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Introduction: Nirmatrelvir/ritonavir is a new medication approved for the treatment of COVID-19 infection. It prevents viral replication by inhibiting the SARS-CoV-2 main protease. While mild adverse effects were described, including dysgeusia, diarrhea, hypertension and myalgia1, there were no reported cases of pancreatitis. Case Description/Methods: An 81-year-old female with a past medical history of hypertension and COPD presented to the hospital complaining of abdominal pain and nausea for one day. She had no history of alcohol, tobacco or marijuana use, recent travel, or trauma. Her medications included lisinopril and prednisone, and she had completed a 5-day course of nirmatrelvir/ritonavir for the treatment of COVID-19 infection 2 days prior to presentation. On abdominal exam, she had left upper and lower quadrant tenderness. Blood tests revealed an amylase of 1333 U/L, lipase of 3779 U/L, triglycerides of 297 mg/dL and calcium of 8.7 mg/dL. CT scan revealed an indurated pancreatic body and tail with peripancreatic fluid along the paracolic gutter. Ultrasound of the abdomen and MRCP did not reveal any acute findings. IgG subclasses 1-4 were normal. Discussion(s): According to the revised Atlanta criteria, the patient had clinical findings consistent with acute pancreatitis. Common causes such as gallstone, alcohol, autoimmune and hypertriglyceridemiainduced pancreatitis were ruled out. There were no masses or structural abnormalities on imaging that might have explained her diagnosis. There have been at least 2 reported cases of lisinopril and prednisone induced pancreatitis, however according to Badalov et al.2 both of these medications are class III drugs that lack any rechallenge in the literature. Moreover, the patient had been taking these medications for many years, making them an unlikely cause of the presenting diagnosis. There are no reports of nirmatrelvir/ritonavir associated pancreatitis or known pharmacologic interaction with her home medications, and a meta-analysis conducted by Babajide et al. revealed no association between acute pancreatitis and COVID-19 infection (3). Given the negative findings stated above and the recent initiation of a new medication, nirmatrelvir/ritonavir was the likely cause of acute pancreatitis.
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BACKGROUND: The pathogenesis of angioedema induced by angiotensin-converting enzyme inhibitors is based on the accumulation of bradykinin as a result of angiotensin-converting enzyme blockade. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the angiotensin-converting enzyme 2 receptor, which may inhibit its production and thereby lead to an increase in bradykinin levels. Thus, SARS-CoV-2 infection may be a likely trigger for the development of angioedema. AIMS: This study aimed to analyze cases of hospitalizations of patients with angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers during the coronavirus disease 2019 (COVID-19) pandemic. MATERIALS AND METHODS: This study retrospectively analyzed medical records of patients admitted to the Vitebsk Regional Clinical Hospital between May 2020 and December 2020 with isolated (without urticaria) angioedema while receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. In all patients, smears from the naso and oropharynx for COVID-19 were analyzed by polymerase chain reaction. RESULT(S): Fifteen inpatients (9 men and 6 women) aged 44-72 years were admitted because of emergent events, of which 53.6% had isolated angioedema. In two cases, a concomitant diagnosis of mild COVID-19 infection was established with predominant symptoms of angioedema, including edema localized in the face, tongue, sublingual area, and soft palate. All patients had favorable disease outcomes. CONCLUSION(S): Patients with angiotensin-converting enzyme inhibitor-induced angioedema may require hospitalization to monitor upper respiratory tract patency. There were cases of a combination of angiotensin-converting enzyme inhibitor-induced angioedema and mild COVID-19. Issues requiring additional research include the effect of SARS- CoV-2 infection on the levels of bradykinin and its metabolites, the triggering role of COVID-19 in the development of angioedema in patients receiving angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, recommendations for the management of patients with angiotensin-converting enzyme inhibitor-induced angioedema, and a positive result for COVID-19.Copyright © 2020 Pharmarus Print Media All rights reserved.
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Though not common, drug-induced pericarditis is a serious condition, since pericardial tamponade, should it develop, may be life-threatening. As the number of drugs is constantly expanding, so does the proportion of those capable of causing pericarditis. The authors reviewed the relevant literature in the PubMed database and complemented it with information from the VigiBase database. In their article, the authors present current knowledge about the mechanisms of origin and level of risk of drug-induced pericarditis and discuss relevant information on individual drugs divided into 7 classes. Some medicines are associated with a high risk of developing pericarditis, a fact to be taken into account when treating patients with these agents. © 2022 Czech Society of Cardiology Z.S. All rights reserved.
