Coronaviruset i verden: Nyheter og diskusjon

[G]

4 hours ago, Snikpellik said:

OUS isolerer alle pasienter med magesmerter: Oppdaget at flere hadde ukjente corona-symptomer

Ni pasienter ved Oslo Universitetssykehus fikk påvist corona som følge av magesmerter. Ingen av pasientene hadde luftveissymptomer.

I en studie som ble publisert i det anerkjente tidsskriftet British Journal of Surgery mandag presenterer norske leger ved Oslo Universitetssykehus overraskende funn:

Ved OUS fikk flere pasienter som ble innlagt med magesmerter i løpet av de to siste ukene i mars, påvist corona. Viruset ble oppdaget ved henvising til CT-undersøkelse av magen/buken.

Pasientene hadde ingen typiske symptomer på covid-19, men klaget på smerter i magen, forteller overlege ved avdelingen for gastro- og barnekirurgi på Oslo Universitetssykehus, Usman Saeed, til VG.

– Funnene våre indikerer at covid-19 kan gi magesmerter alene, uten å gi de vanlige symptomene som feber og luftveissymptomer, sier overlegen.

– Ingen av disse hadde pasientene luftveissymptomer ved innleggelse. Kun en har utviklet dette senere.

Mer: https://www.vg.no/nyheter/innenriks/i/jdE2ze/ous-isolerer-alle-pasienter-med-magesmerter-oppdaget-at-flere-hadde-ukjente-corona-symptomer

 

En artikkel fra legeforeningen:

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Studies have increasingly reported symptoms from the gastrointestinal tract in COVID-19 patients (6, 7, 9). In a large study of 1099 patients with COVID-19, 5 % had nausea and 3.8 % vomiting. The study also found that 8.9 % never developed viral pneumonia (7). In a recently published study of 204 patients with confirmed COVID-19, it was reported that about half of the patients had symptoms of loss of appetite, diarrhoea, vomiting and abdominal pain. It was found that the period of time from onset of symptoms to hospitalisation was longer for patients with gastrointestinal symptoms than for patients with respiratory tract symptoms, and that those with gastrointestinal symptoms had a poorer prognosis (10).

In other infections caused by phylogenetically similar coronaviruses, such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS), it has been reported that 20–25 % of patients initially experienced symptoms from the gastrointestinal tract (11-13).

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Basal pneumonia with pleural effusion may explain pain and discomfort in the upper abdomen. However, it is less likely that basal pneumonia will cause lower abdominal pain and symptoms such as nausea, vomiting and diarrhoea. Other mechanisms must therefore be suspected. Similar to SARS-CoV, SARS-CoV-2 has been shown to have proteins that readily bind to the cell receptor angiotensin-converting enzyme 2 (ACE2) (3). There are many ACE2 receptors on type 2 alveolar cells in the lungs, and the lungs are therefore particularly at risk. Cells in other organs have also been shown to have ACE2 receptors. The virus can therefore invade, multiply and cause infection in several organ systems. A high proportion of ACE2 receptors has been seen in the heart, ileum, oesophagus, kidneys and bladder. In one study, epithelial cells in the ileum were reported to have a very high proportion of ACE2 receptors (30 %, versus 1 % in the lungs) (14).

https://tidsskriftet.no/en/2020/04/kort-kasuistikk/acute-abdomen-early-symptom-covid-19

Endret 29. april 2020 av G

[Peppep]

11 minutes ago, Camlon said:

Påsketallene (0.9 - 1) er basert på trenden.

Nå som vi har åpnet opp skolene og barnehagene, folk har blitt mer avslappet og har ikke gjort noe spesielt siden påsken for å begrense spredningen, så er det forventet at R0 er høyere nå enn i påsken.

Jeg forventer et liten hopp i perioden 20 - 25 april når barnehagene åpnet og et større hopp fra 27 april når 1 - 4 klasse åpnet og barnehagene går tilbake til mer normale rutiner.

