Un medicament din farmacii promite rezultate în tratarea bolii

https://www.dcbusiness.ro/covid-19-un-medicament-din-farmacii-promite-rezultate-in-tratarea-bolii_620464.html 

Reprezentanții Universității Oxford au declarat miercuri că vor studia dacă un medicament indicat pentru afecțiuni reumatice ar putea fi un tratament eficient pentru pacienții cu COVID-19, într-un efort de a utiliza medicamente deja existente ca potențiale terapii împotriva noului coronavirus.

Adalimumab, care este vândut sub numele Humira și este produs de AbbVie, este un tip de antiinflamator cunoscut sub numele de medicament anti-factor de necroză tumorală (anti-TNF). Studii recente au arătat că pacienții cu COVID-19 care iau deja medicamente anti-TNF pentru boli inflamatorii intestinale și artrită inflamatorie sunt mai puțin susceptibili de a ajunge să aibă nevoie de îngrijiri în spital, se spune într-un comunicat al Oxford,

Testele vor avea ca scop tratarea persoanelor din comunitate, în special din aziluri. La acest test se vor înscrie până la 750 de pacienți din instituțiile menționate anterior.

Vaccin, Covid-19. Testări extreme. Cât de morale sunt

Humira este utilizat pentru a trata o serie de afecțiuni, inclusiv artrita reumatoidă, boala Crohn, colita ulcerativă și psoriazisul.

Disponibilitatea unor versiuni biosimilare ale medicamentului ar face ca acesta să fie accesibil și accesibil dacă testarea va avea succes. Novartis produce una dintre alternativele medicamentului care se găsește în farmacii sub numele de Hyrimoz.

Cercetările au identificat unele tratamente pentru pacienții spitalizați cu COVID-19, inclusiv remdesivirul lui Gilead, precum și dexametazonă, un steroid generic.

Cercetătorii au studiat și alte medicamente antiinflamatoare pentru tratarea COVID-19. Se crede că infecțiile severe sunt declanșate de o reacție excesivă a sistemului imunitar, cunoscută sub numele de furtună de citokine, iar medicamentele care suprimă anumite elemente ale sistemului imunitar pot juca un rol în stoparea unei escaladări rapide a simptomelor.

Dacă tocmai ai avut Covid, exercițiul ar putea să nu fie bun pentru tine

 

https://www.wired.com/story/if-youve-just-had-covid-exercise-might-not-be-good-for-you/?fbclid=IwAR2ZWQFQxSFEhp7Fyrv4E4W1qNIwxFQqSYlmmnk_KgW8oMm8vABTzlLWMDI

Dacă tocmai ai avut Covid, exercițiul ar putea să nu fie bun pentru tine

Un număr tot mai mare de studii ridică îngrijorări cu privire la efectele pe termen lung ale coronavirusului asupra inimii. Sportivii trebuie să țină cont în special de avertismente.

DIN IMAGINIscanărilor toracice tulbure și a pacienților gâfâiți conectați la ventilatoare , am fost condiționați să ne gândim la Covid-19 ca la o boală respiratorie. Dar nu este vorba doar de plămâni. Chiar și din primele zile ale pandemiei, medicii au descoperit că o nouă infecție cu coronavirus ar putea distruge alte părți ale corpului, inclusiv creierul , vasele de sânge și inima. Datele din focarele inițiale din China, New York și statul Washington au sugerat că 20 la 30 la sută dintre pacienții spitalizați cu Covid-19 au prezentat semne de leziuni cardiace.


