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Abstract

Pegylated interferons alfa are increasingly used in patients with myeloproliferative neoplasms (MPN) due to their potential disease-modifying effect. Ropeginterferon alfa-2b has been approved for patients with polycythemia vera (PV) with no symptomatic splenomegaly as first-line cytoreductive therapy, based on the results of the PROUD-PV/CONTINUATION-PV studies, documenting significantly higher rates of complete hematologic response (CHR) compared with hydroxyurea from 2-year timepoint onward. Although safety profile of pegylated interferons is overall good, interferon-related toxicities can occur. Focus of this article is on interferon-mediated autoimmune diseases. We describe two patients with PV treated with pegylated interferons alfa, one patient developed a cutaneous, paranasal sarcoidosis without any systemic symptoms and was successfully treated with topical steroids. The other patient developed widespread psoriatric skin lesions, which were treated with moderate effect with topical therapy with calcipotriene and betamethasone dipropionate foam, antidry calm lotion and in the course of the disease with ultraviolet light therapy (UVB). Only with methotrexate she achieved a nearly complete remission of the psoriasis. In both patients pegylated interferon was continued in view of the CHR and therefore the beneficial effect on MPN. We review the pertinent literature on the management of interferon-mediated autoimmune diseases in patients with MPN. As there is little published evidence on that topic, we propose multidisciplinary clinical practice recommendations based on available evidence and clinical experience in the management of patients with MPN treated with pegylated interferon alfa.

Keywords

autoimmune diseases case report myeloproliferative neoplasms pegylated interferons polycythemia vera

Case report

Relevant Equator guidelines were followed using the CARE checklist when writing our report (Supplemental Material).

Case report 1

In March 2018 a 47-year-old lady was diagnosed with polycythemia vera (PV) according to the WHO classification 2016. Main symptoms were headaches and aquagenic pruritus. Physical examination revealed no palpable splenomegaly, and there was no splenomegaly on abdominal ultrasonography. She was treated with acetylsalicylic acid (ASA) and phlebotomy, which was poorly tolerated and lead to the development of symptomatic latent iron deficiency with tiredness, fatigue, and restless legs. Due to the symptoms, and although this was a low-risk disease, she was treated with pegylated interferon. Before treatment start, functional status of the thyroid gland and transaminases were within normal limits. The patient initially received Peginterferon alfa-2a in a dose of 135 µg weekly subcutaneously (s.c.). She achieved a complete hematologic response (CHR) without the necessity of phlebotomy despite intravenous iron supplementation and her symptoms disappeared with a consequently marked improvement of her quality of life. Therefore, dose reduction since December 2022 was possible, with a present dose of 135 µg of Peginterferon alfa-2a monthly. In January 2024, however, she developed a cutaneous, paranasal sarcoidosis without any systemic symptoms. The clinical, laboratory, and imaging work-up of the patient could exclude involvement of the eyes, lung, and heart, and there was no palpable lymphadenopathy. Topical steroids were applied with good effect, and treatment with Peginterferon alfa-2a will be continued with close follow-up (FU) by all involved specialists, as long as there is no evidence of restriction of organ function.

Case report 2

A 59-year-old female, who was complaining of dizziness, tinnitus, and aquagenic pruritus, was diagnosed with PV according to the WHO classification 2016 in April 2021. There was no palpable spleen on physical examination, which was also otherwise uneventful. The family history revealed that her mother had suffered from a myelodysplastic neoplasm with 5q deletion, which was successfully treated with lenalidomide. The patient was initially treated with ASA and phlebotomy as risk stratification revealed a low-risk situation. With the age of 60 years and the presence of cardiovascular risk factors such as arterial hypertension and hypercholesterolemia, discussion of cytoreductive therapy became necessary in view of the transformation into a high-risk situation. Before starting the patient on Ropeginterferon alfa-2b (ropegIFNα-2b) 125 µg every 2 weeks s.c. very scarce psoriatric skin lesions at both elbows were noted. There was no evidence for arthritis. The autoimmune panel including antinuclear antibodies (ANA), anti-ds-DNA-antibodies, and rheumatoid factor was normal, as were the functional status of the thyroid gland and the transaminases. Two months after commencing therapy with ropegIFNα-2b psoriatric skin lesions became widespread involving mainly upper and lower extremities. The patient was seen by a dermatologist, who installed topical therapy with calcipotriene and betamethasone dipropionate foam (Enstilar^®) together with an antidry calm lotion. This therapy improved the psoriatric plaques considerably, but they remained bothersome for the patient. In view of a CHR of PV without need of phlebotomy it was decided to continue with the interferon (IFN)-treatment and to accelerate the treatment of psoriasis. After the psoriatric plaques remained unchanged with ultraviolet light therapy, she is treated with methotrexate since July 2024, presently 12.5 mg/week, with a nearly complete remission of the psoriasis.