Tja, av alt som Sverige har gjort annerledes enn oss, så er vel skoler og barnehager det minst kontroversielle? FHI sier at det er usikkert om det i det hele tatt har en påvirkning på spredningen og i så fall hvor mye. Min ukvalifiserte magefølelse er enig med deg i at Re gikk opp i påsken (på tross av stengte skoler), men tror at den gikk ned igjen etterpå (på tross av åpne skoler). De mest effektive tiltakene er fortsatt hånd-/hostehygiene, rengjøring og avstand. Alt som blir gjenåpnet nå er med veiledere for å unngå smitte. Veilederne er ikke perfekte, men de reduserer garantert smitten som hadde vært (samme sted) uten de tiltakene. Synes også jeg hører mer og mer om folk som får beskjed om at det blir hjemmekontor ut året o.l. På busser og baner har de begynt å blokkere annethvert sete i sikksakk-mønster. På handleturene mine kan jeg ikke huske sist jeg var under 2 meter fra noen i mer enn noen sekunder. Der det ikke er håndsprit ved døren står folk i kø - med flere meters mellomrom - til såpe og vann ved panteautomaten. Disse tingene virker og alt dette kombineres med god nok kapasitet på testing og sporing for tidlig isolering. Andelen positive svar på testene har gått ned de siste ukene, som tyder på at testkapasiteten er god nok. Siden vi er over på synsingen: når "alt" etter hvert skal åpne opp igjen tror jeg dessverre at (ikke-medisinske) munnbind på kollektivtransport og kanskje butikker blir et nødvendig onde for å redusere smitten fra pre- og asymptomatiske, slik bl.a. Tyskland har gjort. Og med alt dette på plass tror jeg at vi klarer å holde Re under 1 i lang tid.

[G]

1 hour ago, Guest 36437...96c said:

Jo, men tenkte at for de profesjonelle monner det lite med et par 50-pakninger med munnbind. Tror også at de har fått kontroll på forsyningene der nå.

Anonymous poster hash: 36437...96c

Prøvd om frisørsalonger behøver slikt?

[Simen1]

Camlon skrev (5 timer siden):

Er det modellen hvor R0 hoppet plutselig fra 3.1 til 0.7 15 mars og ble der? I den modellen så tilpasset de andre faktorene sånn at R0 kan stå bom stille på 0.7.  

Og FHIs modell begynner allerede å bomme. Ifølge deres modell fra 21 april skulle det være ca 100 nå. De får håpe det blir et stort fall snart, eller så kommer de til å bomme igjen.

https://www.fhi.no/contentassets/e6b5660fc35740c8bb2a32bfe0cc45d1/vedlegg/nasjonale-rapporter/2020.21.04---corona_report.pdf

Merkelig graf. Skulle tro de hadde avrundet til heltall i hytt og pine under veis i beregningen.

[G]

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People that develop gastrointestinal symptoms were also likely to experience signs of coronavirus for longer than those with only respiratory symptoms, they added.

https://www.express.co.uk/life-style/health/1272191/coronavirus-symptoms-mild-signs-covid-19-infection-stomach-pain

 

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Patient reports and biopsy data suggest the virus can infect the lower gastrointestinal tract, which is rich in ACE2 receptors. Some 20% or more of patients have diarrhea.

https://www.sciencemag.org/news/2020/04/how-does-coronavirus-kill-clinicians-trace-ferocious-rampage-through-body-brain-toes

Den lenken ser ut å være innholdsrik. Mye informasjon om forskjellige måte kroppen angripes.

 

Spoiler

The coronavirus wreaked extensive damage (yellow) on the lungs of a 59-year-old man who died at George Washington University Hospital, as seen in a 3D model based on computerized tomography scans.

 

GEORGE WASHINGTON HOSPITAL AND SURGICAL THEATER

How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

By Meredith Wadman, Jennifer Couzin-Frankel, Jocelyn Kaiser, Catherine MatacicApr. 17, 2020 , 6:45 PM

Science’s COVID-19 reporting is supported by the Pulitzer Center.

On rounds in a 20-bed intensive care unit one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? “Taking a systems approach may be beneficial as we start thinking about therapies,” says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).

Related story

• 

  For survivors of severe COVID-19, beating the virus is just the beginning

What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no pathogen humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. “We need to keep a very open mind as this phenomenon goes forward,” says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. “We are still learning.”

The infection begins

When an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell’s machinery, making myriad copies of itself and invading new cells.

As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.

If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.

Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration (see graphic). Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.

But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computed tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells.