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SARS-CoV-2 causes Coronavirus Disease 2019 (COVID-19), an infectious condition that can present none or one or more of these symptoms: fever, cough, headache, sore throat, loss of taste and smell, aches, fatigue and musculoskeletal pain. For the prevention of COVID-19, there are vaccines available including those developed by Pfizer, Moderna, Sinovac, Janssen, and AstraZeneca. Recent evidence has shown that some COVID-19-vaccinated individuals can occasionally develop as a potential side effect Guillain-Barre syndrome (GBS), a severe neurological autoimmune condition in which the immune response against the peripheral nerve system (PNS) can result in significant morbidity. GBS had been linked previously to several viral or bacterial infections, and the finding of GBS after vaccination with certain COVID-19, while rare, should alert medical practitioners for an early diagnosis and targeted treatment. Here we review five cases of GBS that developed in different countries after COVID-19 vaccination.Copyright © 2021
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The great use of telecommunication technology propels new healthcare system of telemedicine through which diagnosis as well as treatment can be done in the remote areas. The ancient Greek language explain the terminology of telemedicine in the phrase of distance healing. As per WHO, Telemedicine is the delivery of health-care services, where distance is a critical factor, by all health-care professionals using information and communications technologies for the exchange of valid information for diagnosis, treatment and prevention of disease and injuries, research and evaluation, and the continuing education of health-care workers, with the aim of advancing the health of individuals and communities. Historically the concept of teleconsultation was evolved in the first half of twentieth century when the data of ECG was communicated through telephone lines, this can be traced as first evidence of this unique healthcare system. Further the introduction of electrical system of telegraph as well as evolution of telephone revolutionized this system of healthcare. when the Technology of telemedicine help both patients as well as service providers in multiple ways involving physicians, surgeons, pharmacists, paramedical staff, IT and electronics engineers, government, hospitals and end user public Location is now a days no problem and therefore there is no limitation of the availability of healthcare facilities to such location or remote location. The biggest role in such development is played by the communication technology which may provide healthcare services to every nook and corner of the location. It can decrease the health staff pressure because in India WHO guidelines ask to maintain the ratio 1:1000 of doctor and Indian public compared to present 0.62:1000 ratio of doctor and public. The great advantage of this system is that in case of epidemic or pandemic like COVID 19 Telemedicine can keep the health staff are well general public free from contagious infection (COVID-19). There are a number of networking communication modes that can be applied, which may improve the patient compliance,dosage regimen can be managed in better fashion thus increase the longevity of person life. Disasters management during pandemics present unique challenges which can be addressed effectively as happened during the lockdown. This technology-based practice can break the infectivity chain of the transmission of communicable diseases This chapter incorporates basic concept of telemedicine, its origin and types, communication technologies, services by telemedicine, types of telemedicine, tools of telemedicine, telemedicine software's and guidelines related to practicingtelemedicine in reference to Indian context. Copyright © RJPT All right reserved.
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Aim. To evaluate the effect of taking a single pill combination of amlodipine, lisinopril and rosuvastatin on blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) in hypertensive patients with or without severe hypercholesterolemia. Material and methods. Articles published in Russian were selected for analysis. Six articles that met the criteria for inclusion in a systematic review were found by searching the eLibrary database for the keyword "equamer". The results of 5 observational clinical studies were presented in these articles. The effectiveness of the fixed combination of amlodipine, lisinopril and rosuvastatin was assessed mainly by changes in the level of systolic and diastolic blood pressure, the concentration of LDL cholesterol. In addition, the effects of fixed-dose amlodipine, lisinopril, and rosuvastatin on central aortic pressure and its increment index, as well as carotid-femoral pulse wave velocity, were studied in part of the studies. The effect of the fixed combination of amlodipine, lisinopril and rosuvastatin on blood pressure and LDL-C concentration, as well as on these additional indicators, in patients who had a coronavirus infection with severe lung damage was studied in one study. Results. Evidence from a systematic review demonstrates the efficacy of single pill combination amlodipine, lisinopril and rosuvastatin in reducing blood pressure and LDL-C in a wide range of patients with different baseline risk of developing cardiovascular complications and different baseline levels of blood pressure and LDL-C. Conclusion. The data obtained confirm the feasibility of more frequent prescription of the single pill combination of amlodipine, lisinopril and rosuvastatin in clinical practice for the treatment of hypertensive patients with high or moderate risk of developing cardiovascular diseases, including patients with concomitant hypercholesterolemia.
