Baba Inusa, MBBS, is a Consultant Paediatrician in the School of Life Course & Population Sciences at King's College London.

Using SWAY’s Global Sickle Cell Data to Close Access, Treatment Gaps

Multinational data from SWAY points to an increased incidence of sickle cell in Sub-Saharan Africa despite persistent gaps in treatment access.

Senior study investigator Baba Insusa, MBBS, points clinicians toward actionable solutions, including global support for medications like hydroxyurea and penicillin, along with collaboration between sub-Saharan Africa (SSA), low- and middle-income countries (LMICs), and high-income countries (HICs), in this interview with 

The SWAY data analysis aimed to compare the impact of sickle cell disease—including symptoms, complications, and quality of life—on patients in SSA compared with those in LMICs and HICs.

The study included 2,145 patients aged 12 years and older across three regions: SSA (n = 519), LMICs (n = 422), and HICs (n = 1,204). Patients in SSA were younger overall, with a median age of 15 years, compared with 19 years in LMICs and 29 years in HICs.

“Funding is very important, but what we really need is a joined-up approach that provides a standard framework countries can use—so we can learn from each other and apply best practices across the board,” Inusa said.

Catch up with Part 1 of our conversation here!

Across regions, patients reported broadly similar symptom patterns and complications, suggesting a consistent global clinical phenotype of sickle cell disease. The most common symptoms included fatigue (34%–77%), headache (39%–58%), and bone aches (32%–58%), while complications such as fever (60%–75%), infections (37%–66%), and joint-related issues (29%–65%) were also consistently observed, reinforcing the multisystem burden of disease.

Despite this consistency, differences emerged in acute disease burden and treatment access. More than five vaso-occlusive crises (VOCs) in the prior year were reported in 30% of patients in SSA, compared with 22% in LMICs and 27% in HICs, notably within a younger SSA cohort. Treatment utilization also varied substantially, with lower opioid (26%) and over-the-counter analgesic use (30%) in SSA compared with HICs (73% and 64%, respectively), highlighting disparities in access and care delivery.

Expanding Access Through Essential Medicines

He emphasized that improving access to foundational therapies like hydroxyurea and penicillin should be a global priority, noting that positioning them as essential medicines—and securing support from major funding bodies—could reduce costs and improve both access and utilization.

He highlighted the need for more structured care systems, in which specialist centers are supported by generalist sites with the capacity to treat patients appropriately, helping expand access while maintaining quality of care.

He underscored the importance of incorporating patient perspectives into care and research, noting that symptoms like fatigue—historically underrecognized—are now being identified by patients as a major burden.

Looking Beyond Pain in Sickle Cell Disease

While pain remains central, he stressed that sickle cell disease extends beyond pain alone, pointing to organ damage and broader quality-of-life impacts as critical areas for both care and research.

Driving Investment and Global Collaboration

He concluded that improving outcomes will require stronger investment and collaboration across countries, organizations, and stakeholders, alongside continued efforts to standardize care frameworks and expand access globally.

“There is enough in this study to show we need better access, better investment, and prioritization of these treatments as essential medicines,” he concluded.

Editor’s Note: Inusa reports relevant disclosures with Novo Nordisk A/S.

Inusa B, Andemariam B, Minniti C, et al. Sickle Cell Disease Burden in Sub-Saharan Africa Compared to Other Regions: Results from the SWAY Survey. 

. Published online April 2026:100092. doi:

https://doi.org/10.1016/j.bglo.2026.100092

Inusa B. Increased Sickle Cell Pain Burden in Sub-Saharan Africa Despite Younger Patients. HCPLive. Published April 28, 2026. Accessed April 29, 2026. 

https://www.hcplive.com/view/increased-sickle-cell-pain-burden-in-sub-saharan-africa-despite-younger-patients

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Inusa discusses how clinicians can close gaps in sickle cell disease care and global disparities. 

