<h3>KEY TAKEAWAY</h3>
This article discussed 38 EBMT consensus recommendation*&nbsp;statements for use in the routine management of GVHD in allogeneic SCT in adult patients with hematological malignancies with the following key updates to the 2014 EBMT recommendations.

Rabbit anti-thymocyte globulin (rATG) is recommended for preventing GVHD in patients undergoing matched unrelated donor (MUD) allogeneic SCT (Category 1†; 100% consensus)

Grade 2 acute GVHD (aGVHD) with isolated skin or upper gastrointestinal tract (GIT) manifestations can be treated with lower steroid doses, such as 1 mg/kg per day methylprednisolone or prednisone (Category 1; 100% consensus)

As an initial treatment of bronchiolitis obliterans syndrome, the fluticasone montelukast regimen is recommended in combination with systemic steroids; however, prolonged use of azithromycin after resolution of bronchiolitis obliterans syndrome in chronic GVHD (cGVHD) is not recommended because of the possibility of increased risk of relapse (Category 2A‡; 100% consensus)

Addition of novel drugs in the available treatment options is recommended for steroid-refractory aGVHD (Category 2A; 100% consensus) and cGVHD (Category 2B§; 95% consensus)

In 2014, EBMT and European Leukemia Net (ELN) working group published recommendations on management of GVHD to harmonize clinical practice 
 and address unmet medical need

Several important studies, impacting GVHD prophylaxis and therapy were published following the 2014 recommendations

A&nbsp;<a href="https://www.nature.com/articles/bmt2016298">follow up study</a>&nbsp;by EBMT-ELN working group highlighted several 
 shortcomings in the 2014 recommendations

Thus, these guidelines were updated, and the present article discussed recommendations from the updated EBMT guidelines

EBMT task force developed 38 statements (29: 100% consensus; 9: 95% consensus), to update the 2014 GVHD recommendations related to GVHD prophylaxis, drug management during GVHD prophylaxis, and treatment of aGVHD and cGVHD.

<h3 style="text-align: center;">Prophylaxis of GVHD</h3>

<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td colspan="1" rowspan="1" style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Category of evidence, 
 Consensus (100%)</td>
 <td style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Recommendations</td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Category 1</td>
 <td style="background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Patients undergoing MRD or MUD allogeneic transplant should receive GVHD prophylaxis with a calcineurin inhibitor plus an antimetabolitea</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>Tacrolimus or ciclosporin can be used in the setting of sibling or MUD transplants. The choice should be made based on experience at the center (e.g., ciclosporin is the standard calcineurin inhibitor adopted in most European centres)</td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Category 1</td>
 <td style="background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Methotrexate is the recommended antimetabolite for patients receiving MAC</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>Mycophenolate mofetil can be used instead of methotrexate for patients receiving MAC in case of contraindications to methotrexate or for those patients who need rapid engraftment (e.g., those with aspergillosis)</td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Category 2A</td>
 <td style="background-color: rgb(244, 242, 246); border-color: rgb(244, 242, 246);">Mycophenolate mofetil is the recommended antimetabolite for patients receiving non-MAC and RIC</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>rATG should is recommended for preventing GVHD in patients undergoing MUD allogeneic SCTb</td>
 </tr>
 <tr>
 <td colspan="2">
 aIn children (&lt;18 years) many centres use calcineurin inhibitor as a single agent;&nbsp;bIn children (&lt;18 years) many centres use rATG in MUD allogeneic SCT. MAC, myeloablative conditioning; MRD, matched related donor; MUD, matched unrelated donor; RIC, reduced intensity conditioning.</td>
 </tr>
 </tbody>
</table>

