and primary causes also investigated: ADAMTS13 activity, complement factor B and I were within normal range, slight decrease of factor H with normal anti factor H antibody. The molecular studies of complement genes were performed by NGS-based gene panel revealing a rare heterozygous missense mutation on gene CFB, c.1189G>A (p.Asp397Asn), described as a genetic risk factor of CM-TMA in the presence of a trigger. Result(s): Treatment with eculizumab was started and the patient showed signs of kidney recovery allowing KRT suspension 1 month later (sCr 5.53mg/dL). Of note, the patient never presented MAHA or thrombocytopenia. After 5 months, renal function improved to sCr 3.9mg/dL. Conclusion(s): We report a case of CM-TMA with isolated kidney injury without laboratory hallmarks of TMA. Patients usually require a secondary trigger for the disease to manifest, and in this case SARS-CoV-2 infection may have been the causative agent. A mutation in gene CFB may have predisposed the patient to the outcome. KB was crucial for diagnosis and prompted the treatment with eculizumab with partial recovery without the need for chronic KRT. No conflict of interestCopyright © 2023
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Serum uric acid levels are altered by kidney disorders because the kidneys play a dominant role in uric acid excretion. Here, major kidney disorders which accompany hyperuricemia or hypouricemia, including their pathophysiology, are discussed. Chronic kidney disease (CKD) and hyperuricemia are frequently associated, but recent clinical trials have not supported the pathogenic roles of hyperuricemia in CKD incidence and progression. Diabetes mellitus (DM) is often associated with hyperuricemia, and hyperuricemia may be associated with an increased risk of diabetic kidney disease in patients with type 2 DM. Sodium-glucose cotransporter 2 inhibitors have a uricosuric effect and can relieve hyperuricemia in DM. Autosomal dominant tubulointerstitial kidney disease (ADTKD) is an important hereditary kidney disease, mainly caused by mutations of uromodulin (UMOD) or mucin-1 (MUC-1). Hyperuricemia and gout are the major clinical manifestations of ADTKD-UMOD and ADTKD-MUC1. Renal hypouricemia is caused by URAT1 or GLUT9 loss-of-function mutations and renders patients susceptible to exercise-induced acute kidney injury, probably because of excessive urinary uric acid excretion. Hypouricemia derived from renal uric acid wasting is a component of Fanconi syndrome, which can be hereditary or acquired. During treatment for human immunodeficiency virus, hepatitis B or cytomegalovirus, tenofovir, adefovir, and cidofovir may cause drug-induced renal Fanconi syndrome. In coronavirus disease 2019, hypouricemia due to proximal tubular injury is related to disease severity, including respiratory failure. Finally, serum uric acid and the fractional excretion of uric acid are indicative of plasma volume status; hyperuricemia caused by the enhanced uric acid reabsorption can be induced by volume depletion, and hypouricemia caused by an increased fractional excretion of uric acid is the characteristic finding in syndromes of inappropriate anti-diuresis, cerebral/renal salt wasting, and thiazide-induced hyponatremia. Molecular mechanisms by which uric acid transport is dysregulated in volume or water balance disorders need to be investigated.
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Traditional Chinese medicine (TCM) is the key to unlock treasures of Chinese civilization. TCM and its compound play a beneficial role in medical activities to cure diseases, especially in major public health events such as novel coronavirus epidemics across the globe. The chemical composition in Chinese medicine formula is complex and diverse, but their effective substances resemble "mystery boxes". Revealing their active ingredients and their mechanisms of action has become focal point and difficulty of research for herbalists. Although the existing research methods are numerous and constantly updated iteratively, there is remain a lack of prospective reviews. Hence, this paper provides a comprehensive account of existing new approaches and technologies based on previous studies with an in vitro to in vivo perspective. In addition, the bottlenecks of studies on Chinese medicine formula effective substances are also revealed. Especially, we look ahead to new perspectives, technologies and applications for its future development. This work reviews based on new perspectives to open horizons for the future research. Consequently, herbal compounding pharmaceutical substances study should carry on the essence of TCM while pursuing innovations in the field.