An invader’s impact

In serious cases, SARS-CoV-2 lands in the lungs and can do deep damage there. But the virus, or the body’s response to it, can injure many other organs. Scientists are just beginning to probe the scope and nature of that harm. Click on organ name for more.

 

 

(SLETTET denne interaktive greia som ikke lot seg kopiere så lett)

 

Some clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.

Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.

But others aren’t convinced. “There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven’t really seen convincing data that that is the case,” says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.

He’s also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. “There’s a real risk that we allow more viral replication,” Levitt says.

Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients’ rapid deterioration: the heart and blood vessels.

Striking the heart

In Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle—normally the powerhouse chamber of the heart—so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.

How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 36 patients admitted to the ICU had arrhythmias.

The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.

“The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says.

Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death.

The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19.

Behnood Bikdeli, Columbia University Irving Medical Center

In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,” Levitt says.

If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.

Mangalmurti says she has been “shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. “It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.”

Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.

“We’re still at the beginning,” Krumholz says. “We really don’t understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly … and why it is so hard [for some] to recover.”

Multiple battlefields

The worldwide fears of ventilator shortages for failing lungs have received plenty of attention. Not so a scramble for another type of equipment: dialysis machines. “If these folks are not dying of lung failure, they’re dying of renal failure,” says neurologist Jennifer Frontera of New York University’s Langone Medical Center, which has treated thousands of COVID-19 patients. Her hospital is developing a dialysis protocol with different machines to support additional patients. The need for dialysis may be because the kidneys, abundantly endowed with ACE2 receptors, present another viral target.

According to one preprint, 27% of 85 hospitalized patients in Wuhan had kidney failure. Another reported that 59% of nearly 200 hospitalized COVID-19 patients in China’s Hubei and Sichuan provinces had protein in their urine, and 44% had blood; both suggest kidney damage. Those with acute kidney injury (AKI), were more than five times as likely to die as COVID-19 patients without it, the same Chinese preprint reported.

Medical staff work to help a COVID-19 patient in an intensive care unit in Italy.

 

ANTONIO MASIELLO/GETTY IMAGES

“The lung is the primary battle zone. But a fraction of the virus possibly attacks the kidney. And as on the real battlefield, if two places are being attacked at the same time, each place gets worse,” says Hongbo Jia, a neuroscientist at the Chinese Academy of Sciences’s Suzhou Institute of Biomedical Engineering and Technology and a co-author of that study.

Viral particles were identified in electron micrographs of kidneys from autopsies in one study, suggesting a direct viral attack. But kidney injury may also be collateral damage. Ventilators boost the risk of kidney damage, as do antiviral compounds including remdesivir, which is being deployed experimentally in COVID-19 patients. Cytokine storms also can dramatically reduce blood flow to the kidney, causing often-fatal damage. And pre-existing diseases like diabetes can increase the chances of kidney injury. “There is a whole bucket of people who already have some chronic kidney disease who are at higher risk for acute kidney injury,” says Suzanne Watnick, chief medical officer at Northwest Kidney Centers.

Buffeting the brain

Another striking set of symptoms in COVID-19 patients centers on the brain and central nervous system. Frontera says neurologists are needed to assess 5% to 10% of coronavirus patients at her hospital. But she says that “is probably a gross underestimate” of the number whose brains are struggling, especially because many are sedated and on ventilators.

Frontera has seen patients with the brain inflammation encephalitis, with seizures, and with a “sympathetic storm,” a hyperreaction of the sympathetic nervous system that causes seizurelike symptoms and is most common after a traumatic brain injury. Some people with COVID-19 briefly lose consciousness. Others have strokes. Many report losing their sense of smell. And Frontera and others wonder whether in some cases, infection depresses the brain stem reflex that senses oxygen starvation. This is another explanation for anecdotal observations that some patients aren’t gasping for air, despite dangerously low blood oxygen levels.

ACE2 receptors are present in the neural cortex and brain stem, says Robert Stevens, an intensive care physician at Johns Hopkins Medicine. But it’s not known under what circumstances the virus penetrates the brain and interacts with these receptors. That said, the coronavirus behind the 2003 severe acute respiratory syndrome (SARS) epidemic—a close cousin of today’s culprit—could infiltrate neurons and sometimes caused encephalitis. On 3 April, a case study in the International Journal of Infectious Diseases, from a team in Japan, reported traces of new coronavirus in the cerebrospinal fluid of a COVID-19 patient who developed meningitis and encephalitis, suggesting it, too, can penetrate the central nervous system.