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Background and Aim: The European Medicines Agency has approved mRNA vaccines developed by Pfizer/BioNTech and Moderna for the vaccination of adolescents against the SARS-CoV-2 infection. Cases of myocarditis and pericarditis have been described as rare postvaccination complications. We describe the Latvian experience with adolescents suffering from myocarditis following COVID-19 vaccination. Method(s): From June to December 2021 four cases consistent with postvaccination myocarditis were admitted to the Children's Clinical University Hospital, which is the only centre with special-ized paediatric cardiology care in Latvia. The Pfizer/BioNTech vaccine had been used in all. An ECG, Holter monitoring and ECHO was done, HS Troponin I levels checked, the most common infectious causes of myocarditis were excluded, and a cardiac MRI was performed in all cases. Result(s): Case 1: 12-year-old girl, developed chest pain on postvac-cination day Nr 4 (PVD4) after the 1st dose. Holter monitoring revealed rare non-sustained ventricular tachycardia (NSVT), ECHO showed moderate mitral insufficiency, and a hyperecho-genic papillary muscle, troponin level peaked at 5339 pg/ml (PVD6), MRI (PVD 7) showed widespread myocardial oedema, transmural fibrosis. Symptoms resolved in 1 day, metoprolol suc-cinate and lisinopril were prescribed. Mitral insufficiency persists 5 months later. Case 2: 15-year-old boy, developed chest pain after the 2nd dose on PVD2 and lasted for 7 days, he was admitted on PVD11 with a peak troponin level of 19pg/ml. MRI (PVD15) showed widespread myocardial oedema. Metoprolol succinate was prescribed. Case 3: 15-year-old boy, developed chest pains on the day of the 1st dose and persisted for 35 days, he was admitted on PVD24 with peak troponin level 15ng/ml. MRI (PVD29) showed mild myocardial oedema, myocardial and pericardial fib-rosis. Case 4: 13-year-old boy, developed chest pain on PVD2, which lasted for 65 days, he had an episode of syncope. Holter monitoring showed frequent PVCs, and NSVT, on PVD34 tro-ponin level was 2,5pg/ml. The child received a course of NSAIDs and was referred to us on PVD68. MRI (PVD69) revealed wide-spread myocardial oedema, fibrosis, and pericarditis. Methylprednisolone was given, and betaxolol was prescribed. Conclusion(s): Our case series show that some cases of postvaccination myocarditis develop complications requiring long-term treatment.
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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
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In response to the COVID-19 pandemic, worldwide efforts contributed to the largest vaccination campaign in history. Thus far, 17 cases of IgA nephropathy (IgAN) following COVID-19 vaccine were reported in adults, all after mRNA vaccines. Most patients had gross hematuria (GH) and sub-nephrotic range proteinuria (SNRP) within 2 days after the second dose. A 23-year-old White female with recent mild COVID-19 infection developed asymptomatic GH with SNRP 2 days after receiving the first and the second dose of Pfizer-BioNTech vaccine. Laboratory studies showed normal kidney function and serum albumin. Negative rheumatologic workup. Urinalysis revealed proteinuria, dysmorphic red blood cells, and rare granular casts. Urine protein-creatinine ratio (UPr/Cr) was 1,4g/g. Within 1 week the GH self-resolved, however, she continued to have persistent microscopic hematuria and subnephrotic proteinuria. Kidney biopsy showed IgAN. The Oxford MEST-C score was M1E0S1T0C0. She was started on Lisinopril. Upr was 976mg/24h. Subsequently, 2 days after the booster vaccine she developed GH, Upr increased to 2063mg/24h and was started on Dapagliflozin. This is the first reported case of de novo IgAN following each dose of COVID-19 vaccine and booster presenting with recurrent GH and SNRP. This case illustrates the need for pharmacovigilance and whether we should use non-mRNA or a different vaccine schedule in this vulnerable population. The new-onset and recurrence of GH shortly after the COVID-19 vaccines suggests a potential association with the development of IgAN and relapses. Further studies are needed to understand the pathophysiology of the vaccine-associated glomerular diseases, optimize vaccine strategies and guide optimal therapeutic management. (Figure Presented)
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CASE: 74 year old woman with history of anxiety, depression, and nonsecretory adrenal adenoma presented with two months of progressive night sweats. Initially, she described waking up damp all over, but without needing to change her sheets. Her weight had been stable, and she denied recent travel. Her recent health changes included starting sertraline and receiving the Moderna COVID vaccines. Her other medications included atorvastatin and lisinopril. Her vital signs were all within normal range and her physical exam was unremarkable. Night sweats described were mild, so work up began with checking a CBC with differential and a TSH level. Initial labs were normal. However, the patient called a week later with night sweats that were worsening. She also recalled being treated for tuberculosis at age