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Background: Coronavirus disease causes a proximal tubule dysfunction of kidneys, inducing uric acid loss [1]. It has been established that several changes in laboratory markers (C-reactive protein (CRP), ferritin, interleukin-6 (IL-6)) can predict the severity of Covid-19 [2]. The purpose of this retrospective study was to analyze whether uric acid could act as another predictor of severe Covid-19. Objectives: To evaluate the relationship between the severity of Covid-19 and uric acid levels on admission to the hospital. Methods: This retrospective study included 150 hospitalized patients with con-frmed Covid-19 (mean age 60.3±14.6 years;52% were men), the severity of which was determined by the presence and type of oxygen support: (1) without O2, (2) O2 by mask or nasal cannula, (3) continuous positive airway pressure, (4) positive bi-pressure in the airways or high-fow oxygen, (5) invasive ventilation. Among them, 90 subjects required oxygen support, and 60 people didn't. The mortality rate in our study was 9.3%. The average uric acid level was compared with patients without Covid-19 (40 subjects). The study included patients who didn't receive urate-lowering therapy. Levels of CRP, ferritin, IL-6, D-dimer were also determined on admission. The Spearman's rank coefficient was used for measuring correlation. Results: The mean uric acid level in patients with coronavirus disease was 251.5±104.1 μ mol/L;without Covid-19 it was signifcantly higher - 328.6±96.9 μ mol/L (p<0.001). Approximately one in four (24.6%) Covid-19 patients had uric acid levels below the lower limit of normal (208 μ mol/L for men, 155 μ mol/L for women). A decrease in serum uric acid levels was also observed in patients suffering from asymptomatic hyperuricemia or gout. However, there was no correlation between uric acid levels and disease severity (r=0.01, p=0.88). Also, uric acid levels did not correlate with other laboratory markers of severe Covid-19 (CRP: r=0.07, p=0.73;ferritin: r=0.15, p=0,07;IL-6: r=0.11, p=0,22;D-dimer: r=0.02, p=0,79). Conclusion: Low uric acid levels are common in patients with Covid-19, but are not predictive of a more severe course of this disease. A correlation between uric acid and the level of other laboratory markers of severe Covid-19 was not found.
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Background: Adverse event studies of favipiravir used to treat COVID-19 have been ongoing since it was established as a treatment option. A better understanding of the side effects of favipiravir from recent studies is important for developing and assessing the introduction of effective treatments for COVID-19. Method: The author conducted a systematic review based on research studies and case reports on favipiravir monotherapy in COVID-19. Access to the included studies is via PubMed, SCOPUS, Science Direct, SpringerLink, and MedRxiv.
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OBJECTIVES: This study aimed to identify the relationship between abnormal serum uric acid levels or a history of hyperuricemia and COVID-19 severity in the Japanese population. METHODS: We included 1523 patients enrolled in the Japan COVID-19 Task Force cohort between February 2020 and May 2021. We compared the clinical characteristics, including co-morbidities, laboratory findings, and outcomes, particularly invasive mechanical ventilation (IMV), among patients with and without abnormal uric acid levels or a history of hyperuricemia. RESULTS: Patients with high serum uric acid levels were older and had higher body weight and body mass index than those without. In addition, the multiple logistic regression analysis revealed a significant association between high serum uric acid levels or a history of hyperuricemia and an increased risk of IMV (odds ratio [OR] = 1.77; P = 0.03/OR = 1.56; P = 0.04). Moreover, patients with low uric acid levels on admission were also associated significantly with the requirement of IMV (OR = 5.09; P <0.0001). CONCLUSION: Abnormal serum uric acid levels or a history of hyperuricemia were significantly associated with COVID-19 severity in the Japanese cohort.