Luna trecută, când comisarii ligii de la conferințele universitare Big Ten și Pac-12 au anunțat că vor amâna sezonul sportiv de toamnă 2020, unul dintre factorii majori pe care i-au 
citat au fost îngrijorările legate de ceva numit miocardită. Este vorba despre cardiolog, pentru ceea ce se întâmplă atunci când pereții musculari ai inimii se inflamează, slăbind organul și făcând mai dificilă pomparea sângelui. Nu este o afecțiune descoperită recent și apare destul de rar, dar atunci când se întâmplă, este cel mai adesea declanșată de o infecție. S-a demonstrat că virusurile, bacteriile, chiar și amibele care invadează, drojdiile și viermii o cauzează.Faptul că acești pacienți au avut tendința de a se îmbolnăvi și au murit mai des decât pacienții fără complicații cardiace nu a declanșat alarmele imediate. 
La urma urmei, aceștia erau persoane cu cazuri grave de Covid-19 - suficient de grave pentru a ajunge la spital. Majoritatea persoanelor care contractă virusul experimentează 
un spectru de simptome mai puțin severe . Unul din trei nu se simte niciodată rău . Dar acum, există dovezi că virusul poate provoca leziuni cardiace chiar și la persoanele care au avut simptome ușoare sau deloc, mai ales dacă acei oameni fac exerciții fizice în timp ce sunt infectați.

Ceea ce au în comun este că scot sistemul imunitar al organismului în modul atac, ducând la inflamație. Dacă o persoană se odihnește în timp ce este bolnavă și în timpul recuperării, de cele mai multe ori inflamația se retrage și mușchiul inimii se vindecă singur. Dar activitatea intensă în timp ce inima este slăbită poate provoca umflături la nivelul picioarelor, amețeli, dificultăți de respirație și - în cazuri grave - bătăi neregulate ale inimii, stop cardiac și moarte subită.

Aceste rezultate mai extreme sunt observate cel mai adesea la sportivii competitivi. De aceea, cardiologii au cerut prudență cu privire la revenirea pandemiei medii la sport. Chiar luna trecută, fostul jucător de baschet din statul Florida, Michael Ojo, a murit din cauza aparentelor complicații cardiace în timp ce juca într-o ligă profesionistă din Serbia, la scurt timp după ce tânărul de 27 de ani își revenise din Covid-19.

Pentru a preveni pandemia să conducă la leziuni cardiace la fel de tragice în rândul studenților sportivi, medicii de la Universitatea de Stat din Ohio au dezvoltat un nou protocol, spune Saurabh Rajpal, cardiolog și profesor asistent de medicină internă la OSU. Protocolul impune oricărui jucător diagnosticat cu Covid-19 să primească un examen clinic, test de sânge, electrocardiogramă și RMN - o tehnologie de imagistică costisitoare și puțin folosită - înainte de a reveni la joc. Între iunie și august, 26 de bărbați și femei din echipele școlii de fotbal, fotbal, lacros, baschet și pistă s-au prezentat pentru a fi examinați după recuperarea de la Covid-19. RMN-urile au determinat inflamația mușchiului inimii - un semn al miocarditei - în patru dintre ele. Dintre aceștia, doi nu au experimentat niciodată simptome ale Covid-19. Seria de cazuri a fost raportatăVineri în revista JAMA Cardiology.

Deoarece inimile sportivilor nu au fost imaginate înainte de infecțiile cu Covid-19 și pentru că nu au fost potrivite cu controale - persoane similare care nu au contractat virusul - este imposibil să se spună cu siguranță dacă virusul a cauzat daunele observate . Dar Rajpal, unul dintre coautorii studiului, spune că alte infecții virale provoacă miocardită, iar SARS-CoV-2 nu este diferit. „Este important ca oamenii să știe că Covid-19 poate afecta inima”, spune el.

Exact cât și cât de des, bine, nimeni nu știe asta încă, spune Topol, care conduce Institutul de Traducere Scripps Research din La Jolla, California. „Aceasta este o frontieră neexplorată”, spune el. Dovezile sunt încă în mare parte anecdotice. Ar dori să vadă guvernele și alți finanțatori de cercetare care pun bani deoparte pentru a studia mai sistematic cohorte mari de oameni pentru a vedea ce se întâmplă cu inimile lor după ce obțin Covid-19. Dar până acum nu pare o prioritate. Poate asta pentru că o mulțime de alți viruși pot provoca miocardită, speculează Topol. Dar diferența aici - și ceea ce ar trebui să stimuleze un studiu mai urgent, crede el - este că majoritatea virușilor nu infectează zeci de milioane de oameni în decurs de șase luni.