fifteen. This prompted additional bloodwork including Quantiferon, ACTH, androstenedione, estradiol, testosterone, progesterone, and DHEAS levels, as well as urine catecholamines and metanephrines. Additionally, it was noted sertraline could be a potential cause of night sweats. The dose was halved with the goal to taper off and discontinue the medication. All lab results came back within normal limits, so CT scans of the chest/ abdomen/ pelvis were ordered, and blood cultures collected. Imaging showed an unchanged adrenal adenoma and blood cultures had no growth. Ultimately, after five months of symptoms, her night sweats completely resolved five weeks after stopping sertraline. IMPACT/DISCUSSION: When working up night sweats, first, the severity of symptoms should be determined and medications reviewed. Mild night sweats with no associated red flag symptoms (weight loss, lymphadenopathy, and fever) do not need immediate or extensive work up. Further work up is essential in the setting of any red flag symptoms. Without a clear etiology, the work up includes the following items: chest radiography along with bloodwork including Quantiferon test, CBC, TSH, HIV serology, and CRP. If these results are normal then a CT of the chest, abdomen, and pelvis could be obtained as well as a bone marrow biopsy. Little evidence exists to guide an exact order of workup for night sweats, so it remains the clinician's responsibility to determine which tests to prioritize. Classes of medications that tend to cause night sweats are cholinergics and anti-depressants. Anti-depressants most associated with night sweats include TCAs and SNRIs. Sertraline has been implicated as a cause of night sweats, but little data exists as to how often this occurs and how often severe presentations like the one described occur. Given that selective serotonin reuptake inhibitors are a first line treatment in depression, recognizing this adverse effect is important in primary care and could prevent unnecessary extensive work ups for night sweats. CONCLUSION: -An initial step in evaluating persistent night sweats should be medication review -Many antidepressants including sertraline can have night sweats as an adverse effect.
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CASE: A 58-year-old female with a history of hypertension, type 2 diabetes and hyperlipidemia presented with a two- week history of abdominal pain and fevers. Per the patient, family history was unremarkable, and she denied alcohol, tobacco, or recreational drug use. She denied recent travel or sexual activity and had moved to the U.S. in the 1970s from Cambodia. Medications included amlodipine, atorvastatin, dapagliflozin, lisinopril, metformin and sitagliptin. Physical exam was notable for bilateral axillary lymphadenopathy, hepatomegaly, and right sided abdominal tenderness. Laboratory data was notable for microcytic anemia, thrombocytopenia, and elevated transaminases, D-dimer, and C- reactive protein. Urinalysis demonstrated microscopic hematuria and proteinuria. Imaging showed diffuse lymphadenopathy and hepatomegaly. Autoimmune work-up was strongly positive for ANA, anti-histone, and anti DS DNA. Kidney biopsy was suggestive of glomerulonephritis. Liver biopsy was suggestive of drug induced liver injury or autoimmune hepatitis. A diagnosis of DIL and SLE was not reached until additional historical data from the patient's son was provided on hospital day 4;namely that the patient had a 30-lb unintentional weight loss, took unknown herbal supplements and had a daughter who passed away from complications of lupus. IMPACT/DISCUSSION: DIL is a rare adverse reaction to many drugs that generally manifests with mild systemic symptoms such as low-grade fevers, anorexia, and fatigue and rarely involves classic symptoms of SLE such as skin findings and major organ involvement. Notably, DIL can unmask clinically silent SLE and thereby lead to lupus like syndromes. This patient presented with mild symptoms and underwent an extensive workup due to missing key historical data which led to a delayed diagnosis. Due to COVID-19 restrictions on visitation, it was not until hospital day 4 when the patient's son visited that the team became aware of an unintentional 30-lb weight loss, unknown herbal supplement use, and a family history of SLE. The lack of such critical information stemmed from the fact that we did not ask about the use of supplements properly and never revisited it in a different manner. The patient did not share the cause of her daughter's passing as she was unaware of it, which may speak to cultural limitations in sharing health information among family members. It is imperative that as clinicians we constantly revisit the history and diversify our questions. A more complete history would optimize our workup and limit unnecessary testing, including blood draws and painful biopsies, which unfortunately occurred in this patient. CONCLUSION: A thorough history is important to achieving a timely diagnosis and to avoid excessive testing and procedures. Revisiting the history is necessary to finding key information and clinicians should consider incorporating available family members early in the diagnostic work up, especially if the diagnosis is unclear.