Subject(s)
COVID-19 , Hyperuricemia , Cohort Studies , Humans , Hyperuricemia/complications , Hyperuricemia/epidemiology , Japan/epidemiology , Risk Factors , Uric AcidABSTRACT
Background and aims: Person-in-a-barrel syndrome (PIBS) is clinically characterized by brachial diparesis, with preserved cranial and crural muscle strength. It is a rare neurological syndrome most commonly caused by bilateral and symmetric injury of the motor neurons that control the upper limb movements, including bilateral injury to the brain hemispheres, brainstem, cervical spinal cord, brachial plexus, or peripheral nerves. Methods: N/A Results: A 70-year-old male patient with a history of hypertension, dyslipidaemia and hyperuricemia was admitted with an acute and rapidly progressive (10 days of evolution) bilateral upper limb weakness. The patient denied respiratory or gastrointestinal symptoms, fever or recent cervical trauma/pain. Two weeks earlier he was given the first dose of the Pfizer-BioNTech™ vaccine for COVID- 19. The neurological examination revealed severe brachial diparesis and generalized hyporeflexia. Ancillary testing revealed positive serum anti-GM1 and GD1b antibodies. The PCR for SARS-CoV-2 was negative (with positive serum T-Spike antibodies). CSF analysis and Brain/Spinal MRI were normal. The electromyography and nerve conduction studies disclosed diffuse motor conduction blocks in the upper extremities, ultimately fulfilling criteria for Acute Motor Axonal Neuropathy (AMAN) with reversible conduction failure. Intravenous human immunoglobulin (0.4g/kg/day, 5 days) and rehabilitation were started, with subsequent motor improvement. Conclusion: To our knowledge this is the first case of AMAN presenting as PIBS. We intend to highlight that AMAN should be added to the list of causes of this syndrome. The role of the COVID-19 vaccine in this case remains uncertain, and it is not possible, at this moment, to infer causality.
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Introduction. Comorbid diseases significantly exacerbate gout burden, represent an even more elevated risk of hospitalization and mortality rates owing to the coronavirus disease 2019 (COVID-19) than gout itself. Objectives. To evaluate the influence of the modified Rheumatic Disease Comorbidity Index (mRDCI) on the clinical course of gout and COVID-19. Methods. Using data from 136 male participants with gout, we distributed the cohort according to values of the mRDCI as follows: 0 - without comorbidities, 1-2 - low comorbidity index (CI), 3-4 - moderate CI and ≥5 - high CI. “Treat-to-target” approach for gout, the association of mRDCI with the clinical course of gout, lipid metabolism, and severity of COVID-19 were analyzed. Results. According to mRDCI scores, almost every second gout patient (45.6%) had moderate CI, every fifth (19.1%) - high CI, and 14.7% - low CI. Greater mRDCI was associated with the higher severity of COVID-19 (p=0.003), limited physical functioning (r=0.5, p<0.001), higher body mass index (r=0.63, p<0.001), hyperuricemia (r=0.37, p<0.001), increased low-density lipoprotein cholesterol (LDL-C) (r=0.38, p<0.001), higher gout activity (r=0.4, p<0.001), more frequent acute flares in the preceding year (r=0.39, p<0.001), number of tophi (r=0.31, p<0.001), longer duration of gout (r=0.34, p<0.001), reduced glomerular filtration rate (r =-0.39, p<0.001), and daily excretion of uric acid (UA) (r=-0.28, p=0.001). The target level of serum UA was achieved in 22.1%. The majority of patients were not controlled for LDL-C (83.7%), blood pressure (75.5%), and glucose (69.44%) in the cohort with dyslipidemia, hypertension, and diabetes respectively. Conclusion. The high prevalence of comorbidities in gout patients was associated with the severity of COVID-19. We have established the following three patterns of comorbidity predictors: anthropometric, disease-related, and dysmetabolic. The management of gout requires a multidisciplinary approach. © Svitlana Smiyan, Olha Makhovska, 2022