<h3 style="text-align: center;">Drug management during prophylaxis of GVHD</h3>

<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td colspan="1" rowspan="1" style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Category of evidence, 
 Consensus (100%)</td>
 <td style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Recommendations</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>Ciclosporin concentration should be carefully monitored. When using the two daily doses regimen, the target concentration in the first-week post-transplant should be 200–300 μg/L to efficiently prevent aGVHD</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>Ciclosporin concentrations should be monitored with whole blood sampling for 12 h after a dose; sampling from the lines used for ciclosporin infusion should be avoided</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>The standard duration of ciclosporin prophylaxis is 6 months; however, it needs to be adjusted to the risk of relapse, chimerism, and presence or absence of GVHD. If no GVHD is reported, ciclosporin dose is tapered from 4 months until the regimen is stopped. Faster tapering is recommended if the risk of relapse is high and a bone marrow graft is provided, especially if complete chimerism is reported. The dose is not tapered, if there are signs of aGVHD or cGVHD with the exception of mild cutaneous aGVHD. In cases of persistent disease or relapse and no GVHD, ciclosporin dose can be carefully tapereda</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>Methotrexate is given as a bolus intravenous injection. In MAC transplants, initial methotrexate dose is 15 mg/m2 given on the first day after the transplant; however, lower doses of methotrexate have also been reported in RIC transplants. In MAC transplants, two additional doses of 10 mg/m2 are given on day three and six after the transplant, an additional dose at 11 days after transplant can be administered. Lower doses are usually administered in RIC transplants on 3 and 6 days after the transplant</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>On the basis of expert opinion, we recommend leucovorin rescue after prophylactically given methotrexate; however, no definite evidence supports leucovorin rescue for preventing methotrexate toxicity or enhancing methotrexate efficacy</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>The leucovorin regimen is usually started 24 h after each dose of methotrexate; on the first day after the transplant the leucovorin should be three 15 mg doses every 6 h, the dose should then increase to four 15 mg doses every six hr after methotrexate doses 3-, 6-, and 11-days after the transplant; leucovorin should be administered by intravenous injection</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>Mycophenolate mofetil should be administered intravenously or orally in three 10–15 mg/kg daily doses; the dose should be adapted according to toxicity</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>The recommended total dose of rATG ranges from 2.5–5.0 mg/kg in MRD and 4.5–6.0 mg/kg in MUD transplants; higher doses are associated with a higher risk of infectious complications</td>
 </tr>
 <tr>
 <td colspan="2">
 aIn children (&lt;18 years) with allogeneic SCT for non-malignant diseases, a longer duration of calcineurin inhibitor is often applied. MAC, myeloablative conditioning; RIC, reduced intensity conditioning.</td>
 </tr>
 </tbody>
</table>

<h3 style="text-align: center;">Treatment of aGVHD¶</h3>

<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td colspan="1" rowspan="1" style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Category of evidence, 
 Consensus (100%)</td>
 <td style="text-align: center; background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76);">Recommendations</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>Systemic treatment is initiated for grade 2 or higher aGVHD</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>First-line treatment of aGVHD is methylprednisolone with an initial dose of 2 mg/kg per day; prednisone in a dose of 2.0–2.5 mg/kg per day is regarded as equivalent to methylprednisolone 2.0 mg/kg per day dose</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>Grade 2 aGVHD with isolated skin or upper GIT manifestations can be treated with lower steroid doses, such as 1 mg/kg per day methylprednisolone or prednisone</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>No reduction in the prednisolone dose is recommended during the first 7 days after transplant, but parenteral steroids can be stopped, and oral steroids can be used until all signs of aGVHD have disappeared. Tapering of the dose is a slow, response dependent process: In cases of complete response, steroid dose should be gradually reduced to 10% of the initial dose over a period of approximately four weeks. In cases of steroid-resistant GVHD, long-term use of steroids might cause major complications; therefore, second-line therapy is recommended</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 1</td>
 <td>Non-absorbable oral steroids, such as budesonide (9 mg per day) or oral beclomethasone (1.3–2.0 mg four times a day), can be given in addition to systemic corticosteroids as treatment of gastrointestinal aGVHD</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>There is no standard second-line treatment for aGVHD. Current practice is to prescribe one of the following drugs: Alemtuzumab, α1-antitripsin, basiliximab, cellular therapies (eg, mesenchymal cells and regulatory T-cells) daclizumab, extracorporeal photopheresis, faecal microbiota transplantation, JAK inhibitors (eg, ruxulotinib which is FDA approved), mycophenolate mofetil, methotrexate, pentostatin, rATG, sirolimus, or vedolizumab; for second-line treatment of aGVHD, centres should follow their institutional guidelines, and patients should be treated in clinical trials when possible</td>
 </tr>
 <tr>
 <td colspan="2">
 FDA, US Food and Drug administration; JAK, Janus kinase</td>
 </tr>
 </tbody>
</table>