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CASE: This is a 41-year-old man who was admitted to the medical floor with mild COVID-19 symptoms without hypoxia. He had End Stage Renal Disease (ESRD) on Hemodialysis (HD), failed renal transplant, Hypertension and Schizophrenia. Patient had no relevant family history. Medications included Aspirin, Atorvastatin, Nifedipine, Benztropine, and Haloperidol. Patient had allergy to shellfish products. He tested positive a week prior to admission with mild cough no fever or hypoxia. As symptoms worsened, he presented to emergency department and was admitted because of his immunocompromised status. The night of admission, he developed wheezing and stridor, swelling of face and lips, and altered mental status. It was difficult to pass endotracheal tube due to swollen airways. Vital signs were stable except for a low oxygen saturation. Physical examination significant for stridor and swelling of the face and lips. Laboratory values were not significant. We reviewed and none of them was newly started or associated with risks of angioedema. He had no history of previous similar episodes. Patient was given anti-histamines and steroids with slight improvement. Flexible laryngoscopy was performed showing swollen epiglottis and aryepiglottic folds. He ended up getting a tracheostomy as he was regarded as a high risk to be liberated from intubation. IMPACT/DISCUSSION: Few other cases of COVID-associated angioedema have been reported in the literature, majority of the cases explained were in African American patients. The features of angioedema reported like the traditional angioedema, swelling of the face, lips and airways. This angioedema developed within 7 days of detection of COVID-19 in our case and >10 days in the previously reported cases. Angioedema develops due to increased levels of Bradykinin (BK) and its metabolites due to increased expression or decreased degradation. Angiotensin Converting Enzyme (ACE) with other enzymes prevent angioedema by degradation of BK and its metabolites . African Americans, have genetic susceptibility which leads to lower levels of other enzymes involved in the Bradykinin metabolism, thus ACE blockade put them at a higher risk of angioedema. The association of COVID-19 with ACE2 and its subsequent disruption of ACE activity is thought to be the reason behind the development of angioedema. Most of the published articles are either observational or sporadic case reports. More thorough study might help identify further mechanisms and if there is a direct true causal relationship between COVID-19 infection and angioedema or if it is the result of a “second hit,” as it was called by authors of another case that involved a Caucasian male with hypertension who has been using Lisinopril for years with no previously reported complaint. CONCLUSION: SARS CoV-2 should be suspected as cause for angioedema. Further studies needed to establish modalities for diagnosis, management and prevention in high-risk patients.