„În SUA, se estimează că peste 50 de milioane de oameni au fost infectați cu acest virus”, spune el. (Au existat 6,5 milioane de cazuri confirmate , dar datorită infrastructurii de testare a SUA , experții estimează că numărul real este mai aproape de 10 ori mai mare decât acesta .) Chiar dacă doar 1% dintre americani se confruntă cu un fel de problemă cardiacă, aceasta este încă 500.000 de oameni . „Asta pierd oamenii aici”, spune Topol. „Nu este nevoie de prea multe incidențe atunci când acest virus a trecut prin atât de mulți oameni pentru a fi o povară imensă. De aceea trebuie să punem brațele în jurul nostru și să înțelegem acest lucru cât mai curând posibil. 

De asemenea, oamenii de știință încă nu știu dacă inflamația observată la pacienții cu Covid-19 este afectarea colaterală a răspunsului imun al organismului sau virusul care infectează direct țesutul cardiac. Celulele musculare cardiace exprimă ACE2 , ușa moleculară pe care coronavirusul o folosește pentru a invada noi gazde. Și studiile de autopsie au descoperit virusul în inimile pacienților decedați cu Covid-19. (Deși, în special, nu tipurile de celule imune asociate cu un răspuns inflamator.) La începutul acestei luni, oamenii de știință de la Institutele Gladstone din San Francisco au descoperit că virusul, atunci când a fost adăugat la celulele cardiace umane într-o cutie Petri, a mărunțit lungul fibre musculare care fac ca inimile să bată. Bruce Conklin, unul dintre coautorii studiului , a declarat pentru STAT„masacrul” nu s-a asemănat cu nimic care a fost văzut vreodată cu alte boli. Dar sunt necesare mai multe cercetări pentru a înțelege mai bine dacă acest lucru este reprezentativ pentru ceea ce se întâmplă de fapt în interiorul corpurilor persoanelor cu infecții cu Covid-19.

Nevoia este deosebit de critică, deoarece atât de mulți oameni care se infectează cu coronavirus nu o știu. Și ar putea, fără să vrea, să facă lucruri - cum ar fi exercițiile fizice - care le-ar putea deteriora inima în timpul sau imediat după infectarea lor. Sportivii amatori în special, cum ar fi maratonistii, ultrarunnerii, triatletele și alții care urmăresc o mulțime de kilometri, dar nu au acces la screening-uri cardiace regulate, s-ar putea să nu fie suficient de conștienți de riscuri pentru a face aprecieri cu privire la siguranța regimurilor lor de antrenament.

De aceea, Rajpal sugerează să acordați o atenție deosebită corpului dvs. dacă mergeți la o alergare grea, la plimbare cu bicicleta sau la alte activități sportive, mai ales dacă aveți vreo boală. "Dacă aveți simptome suspecte - dureri în piept, dificultăți de respirație sau palpitații cardiace - contactați medicul", spune el. Și dacă ați dat rezultate pozitive pentru Covid-19, spune el, ar trebui să vă luați câteva săptămâni libere înainte de a reveni treptat la nivelul de antrenament la care erați înainte.

La OSU, sportivii care au prezentat semne de miocardită la RMN au fost supuși unei odihnă obligatorie de trei luni. La sfârșitul acestui lucru, vor fi rescanate pentru a se asigura că inflamația s-a calmat și abia atunci, spune Rajpal, vor fi autorizați să joace.


Mai multe de la WIRED pe Covid-19

supplements-singaporean-researchers-say-that-vitamin-d,-magnesium-and-vitamin-b12-combo-may-reduce-severity-in-older-covid-19-patients

https://www.thailandmedical.news/news/supplements-singaporean-researchers-say-that-vitamin-d,-magnesium-and-vitamin-b12-combo-may-reduce-severity-in-older-covid-19-patients

Famotidine use and quantitative symptom tracking for COVID-19 in non-hospitalised patients: a case series

 https://gut.bmj.com/content/69/9/1592


Abstract

Objective Treatment options for non-hospitalised patients with coronavirus disease 2019 (COVID-19) to reduce morbidity, mortality and spread of the disease are an urgent global need. The over-the-counter histamine-2 receptor antagonist famotidine is a putative therapy for COVID-19. We quantitively assessed longitudinal changes in patient reported outcome measures in non-hospitalised patients with COVID-19 who self-administered high-dose famotidine orally.