A 58-year-old woman with COVID-19 developed encephalitis, resulting in tissue damage in the brain (arrows).

 

N. POYIADJI ET AL., RADIOLOGY, (2020) DOI.ORG/10.1148/RADIOL.2020201187

But other factors could be damaging the brain. For example, a cytokine storm could cause brain swelling, and the blood’s exaggerated tendency to clot could trigger strokes. The challenge now is to shift from conjecture to confidence, at a time when staff are focused on saving lives, and even neurologic assessments like inducing the gag reflex or transporting patients for brain scans risk spreading the virus.

Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus’ impact on the nervous system, including the brain.

Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb—explaining reports of a loss of smell—which connects to the brain. “It’s a nice sounding theory,” she says. “We really have to go and prove that.”

Most neurological symptoms “are reported from colleague to colleague by word of mouth,” Chou adds. “I don’t think anybody, and certainly not me, can say we’re experts.”

Reaching the gut

In early March, a 71-year-old Michigan woman returned from a Nile River cruise with bloody diarrhea, vomiting, and abdominal pain. Initially doctors suspected she had a common stomach bug, such as Salmonella. But after she developed a cough, doctors took a nasal swab and found her positive for the novel coronavirus. A stool sample positive for viral RNA, as well as signs of colon injury seen in an endoscopy, pointed to a gastrointestinal (GI) infection with the coronavirus, according to a paper posted online in The American Journal of Gastroenterology (AJG).

Her case adds to a growing body of evidence suggesting the new coronavirus, like its cousin SARS, can infect the lining of the lower digestive tract, where the crucial ACE2 receptors are abundant. Viral RNA has been found in as many as 53% of sampled patients’ stool samples. And in a paper in press at Gastroenterology, a Chinese team reported finding the virus’ protein shell in gastric, duodenal, and rectal cells in biopsies from a COVID-19 patient. “I think it probably does replicate in the gastrointestinal tract,” says Mary Estes, a virologist at Baylor College of Medicine.

Recent reports suggest up to half of patients, averaging about 20% across studies, experience diarrhea, says Brennan Spiegel of Cedars-Sinai Medical Center in Los Angeles, co–editor-in-chief of AJG. GI symptoms aren’t on CDC’s list of COVID-19 symptoms, which could cause some COVID-19 cases to go undetected, Spiegel and others say. “If you mainly have fever and diarrhea, you won’t be tested for COVID,” says Douglas Corley of Kaiser Permanente, NorthernCalifornia, co-editor of Gastroenterology.

The presence of virus in the GI tract raises the unsettling possibility that it could be passed on through feces. But it’s not yet clear whether stool contains intact,

infectious virus, or only RNA and proteins. To date, “We have no evidence” that fecal transmission is important, says coronavirus expert Stanley Perlman of the University of Iowa. CDC says that based on experiences with SARS and with the virus that causes Middle East respiratory syndrome, another dangerous cousin of the new coronavirus, the risk from fecal transmission is probably low.

The intestines are not the end of the disease’s march through the body. For example, up to one-third of hospitalized patients develop conjunctivitis—pink, watery eyes—although it’s not clear that the virus directly invades the eye. Other reports suggest liver damage: More than half of COVID-19 patients hospitalized in two Chinese centers had elevated levels of enzymes indicating injury to the liver or bile ducts. But several experts told Science that direct viral invasion isn’t likely the culprit. They say other events in a failing body, like drugs or an immune system in overdrive, are more likely driving the liver damage.

This map of the devastation that COVID-19 can inflict on the body is still just a sketch. It will take years of painstaking research to sharpen the picture of its reach, and the cascade of cardiovascular and immune effects it might set in motion. As science races ahead, from probing tissues under microscopes to testing drugs on patients, the hope is for treatments more wily than the virus that has stopped the world in its tracks.

*Correction, 20 April, 12:25 p.m.: This story has been updated to correct the description of a sympathetic storm. It has also been updated to more accurately describe the geographic locations of the patients found to have protein and blood in their urine.