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Sickle Cell condition center page, resources on the topics of medical news and expert insight into sickle cell disease can be found. Content includes articles, interviews, videos, podcasts, and breaking news on sickle cell research, treatment, and drug development.

Using SWAY’s Global Sickle Cell Data to Close Access, Treatment Gaps 

Shashank Joshi, MD, is a consultant endocrinologist at Liavati Hospital and Joshi Clinic in Mumbai.

Navigating Iodine Deficiencies and Excesses in Thyroid Health, With Shashank Joshi, MD

 risk from both under- and overconsumption, iodine intake must be carefully monitored – particularly given the small doses hidden in many popular supplements.

American Association of Clinical Endocrinology (AACE) Annual Meeting 2026

 in Las Vegas, Nevada, by Shashank Joshi, MD, a consultant endocrinologist at Lilavati Hospital and Joshi Clinic in Mumbai, this talk details the risks of both excess iodine and iodine deficiency. Joshi highlights the various diseases born from iodine’s interaction with the thyroid, triggered both by too little and too much iodine in the system.

“Iodine biology becomes immunology. So, what happens when you have too much iodine or too little iodine?” Joshi told 

 in an exclusive interview. “The iodine behaves like an immunogen, and the body identifies it as an immunogen, and it attacks it through antibody production. If there is downregulation, then you get hypothyroidism or Hashimoto’s thyroiditis. If it’s upregulated, you will have Graves’ disease.”

Iodine deficiency is a well-studied contributor to goiter and hypothyroidism, as it plays a direct role in the production of thyroid hormone. Mild-to-moderate iodine deficiency can potentially be compensated by increased thyroid activity; however, chronic stimulation of the thyroid eventually increases the prevalence of toxic nodular goiter and hyperthyroidism. Additionally, iodine deficiency can directly impair cognitive function, as thyroid hormones are required for neuronal migration, glial differentiation, and myelination of the central nervous system.

However, the other side of the coin is similarly damaging. Iodine excess, the less-studied extreme of iodine intake, can lead to Graves’ disease and Hashimoto’s thyroiditis, both of which are driven by immune cell polarization and alterations in gut microbiota. The risk of cardiovascular diseases like hypertension and atherosclerosis is also increased due to endothelial dysfunction, inflammation, and oxidative stress. Further down the line, the development of thyroid cancer can also be influenced by excess iodine, as can learning and memory through neurotoxic effects.

To address these potential outcomes, Joshi highlights a narrow iodine window, pointing out the thyroid’s intolerance of extremes in either direction. He notes a bell curve in the biology of iodine, with early symptoms of both insufficient and excessive iodine intake appearing similar. The optimal range of iodine for thyroid health, therefore, occupies a relatively narrow space.

Additionally, Joshi points out the risk of iodine excess posed by everyday intake. Micronutrient supplements, despite being widely used and sold over the counter, are not directly approved by the US Food and Drug Administration (FDA). Because of this, they lack warnings for excess iodine content and can thus stealthily raise levels in a patient’s body. Additionally, iodized salt has become popular over the last few years, leading to another prominent source of iodine without any kind of warning on the risks of excess.

“Whenever a patient is taking any supplement over the counter, they need to read the label and see how much iodine is contained in it,” Joshi said. “You’re taking iodine sometimes through your salt, through your food, and an extra supplement could be creating that perfect storm which you want to avoid. Remember that excess thyroid production or cancer can be a byproduct of excess iodine intake.”

Editors’ Note: Joshi reports disclosures with Abbott, Lilly, Novo Nordisk, Sanofi, Torrent, Celagenex, and others.

Joshi S. Impact of Iodine on Thyroid Autoimmunity, Goiter and Oncogenesis (Hossein Gharib, MD, Lectureship). Presented at the American Association of Clinical Endocrinology Annual Meeting 2026, Las Vegas, NV. April 22-24, 2026.

Zimmermann MB, Boelaert K. Iodine deficiency and thyroid disorders. 