<h3 style="text-align: center;">Treatment of cGVHD#</h3>

<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td colspan="1" rowspan="1" style="background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76); text-align: center;">Category of evidence, 
 Consensus (100%)</td>
 <td style="background-color: rgb(35, 0, 76); border-color: rgb(35, 0, 76); text-align: center;">Recommendations</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>The first-line treatment of newly diagnosed cGVHD is steroids</td>
 </tr>
 <tr>
 <td style="text-align: center;">Category 2A</td>
 <td>As an initial treatment of bronchiolitis obliterans syndrome, the fluticasone montelukast regimen is recommended in combination with systemic steroids; however, prolonged use of azithromycin after resolution of bronchiolitis obliterans syndrome is not recommended because of the possibility of increased risk of relapse</td>
 </tr>
 </tbody>
</table>

*Please refer to the source publication <a href="https://www.sciencedirect.com/science/article/pii/S235230261930256X?via%3Dihub">Penack O, et al. </a> for additional details.
The National Comprehensive Cancer Network classification of evidence and consensus was used to define consensus recommendations; †Category 1: High-level evidence (randomized trials or meta-analyses) and 100% consensus; ‡Category 2A: Lower-level evidence (small, randomized trials) and 100% consensus; §Category 2B: Lower-level evidence (small, randomized trials) and 80–100% consensus; ¶aGVHD was defined using the Mount Sinai Acute GvHD International Consortium group criteria; #cGVHD was defined using the National Institutes of Health 2014 criteria

Reference

Updated European Society of Blood and Marrow Transplantation consensus recommendations for GVHD prophylaxis and management in hematological malignancies after stem-cell transplantation

CHRONIC-GRAFT-VERSUS-HOST-DISEASE-CGVHD

TRANSPLANT

<h3>KEY TAKEAWAY</h3>
Dr. Mohty discussed the pathophysiology, therapeutic targets, and diagnostic biomarkers for the management of cGVHD, based on published evidence and highlighted that:

The pathophysiological continuum of cGVHD involves early thymic damage leading to dysfunctional selection of T and B cells with subsequent production of autoantibodies and tissue fibrosis

Understanding pathways allows more diverse and more specific therapeutic approaches for cGVHD
<ul>
 <li>Therapeutic targets (e.g., ROCK2) and microbiome-derived protection from cGVHD may be explored</li>
</ul>

There exists a lack of clarity regarding organ specificity for organ-specific damage, the role of microbiota, and tissue-specific antigens and antibodies

Various studies have demonstrated diagnostic biomarkers for cGVHD, but prospective validation is needed

In this presentation, Dr. Mohty provided insights into the biology and pathophysiology of cGVHD and suggested diagnostic biomarkers and therapeutic targets for its management, based on published scientific evidence.

<h3>KEY HIGHLIGHTS</h3>
Definition of cGVHD (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6786777/">Schoemans HM, et al. 2018</a>)

<ul>
 <li>While the historical perception was that acute GVHD (aGVHD) occurs in the first three months after transplant and cGVHD thereafter, a consensus was provided to capture various cGVHD entities including an overlap cGVHD</li>
</ul>

<ul>
 <li>Manifestations of aGVHD are limited to skin, liver, and GI tract, while manifestations of cGVHD (meeting NIH 2014 diagnostic criteria) cover a wider list*</li>
</ul>

<ul>
 <li>Undefined other cGVHD includes atypical signs and symptoms of alloreactivity falling outside the NIH 2014 diagnostic criteria</li>
</ul>