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Background: Dysgeusia is a distortion of taste sensation. Etiologies can include medications and Covid-19, among others. Dysgeusia may lead to appetite loss which is nonspecific and can have multiple causes, including major depressive disorder (MDD) (Coulter, 1988). Although post-marketing data revealed no association between nifedipine and dysgeusia (Ackerman, 1997), case reports of dysgeusia from nifedipine exist (Ackerman, 1997). We present a case of nifedipine-induced dysgeusia mistaken for depression. Case Report: A 42-year-old man with hypertension and diabetes was admitted to the hospital following right thalamocapsular and intraventricular hemorrhages. Hypertension was managed with metoprolol, lisinopril, nifedipine, and chlorthalidone. Levetiracetam was started for seizure prophylaxis. Medications included pantoprazole, simethicone, transdermal lidocaine, insulin, metformin, docusate, senna, and subcutaneous heparin. Psychiatric consultation was requested out of concern that appetite loss indicated depression. The day before psychiatric evaluation, mirtazapine 15 mg at bedtime for mood and appetite was started. Nifedipine 90 mg daily had been started 9 days prior to his first complaint of decreased appetite. The patient reported feeling disconnected from his family and “sad" for ∼10 years, complaining that family members “talk behind his back.” He was otherwise without paranoia. He denied insomnia, anhedonia, hopelessness, poor concentration, suicidal ideation, homicidal ideation, guilt, mania, or hallucinations. He reported poor appetite due to epigastric discomfort and bad taste to foods. Covid-19 testing was not yet widely available. No other signs or symptoms suggestive of Covid-19 were present. Although alert and fully oriented, concentration was impaired with sometimes tangential thought processes. Affect was full without depression. A diagnosis of adjustment disorder was made. The psychiatry team suspected nifedipine-induced dysgeusia and advised discontinuing nifedipine. Appetite improved two days later. Discussion: This case highlights the importance of considering alternative causes of nonspecific symptoms of depression, including decreased appetite, that may have non-psychiatric causes. Dysgeusia is widely recognized as a symptom of Covid-19. Other causes, including medications may be underrecognized and amenable to intervention. Conclusion: It would be helpful to consider medication side-effects as potential causes for taste distortion alongside psychiatric diagnoses, and COVID-19. References: 1. Coulter DM: Eye pain with nifedipine and disturbance of taste with captopril: a mutually controlled study showing a method of post marketing surveillance BMJ 1988;296: 1086–8. 2. Ackerman BH, Kasbekar N: Disturbances of taste and smell induced by drugs. Pharmacotherapy 1997;17(3):482-96.
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Aim. To study the dynamics of the lipid profile of hypertensive patients with dyslipidemia who underwent COVID-19. Material and methods. Hypertensive patients with dyslipidemia who underwent COVID-19 [n=126;58 men and 68 women;median age 60 (56.0;65.5) years] examined. Patients were included into two groups: group 1 (n=64) received a single pill combination of lisinopril + amlodipine + rosuvastatin;2 groups (n=62) continued the previous drug treatment. Clinical, demographic, office blood pressure (BP), total cholesterol (TC), low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol, triglycerides, C-reactive protein (CRP) levels were assessed in all patients in 3 visits within 24 weeks. Results. The groups did not differ in prior antihypertensive therapy (except for more frequent use of angiotensin II receptor blockers in group 2, p<0.05), lipid profile and blood pressure parameters at study entry. A decrease in systolic (by 9.5%) and diastolic blood pressure (by 12.1%) after 24 weeks was found in group 1 compared with 4.29% and 5.56%, respectively, in group 2 (p<0.05). A decrease in the level of total cholesterol by 14.5% and LDL-c by 31.4% after 24 weeks was found in group 1 compared with 11.2% and 9.7%, respectively, in group 2 (p<0.05). The level of CRP during the observation period decreased by 53.7% in group 1 versus 43.4% in patients of group 2 (p<0.05). Conclusion. The single pill combination of lisinopril/amlodipine/rosuvastatin in hypertensive patients with dyslipidemia who underwent COVID-19 led to an improvement in lipid profile and blood pressure control.
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Distal sensory peripheral neuropathy (DSPN) in Type 2 diabetes mellitus (T2DM) is a painful chronic condition that affects one’s quality of life. People with DSPN experience pain, numbness, tingling, sensory loss, absent or reduced reflexes, and muscle weakness. Distal sensory peripheral neuropathy in T2DM is typically managed with tricyclic antidepressants, anticonvulsants and opiates. However, side effects can occur with pharmaceuticals, therefore a non-invasive symptom management approach such as moxibustion is worthy of consideration. Unfortunately, moxibustion is often overlooked and not considered a viable method for managing symptoms associated with DSPN. This case report illustrates the success of six moxibustion treatments conducted twice weekly for three weeks. The treatments reduced pain related to DSPN and improved indices of neurosensory testing.