Khudair A, Khudair A, Niinuma SA, Habib H, Butler AE. Beyond thyroid dysfunction: the systemic impact of iodine excess. 

Joshi explains the narrow window of optimal iodine levels, highlighting the risk posed by supplements and iodized salt in tipping the scales toward health risks.

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The HCPLive endocrinology page is a comprehensive resource for clinical news and insights on endocrine system conditions. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for diabetes, hormonal disease, and more.

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Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for HCPLive. He is also the executive producer of two podcasts: Skin of Color Savvy and The Medical Sisterhood. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

 research and care: the lack of universally accepted definitions for several key treatment outcomes, such as low disease activity (LDA), very low disease activity (vLDA), and disease remission.

Atopic dermatitis, often referred to as atopic eczema, is a relapsing inflammatory skin disease with clinical manifestations known to be both variable and dependent on patient’s age.

 It is also 1 of the most common skin disorders around the world.

This new statement regarding disease definitions for key outcomes in atopic dermatitis was authored by such investigators as Joseph Merola, MD, MMSc, of the Department of Dermatology and Department of Medicine at UT Southwestern Medical Center and O’Donnell School of Public Health in Dallas. Merola et al noted that, although recent advances in targeted medications have led to higher levels of disease control being more attainable, variability in the ways outcomes are defined has complicated clinical trial comparisons.

It has also made regulatory decision-making and treatment goal-setting difficult. In order to address this concern, the team of investigators with the International Eczema Council set out to determine what will become the standardized, consensus-driven definitions to be applied across both research and clinical practice around the world.

“This modified Delphi initiative establishes a globally endorsed, expert-derived framework defining LDA, vLDA, on-drug complete control, and off-drug remission in [atopic dermatitis],” Merola and coauthors wrote.

The initiative was led by a steering committee from the International Eczema Council, which began by conducting a focused systematic literature review. Using PubMed, the group identified relevant studies published between 2004 and 2024 that examined clinician-reported and patient-reported outcomes, disease activity measures, and pruritus severity in patients with atopic dermatitis.

The quality of evidence was evaluated using established criteria from the Oxford Centre for Evidence-Based Medicine. These findings informed the development of key conceptual domains that would guide a structured consensus-building process. In order to ensure agreement among the team’s set of experts, Merola et al employed a modified Delphi method consisting of 3 sequential survey rounds. They conducted their development of this statement in the period between January - July 2025.

Those who took part included a set of members currently involved with the International Eczema Council who also had recognized expertise in atopic dermatitis. Across the 3 rounds, those involved as panelists looked over the proposed definitions, providing various levels of feedback and refining the thresholds for disease activity measures. The process incorporated a set of predefined criteria to determine the levels of agreement, with 70% consensus at minimum being required for the adoption of a definition.

There were 151 experts in total who were invited to take part, with varying response rates across rounds. Those taking part represented a broad global distribution, including Europe, North America, Asia-Pacific, Latin America, and areas around Africa and the Middle East. The expert panel was made up primarily of clinician-researchers and practicing clinicians, in addition to a smaller proportion of researchers and individuals representing patient perspectives or advocacy groups.

One of the key outcomes of panel’s process was strong support for a modular framework that distinguishes between clinician-assessed signs and patient-reported symptoms as separate but complementary elements related to disease control. This approach allows for more nuanced categorization of remission, including distinctions between improvement in patients’ visible disease and relief of symptoms such as itch.

Overall, Merola and colleagues noted the final consensus definitions laid out specific thresholds using commonly utilized clinical tools. Low disease activity was defined by the panelists as moderate but controlled disease, based on validated global assessment scores or limited atopic dermatitis extent combined with manageable levels of itch. Very low disease activity reflected minimal or near-clear skin alongside little to no itch.

The team of experts also defined “on-drug complete control,” describing individuals who attain full disease clearance and resolution of symptoms while continuing medication use for a sustained timeframe. In contrast, “off-drug remission” was defined by the panelists as the maintenance of such outcomes for an extended time period following the discontinuation of a treatment.

