Prevalence of type 2 diabetes among American youth has nearly doubled over the past 20 years, a new study found.
Since the turn of the century, the estimated prevalence of type 2 diabetes among Americans ages 10 to 19 years increased by a relative 95.3% (95% CI 77.0%-115.4%), reported Jean Lawrence, ScD, MPH, MSSA, of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland, and colleagues.
In 2001, a total of 588 of 1.73 million youth had type 2 diabetes. This number steadily increased to 814 of 1.85 million youth in 2009, and subsequently hit 1,230 of 1.85 million by the year 2017, according to the findings in JAMA.
This translated to an absolute increase of 0.32 per 1,000 estimated youths (95% CI 0.30-0.35) diagnosed with type 2 diabetes during this time:
2001: 0.34 per 1,000 (95% CI 0.31-0.37)
2009: 0.46 per 1,000 (95% CI 0.43-0.49)
2017: 0.67 per 1,000 (95% CI 0.63-0.70)
Delving deeper into these rising type 2 diabetes trends among youth, Lawrence's group found some differences by race and ethnicity. Specifically, the steepest absolute increases in type 2 diabetes prevalence from 2001 to 2017 were seen among non-Hispanic Black (0.85 per 1,000; 95% CI 0.74-0.97) and Hispanic (0.57 per 1,000; 95% CI 0.51-0.64) youth.
This steady rise in diabetes prevalence wasn't just isolated to type 2 diabetes, either.
When looking at American youth under the age of 20, a total of 4,958 of 3.35 million youth had type 1 diabetes in 2001. Mirroring trends seen for type 2 diabetes, this number crept up to 6,672 of 3.46 million youth in 2009 and rounded out at 7,759 of 3.61 million youth in 2017.
This translated to a 45.1% (95% CI 40.0%-50.4%) relative increase in type 1 diabetes diagnoses over 16 years for American youth. Paired with this, there was an absolute increase of 0.67 per 1,000 (95% CI 0.64-0.70) estimated youths diagnosed with type 1 diabetes from 2001 to 2017:
2001: 1.48 per 1,000 (95% CI 1.44-1.52)
2009: 1.93 per 1,000 (95% CI 1.88-1.98)
2017: 2.15 per 1,000 (95% CI 2.10-2.20)
This increase in type 1 diabetes prevalence followed a slightly different pattern than seen with type 2 diabetes, as non-Hispanic white youth saw the greatest absolute increase in diagnoses during this time (0.93 per 1,000; 95% CI 0.88-0.98). Non-Hispanic Black youth had the second steepest rise in type 1 diabetes cases, increasing by 0.89 per 1,000 (95% CI 0.88-0.98) from 2001 to 2017.
"Increases in prevalence can be driven by increased incidence, declining mortality, or both," the researchers explained. That being said, though, the team noted, one of the main drivers of this increased incidence is likely due to the rising childhood obesity rates in America -- growing from 13.9% in 1999-2000 to 18.5% in 2015-2016.
And stemming from this, Black and Mexican American teenagers saw some of the largest spikes in obesity prevalence during this time, likely underlying the simultaneous increases in type 2 diabetes.
For this cross-sectional observational study, Lawrence's group looked at both incidence rates and prevalence estimates from the SEARCH for Diabetes in Youth Study, which included data from six U.S. areas: California, Colorado, Ohio, South Carolina, Washington State, and Indian Health Services users in certain areas of Arizona and New Mexico.
The type 1 and type 2 diabetes cases in the study were diagnosed by physicians. Type 1 diabetes was classified as having a presence of at least one autoantibody -- glutamic acid decarboxylase antibody, zinc transporter 8 antibody, or insulinoma-associated antibody -- identified using harmonized assays or antibody-negative and insulin-sensitive based on a clamp validated index. Type 2 diabetes was classified as having no evidence of diabetes autoimmunity or the presence of insulin resistance.