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A 46-years old Egyptian man was admitted to our department because of the onset of worsening dyspnea. In his clinical history were present: hypothyroidism, obesity, hyperuricemia, hypertension and recent Sars-Cov2 infection. Bilateral pleuric effusion was suspected during physical examination and confirmed by chest CT. Blood data showed mild macrocytic anemia, increased levels of creatinine, transaminases, pro-BNP (3574 pg/ml cut-off 0-125) and D-dimer. Multiple molecular swabs for research of Sars-Cov2 were negative. ECG showed sinus rhythm and non specific atypia of repolarization. An eco-fast was performed at bedside and revelead left ventricular dilatation and severe systolic disfunction due to diffuse hypokinesia (EF 30%). Diuretic therapy was set up with improvement of the clinical status. In order to exclude ischaemic genesis of the cardiopathy a coronary angiography was performed without evidence of obstructive lesions. An echocardiogram was repeated and it showed a parietal ipertrabeculation of the left ventricle. This aspect was suggestive of non-compact myocardium, a rare disease due to the arrest of the myocardial maturation process during fetal development, leading to the persistence of embryonic structures in the heart muscle. Genetic inheritance arises in 30-50% of patients and are involved genes that generally seem to encode sarcomeric or cytoskeletal proteins.Cardiac MRI is planned in order to have further confirmation of our diagnostic hypothesis. In the meantime wearable defibrillator was prescribed for the prevention of sudden death.
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Objective To explore the occurrence and influencing factors of serum uric acid elevation in patients with coronavirus disease 2019 (COVID⁃19) treated with favipiravir. Methods Medical records of patients with COVID⁃19 who were hospitalized in Beijing Ditan Hospital between June 1, 2020 and June 30, 2021 and treated with the 5- or 10-day regimen of favipiravir were collected and retrospectively analyzed. After favipiravir withdrawal, if the elevation in serum uric acid was ≥30% of baseline level, it was defined as serum uric acid elevation. Then patients were divided into serum uric acid elevation group and non-serum uric acid elevation group. The clinical characteristics such as gender, age, body mass index, comorbidities, smoking and drinking behavior, COVID⁃19 grade, favipiravir regimen, and serum uric acid level and renal function before treatment in patients between the 2 groups were compared. Influencing factors of favipiravir⁃associated serum uric acid elevation was analyzed using multivariate logistic regression method. Results A total of 179 patients were included in the analysis, including 104 (58.1%) males and 75 (41.9%) females, aged from 19 to 70 years with a median age of 43 years. The level of serum uric acid in 179 patients after favipiravir treatment was significantly higher than before [(451±119) μmol/L vs. (332±94) μmol/L, P<0.001]. The change rate of serum uric acid from baseline level ranged from -57.1% to 157.8% with the median of 38.6%. The elevation in serum uric acid of ≥ 30% of baseline level occurred in 108 (60.3%) patients. The incidences of serum uric acid elevation in patients treated with 5-day and 10-day regi⁃ mens of favipiravir were 46.8% (36/77) and 70.6% (72/102), respectively, and the difference between them was significant (P=0.001). Multivariate logistic regression analysis showed that body mass index 24.0 to <28.0 kg/m2 (OR=3.109, 95%CI: 1.209-7.994, P=0.019) and 10-day regimen of favipiravir (OR=3.017, 95%CI: 1.526-5.964, P=0.001) were independent risk factors for favipiravir⁃associated serum uric acid elevation. Conclusions More than half of COVID⁃19 patients treated with favipiravir can develop serum uric acid elevation. Overweight and 10-day regimen of favipiravir are independent risk factors for serum uric acid elevation in patients. © 2022 Adverse Drug Reactions Journal.