 

Endret 29. april 2020 av G

[Benbjo]

1 hour ago, G said:

 

En artikkel fra legeforeningen:

https://tidsskriftet.no/en/2020/04/kort-kasuistikk/acute-abdomen-early-symptom-covid-19

Så over 91% får lungebetennelse altså? Interessant. Det passer jo dårlig med at de fleste får milde/ingen symptomer. 

 

Endret 29. april 2020 av Benbjo

[G]

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Studies have increasingly reported symptoms from the gastrointestinal tract in COVID-19 patients (6, 7, 9). In a large study of 1099 patients with COVID-19, 5 % had nausea and 3.8 % vomiting. The study also found that 8.9 % never developed viral pneumonia (7). In a recently published study of 204 patients with confirmed COVID-19, it was reported that about half of the patients had symptoms of loss of appetite, diarrhoea, vomiting and abdominal pain. It was found that the period of time from onset of symptoms to hospitalisation was longer for patients with gastrointestinal symptoms than for patients with respiratory tract symptoms, and that those with gastrointestinal symptoms had a poorer prognosis (10).

In other infections caused by phylogenetically similar coronaviruses, such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS), it has been reported that 20–25 % of patients initially experienced symptoms from the gastrointestinal tract (11-13).

 

Vet ikke helt hvordan man tolker disse. Men, man har jo mange tallgymnaster her, så kanskje de kan tolke det? Artikkelen er full av lenker ut til andre kilder:

Quote

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Folkehelseinstituttet. Definisjon av nærkontakter til personer som har fått påvist covid-19. https://www.fhi.no/nettpub/coronavirus/helsepersonell/definisjoner-av-mistenkte-og-bekreftede-tilfeller-med-koronavirus-coronavir/Accessed 25.3.2020.

 

2

Tan W, Zhao X, Ma X et al. A Novel Coronavirus Genome Identified in a Cluster of Pneumonia Cases – Wuhan, China 2019−2020. China CDC Weekly 2020; 2: 61–2. http://weekly.chinacdc.cn/en/article/id/a3907201-f64f-4154-a19e-4253b453d10c Accessed 30.3.2020.

 

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Lu R, Zhao X, Li J et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet 2020; 395: 565–74. [PubMed][CrossRef]

 

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Verdens helseorganisasjon. WHO Director-General’s opening remarks at the media briefing on COVID-19 – 11 March 2020. https://www.who.int/dg/speeches/detail/who-director-general-s-opening-remarks-at-the-media-briefing-on-covid-19–11-march-2020 Accessed 27.3.2020.

 

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Huang C, Wang Y, Li X et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395: 497–506. [PubMed][CrossRef]

 

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Chen N, Zhou M, Dong X et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395: 507–13. [PubMed][CrossRef]

 

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Guan WJ, Ni ZY, Hu Y et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med 2020; 382: 382. [PubMed][CrossRef]

 

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Borén HK, Kjøstolfsen GH, Aaløkken TM et al. En mann i 90-årene med feber og tørrhoste. Tidsskr Nor Legeforen 2020; 140. doi: 10.4045/tidsskr.20.0218. [CrossRef]

 

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Wang D, Hu B, Hu C et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 2020; 323: 1061. [PubMed][CrossRef]

 

10

Pan L, Mu M, Ren HG et al. Clinical characteristics of COVID-19 patients with digestive symptoms in Hubei, China: a descriptive, cross-sectional, multicenter study. Am J Gastroenterol 20.3.2020. https://journals.lww.com/ajg/Documents/COVID_Digestive_Symptoms_AJG_Preproof.pdf Accessed 25.3.2020.

 

11

Assiri A, Al-Tawfiq JA, Al-Rabeeah AA et al. Epidemiological, demographic, and clinical characteristics of 47 cases of Middle East respiratory syndrome coronavirus disease from Saudi Arabia: a descriptive study. Lancet Infect Dis 2013; 13: 752–61. [PubMed][CrossRef]

 

12

Leung WK, To KF, Chan PKS et al. Enteric involvement of severe acute respiratory syndrome-associated coronavirus infection. Gastroenterology 2003; 125: 1011–7. [PubMed][CrossRef]

 

13

Zumla A, Hui DS, Perlman S. Middle East respiratory syndrome. Lancet 2015; 386: 995–1007. [PubMed][CrossRef]

 

14

Zou X, Chen K, Zou J et al. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Front Med 12.3.2020. https://link.springer.com/10.1007/s11684-020-0754-0 Accessed 23.3.2020.