The researchers also pointed out that the 2010 change in diagnostic criteria by the American Diabetes Association, which then recommended an HbA1c reading of at least 6.5% when diagnosing adults, likely did not have any impact on these prevalence trends, since they did not apply to pediatric patients
Disclosures
The study was supported by Kaiser Permanente Southern California's Marilyn Owsley Clinical Research Center, the South Carolina Clinical & Translational Research Institute at the Medical University of South Carolina, NIH/National Center for Advancing Translational Sciences, Seattle Children's Hospital, the University of Washington, University of Colorado Pediatric Clinical and Translational Research Center the Barbara Davis Center, the University of Cincinnati, and the Children with Medical Handicaps program.
Shares of Bio-Path Holdings (BPTH) - Get Report jumped Tuesday afternoon after the company announced that the U.S. Food and Drug Administration has reviewed and cleared its investigational leukemia treatment.
The company's second drug candidate BP1002 has been cleared for an initial Phase 1/1b clinical trial that will evaluate its ability to treat refractory/relapsed acute myeloid leukemia patients.
"Preclinical studies indicate that the BP1002 and decitabine combination is effective against venetoclax-resistant cell lines, suggesting that the BP1002 and decitabine combination therapy may provide benefits to patients who have relapsed from venetoclax-based treatment," said CEO Peter Nielsen.
The company says that by targeting its treatment at the DNA level rather than the protein, BP1002 might "overcome and prevent some of the mechanisms of resistance that affect venetoclax."
Phase 1/1b clinical trials feature humans and provide the first introduction of a pharmaceutical product into patients having the disease of interest. The primary endpoint of the trial is determining safety, metabolism and pharmacokinetic properties of the product.
The investigational new drug review process was performed by the FDA's Office of Oncologic Disease Division of Hematologic Malignancies and involved the agency conducting a comprehensive review of data submitted by the company.
“We are excited to move into these advanced clinical studies and look forward to generating data that not only support the DNAbilize platform but bring us one step closer to bringing these potentially lifesaving drugs to patients,” said Jorge Cortes, chairman of Bio-Path's scientific advisory board.
Vaccine specialistDynavax(NASDAQ:DVAX)climbed more than 14% higher on Monday. It's little wonder: The company announced the coronavirus jab it co-developed with Taiwan's Medigen has been rolled out in the populous Asian nation.
Every Dynavax watcher knew this day was coming; still, it's encouraging that MVC-COV1901 has been efficiently produced and launched. After all, the vaccine received its Emergency Use Authorization (EUA) from Taiwan's health ministry barely over one month ago.
In its press release trumpeting the news, Dynavax said that roughly 600,000 people in the large island nation will be inoculated with the vaccine this week. Similar to the more high-profile coronavirus vaccines made by Pfizer/BioNTech and Moderna, MVC-COV1901 is a two-shot solution.
Dynavax makes the adjutant -- an ingredient used to stimulate a stronger immune response in vaccines -- utilized in the Medigen jab.
"We are very excited for this first, of hopefully multiple, EUAs and approvals for COVID-19 vaccines that include CpG 1018 adjuvant," the biotech company quoted CEO Ryan Spencer as saying.
"Considering the limitations of current vaccines and the global vaccine shortage, we believe adjuvanted vaccines can contribute significantly to current vaccination efforts," he added.
The ball is certainly rolling for MVC-COV1901. Indeed, now that the shot has won its first authorization from a national health authority and will soon be jabbed into arms, it's likely other authorizations will follow.
Nevertheless, Dynavax bulls should temper their enthusiasm by recognizing that other vaccines -- notably Pfizer/BioNTech's newly fully approved Comirnaty -- have been on the market for quite some time and are well established throughout the world.
Her husband collapsed just before reaching the top of the stairs in their small one-bedroom house in São Paulo, Brazil. Frantic, Thais Andrade grabbed the portable pulse oximeter she had purchased after hearing that a low oxygen reading could be the first sign of the novel coronavirus. Erik’s reading was hovering eight points lower than it had that morning. He also looked feverish.