Pathophysiology of cGVHD and role of T and B cells 
 &nbsp;
<ul>
 <li><a href="https://www.sciencedirect.com/science/article/pii/S1470204509702256?via%3Dihub">Finke J, et al. 2009</a>&nbsp;reported that the addition of ATG-F to GVHD prophylaxis lowered the incidence of cGVHD (limited/extensive and extensive) vs control by depleting the T cells</li>
 <li><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC9642318/">Meyer E, et al. 2022</a>&nbsp;showed that Orca-T, an engineered allograft, resulted in high GVHD- free and relapse-free survival (at one year) following myeloablative conditioning for hematological malignancies vs CIBMTR control (71% vs 34%) 
 <ul>
 <li>Incidence of moderate to severe cGVHD (as per NIH Consensus Grading) through day +365 was reduced with Orca-T vs CIBMTR control (5% vs 38%)</li>
 </ul></li>
 <li>As per Dr Mohty, the risk factors† for cGVHD analyzed by&nbsp;<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062319/">Flowers M, et al. 2011</a>&nbsp;highlight its pathophysiology including HLA mismatching, minor HLA antigen, number of T cells, insult by the conditioning regimen and GVHD prophylaxis regimen, and thymic damage and immune reconstitution</li>
 <li>To avoid cGVHD, a normal immune reconstitution needs to be achieved. However, transplant patients can suffer from other complications highlighted by&nbsp;<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6020045/">Cooke KR, et al. 2017</a>&nbsp;where the T cells can be impacted leading to immune dysregulation and abnormal proliferation of alloreactive T cells</li>
 <li>Injury to the thymus and the subsequent T cell recovery especially the naïve T helper cells plays an important role in T cell reconstitution (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7412601/">Gaballa A, et al. 2020</a>)</li>
 <li>An unbalanced reconstitution of donor-derived regulatory T cells (Tregs) as well as effector/ conventional T cells (Tcons) and CD8 T cells, observed after nine months of transplant, was associated with cGVHD (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4742552/">Alho AC, et al. 2016</a>) 
 <ul>
 <li>Thymic damage prevented recovery of naïve Tregs</li>
 </ul></li>
 <li>Findings from&nbsp;<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8049519/">McManigle W, et al. 2019</a>&nbsp;highlighted that in cGVHD, after allogeneic HCT, B cell recovery occurs under constant exposure to chronic alloantigen and a high B-cell activating factor: B cells ratio, leading to altered peripheral B-cell with constitutive activation and survival signaling</li>
 <li>Also, as shown by&nbsp;<a href="https://rupress.org/jem/article-abstract/199/8/1133/40065/Minor-Histocompatibility-Antigen-DBY-Elicits-a?redirectedFrom=fulltext">Zorn E, et al. 2004</a>, after allogeneic SCT, T cell response, was blocked by anti-DRB1501; recognized endogenously processed peptide on female and male dendritic cells; and was followed by B cell response</li>
 <li><a href="https://ashpublications.org/blood/article/103/1/353/17591/Antibody-response-to-DBY-minor-histocompatibility">Mikios DB, et al. 2004</a>&nbsp;examined the magnitude of antibody responses to recombinant DBY and DBX and found anti-DBY response to be higher in male patients with female donors vs male patients with male donors</li>
 <li><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5016705/">Sarvaria A, et al. 2016</a>demonstrated that IL-10+ regulatory B cells, enriched in cord blood, may protect against cGVHD after cord blood transplantation</li>
 <li>In general, the pathophysiology of cGVHD as per&nbsp;<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6020045/">Cookee KR, et al. 2016</a>&nbsp;involves: 
 <ul>
 <li>Phase 1: Acute inflammation, tissue injury, and involves innate immunity</li>
 <li>Phase 2: Chronic inflammation and dysregulated immunity and involves adaptive immune system (including T cells, B cells, antigen-presenting cells, NK cells, and regulatory cells: Tregs, Bregs, and Tr1 cells)</li>
 <li>Phase 3: Marks aberrant tissue repair and fibrosis and involves innate and adaptive immunity</li>
 </ul></li>
</ul>