Design Patients were enrolled consecutively after signing written informed consent. Data on demographics, COVID-19 diagnosis, famotidine use, drug-related side effects, temperature measurements, oxygen saturations and symptom scores were obtained using questionnaires and telephone interviews. Based on a National Institute of Health (NIH)-endorsed Protocol to research Patient Experience of COVID-19, we collected longitudinal severity scores of five symptoms (cough, shortness of breath, fatigue, headaches and anosmia) and general unwellness on a four-point ordinal scale modelled on performance status scoring. All data are reported at the patient level. Longitudinal combined normalised symptom scores were statistically compared.

Results Ten consecutive patients with COVID-19 who self-administered high-dose oral famotidine were identified. The most frequently used famotidine regimen was 80 mg three times daily (n=6) for a median of 11 days (range: 5–21 days). Famotidine was well tolerated. All patients reported marked improvements of disease related symptoms after starting famotidine. The combined symptom score improved significantly within 24 hours of starting famotidine and peripheral oxygen saturation (n=2) and device recorded activity (n=1) increased.

Conclusions The results of this case series suggest that high-dose oral famotidine is well tolerated and associated with improved patient-reported outcomes in non-hospitalised patients with COVID-19.

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Significance of this study

What is already known on this subject?

  • COVID-19 is a global pandemic caused by the severe acute respiratory syndrome coronavirus 2. COVID-19 is highly contagious and causes a spectrum of disorders ranging from relatively mild symptoms to life-threatening conditions. Medical therapies that interrupt COVID-19 progression in non-hospitalised symptomatic patients are therefore highly sought.

What are the new findings?

  • We devised a method to quantitatively follow six common symptoms in non-hospitalised patients with COVID-19 over the course of their illness. The individually normalised patient symptoms revealed that the self-administration of the histamine-2 receptor antagonist famotidine is associated with symptomatic improvements in a case series of 10 consecutive patients.

How might it impact on clinical practice in the foreseeable future?

  • Our findings support the rigorous evaluation of famotidine as a potential therapy and of the use of symptom tracking for non-hospitalised patients with COVID-19.

Introduction

Management of patients with coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), poses a major challenge to the biomedical community, governments and global population. Currently, most research focuses on vaccine development or pharmacological treatment strategies for hospitalised patients with COVID-19.1 However, to reduce global morbidity and mortality, effective treatment strategies for non-hospitalised patients are required.

Famotidine may be a candidate medication for this. Famotidine is a histamine-2 receptor antagonist, widely available over the counter at low cost, does not interact with other medications and has been safely used for suppression of gastric acid production over a wide range of oral doses from 20 mg once daily to 160 mg four times daily.2 In computer simulations, famotidine was identified as a potential inhibitor of the 3-chymotrypsin-like protease,3 and this and other potential mechanisms of action for famotidine in COVID-19 are an area of current research. In a propensity score matched retrospective cohort study a significantly reduced risk for death or intubation (adjusted HR 0.43, 95% CI 0.21 to 0.88) was identified for patients with COVID-19 who were incidentally taking famotidine before or at the point of hospital admission.4

The incentive for the retrospective cohort study were the unexpected positive results from a group of 10 patients who took famotidine following onset of symptoms for COVID-19. Here, we summarise this series of 10 patients with COVID-19 who self-medicated with famotidine as outpatients. The patient-reported demographics, clinical course, drug tolerability and longitudinal symptom scores are provided.