“When he hit 90% [on the oximeter], I said we can’t wait anymore,” Andrade recalled. “I called an ambulance.”
At the hospital that day in June 2020, a CT scan showed multiple lesions in her husband’s lungs — an indication of severe Covid-19 infection – which was later confirmed via a blood test. Erik, 44, had likely contracted the virus up to a week earlier, from a friend who had visited their home.
He spent the next several weeks on oxygen in the ICU, a stay that was complicated by blood clots before he was discharged. But it wasn’t his sudden decline and subsequent recovery that is notable: It’s that Andrade had been sharing the same close quarters with her husband while he was infected and able to transmit the virus. She never wore a mask in the home with him. They shared the same bed. They were physically intimate. Yet when tested for an active or past infection — twice — her bloodwork came up negative.
And that wasn’t the only time she was potentially exposed. As part of her research work as a veterinary neurologist, she went to a meeting at the University of São Paulo where an infected attendee set off a chain reaction of positivity – but Andrade dodged it. Her tests were again negative.
Both experiences suggest that Andrade may have won a sort of biological lottery — that she’s one of a lucky few “resistant” to the virus that has killed more than 4 million people. But how? That’s the mystery researchers around the world have set out to unravel.
The question of viral resistance has perplexed Mayana Zatz, a University of São Paulo genetics professor, for years, beginning with exploring the clinical variability of genetic diseases in patients who carried the same pathogenic mutation. She began with neuromuscular disorders like Duchenne muscular dystrophy, and then expanded to exploring why the Zika virus caused severe brain damage in some newborns while others were healthy.
In 2018, she published a study of nine sets of twins — seven fraternal and two identical — born to Zika-infected mothers; in each pair, one twin was born with microcephaly and developmental delay while the other was spared. Zatz suspected the answer to Zika resistance lay in their genes. To test this hypothesis, she collected blood from three of the pairs and reprogrammed their cells in the lab to generate induced pluripotent stem (iPS) cells and immature brain cells called neuroprogenitor cells (NPCs) that had genomes identical to those of the resistant and non-resistant infants. Then, her team infected the NPCs with Zika and found that the virus destroyed the NPCs of only those who were not resistant — supporting the idea that resistance is genetic.
It was a serendipitous moment in early February 2020, on her daily walk, that caused Zatz to turn her interest to exploring resistance to the Covid-19 virus.
Zatz often passed a middle-aged couple that lived nearby. After noticing the husband’s absence for several days, she stopped to ask after him. It turned out he had been gravely ill with Covid, yet his wife remained symptom-free. Zatz wondered: Along the same lines as the twin study, could discordant couples — where one is infected and the other not — be studied to potentially isolate gene associations for resistance?
Appearing on Brazilian TV a few days later, Zatz appealed for such couples to sign up for a study. “We received almost 3,000 emails of discordant couples, where one was infected and symptomatic while the partner was asymptomatic and seronegative,” Zatz told me.
After confirming the infection status of couples, her research team chose 100 of them to have their genes sequenced, in hopes of identifying mutations that are more frequent in key areas of the genomes of uninfected participants.
Zatz’s work is part of a growing effort to identify factors that may make people resistant to Covid, with the goal of finding clues to treatments, as well as understanding resistance against viruses more broadly. Other scientists have run lab experiments using CRISPR genome-editing technology to disable genes, in search of ones that could be manipulated to perhaps protect those of us not fortunate enough to have natural resistance against the coronavirus.
“The biological implications [of identifying a resistance gene] are important because it will provide one more piece in the assembly of the puzzle of the pathogenesis of Covid,” said pediatric immunologist Jean-Laurent Casanova of Rockefeller University, who has been studying the genes involved in Covid-19 severity, but is now shifting to look at elements of resistance. “Medically, if you knew you’re resistant, you know, you’d be relaxed. You would feel like King Kong right? The second possibility is that in people who are not genetically resistant, you can think of blocking the very same component on the surface of cells that you don’t have genetically.”