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Background: Vaccine-associated Myocarditis (VAM) is increasingly documented as a complication of COVID-19 mRNA vaccines. In the United States, as of 10/16/2021 188.9 million are fully vaccinated with mRNA vaccines. VAM has an incidence of 4.8 cases per million post 2nd dose of mRNA vaccines. We present a case of mRNA VAM in a young male and challenges faced in screening and management of this rare condition in a time where clearer guidelines are needed. Case: 45 y/o male with no PMH presented with acute onset sharp midsternal chest pain associated with dyspnea and diaphoresis. Patient received the 2nd dose of the Moderna vaccine three days prior. Initial EKG: ST-elevations in leads V2-V4;troponin 4.37 (peaked at 7.3);CRP 25.8. Coreg was initiated. Emergent cardiac catheterization: nonobstructive CAD, mildly reduced systolic function 50%. Subsequent echo: EF 40% with mild hypokinesis in apical segments. Colchicine was started. Symptoms resolved and patient was discharged with avoidance of strenuous activity. 1st follow-up: improved symptomatology. Lisinopril was added. Repeat echo: EF 60%. 2nd follow-up 2 weeks later: he had presyncope. Holter: no arrhythmia. Cardiac MRI: multifocal mid-myocardial and subepicardial late gadolinium enhancement in apical and basal segments consistent with myocarditis. After 2 months, the patient was asymptomatic and exercise tolerant. Decision-making: New data from the CDC, and the Israeli National Database indicate a causal relationship between the new mRNA vaccines and the increase in VAM. This complication predominantly affects young males like this patient within 7 days post 2nd dose. In this age group, observed numbers of VAM were > 10 times more than expected. This data incited a high index of suspicion which led to the diagnosis. Conclusion: Since this vaccine technology will likely monopolize future vaccine production, this condition is expected to increase in prevalence and the medical community needs to remain vigilant. Better guidance is needed on how best to screen and manage. Further research is thus warranted. We maintain that mRNA vaccines provide benefits which far outweigh this often self-limited complication.
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Case presentation A 36-year-old with recent vaginal delivery cocaine abuse, and COVID-19 infection was admitted for new acute systolic heart failure. Etiology of heart failure was suspected as peripartum cardiomyopathy, cocaine-induced, or COVID myocarditis. EKG had no ischemic changes and echocardiography revealed an ejection fraction (EF) of 10-15% with severe global hypokinesis. Additional diagnostics showed a BNP of 3600 and a stable high-sensitivity troponin with a negative delta of 60-65. No arrhythmia on telemetry noted as well. Cardiac MRI was suggestive of myocarditis and no evidence of ischemia on stress MRI (figure 1). The patient received diuresis until euvolemia and tolerated lisinopril and carvedilol. With a diagnosis of clinically suspected non-fulminant COVID myocarditis, she was discharged on a tapered oral dexamethasone for two weeks. On a follow-up telemedicine encounter, the patient denied any chest pain, shortness of breath, and was otherwise asymptomatic Discussion Currently, there remain no guidelines of treatment for COVID-19 myocarditis. Many published management strategies are focused on use of IV corticosteroids and other immunosuppression for cases of fulminant myocarditis. However there is limited data on outpatient management of nonfulminant myocarditis associated with COVID-19. In our case report, we demonstarte successfully managing a patient with non-fulimant myocarditis in the setting of severely reduced EF with an outpatient steroid regimen. Of note, her systolic dysfunction was not exclusively from myocarditis as the patient also had a history of cocaine abuse and possible peripartum cardiomyopathy. At the time of hospital discharge, she was clinically stable, euvolemic, tolerated guideline-directed medical therapy, and her troponins suggested no on-going myocardial injury.
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Aim. To evaluate the potential of a fixed-dose combination of lisinopril+amlodi-pine+rosuvastatin (Equamer® ) in achieving additional vascular protection in patients with hypertension and high pulse wave velocity (PWV) after severe and very severe coronavirus disease 2019 (COVID-19), complicated by bilateral multisegmental viral pneumonia, with the use of biological therapy, who had not previously received combination antihypertensive therapy. Material and methods. This 12-week open-label observational study included 30 patients with or without antihypertensive therapy. The patients underwent 24-hour blood pressure monitoring, applanation tonometry (determination of the augmentation index (AI) and central blood pressure (CBP)), PWV measurement, blood laboratory tests (lipid profile, fasting glucose, C-reactive protein, complete blood count, ferritin, fibrinogen, D-dimer, alanine aminotransferase, aspartate aminotransferase, creatinine, uric acid) before and after switch to a fixed-dose combination of lisinopril+amlodipine+rosuvastatin. Results. At baseline, the patients had an increase in office blood pressure (BP) up to 152,6/89,1 mm Hg. After prescribing a fixed-dose combination of lisinopril+amlo dipine+rosuvastatin, there was a decrease in systolic blood pressure (SBP) by 15,8% and diastolic blood pressure (DBP) by 12,2%. According to 24-hour blood pressure monitoring, the decrease in SBP was 15%, DBP — by 9%, PWV — by 23,8%, AI — by 9%, CBP — by 12,4% (p<0,05 for all compared to baseline values). Vascular age (VA) was initially increased to 41,9 years with a chronological age of 35,03 years. After the end of therapy, there was a significant decrease in VA to 36,5 years, low-density lipoproteins by 46,8%, triglycerides by 16,8% and an increase in high-density lipoproteins by 10,7% (p<0,05 for all compared to baseline values). In addition, the levels of C-reactive protein, fibrinogen, D-dimer, glucose, and uric acid significantly decreased. Conclusion. The fixed-dosed combination of lisinopril+amlodipine+rosuvastatin provides better blood pressure control, improved vascular elasticity parameters (AI, PWV, CBP, decrease in VA), and also improves lipid and carbohydrate metabolism, reduces inflammation in patients with hypertension and hyperlipidemia after severe COVID-19.