Methods

Consecutive patients were enrolled in this study after signing written informed consent for study participation and for deidentified data being reported in a published case series. No participant was excluded. Data were collected by two telephone interviews and two written questionnaires. Information on patient demographics, comorbidities, COVID-19 test results, famotidine use, drug-related side effects, temperature measurements, oxygen saturations and symptom scores were obtained. We collected longitudinal severity scores on five symptoms (cough, shortness of breath, fatigue, headaches and anosmia), based on an NIH endorsed Protocol to research Patient Experience of COVID-19, in addition to general unwellness.5 Symptom scores were retrospectively provided by patients on an ordinal scale: 1=not affected, 2=little affected, 3=affected and 4=severely affected. This four-point scale was based on performance status scoring in patients with cancer who are systemically affected by illness or treatment. We adapted the first four scale points of the Eastern Cooperative Oncology Group performance status (ECOG PS) scale6 and provided explanatory text to the patients as part of the symptom questionnaire. We chose only those scale points of the ECOG PS as measures of grades of severity that are relevant to a severity of COVID-19 illness that does not require hospitalisation. The relevant sections of the questionnaire with the introduction to the scale and scoring system were provided to the participants and are included in the online supplementary methods section. Longitudinal symptom scores for the time prior to the COVID-19 illness (baseline, B), the day before starting famotidine (day −1), the day famotidine was started (day 0) and days 1, 2, 7 and 14 after starting famotidine were recorded. Longitudinal temperature recordings, pulse oximetry and activity monitoring data were recorded when available.

Supplemental material

Results

Patient characteristics

Ten individuals with the clinical diagnosis of COVID-19 who self-medicated with high dose oral famotidine were identified. Eight patients were from New York State, one from New Jersey and one from Sweden. The characteristics of all study participants are summarised in table 1. The study participants were diverse with regard to known risk factors for severity of COVID-19 illness: age, sex, ethnicity and body mass index (BMI).7 Seven patients had positive PCR-based diagnoses from nasal swabs for SARS-CoV-2, two patients had positive serological tests for antibodies directed against the virus and one patient had a clinical diagnosis without molecular confirmation (table 1). All started taking famotidine while feeling unwell with COVID-19. The most commonly used dose was 80 mg oral famotidine three times daily (n=6), and the dose ranged from 20 mg three times daily to 80 mg three times daily. Median duration of famotidine self-administration was 11 days (range 5–21 days). The time period between onset of symptoms and starting treatment differed widely between patients, ranging from 2 days to 26 days (figure 1).

Figure 1

Symptomatic days before famotidine start. The durations of symptoms prior to starting famotidine are displayed in ascending order for individual patients.

Table 1

Patient characteristics

Patient-reported toxicity

Seven patients did not experience any adverse events. One patient reported grade 1 dizziness and very occasional perceptions of a racing heartbeat. Another patient experienced grade 1 dizziness, dry skin and insomnia. A third patient reported grade 1 gastroenterological symptoms and temporary forgetfulness (table 1). Other than forgetfulness, all of these side effects are listed in the prescription information for famotidine,2 and all side effects resolved on discontinuation of famotidine.

Patient-reported outcomes and symptoms

No hospitalisations were reported by any of the participants, and at the point of submission of this manuscript, patients reported feeling fully recovered apart from persistent anosmia in two cases. All patients were asymptomatic prior to developing COVID-19. They all were affected by a wide range of symptoms when they were feeling worst, and this was comparable with how they felt on the day prior to starting famotidine. On starting famotidine, all patients reported improvement of symptoms within 24–48 hours (case synopses and figure 2). When we analysed the changes of the normalised total symptom score across all patients, we found no significant difference for the day before starting famotidine compared with the day of starting famotidine, but a significant improvement in the symptom score was reported within 24 hours of starting famotidine and symptoms continued to improve and nearly normalised to preillness levels at 14 days after first famotidine use (figure 3). The improvement of symptoms was across all categories, but airway-related symptoms such as cough and shortness of breath were reported to improve more rapidly than systemic symptoms such as fatigue (figure 2).

Figure 2

Patient level symptom scores. The longitudinal data for all reported symptoms are shown for individual patients. The mean is indicated as a dashed black line. The baseline scores are indicated adjacent to the y-axis. All patients reported baseline symptoms at 1. Colour-coded lines and dots for respective symptoms are ordered alphabetically and are slightly offset to avoid overlap. Day 0 indicates the day at which patients took the first dose of famotidine. Severity score: 1=not affected, 2=little affected, 3=affected, 4=severely affected. B, baseline; Pt, patient.