Veterinarian Thais Andrade poses for a portrait at the University of São Paulo, one of the places where she works.PATRÍCIA MONTEIRO FOR STAT
The first disease-resistance gene was discovered in 1905, when Cambridge University botanist Sir Rowland Biffen published a study isolating a single recessive gene for resistance to the fungus P. striiformis in wheat. The study has been pivotal in our understanding of genetically modified crops. A similar approach has since been applied to understanding children’s resistance to severe genetic diseases, and, more recently, to cancer. But when it comes to viruses, diseases that don’t arise within us but out of the environment and exposures, the picture becomes a bit more complex.
It’s hard to gauge how much you were exposed, and it’s not always clear when a virus makes someone sick. That’s especially true with SARS-CoV-2; the basic biology of how the virus attacks our bodies is still poorly understood, and its effects on people vary widely. Some people become infected but their immune systems spontaneously clear the virus, keeping them from developing the actual disease. These individuals may be asymptomatic, but this is not the same as resistance; an antibody test would generally detect evidence of a prior infection. Instead, resistance is broadly understood as having cleared a virus before it enters cells and gets a foothold – preventing infection, in other words, not just disease.
Resistance has been demonstrated against other viruses. In 1994, doctors found that a man named Stephen Crohn, despite having been exposed to numerous HIV-positive partners, was found to have no signs of HIV infection during multiple rounds of testing. Researchers later discovered he had a “delta 32” genetic mutation, which prevented HIV from entering his cells. However, later studies have suggested that resistance to HIV is rarely as simple as one mutation – there may be several genes and proteins that confer resistance, as found in research among sex workers in Kenya.
A team of scientists at New York University and the Icahn School of Medicine at Mount Sinai were the first to report finding genes possibly tied to resistance to Covid-19. In early 2020, Benjamin tenOever, a professor of microbiology at Mount Sinai, along with Neville Sanjana, an assistant professor of biology at NYU, and colleagues at the New York Genome Center set out to sort through the potential genetic factors underlying Covid resistance. To do this, they used CRISPR genome editing technology to disable each of the 20,000 human genes in lung cells and then exposed them to SARS-CoV-2. Most of the cells died within a few days. “Anything that lives,” tenOever explained, “is clearly missing something essential for a virus, and so potentially has a significant gene mutation.”
In January 2021, the group published a paper in Cell, reporting that RAB7A, a gene important for the movement of cargo from inside the cell to the cell surface, topped their quantitative ranking of genes the coronavirus can’t do without. Inhibiting RAB7A reduces SARS-CoV-2 infection by ensuring ACE2 receptors are retained inside the cell, making them unavailable as the required point of attachment for the spike protein of SARS-CoV-2 (which attaches and then enters the cell).
Although mutations in RAB7A are very rare, according to Sanjana, drugs that inhibit this gene or others required for viral infection could, in theory, be used as a treatment or even be used as a post-exposure prophylactic.
“Amazingly,” Sanjana said, “we found many genes whose loss reduces viral infection. For a subset of these, we identified existing drugs that can be repurposed to inhibit these genes. Some of them are already FDA-approved.”
But tenOever isn’t so sure their results will translate to therapies, noting that despite identifying the mutation that blocked HIV infection years ago, and spending billions of dollars since, we haven’t come up with a workable way to make people resistant to HIV. “Even if you found an inert protein that could be erased from our biology without major impact,” he said, “it doesn’t [necessarily] translate to any meaningful therapeutic.”
Casanova disagrees, believing that identifying mutations governing resistance can have a meaningful impact on therapeutics, but it involves re-imagining exactly where to target drugs.