Overall, the consensus statement was described by Merola and colleagues as representing 1 of the first globally coordinated attempts to standardize treatment outcome definitions in the atopic dermatitis space. Through the establishment of clinically meaningful and clear benchmarks, the team’s framework is designed to allow for improvement of consistency across clinical trials, support regulatory assessment of novel treatments, and facilitate long-term comparative research. Ultimately, the set of definitions may also allow for guidance in a more structured, treat-to-target approach in clinical practice.

Merola JF, Childs BA, Bartley BR, et al. International Eczema Council Definitions of Low Disease Activity and Remission in Atopic Dermatitis: A Consensus Statement. JAMA Dermatol. Published online April 15, 2026. 

Jeskey J, Kurien C, Hostoffer R, et al. Atopic Dermatitis: A Review of Diagnosis and Treatment. J Pediatr Pharmacol Ther. 2024 Dec;29(6):587-603. 

. Epub 2024 Dec 9. PMID: 39659858; PMCID: PMC11627575.

Articles

A globally endorsed consensus statement from the International Eczema Council establishes standardized definitions for low disease activity, very low disease activity, on-drug complete control, and off-drug remission in atopic dermatitis. A steering committee conducted a 2004–2024 literature review, graded evidence per Oxford criteria, and used a three-round modified Delphi process (January–July 2025) requiring ≥70% agreement. The framework is modular, separating clinician-assessed signs from patient-reported symptoms, and sets thresholds using common validated instruments to support trial comparability, regulatory evaluation, and treat-to-target care.

The International Eczema Council set out to create a set of consensus-based definitions of remission, LDA, and vLDA in atopic dermatitis.

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International Eczema Council Releases Definitions of Remission, Low Disease Activity

Linda Stein Gold, MD, is a dermatologist at Henry Ford Health. 

Eingun James Song, MD, is the director of clinical research for Frontier Dermatology. 

IL-17 Inhibition and Long-Term Outcomes in Psoriasis

In this episode, ‘IL-17 Inhibition and Long-Term Outcomes in Psoriasis,’ the panelists provide a deeper exploration of IL-17–targeted therapies in psoriasis, focusing on the biological rationale behind different mechanisms of action and how these translate into clinical outcomes. The faculty explored the distinction between selective IL-17A inhibition and dual inhibition of IL-17A and IL-17F, highlighting the evolving understanding of the IL-17 cytokine family and its role in driving inflammation. While IL-17A has historically been considered the primary therapeutic target, emerging insights suggest that IL-17F may also play a significant role due to its higher abundance in psoriatic lesions, raising the possibility that broader pathway inhibition may offer additional clinical benefit.

The faculty examined the complexities of interpreting long-term efficacy data across therapies. While individual clinical trials demonstrate sustained responses over multiple years, they emphasized that differences in study design, patient populations, and statistical methodologies make cross-trial comparisons challenging. Factors such as responder enrichment, rescue criteria, and analytic approaches can significantly influence reported outcomes, underscoring the need for careful interpretation of long-term extension data.

Additionally, the panelists explore the role of real-world evidence as a complementary perspective to clinical trial findings. Although real-world data may introduce variability, it can provide valuable insights into treatment durability and performance in broader patient populations. They also highlight both the benefits and limitations of evaluating therapies aimed at achieving sustained remission in psoriasis.

The next episode in this series, ‘Rapid Response in Psoriasis Treatment,’ the panelists examine the role of rapid treatment response in psoriasis and how speed of efficacy influences treatment decisions and patient satisfaction. It highlights differences within IL-17 inhibitors and the ability to achieve both rapid and sustained disease control without compromising outcomes.

Expert panel weighs IL‑17 vs IL‑23 biologics for psoriasis, highlighting fast onset, durability, and why switching within class may work.