Review of the literature and multidisciplinary clinical practice recommendations

IFN, and especially the two available pegylated interferons alfa, Peginterferon alfa-2a and ropegIFNα-2b, is increasingly used in patients with myeloproliferative neoplasms (MPN).¹ RopegIFNα-2b has been approved for patients with PV with no symptomatic splenomegaly as first-line cytoreductive therapy, based on the results of the PROUD-PV/CONTINUATION-PV studies, documenting significantly higher rates of CHR compared with hydroxyurea from 2-year timepoint onward.^2,3 There was also a superior molecular response, with about 20% of patients treated with ropegIFNα2b achieved a JAK2^V617F variant allele frequency of <1% at 6 years.⁴ There is evidence that even in low-risk patients with PV fixed dose of ropegIFNα-2b is beneficial in terms of maintaining hematocrit values on target of 45% or lower without progressive disease compared to phlebotomy alone.⁵

Although safety profile of pegylated interferons alfa is overall good, IFN-related toxicities can occur, however, etiology of toxicities is variable. Next to mood depression (where there is no dose dependency of IFN), these are especially flu-like symptoms, neurological diseases (e.g., polyneuropathy, motoric neuropathy (an absolute contraindication for IFN), vasculitis in the brain), cardiovascular diseases (e.g., atrial fibrillation, myocardial infarction, cardiomyopathy or ischemic heart disease), respiratory diseases (e.g., pneumonitis, lung infiltration, pulmonary arterial hypertension), and rare visual diseases (e.g., retinal bleeding, retinal exudates, retinopathy, vascular occlusions, or retinal detachment).^2,3

Although MPN themselves are related to autoimmune diseases, the focus of this article is on common IFN-related autoimmune diseases. It is important to establish (1) clinical and laboratory screening parameters before start of IFN-treatment, (2) frequency and kind of laboratory parameters during IFN-treatment, and (3) management strategies in case of evidence of IFN-related autoimmune diseases. Table 1 summarizes clinical evaluation and laboratory screening parameters before start of IFN-treatment. Table 2 contains frequency of clinical evaluation and analysis of laboratory parameters during treatment with IFNα.

Table 1.

Clinical evaluation and laboratory screening parameters before start of treatment with IFNα in patients with MPN. Traffic light scheme.