In a paper accepted for publication in Nature Immunology, Casanova, Zatz, and colleagues with the COVID Human Genetic Effort propose several potential sites in the genome that could govern resistance to SARS-CoV-2, and suggested undertaking large genome-wide association studies that screen large populations for gene variants associated with resistance to SARS-CoV-2.
Casanova points to a limitation in the field of microbiology, which explains why therapeutics for infectious diseases have focused primarily on the disease-causing organism, instead of the host.
“The history of infectious diseases is essentially characterized by the idea that the microbe [alone] is causal, and you can prevent disease by vaccinating against the microbe, or by interfering with the microbe (via drugs). In my work, we see we can prevent or treat infectious diseases, not [just] by hammering the microbe, or playing with adaptive immunity (via vaccines or monoclonal antibodies), but by restoring deficient immunity, which accounts for life-threatening disease,” Casanova said.
This is the core reason why studying those who appear “resistant” to SARS-CoV-2 is of interest, he said.
Mayana Zatz, a molecular biologist and geneticist, in her office at the University of São Paulo.PATRÍCIA MONTEIRO FOR STAT
This point underlies Zatz’s focus as well: In her Covid studies, she’s looking for mutations in genes that regulate the immune response to viruses. She hypothesized that two main biological pathways could be involved in resistance. The first is the major histocompatibility complex (MHC), which includes various genes that govern how the immune system recognizes and latches on to viral proteins. Another factor is the leukocyte receptor complex (LRC), which is involved in how various types of white blood cells – such as natural killer (NK) cells — respond to pathogens.
In April 2021 Zatz’s team published the initial results of the discordant couples study in a preprint posted to medRxiv. Contrary to the lab’s hypothesis, no single gene mutation in these pathways was responsible for Covid-19 resistance. In July, Zatz’s lab re-analyzed the results. Among the genes related to immune modulation, 46 variants in the MICA and MICB genes were associated with symptomatic infections, all which influenced NK cell activity in infected individuals but not in their resistant partners. Zatz found that NK activity was less efficient in symptomatic individuals. The resistant individuals were mostly women, with professions ranging from physicians to teachers to the trades. In other words: the ‘super-resisters’ could be anyone. This study has been peer-reviewed and is awaiting publication in the journal Frontiers in Immunology.
Overall, the findings echo that of the Kenyan sex worker study for HIV: Several gene mutations, working together, may confer resistance. Zatz hopes that this research, and the studies that follow, will shed light on future Covid treatments.
Her earlier Zika work, she says, illustrates how understanding resistance can lead to novel therapeutic approaches. Using the findings from the study of twins’ neuroprogenitor cells, and knowing that certain brain tumors of embryonic origin are largely comprised of the same NPCs, her team decided to test whether the Zika virus might be used to attack cancer cells. Hence a new experiment was born: Brain tumors in mice, “treated” with Zika, showed significant shrinkage — and in one-third, the cancer cells disappeared completely. When Zatz’s team repeated the experiment in dogs, the reduction in tumor size extended their lives for many months without side effects.
“Our enemy — the virus — became our ally,” Zatz said.
While Zatz and other researchers pursue ways to make all of us — as Casanova put it — feel like King Kong, Andrade doesn’t see herself as being endowed with superhuman abilities to combat the pandemic.
“It’s still not clear if I can spread Covid or carry the virus to someone, even though I am ‘resistant’ to it. Erik is clearly vulnerable, so it doesn’t feel like much of an advantage if my loved ones are not resistant,” Andrade wrote in an email. “And with new, more contagious variants complicating the slow rate of general population vaccination in Brazil, it’s really hard to be more relaxed about it.”
For Car-T therapy to become anything other than a niche hospital procedure it has to move into early treatment lines. Novartis’s Kymriah seems unlikely to secure such an accolade, however, having today failed to beat autologous stem cell transplantation in a second-line lymphoma study.