Therapeutic targets for cGVHD
<ul>
 <li>Dr. Mohty mentioned the therapeutic targets that could be considered while managing cGVHD</li>
 <li>He highlighted ROCK2‡, a critical regulator of immune modulation and fibrosis, and an emerging therapeutic target in cGVHD which can be effectively inhibited by drugs (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8456981/">Zannin-Zhorav A, et al. 2021</a>)</li>
 <li>Microbiota and dysbiosis in local organs after HCT can influence GVHD. Findings from&nbsp;<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7332893/">Markey KE, et al. 2020</a>&nbsp;showed that microbe-derived short-chain fatty acids butyrate and propionate at day 100 were associated with protection from cGVHD</li>
</ul>

Diagnostic biomarkers for cGVHD
<ul>
 <li>The cGVHD biomarkers can aid in refining diagnosis, anticipating severity, and in guiding treatment</li>
 <li>Evaluation of diagnostic biomarker values (<a href="https://ashpublications.org/bloodadvances/article/7/14/3612/486749/A-diagnostic-classifier-for-pediatric-chronic">Cuvellier GDE, et al. 2023</a>) have shown that: 
 <ul>
 <li>At the onset of cGVHD, various populations of T cells§&nbsp;decreased, indicating thymic damage, whereas various cytokines and chemokines increased indicating effector T cell recruitment and cGVHD tissue damage</li>
 <li>Similar patterns of biomarkers were seen at the onset of moderate-severe GVHD except for a decrease in NKreg cells</li>
 </ul></li>
 <li>Assessment of cGVHD risk at three months after HCT identified cGVHD biomarkers including some key molecules including CXCL9, and fibrotic biomarkers like MMP3 and DKK3 (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10378149/">Logan BR, et al. 2023</a>)</li>
</ul>
*skin, nails, scalp, body hair, mouth, eyes, esophagus, lungs, muscles, joints, fascia, genitalia;&nbsp;†matched unrelated donor, mismatched related donor, mismatched unrelated donor, female donor/male recipient, mobilized blood cell graft, diagnosis of CML, total body irradiation, conditioning with rabbit ATG, patient age (per decade), donor age (per decade);&nbsp;‡Rho-associated coiled-coil–containing protein kinase;&nbsp;§&nbsp;naïve Th cells, naive Treg cells, NKreg cells, and cytolytic NK cells.
Disclaimer: Dr Ernst Holler is the author of this presentation. However, in his absence, it was presented by Dr Mohamad Mohty at the conference.
ABBREVIATIONS 
 ATG, anti-T-cell globulins; ATG-F, ATG-Fresenius; Breg, B regulatory cells; CD8, cluster of differentiation 8; CIBMTR, The Center for International Blood and Marrow Transplant Research; CML, chronic myeloid leukemia; CXCL9, chemokine (C-X-C motif) ligand 9; DBX, dead box RNAhelicase X; DBY, dead box RNAhelicase Y; DKK3, dickkopf-3; ELISA, enzyme-linked immunosorbent assay; GI, gastro-intestinal tract; GVHD, graft-versus-host disease; HCT, hematopoietic cell transplantation; HLA, human leukocyte antigen; HSCT, hematopoietic stemcell transplantation; IL-10, interleukin 10; MMP3, matrix- metalloproteinase 3; NIH, National Institutes of Health; NK, natural killer; NKreg, natural killer regulatory; SCT, stem cell transplantation; Tcons, conventional T cells; Th, T helper; Treg, T regulatory cells; Tr1, IL-10 producing regulatory T cells.

Advances in the biology of chronic GVHD

ACID-SPHINGOMYLENASE-DEFICIENCY-NIEMANN-PICK

RARE-DISEASE

What is ASMD?

This video explains the different types of the disease, its causes and its symptoms.