 

Endret 29. april 2020 av G

[xRun]

Benbjo skrev (23 minutter siden):

Så over 91% får lungebetennelse altså? Interessant. Det passer jo dårlig med at de fleste får milde/ingen symptomer. 

 

8,9% av pasienter på sykehus med påvist COVID-19 har ikke respiratoriske symptomer.

[G]

1 minute ago, xRun said:

8,9% av pasienter på sykehus med påvist COVID-19 har ikke respiratoriske symptomer.

Eller kan det tolkes til at 8,9 % av de med magesmerter ikke har symptomene ved lungeinfeksjon? De kan likevel ha noe lungeinfeksjon. Blir ikke klok på det der jeg fra legeforeningen.

[Benbjo]

3 minutes ago, xRun said:

8,9% av pasienter på sykehus med påvist COVID-19 har ikke respiratoriske symptomer.

Det står det jo ikke noe om? Av de over tusen smittede de fulgte så fikk 91.1% lungebetennelse. Står ikke noe om at det var innlagt? 

[Svein M]

En liten sammenligning av utviklingen i Norge, Sverige, Danmark, Finland

Ut fra kurven anslår jeg at i Sverige er antall døde per 1 mill innbyggere ca 10, mens i Norge og Danmark er den under 2. (jeg ser bort fra de siste 4 dager da data ofte tar noen dager på å bli justert)

Forventet antall Corona-dødsfall i Sverige har da kommet opp til ca 100 per dag.

 

Vi ser at Sverige øker fortsatt brattest opp, mens de andre landene her har greid å begrense økningen.

 

Endret 29. april 2020 av Svein M

[Kazuo]

Mye snakk om ACE2 reseptorer, kan forklare hvorfor de med mørk hudfarge ofte havner på sykehus i typ land som Frankrike ,  de sleit mye med ha kontroll på karantene nettopp i områder med stor andel minoritets befolking.

Mulig dette også gjelder Belgia, Frankrike, UK osv.

Benbjo skrev (26 minutter siden):

Så over 91% får lungebetennelse altså? Interessant. Det passer jo dårlig med at de fleste får milde/ingen symptomer. 

 

Du klarer virkelig vri alt til noe negativt, de fleste får milde symptomer og flere utvikler ikke symptomer i det hele tatt.

 

[xRun]

Benbjo skrev (3 minutter siden):

Det står det jo ikke noe om? Av de over tusen smittede de fulgte så fikk 91.1% lungebetennelse. Står ikke noe om at det var innlagt? 

Det står pasienter, og disse må etter alt å dømme ha blitt undersøkt av lege.
De dukker ikke opp om de ikke har symptomer, eller har så milde symptomer at de ikke mener de trenger lege.

Endret 29. april 2020 av xRun

[G]

9 minutes ago, DaniNichi said:

Mye snakk om ACE2 reseptorer, kan forklare hvorfor de med mørk hudfarge ofte havner på sykehus i typ land som Frankrike ,  de sleit mye med ha kontroll på karantene nettopp i områder med stor andel minoritets befolking.

Mulig dette også gjelder Belgia, Frankrike, UK osv.

Du klarer virkelig vri alt til noe negativt, de fleste får milde symptomer og flere utvikler ikke symptomer i det hele tatt.

 

Man må vel ut å lese de andre kildeartiklene, pkt. 6, 7 og 9 for å bli helt klok på hva som gjelder?

Quote

6

Chen N, Zhou M, Dong X et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet 2020; 395: 507–13. [PubMed][CrossRef]

 

7

Guan WJ, Ni ZY, Hu Y et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med 2020; 382: 382. [PubMed][CrossRef]

 

8

Borén HK, Kjøstolfsen GH, Aaløkken TM et al. En mann i 90-årene med feber og tørrhoste. Tidsskr Nor Legeforen 2020; 140. doi: 10.4045/tidsskr.20.0218. [CrossRef]

 

9

Wang D, Hu B, Hu C et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 2020; 323: 1061. [PubMed][CrossRef]

Spesiellt kilde 7 siden tallet lenkes til (7). Da får man denne oppsummeringen derfra:

Quote

BACKGROUND

Since December 2019, when coronavirus disease 2019 (Covid-19) emerged in Wuhan city and rapidly spread throughout China, data have been needed on the clinical characteristics of the affected patients.