For the Swiss group this is especially galling as Kymriah’s two big competitors, Bristol Myers Squibb’s Breyanzi and Gilead’s Yescarta, have just succeeded in similar trials. Still, it will be important to bear in mind trial design differences, though one take is that important fault lines are emerging between CD19-directed Car-T therapies.
On a cross-study basis this was already becoming apparent in these treatments’ approved salvage uses in second-line or later lymphoma, where for instance Yescarta and Breyanzi boast overall remission rates above 70% while Kymriah’s is 50%, according to US prescribing information.
Second line
Now the battle lines move to second-line lymphoma, an important setting where patients have relapsed after or are refractory to front-line Rituxan plus chemo.
Belinda, the trial Novartis today said had failed, compared giving these patients Kymriah head to head against the standard of care of chemo followed, in responders, by autologous transplant. Novartis said Belinda’s primary endpoint, event-free survival (EFS), failed to show a benefit for Kymriah.
An important point is that Belinda allowed the option of platinum-based immunochemotherapy before dosing Kymriah or the standard of care, a fact that might have rendered any subsequent benefit statistically insignificant.
Bristol’s corresponding Transform and Gilead’s Zuma-7 studies had similar designs and also tested EFS as primary endpoint, though they did not have the immunochemotherapy option. On June 10 Bristol said Breyanzi had beaten chemo plus transplant in terms of EFS, as well as in terms of complete response rates.
Two weeks later Yescarta scored in Zuma-7, with Gilead quantifying the EFS benefit versus chemo and transplant as a 60% reduction in event risk (p<0.0001). There was also a benefit in overall remission rate; overall survival was insufficiently mature for Transform and Zuma-7 alike.
Note: *all 2nd line after Rituxan + chemo, compared against standard of care/autologous transplant in responders; **included the option of platinum immunochemotherapy before Kymriah or SoC. BCL=B-cell lymphoma; DLBCL=diffuse large B-cell lymphoma. Source: company statements.
Next it will be time to pick apart the data, with a clear focus falling on the possible effect of Belinda's addition of platinum immunochemotherapy.
In terms of disease criteria, for instance, Zuma-7 enrolled only diffuse large B-cell lymphoma patients, while Transform and Belinda both specified aggressive B-cell lymphoma but allowed subjects with grade 3B follicular lymphoma, a less aggressive type.
The precise balance of baseline characteristics will be scrutinised to see whether the studies offer an apples-to-apples comparison. A similar thing goes for subsequent therapy. How many patients in each study’s control cohorts went on to receive Car-T, and did this influence outcomes? How durable are responses and what will the gold standard of median overall survival tell us once it is reached?
Some answers should be forthcoming when full data from these recent interim analyses are presented, perhaps at December’s Ash meeting. In the meantime doctors and analysts alike will digest the emerging data suggesting that Kymriah, the first Car-T therapy to make it to market, might not be the best.
What a difference a year makes. The second quarter of 2020 took a tremendous toll on many device makers, principally those whose technologies are used in elective procedures, as non-urgent care was deprioritised to allow hospitals to focus on treating Covid-19 patients.
Companies whose sales were hit hardest are now riding high, with orthopaedics and cardiovascular players leading the revenue renaissance among the 10 biggest groups. But a comparison with the second quarter of 2019, as a means of benchmarking companies’ 2021 performance against a more normal year, suggests that the real winners from the pandemic era are the diagnostics companies.
Medtronic reported a return to growth today, unveiling a 23% increase in quarterly sales from the same period in 2020; this time last year, the pandemic caused the company's sales to shrink 13% on 2019's level. The group cited "strong recovery" in elective operations, adding that most of its businesses are now at or above pre-Covid levels.
Still, that 23% makes Medtronic’s performance pretty average, compared to other big medtechs. In a neat reversal of the situation in 2020, the orthopaedics players Johnson & Johnson and Stryker and the cardiovascular specialist Boston Scientific now lead the charge – these three, in the same order, posted the worst revenue losses of the second quarter last year (Orthopaedics companies’ nightmare quarter, August 25, 2020).