Laboratory screening parameters and clinical evaluation
Laboratory screening parameters and clinical evaluation	Go—Treat	Warning—Treat with more frequent follow-up (2 months)	Stop—Do not treat. Patient needs specialist assessment
Autoimmunity screening
Antinuclear antibodies	Absent	Present and without clinical correlate	Present or clinical correlate → Referral to rheumatologist
Anti-ds-DNA-antibodies	Absent	Present and without clinical correlate	Present or clinical correlate → Referral to rheumatologist
Rheumatoid factor	Absent	Present and without clinical correlate	Present or clinical correlate → Referral to rheumatologist
Thyroid
Thyroid stimulating hormone	Normal	Elevated or suppressed	Elevated or suppressed → Referral to endocrinologist
Free T4	Normal	Normal	Elevated or suppressed → Referral to endocrinologist
Thyroid peroxidase antibodies	Absent	—	Present → Referral to endocrinologist
Thyroglobulin (Tg) antibodies	Absent	—	Present → Referral to endocrinologist
Liver
Transaminases	Normal	—	Elevated → Referral to hepatologist
Antiphospholipid antibodies
Lupus anticoagulant	Absent	Low titer and without clinical correlate	Intermediate/high titer or clinical correlate → Referral to specialist
Anticardiolipin antibodies IgM and IgG	Absent	Low titer and without clinical correlate	Intermediate/high titer or clinical correlate → Referral to specialist
Anti-β2-glycoprotein antibodies IgM and IgG	Absent	Low titer and without clinical correlate	Intermediate/high titer or clinical correlate → Referral to specialist
Renal
Glomerular filtration rate (ml/min/1.73 m²)	>60	45–60	<45 → Referral to nephrologist
Hematuria	Absent	—	Present → Referral to nephrologist
Albuminuria	Absent	—	Present → Referral to nephrologist
Clinical
History of psychiatric disease	Absent	—	Present → Referral to psychiatrist
History of cardiovascular disease	Absent	—	Present → Referral to cardiologist
History of eye disease	Absent	—	Present → Referral to ophthalmologist
Psoriasis	Absent	Scarce skin lesions without evidence of arthritis	Widespread skin lesions or evidence of arthritis → Referral to dermatologist

IFN, interferon; Ig, immunoglobulin; MPN, myeloproliferative neoplasms.

Table 2.

Frequency of clinical evaluation and of laboratory analyses during treatment with IFNα in patients with MPN and management consequences.

Laboratory analyses and clinical evaluation	Frequency of analysis	Management consequences
Rheumatological diseases
Anti-SSA(Ro)/SSB(La)-antibodies	If clinical suspicion is suggestive of Sjögren syndrome	Referral to rheumatologist. Stop IFNα
Antinuclear antibodies	If clinical suspicion is suggestive of rheumatological disease	Referral to rheumatologist. Stop IFNα
Anti-ds-DNA-antibodies	If clinical suspicion is suggestive of rheumatological disease	Referral to rheumatologist. Stop IFNα
Rheumatoid factor	If clinical suspicion is suggestive of rheumatological disease	Referral to rheumatologist. Stop IFNα
Thyroid
Thyroid stimulating hormone	Every 3–6 months	Referral to endocrinologist if elevated or suppressed with elevated or suppressed free T4
Free T4	Every 3–6 months	Referral to endocrinologist if elevated or suppressed
Liver
Transaminases	Every 3–6 months	Referral to hepatologist if >5 × the ULN despite dose decrease. Stop IFNα
Diabetes mellitus
Fasting blood glucose	Every 6–12 months	Referral to endocrinologist if >7 mmol/l. Stop IFNα
HbA1c	Every 6–12 months	Referral to endocrinologist if >6.5%. Stop IFNα
Renal
GFR (ml/min/1.73 m²) and albumin-creatinine ratio in spot urine	Every 3–6 months	Referral to nephrologist if progressive decline of GFR ± new hematuria, proteinuria, nephritic/nephrotic syndrome, arterial hypertension. Stop IFNα
Diabetes mellitus
Fasting blood glucose	Every 6–12 months	Referral to endocrinologist if >7 mmol/l. Stop IFNα
HbA1c	Every 6–12 months	Referral to endocrinologist if >6.5%. Stop IFNα
Sarcoidosis
Angiotensin converting enzyme	If clinical suspicion is suggestive	Referral to specialist. Stop IFNα only if restriction of organ function
Calcium in blood and urine	If clinical suspicion is suggestive	Referral to specialist. Stop IFNα only if restriction of organ function
C-Reactive Protein, Erythrocyte Sedimentation Rate, soluble interleukin-2 receptor	If clinical suspicion is suggestive	Referral to specialist. Stop IFNα only if restriction of organ function
Antiphospholipid antibodies
Lupus anticoagulant	If clinical suspicion is suggestive of rheumatological disease or thromboembolic event	Referral to specialist. Stop IFNα in case of rheumatological disease. Anticoagulation in case of thromboembolic event
Anticardiolipin antibodies IgM and IgG	If clinical suspicion is suggestive of rheumatological disease or thromboembolic event	Referral to specialist. Stop IFNα in case of rheumatological disease. Anticoagulation in case of thromboembolic event
Anti-β2-glycoprotein antibodies IgM and IgG	If clinical suspicion is suggestive of rheumatological disease or thromboembolic event	Referral to specialist. Stop IFNα in case of rheumatological disease. Anticoagulation in case of thromboembolic event
Psoriasis
Clinical evaluation	Each FU visit	Referral to dermatologist if widespread skin lesions or evidence of arthritis

FU, follow-up; GFR, glomerular filtration rate; IFN, interferon; Ig, immunoglobulin; MPN, myeloproliferative neoplasms.