METHODS

We extracted data regarding 1099 patients with laboratory-confirmed Covid-19 from 552 hospitals in 30 provinces, autonomous regions, and municipalities in mainland China through January 29, 2020. The primary composite end point was admission to an intensive care unit (ICU), the use of mechanical ventilation, or death.

RESULTS

The median age of the patients was 47 years; 41.9% of the patients were female. The primary composite end point occurred in 67 patients (6.1%), including 5.0% who were admitted to the ICU, 2.3% who underwent invasive mechanical ventilation, and 1.4% who died. Only 1.9% of the patients had a history of direct contact with wildlife. Among nonresidents of Wuhan, 72.3% had contact with residents of Wuhan, including 31.3% who had visited the city. The most common symptoms were fever (43.8% on admission and 88.7% during hospitalization) and cough (67.8%). Diarrhea was uncommon (3.8%). The median incubation period was 4 days (interquartile range, 2 to 7). On admission, ground-glass opacity was the most common radiologic finding on chest computed tomography (CT) (56.4%). No radiographic or CT abnormality was found in 157 of 877 patients (17.9%) with nonsevere disease and in 5 of 173 patients (2.9%) with severe disease. Lymphocytopenia was present in 83.2% of the patients on admission.

CONCLUSIONS

During the first 2 months of the current outbreak, Covid-19 spread rapidly throughout China and caused varying degrees of illness. Patients often presented without fever, and many did not have abnormal radiologic findings. (Funded by the National Health Commission of China and others.)

Eeh, nei. Her klarte jeg bare å finne tallet for de med diaré som var 3,8 % og beskrives som uvanlig. Vel fant ordet diaré igjen i dybdeteksten av samme pkt 7 artikkel:

Quote

The median incubation period was 4 days (interquartile range, 2 to 7). The median age of the patients was 47 years (interquartile range, 35 to 58); 0.9% of the patients were younger than 15 years of age. A total of 41.9% were female. Fever was present in 43.8% of the patients on admission but developed in 88.7% during hospitalization. The second most common symptom was cough (67.8%); nausea or vomiting (5.0%) and diarrhea (3.8%) were uncommon. Among the overall population, 23.7% had at least one coexisting illness (e.g., hypertension and chronic obstructive pulmonary disease).

On admission, the degree of severity of Covid-19 was categorized as nonsevere in 926 patients and severe in 173 patients. Patients with severe disease were older than those with nonsevere disease by a median of 7 years. Moreover, the presence of any coexisting illness was more common among patients with severe disease than among those with nonsevere disease (38.7% vs. 21.0%). However, the exposure history between the two groups of disease severity was similar.

 

Endret 29. april 2020 av G

[Benbjo]

Just now, xRun said:

Det står pasienter, og disse må etter alt å dømme ha undersøkt av lege.
De dukker ikke opp om de ikke har symptomer, eller har så milde symptomer at de ikke mener de trenger lege.

Ja, jeg kikket i kildehenvisnignen, det var alle pasienter som var innlagt på sykehus. Du har rett utrolig dårlig skrevet i artikkelen som ble sitert. 

[Oddvardm]

Siste nytt fra Kina. CCP har nå satt opp informasjons kontorer i krematoriene og begravelse byråene. De har også opprettet informasjons kontorer i alle sykehus  storbyene.

[0laf]

107 dødsfall i Sverige i dag, tallene går ikke nedover.

Ser man på de akkumulerte dødstallene per dag nå, så hevdet Tegnell at toppen var nådd 8. april, men etterhvert som tallene kommer inn, danner det seg nå en ny topp også rundt 15. april, uken etter.

Det kan se ut som det kanskje kommer en topp rundt 22. april også, denne vil nok øke etterhvert, dersom den også kommer opp i over 100, så er det tydelig at disse toppene kun er "midten av uken", og at etterslepet fra helgene gjør at det er flest midt i uken, men at det ligger ganske stabilt på 80-90 døde per dag.