<h2>Are you interested in knowing more about this topic?</h2>

<h2>The clinical objective in PN is to relieve intense itch and heal nodular lesions, which may improve patients’ QoL2-4</h2>

<h2>A multimodal treatment approach is recommended for PN by a US consensus panel2,</h2>
Treatment is selected based on a patient’s clinical presentation, comorbidities, and response to prior treatments and should address both neural and immunologic components of disease, which often requires use of multiple therapeutic agents2,5
<ol>
 <li>Mainly topical therapies</li>
 <li>Widespread skin-directed or systemic therapies</li>
 <li>Experimental therapies</li>
</ol>

There remains an unmet need in the management of PN1

References

There is significant unmet need in the management of PN¹

PRURIGO-NODULARIS

DERMATOLOGY

<h2>PN is characterized by the following:</h2>
<ul>
 <li>Chronic pruritus1,2
 <ul>
 <li>Pruritus lasting ≥6 weeks is required for a diagnosis2</li>
 <li>Most patients (&gt;80%) have pruritus for &gt;6 months and over half of patients experience pruritus for &gt;2 years3</li>
 <li>PN is regarded as having the highest itch intensity among the many diverse&nbsp;types of chronic pruritus4-6</li>
 <li>The most burdensome symptom as rated by patients with PN is itch3&nbsp;</li>
 </ul></li>
</ul>
<ul>
 <li>Presence of multiple, firm, pruriginous lesions1,2,b
 <ul>
 <li>Visibility of skin lesions and bleeding of skin lesions are the second and third most burdensome symptoms as rated by patients3,b 
 &nbsp;</li>
 </ul></li>
 <li>History and/or evidence of repeated scratching, picking, or rubbing (eg, excoriations and scars)2</li>
</ul>

<h2>PN negatively affects many aspects of patients’ quality of life, including7,8:</h2>
<ul>
 <li>
 <h3>Sleep9,c</h3>
 <ul>
 <li>
 Pruritus is often worse in the evening or at night</li>
 <li>Over 60% of patients with PN report that itching disturbs their sleep “to a great extent” 
 &nbsp;</li>
 </ul></li>
 <li>
 <h3>Mental health7,10,11</h3>
 <ul>
 <li>Patients with PN are more likely to have depression or anxiety compared with healthy individuals 
 &nbsp;</li>
 </ul></li>
 <li>
 <h3>Activities of daily living12,d</h3>
 <ul>
 <li>Over 50% of patients report that their everyday life is affected by PN 
 &nbsp;</li>
 </ul></li>
 <li>
 <h3>Social interactions12,d</h3>
 <ul>
 <li>38% of patients report that itch affects their interactions with others</li>
 </ul></li>
</ul>

<h2>PN may be associated with the following comorbidities2,8:</h2>
<ul>
 <li>Chronic conditions eg, Chronic kidney disease</li>
 <li>Dermatological conditions eg, Atopic dermatitis</li>
 <li>Infections eg, HIV</li>
 <li>Psychiatric conditions eg, Depression</li>
</ul>

<h2>PN can arise as a distinct disease in the absence of any of the comorbidities above</h2>
The debilitating signs and symptoms of PN result in significantly reduced quality of life, including negatively impacting sleep, mental health, activities of daily living, and social interactions. In addition, PN may also be associated with a range of comorbidities8

Prurigo Nodularis is a distinct, Chronic, Neural and Immune- Mediated skin disease characterized by intense itch and Nodular Lesions¹

PN Expert Interview Series with Dr. Shawn Kwatra

PN Expert interview with Dr. Shawn Kwatra about his perspective on aspects of PN

MUCOPOLYSACCHARIDOSIS-MPS

MPSI – Rheumatology Case Study

By simulating a real-life Scenario this case study developed to increase the awareness of MPS I, by highlighting familiar symptoms that suggest the possibility of an unfamiliar underlying metabolic disease for Rheumatologist specialty.

<h2>Are you interested in knowing more about this topic?</h2>

MPSI – ENT Case Study

By simulating a real-life Scenario this case study developed to increase the awareness of MPS I, by highlighting familiar symptoms that suggest the possibility of an unfamiliar underlying metabolic disease for ENT specialty.

MPSI – Endocrinology Case Study

By simulating a real-life Scenario this case study developed to increase the awareness of MPS I, by highlighting familiar symptoms that suggest the possibility of an unfamiliar underlying metabolic disease for Endocrinologist specialty.

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The ADCT gives a measure of how controlled the eczema is. Answer these 6 simple questions with your patient to find the ADCT score. It will indicate proper course of action.

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