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Professor of Medicine and Renal Division Chief at the University of Pennsylvania Perelman School of Medicine

April 28th, 2026, was the American Kidney Fund’s third annual APOL1-Mediated Kidney Disease (AMKD) Awareness Day, which urges clinicians to identify high-risk patients of African ancestry with unexplained kidney failure.

More than a decade after the discovery of APOL1 risk variants, translation into clinical care has been slower than many anticipated, with the field reaching an important milestone with the first proof-of-concept data for APOL1-targeted therapies.

As these treatments advance and longstanding questions around risk prediction, screening, and access remain unresolved, the focus is shifting toward how to translate this progress into equitable, real-world care.

In this Q&A, Kirk Campbell, MD, a nephrologist at Penn Medicine, discusses the evolving clinical landscape of APOL1-mediated kidney disease, the challenges that have slowed progress, and what must change to ensure emerging advances reach the patients most at risk.

HCPLive: We’ve known about APOL1’s role in kidney disease for over a decade. Why has translation into clinical practice been so slow and what has that delay meant for patients?

Campbell: It is a long time, but the fact that it took 13 years from the discovery of APOL1 kidney disease genetic association to the first proof-of-concept APOL1 inhibitor efficacy report should be celebrated. At the same time, the many uncertainties around disease pathogenesis have slowed translation in several ways. There are still no approved APOL1-specific therapies, no consensus on population screening, limited ability to predict who among carriers will progress and unresolved questions about “second hits,”

For patients carrying APOL1 high-risk variants, what does “risk” translate to in terms of real-world monitoring and follow-up today?

Approximately 14% of African Americans have the APOl1 high risk genotype. These two APOL1 risk variants confer roughly a 15%–20% lifetime chance of kidney disease, while also emphasizing that about 80% of people with two risk variants do not develop kidney disease

: With AMPLITUDE now in Phase 3 and Maze Therapeutics advancing a Phase 2 program, if one of these therapies succeeds, what needs to happen to ensure equitable access, particularly for patients with the highest genetic risk?

Campbell: Equitable access would require more than drug approval. It would require payer coverage for APOL1 testing, genetic counseling, urine albumin testing, nephrology referral, and the medication itself. It would also require that eligibility be based on genotype and clinical phenotype, not crude racial categories. Otherwise, we risk repeating the same inequities: patients with better insurance and academic-center access get tested and treated, while safety-net, rural, and historically underserved remain underdiagnosed. The highest-burden regions cannot be an afterthought. KDIGO notes that APOL1 kidney disease disproportionately affects communities with limited health-care and research infrastructure, and the report calls for community engagement, education, and clinical-trial participation strategies involving trusted community partners

: There’s ongoing debate about how to frame APOL1 risk, as a biological story, a population genetics story, or one rooted in structural inequities. Where do you land on that, and has your thinking evolved?

I would not choose only one frame. APOL1 is a biological mechanism, a population-genetics story, and a health-equity story at the same time. The biology matters because APOL1 variants can injure kidney cells and are now targetable. The population-genetics story matters because G1 and G2 variants are enriched in people with West and Central African ancestry and likely rose in frequency because of protection against certain trypanosomal infections. But the structural inequity story is just as important. Genetics may help explain susceptibility; it does not explain who gets screened, who has a primary care relationship, who sees a nephrologist early, who gets a transplant evaluation, who is offered genetic counseling, or who can afford a precision medicine.

: The KDIGO conference on APOL1 was held in Accra, Ghana. What does it mean for the field to be having these conversations on the African continent, and does that reflect a meaningful shift toward meeting patients where they are?

Campbell: It matters a lot. West Africa is central to our understanding of APOL1 kidney disease. KDIGO reports very high frequencies of APOL1 high-risk genotypes in West African populations, including up to 37% in Central Ghana and 50% in Southeastern Nigeria, and estimates that more than 100 million people in Sub-Saharan Africa may have two APOL1 high-risk alleles.