 

06.04.2020	90
07.04.2020	84
08.04.2020	113
09.04.2020	86
10.04.2020	91
11.04.2020	99
12.04.2020	98
13.04.2020	85
14.04.2020	91
15.04.2020	110
16.04.2020	107
17.04.2020	80
18.04.2020	81
19.04.2020	86
20.04.2020	75
21.04.2020	59
22.04.2020	68
23.04.2020	65
24.04.2020	50
25.04.2020	39
26.04.2020	45
27.04.2020	35
28.04.2020	17
29.04.2020	4

[G]

Skulle ha søkt på tallet heller 8.9 % fordi da fant jeg dette:

Quote

Conventional routes of transmission of SARS-CoV, MERS-CoV, and highly pathogenic influenza consist of respiratory droplets and direct contact,^18-20 mechanisms that probably occur with SARS-CoV-2 as well. Because SARS-CoV-2 can be detected in the gastrointestinal tract, saliva, and urine, these routes of potential transmission need to be investigated²¹ (Tables S1 and S2).

The term Covid-19 has been applied to patients who have laboratory-confirmed symptomatic cases without apparent radiologic manifestations. A better understanding of the spectrum of the disease is needed, since in 8.9% of the patients, SARS-CoV-2 infection was detected before the development of viral pneumonia or viral pneumonia did not develop.

In concert with recent studies,^1,8,12 we found that the clinical characteristics of Covid-19 mimic those of SARS-CoV. Fever and cough were the dominant symptoms and gastrointestinal symptoms were uncommon, which suggests a difference in viral tropism as compared with SARS-CoV, MERS-CoV, and seasonal influenza.^22,23 The absence of fever in Covid-19 is more frequent than in SARS-CoV (1%) and MERS-CoV infection (2%),²⁰ so afebrile patients may be missed if the surveillance case definition focuses on fever detection.¹⁴ Lymphocytopenia was common and, in some cases, severe, a finding that was consistent with the results of two recent reports.^1,12 We found a lower case fatality rate (1.4%) than the rate that was recently reportedly,^1,12 probably because of the difference in sample sizes and case inclusion criteria. Our findings were more similar to the national official statistics, which showed a rate of death of 3.2% among 51,857 cases of Covid-19 as of February 16, 2020.^11,24 Since patients who were mildly ill and who did not seek medical attention were not included in our study, the case fatality rate in a real-world scenario might be even lower. Early isolation, early diagnosis, and early management might have collectively contributed to the reduction in mortality in Guangdong.

 

Legeforeningen skrev dette:

Quote

Studies have increasingly reported symptoms from the gastrointestinal tract in COVID-19 patients (6, 7, 9). In a large study of 1099 patients with COVID-19, 5 % had nausea and 3.8 % vomiting. The study also found that 8.9 % never developed viral pneumonia (7). In a recently published study of 204 patients with confirmed COVID-19, it was reported that about half of the patients had symptoms of loss of appetite, diarrhoea, vomiting and abdominal pain. It was found that the period of time from onset of symptoms to hospitalisation was longer for patients with gastrointestinal symptoms than for patients with respiratory tract symptoms, and that those with gastrointestinal symptoms had a poorer prognosis (10).

In other infections caused by phylogenetically similar coronaviruses, such as Middle East Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome (SARS), it has been reported that 20–25 % of patients initially experienced symptoms from the gastrointestinal tract (11-13).

Tallet misrepresenteres. Originalartikkel sier aldri det legetidskriftet konkluderer med. Kun dette:

Quote

ORIGINAL-ARTIKKEL:

SARS-CoV-2 infection was detected before the development of viral pneumonia or viral pneumonia did not develop.

Legeforeningen skriver jo noe helt annet enn kilden!!

Endret 29. april 2020 av G

[helsten2]

COVID Symptom Tracker launches in Sweden, coming to India

Quote

The COVID Symptom Tracker app, developed by the health firm ZOE and King’s College London, is now available in Sweden. Rather than feeding information back to the UK, data collected in Sweden will be analysed by Lund University and handled in accordance with the General Data Protection Regulation (GDPR).

https://www.neowin.net/news/covid-symptom-tracker-launches-in-sweden-coming-to-india

[Benbjo]

https://m-en.yna.co.kr/view/AEN20200429007051320

Godt nytt. Ser ikke ut som at positiv - negativ - positiv test skyldes reaktivering eller ny smitte, men pga testen plukker opp døde virus.