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Diabetes mellitus refers to a group of common metabolic disorders that share the phenotype of hyperglycemia. The worldwide prevalence of DM has risen dramatically over the past two decades.Diabetes mellitus is a major cause of mortality and morbidity worldwide. Assay for C-peptide can be used to provide an index of endogenous insulin production and pancreatic beta cell function. MATERIAL: This is a hospital based cross section study involving 50 newly detected diabetic subjects of age group 35-40 years. The subjects were evaluated with their fasting and stimulated c-peptide levels assay, fasting and postprandial blood sugars, HbA1c. OBSERVATION: Eight subjects out of 50 subjects had a fasting serum C-peptide value less than normal value. Thirteen subjects out of 50 subjects had a low stimulated serum C-peptide. CONCLUSION: This study suggests measurement of C-peptide levels in newly detected diabetic subjects especially of younger age group is of value in differentiating type of diabetes and appropriate next line of management. © Journal of the Association of Physicians of India 2011.
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Introduction: Mitochondria are organelles that fulfill the energy requirements for cells, which is essential for their survival and function. Mitochondria function is dependent on both mitochondrial (mtDNA) and nuclear genes (Tucker, 2010). SARS2 is a nuclear gene that encodes the mitochondria seryl-tRNA synthetase precursor. It catalyzes the attachment of serine to tRNA and in the biosynthesis of selenocysteinyl-tRNA in the mitochondria. Pathogenic variation in the gene is associated with HUPRA syndrome, which is characterized by hyperuricemia, pulmonary hypertension, renal failure, and metabolic alkalosis (Rivera, 2013). It is important to recognize this autosomal recessive condition as it presents in infancy, can lead to death, and has recurrence implications for carrier couples. Case Description: We present a term neonate male who experienced tachypnea at birth requiring respiratory support;echocardiogram concerning for pulmonary hypertension and right ventricular hypertrophy requiring ionized nitric oxide. During his hospitalization, he developed lactic acidosis (consistently 10–12 mmol/L, reaching 26 mmol/L), seizures, and his newborn screen results flagged as abnormal for severe combined immunodeficiency (SCID) due to low Tcell count. He was transferred to a tertiary medical center due to continued elevated lactate levels. During admission to the tertiary medical center, he was found to have hyperkalemia, elevated BUN/Cr, and elevated lactate levels. Additionally, pre-prandial and postprandial lactate and pyruvate levels were obtained. It was found that hyperlactatemia was persistent and not related to feedings. The patient developed a presumed pulmonary hypertensive crisis at 8 weeks of age, and in the setting of chronic intrinsic renal dysfunction and chronic lactic acidosis, the family elected to transfer him to the home hospital for compassionate extubation where he died. Notable genetics evaluation findings included urine organic acid results showing markedly and persistently elevated levels of fumaric acid and lactic acid concerning for fumarase deficiency or a mitochondrial oxidative phosphorylation disorder and plasma amino acids showing elevated alanine and proline indicative of lactic acidosis. An array CGH showed 2% areas of homozygosity, consistent with known shared parental ancestry. The results of combined mitochondrial genome and Mitochondrial Nuclear Gene Panel was ordered. The results revealed two SARS2 variants: (c.988C>T,p.R330W and c.173T>A, p.L58Q). Both variants were classified as variants of uncertain significance (VUS) based on ACMG-AMP criteria (Richards, 2015) and parental testing to determine phase is ongoing. Discussion: Pathogenic variants in SARS2 lead to dysfunction of seryltRNA synthetase and is associated with HUPRA syndrome. Our patient harbors two variants in SARS2 classified as VUSes but based on clinical presentation the phenotype is consistent with HUPRA syndrome. The condition was first described in 2011 (Belostotsky, 2011) with 6 reported patients from 3 families (Belostotsky, 2011 and Rivera, 2013). Further study into pathogenic mechanism is important as no treatment exists, and the disease leads to death of the infants affected. Although the disease is very rare, it must be considered in infants with who present with symptoms of failure to thrive, hyperuricemia, pulmonary hypertension, renal failure, and metabolic alkalosis.