The first of the big groups to report, J&J set the tone for a buoyant quarter, its medtech sales up 63% as Ashley McEvoy, chairman of J&J's medical devices unit, hailed “the light at the end of the Covid-19 tunnel”. The group’s orthopaedic sales grew 54%, driven by a near-doubling of revenues from its knee business.
Stryker followed suit a week later, its 55% uptick in second-quarter sales fuelled by the rebound in elective surgery. The group was able to flip its bottom line from a loss of $83m a year ago to a $592m profit.
How the top 10 medtechs have fared in the pandemic era
At the bottom end of the scale, the Dutch giant Philips only managed a meagre 6% second-quarter sales boost. The company had been doing reasonably well until mid-June, when it was forced to recall millions of DreamStation ventilators and sleep apnoea machines owing to health risks posed by the polyester-based polyurethane foam used to muffle the sound of these devices.
Degradation of this foam produces particles that might enter the devices’ air intake and be ingested or inhaled by the user, potentially causing inflammation, headaches, nausea and even carcinogenic effects, the FDA said when designating the recall as class 1, the most serious kind. The foam could also release chemicals that can lead to toxic reactions, difficulty breathing and lack of oxygen in the blood.
The recall prompted a double-digit decline in Philips’s sleep and respiratory care segment in the second quarter. The situation has only got worse since, with two more recalls of different ventilators designated class 1 in August.
Two years
The pattern is not perfect, but the table above shows a clear trend: those groups that did worst in the second quarter of 2020 owing to the strictures of the pandemic did best this past quarter as these pressures eased – and vice versa.
Arguably a better benchmark of underlying performance is given by making a two-year comparison, to before the new coronavirus changed the way the world works. And here the secret to success is clear: Covid-19 diagnostics.
Roche, Abbott and Siemens Healthineers spent huge sums on developing dozens of Covid-19 tests, including highly accurate PCR assays, fast, cheap antigen tests and innovative products including those that can not only detect antibodies to Covid-19 but measure their levels, and tests that can track the transmission of new variants of the virus.
The investment has been worth it. Healthineers, the fourth-largest in vitro diagnostics company by sales of these products, had a scorching second quarter, its Covid-19 test revenues markedly higher than expected at a time when most of its rivals were reporting declining sales of coronavirus assays.
Abbott, for example, when reporting its second-quarter results, cut its full-year guidance by 24% versus what it had forecast in April, blaming falling demand for its suite of Covid-19 tests. But its cardiovascular business, hit hard during the height of the pandemic in early 2020, has already largely recovered.
The group’s sales have increased by 28% since the second quarter of 2019. It seems that diagnostics saw Abbott though the hard times, and now its cardiology, diabetes and neurology units are picking back up.
Inorganic growth and shrinkage have also played their parts in companies’ performance. GE’s sales are down 10% since 2019 largely because it sold its biopharma business to Danaher in 2019. And Healthineers’ top line will have been boosted by its acquisition of Varian, which closed in April.
M&A activity notwithstanding, the correlation between the pandemic taking away in mid-2020 and giving back a year later is stark. If vaccination drives continue, and no frightening new variants of the virus emerge, the second quarter of 2022 might see a return to normality.
Medtronic PLC raised the lower end of its adjusted per-share earnings guidance range for fiscal 2022 and reiterated its revenue growth outlook as Chief Executive Geoff Martha said the company has seen "continued procedure volume recovery, with most of our businesses at or above pre-Covid levels."
The medical-technology company on Tuesday said it expects full-year adjusted earnings of $5.65 a share to $5.75 a share, up from its prior outlook of $5.60 a share to $5.75 a share.
The company continues to expect revenue growing about 9% on an organic basis for the year.