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Background: Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) disease (COVID19) mainly affects the respiratory system, but cardiac complications occur very often. SARS-CoV-2 entry in host cells is mediated by the interaction between the viral Spike (S) glycoprotein and the host angiotensin-converting enzyme 2 (ACE2). The use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 receptor blockers (ARBs) might influence the expression of ACE2 and viral infection, but not much is known about these interactions. Aim: To evaluate the effects of ACEIs and ARBs during active viraemia. Methods: We tested the ACEI Lisinopril (at 100nM and 500nM) and the ARB Valsartan (at 10uM and 50uM) for one week on two cell types: cardiomyocytes derived from hiPSC (hiPSC-CMs) as heart model and a lung epithelial cancer cell line (16HBE) as pulmonary model. The SARS-CoV-2 wild strain was inoculated in the two treated cell types for one hour. Cell viability was measured 72 hours after infection. Supernatants were collected and titrated to verify the presence of infectious virus using a micro-neutralization assay on VERO-E6 cells. Levels of ACE2 mRNA and protein content on cell lysates were quantified after each treatment by RT-qPCR and western blot, respectively. Results: ACEI and ARB at both concentrations affected the viability of neither hiPSC-CMs nor 16HBE cells in the absence of virus. Vice versa, viral infection significantly decreased viability of both hiPSC-CMs (-46%;p<0,01) and 16HBE (-19%;p<0,05). Viral titration revealed that SARSCoV-2 replicated in both cell lines and was actively released in supernatants. Importantly, pretreatment with Valsartan 50uM increased the viability of both hiPSC-CMs and 16HBE after infection, while Lisinopril and the lower dose of Valsartan had neutral effect. Of note, Valsartan 50uM treatment decrease ACE2 mRNA level in both hiPSC-CMs (-47%, p<0,01) and 16HBE (-37%, p<0,01). Also ACE2 protein levels were reduced in cell lysates of hiPSC-CMs and 16HBE treated with Valsartan 50uM. Conclusion: These data suggest that ACEIs and ARBs do not worsen the SARS-CoV-2 infection. On the contrary, Valsartan seems to be protective against SARS-CoV-2 infection, possibly by reducing ACE2 expression.
ABSTRACT
Results of foreign and Russian studies indicate a higher mortality rate of patients with concomitant cardiovascular diseases (CVD) due to the new coronavirus infection COVID-19. It has been proven that arterial hypertension, as one of the significant risk factors for the development of concomitant cardiovascular diseases, is associated with a more severe prognosis of COVID-19. This article presents the results of modern studies and large meta-analyzes of necessity and safety of the use of blockers of the renin-angiotensin-aldosterone system in patients with arterial hypertension and COVID-19. The data of studies show that an angiotensin-converting enzyme inhibitor (ACE inhibitor) and a thiazide-like diuretic is a pathogenetically rational combination. It realizes various ways of lowering blood pressure by reducing the activity of the renin-angiotensin-aldosterone system, which is achieved by using an ACE inhibitor, and natriuresis due to diuretics. As an example, a highly effective fixed combination of drugs is considered, characterized by good tolerance, which consists of an ACE inhibitor lisinopril and a thiazide-like diuretic indapamide of prolonged action. The authors expressed the opinion that the appointment of the fixed combination drug Diroton Plus (Gedeon Richter) will contribute to effective control of blood pressure and organoprotection in conditions of increased thrombogenic and prooxidative potential, characteristic of COVID-19 both in the acute stage and within the post-COVID Syndrome.