Holding the conference in Accra signals that the field is beginning to locate the conversation closer to the populations most affected, rather than treating African populations only as a source of retrospective genetic insight.

: If you had to leave clinicians with one practical implication about APOL1 today, what should it be?

Campbell: APOL1 testing is worth considering when the result can change follow-up, trial eligibility, transplant donor counseling, or future targeted-treatment decisions. But the test should come with counseling, and it should never replace a full kidney-disease workup. KDIGO explicitly says APOL1 testing can guide risk stratification and follow-up, but should not preclude diagnostic evaluation, including biopsy when clinically indicated.

APOL1-Mediated Kidney Disease (AMKD) awareness efforts underscore the lag between discovery of APOL1 risk variants and meaningful clinical translation, despite emerging proof-of-concept inhibitor data and late-stage trials. About 14% of African Americans carry a high-risk genotype, translating to an estimated 15%–20% lifetime kidney-disease risk, while most carriers never progress, highlighting persistent gaps in prediction and “second hit” biology. Equitable implementation will require coverage for testing, counseling, monitoring, referrals, and therapy, plus genotype-driven—not race-based—eligibility and stronger community-engaged infrastructure.

Campbell answers questions about the current research and clinical landscape of APOL1-mediated kidney disease. 

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APOL1 Reaches Turning Point While Clinical, Equity Challenges Persist, With Kirk Campbell, MD

Comparing Biologic Classes and Durability in Psoriasis

Christopher G. Bunick, MD, PhD, is an associate professor of dermatology at Yale University School of Medicine.

This Q&A interview highlights emerging therapies for atopic dermatitis, featuring Christopher G. Bunick, MD, PhD of Yale Medicine.

Positive Signals for Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD

Tatyana Kushner, MD, is an associate professor of medicine in the division of gastroenterology and hepatology at Weill Cornell Medicine.

Brelovitug met the primary endpoint for virologic response and ALT normalization in the phase 2b portion of the AZURE-1 trial.

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Martina J. Porter, MD, is a dermatologist at Beth Israel Deaconess Medical Center.

54-week STOP-HS safety data for the JAK1-selective inhibitor povorcitinib showed no dose-dependent safety signal and few laboratory abnormalities.

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Contextualizing JAK Safety With Povorcitinib in HS, With Martina Porter, MD

Endocrinology experts compare pediatric and adult growth hormone deficiency—causes, testing, MRI use, and transition care tips to improve outcomes.

Recognizing Growth Hormone Deficiency — Symptoms, Presentation, and Quality of Life

Experts compare pediatric vs adult growth hormone deficiency—causes, testing, MRI use, and why retesting matters during transition to adult care.

Unraveling Growth Hormone Deficiency — Etiology and Prevalence

Study investigator Inusa explains the gap in sickle cell disease findings from SWAP, a multinational survey. 

Increased Sickle Cell Pain Burden in Sub-Saharan Africa Despite Younger Patients

Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Isaacs covers the range of AID devices currently available and approved for T2D, providing suggestions for implementation and continuous glycated hemoglobin monitoring.

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Implementing Automated Insulin Delivery in Type 2 Diabetes, With Diana Isaacs, PharmD

In this Q&A interview, Bhatia discusses the FDA's recent acceptance of BLA for imsidolimab for generalized pustular psoriasis (GPP).

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Andrea Cipriani, MD, PhD, from the University of Oxford.

Study showed the PETRUSHKA decision-support tool reduced antidepressant discontinuation, supporting personalized treatment approaches.

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Latest News

Using SWAY’s Global Sickle Cell Data to Close Access, Treatment Gaps

Navigating Iodine Deficiencies and Excesses in Thyroid Health, With Shashank Joshi, MD

International Eczema Council Releases Definitions of Remission, Low Disease Activity

IL-17 Inhibition and Long-Term Outcomes in Psoriasis

APOL1 Reaches Turning Point While Clinical, Equity Challenges Persist, With Kirk Campbell, MD