Figure 3

Normalised symptom scores of all patients. The mean longitudinal normalised symptom score for all patients is shown. The SE of the mean is indicated. Statistical comparisons by two-sided t-test in comparison with day 0, the day of starting famotidine. *P<0.05; ***p<0.001; ****p<0.0001. NS, not significant.

Individual case summaries

Patient 1 is a white woman in her 40s with a medical history of epilepsy for which she takes levetiracetam 1 g daily. She took famotidine 80 mg three times daily for 11 days starting 4 days after first experiencing symptoms of COVID-19. She reported feeling very unwell at this time point. Within 1 day of the first dose of famotidine, she noticed marked improvement of her shortness of breath. This improvement was matched by an increase in her home-monitored pulse oximetry measured oxygen saturation levels from 91%–95% to 97%–98% (figure 4A). She was febrile with a temperature of 37.8°C prior to starting famotidine and afebrile on day 7 of taking famotidine.

Figure 4

Patient-level pulse oximetry and activity results. (A) The pulse oximetry data from two patients are displayed. (B–D) The device software provided display of weekly data relating to three metrices recorded using an Oura Ring are displayed for patient 8. The mean for each metric over the displayed period is indicated by a dashed line. Day 0 and week 0 represent the day and week of starting famotidine, respectively. Pt, patient.

Patient 2 is a Hispanic man in his 40s without pre-existing conditions. He took famotidine 80 mg three times daily for 11 days starting 8 days after first experiencing symptoms of COVID-19. He reported improvement of symptoms within 2 days of treatment. He was febrile with a temperature of 38.3°C prior to starting famotidine and afebrile on day 5 of taking famotidine.

Patient 3 is an Asian man in his 30s without pre-existing conditions. He took famotidine 80 mg three times daily for 7 days starting 9 days after first experiencing symptoms of COVID-19. He experienced severe shortness of breath prior to starting famotidine, and his dyspnoea and other symptoms improved by day 7. His home monitored oxygen saturation levels improved from 89% on day 2 of treatment to 96% on day 5 of treatment (figure 4A). He was febrile with a temperature of 38.9°C prior to starting famotidine and afebrile on day 5 of taking famotidine. He intermittently took paracetamol for fever during illness.

Patient 4 is a black woman in her 60s with a BMI of 38, positive smoking history and hypertension controlled by triple therapy. She took famotidine 50 mg three times daily for 12 days starting 10 days after first experiencing symptoms of COVID-19. She noticed improvement in muscle aches and chest tightness in addition to those recorded in figure 2.

Patient 5 is a white man in his 50s iswith hypertension and hyperlipidaemia, both treated with medications, and positive smoking history. He took famotidine 80 mg three times daily for 8 days starting 6 days after first experiencing symptoms of COVID-19. He described ongoing increase of fatigue for another 7 days after starting famotidine; the only patient to describe worsening of any symptoms during this treatment period. However, he noticed improvement in respiratory symptoms within 2 days of starting famotidine.

Patient 6 is a Hispanic woman in her 20s with no pre-existing conditions. She took famotidine 80 mg three times daily starting 9 days after first experiencing symptoms of COVID-19. She felt markedly better within 2 days of treatment but had mild dizziness and accelerated heart beats intermittently while taking famotidine.

Patient 7 is a black and Hispanic woman in her 20s with a BMI of 41 with no pre-existing conditions. She took famotidine 80 mg three times daily for 12 days starting 6 days after first experiencing symptoms of COVID-19. Within 1 week of treatment, she reported relief of most symptoms. She reported grade 1 dizziness, insomnia and dry skin concurrent with taking famotidine.