Psoriasis

A common autoimmune-mediated side effect of IFN-treatment is psoriasis (⩾1/100, <1/10). If there are scarce skin lesions without evidence for arthritis before IFN-treatment, IFN can still be used, although the risk of exacerbation of existing plaques is increased. IFNα can trigger a dysregulated immune response of the skin in genetically susceptible patients with abnormal proliferation and differentiation of keratinocytes resulting in epidermal hyperplasia.⁶ Withdrawing IFN in such cases has to be discussed in a multidisciplinary approach weighing benefits and risks of IFN-treatment, especially if treatment of psoriasis with topical (steroids, vitamin D, Tacrolimus/Pimecrolimus) or systemic drugs (Methotrexat, Ciclosporin, small molecules (Apremilast) or biologics (Adalimumab, Etanercept, Infliximab, and others)) is beneficial.

Rheumatological diseases

Rheumatological autoimmune diseases, such as myositis, rheumatoid arthritis, Sjögren syndrome, systemic lupus erythromatosus, and systemic sclerosis, are associated with activation of IFN-pathway. Therefore, patients with preexisting rheumatological autoimmune diseases may experience an exacerbation during IFN-therapy. Also, de novo rheumatological autoimmune diseases may develop during IFN-therapy, and Sjögren syndrome commonly occurs with IFN-treatment. In these cases, a clinical assessment with analysis of relevant antibodies is necessary. Additionally, a multidisciplinary discussion is advisable with consideration to stop IFN-treatment and/or to start treatment with corticosteroids and/or disease-modifying anti-rheumatic drugs.⁷

Thyroid

Interferon-induced thyroid (IIT) disease is common in IFN-treated patients. IIT can be classified into autoimmune IIT, with development of thyroid autoantibodies without clinical disease, Hashimoto’s thyroiditis and Graves’ disease (GD), and non-autoimmune IIT, with destructive thyroiditis and nonautoimmune hypothyroidism.⁸

Before starting IFN-treatment, functional status of the thyroid gland has to be assessed. In the presence of autoantibodies, the risk of development of an autoimmune thyroid disease (especially Hashimoto’s thyroiditis) is—next to female sex—increased, and more than half of patients will develop thyroid disease. The negative predictive value of the existence of such autoantibodies pre-treatment is with >90% clinically relevant. Presence of those autoantibodies without thyroid dysfunction should not be regarded as cause for not commencing IFN-treatment, but frequency of clinical and laboratory FU must be increased. Autoantibodies may develop during IFN-treatment in patients who were antibody-negative before IFN-therapy.

The most common cause of IIT during IFN-therapy is autoimmune thyroiditis similar to Hashimoto’s thyroiditis leading to hypothyroidism. Thyroid peroxidase (TPO) antibodies and thyroglobulin antibodies are usually positive. Hypothyroidism can be divided into subclinical (thyroid stimulating hormone (TSH) elevated and fT4 normal) and manifest (TSH elevated and fT4 reduced) hypothyroidism. Treatment with levothyroxine is indicated in manifest hypothyroidism and should be evaluated in subclinical hypothyroidism, especially in patients with TSH-values >7mU/l, increasing TSH-values and high anti-TPO-antibody titers. As stopping of IFN-treatment often does not result in a resolution of hypothyroidism and patients will need levothyroxine supplementation, IFN-treatment can safely be continued.

Hyperthyroidism, however, in IFN-treated patients is unusual. It can mostly be caused by destructive thyroiditis or infrequently by GD.