Patient 8 is a white man in his 70s with history of myocardial infarction, surgery for a benign pancreatic tumour, chronic pancreatitis and chronic back pain. His diagnosis is based on clinical symptoms and signs and being from a high prevalence location, with all family members being clinically affected by COVID-19. He took Famotidine 60 mg two times daily for 5 days starting 26 days after first experiencing symptoms of COVID-19. He reported a rapid improvement and being asymptomatic within 3 days of treatment. He routinely monitors his activity using an Oura Ring device and was able to provide readings on walking equivalence, calorie usage and activity score for the weeks before and after starting famotidine, which all showed marked improvements (figure 4B–D).

Patient 9 is a South Asian ex-smoker man in his 50s with history of hyperlipidaemia controlled by rosuvastatin. He took famotidine 60 mg two times daily for 21 days starting 2 days after first experiencing symptoms of COVID-19. He described improvement in his symptoms within 2 days of starting famotidine. He reported possible famotidine associated mild forgetfulness and gastroenterological symptoms that started while he was on famotidine but resolved before he stopped the medication.

Patient 10 is a white former smoker man in his 60s with a BMI of 37.5 without known pre-existing conditions. He took famotidine 20 mg three times daily for 5 days starting 7 days after first experiencing symptoms of COVID-19. He reported a universal improvement in symptoms within the first week of taking famotidine.

Discussion

This case series provides patient-reported outcome measures for 10 consecutively enrolled non-hospitalised patients with COVID-19. They all noticed improvements in their condition in correlation with famotidine use at doses ranging from 60 mg to 240 mg daily. Based on published pharmacokinetic data for famotidine,8 9 we estimate that these treatment regimens would have resulted in peak plasma concentrations of approximately 0.5–2 µM and average plasma concentrations of approximately 0.15–0.7 µM famotidine, assuming normal kidney function. In concordance with the clinical evidence and consensus that famotidine is safe across a wide range of doses and frequencies, famotidine was very well tolerated by all patients. Given that famotidine has only minimal inhibitory effect on the hepatic cytochrome p450 system and low risk of clinically significant alterations in oxidative drug metabolism,10 11 it may be a safe drug for testing in a trial or clinical setting where patients self-administer the medication.

A pertinent aspect of this work is the exploration and application of graded symptom scores and patient-reported outcome measures in tracking COVID-19 in the non-hospitalised setting using a four-point ordinal scale. Using these symptom scores, we were able to determine that all patients noticed a rapid improvement in their condition within 24–48 hours of starting famotidine. Our quantitative approach to follow symptom severity may be a useful tool, in particular for outpatient studies, but requires validation. In addition, for all patients who were able to provide data, temperature readings, oxygen saturations and activity improved in correlation with taking famotidine. These findings suggest that famotidine may affect the course of COVID-19 but must be considered in the context of several limitations. Placebo effect, enrolment bias and recall bias12 for symptoms may affect our findings as is the case for the outcome measures of any non-blinded, non-controlled study, despite us attempting to minimise bias by asking non-leading questions. An improvement of symptoms was noticed within 48 hours by all individuals in this study, despite the symptomatic period prior to taking famotidine varying widely. There remains the possibility, however, that these changes may reflect treatment independent convalescence, as the natural course of COVID-19 in patients who do not require hospital admission is not well characterised.

Our case series suggests, but does not establish, a benefit from famotidine treatment in outpatients with COVID-19. Future work will investigate potential mechanisms of action and clinical relevance of famotidine. Mechanistically, famotidine could have a viral target, for example, one of the viral proteases, or a host target, resulting, for example, in modulation of the immunological response to the virus. Clinically, we unreservedly share the opinion that well designed and informative studies of efficacy are required to evaluate candidate medications for COVID-19 as for other diseases.13 A randomised phase III trial testing the efficacy of high dose intravenous famotidine three times daily in addition to hydroxychloroquine in hospitalised patients with COVID-19 has recently commenced (NCT04370262). An outpatient study of oral famotidine that investigates efficacy for symptom control, viral burden and disease outcome and assesses effects of medication use on long term immunity should be considered to establish if famotidine may be of use in controlling COVID-19 in individual patients while also reducing the risk of SARS-CoV-2 transmission.

Conclusions

The results presented in this case series suggest that high-dose oral famotidine is well tolerated and associated with improved self-reported outcomes in non-hospitalised patients with COVID-19.