Destructive thyroiditis is a nonautoimmune mediated and self-limiting occurring inflammatory disorder. It leads to an initial phase of hyperthyroidism by leakage of stored thyroid hormones into the circulation, followed by a phase of hypothyroidism and restoration of normal thyroid function at last. Typically, TSH receptor antibodies (TRAb) are negative, and there is a zero to low tracer uptake on thyroid scintigraphy (Sodium-^99mTechnetium-Pertechnetate or ¹²³Iodine). Treatment is symptomatic (beta blocker). Thyreostatic drugs, such as carbimazole or methimazole, are ineffective. Once inflammation has healed and a euthyroid state is present, IFN can be re-commenced.⁹

GD as an autoimmune IIT presents with the pathognomonic feature of positive TRAb and is less frequent. Diffuse goiter can be present, whereas concomitant endocrine orbitopathy seems rare. Scintigraphy demonstrates diffuse enhanced uptake throughout the thyroid gland. Stopping IFN is necessary in clinically manifest hyperthyroidism. Treatment with carbimazole or methimazole and a beta blocker is indicated, a long-term and low-dose thyreostatic treatment seems to be efficient and safe.¹⁰ In case of an euthyroid state without the need for drugs and absence of TRAb, if TRAb were previously detected, a multidisciplinary discussion about advantages and disadvantages of IFN-treatment is indicated, taking the hematologic and molecular remission status into account.

Liver

IFN is contraindicated in patients with autoimmune hepatitis or decompensated cirrhosis. Therefore, before starting IFN-treatment, transaminases should be checked and in case of any elevation patients should be investigated for the presence of autoimmune hepatitis or be referred to a hepatologist. Laboratory analyses include ANA, anti-smooth muscle antibodies, anti-liver-kidney microsomal antibodies, antisoluble liver antigen antibodies, and immunoglobulin G.

During IFN-treatment mild elevated transaminases are common and are generally not due to autoimmunity. If transaminases are ⩽3 × the upper limit of normal (ULN), IFN can usually be continued. If the elevation is 3–5 × the ULN, dose of IFN needs to be decreased by 50%. If, despite dose decrease, transaminases continue to raise, IFN should be stopped and transaminases should be monitored. Immunosuppressive therapy is considered in case of persistently elevated transaminases.¹¹

Diabetes mellitus

In patients with type-1-diabetes mellitus treated with insulin IFN can be used in collaboration with an endocrinologist. However, IFN-related de novo onset of diabetes mellitus can occasionally occur (⩾1/1000, <1/100), but can have a fulminant course with ketoacidosis and is irreversible after long periods of IFN-treatment.¹²

Sarcoidosis

Sarcoidosis is an inflammatory disorder and can occasionally occur during IFN-therapy. Abnormal collections of granulomas can form nodules in any organ, affecting most often lung and lymph nodes. Symptoms are unspecific with fever, painful nodules (erythema nodosum), cough and/or dyspnea, and swelling of lymph nodes.¹³ If there is a functionally restriction of any organ function, IFN-therapy has to be stopped. If this is not the case, and therapy of sarcoidosis is not necessary or can be done with topical steroids only, IFN can be continued with close regular FU of the patient.

Antiphospholipid antibodies

There is no evidence that IFN-therapy can cause a primary antiphospholipid syndrome. However, analysis of lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein antibodies as risk factors for thrombosis is therefore only necessary if an underlying rheumatological disease, most commonly SLE, is suspected, or a thromboembolic event, most commonly a venous thrombosis of the lower limbs (venous site) or a stroke (arterial site), has occurred. Low titer (>95th and <99th percentile) antiphospholipid antibodies without a clinical correlate is not a reason for not starting IFN-treatment, but more frequent clinical and laboratory FU is advisable. If antiphospholipid antibodies have intermediate or high titers and have a clinical correlate with a rheumatological disease, IFN-treatment has to be stopped. Anticoagulation should be started in case of a thromboembolic event, in this situation IFN-treatment can be continued.¹⁴

Renal

Before start of IFN-treatment, glomerular filtration rate (GFR) has to be calculated and hematuria/albuminuria have to be excluded. If GFR is<45 ml/min/1.73 m² a nephrologist should be consulted. The development of autoimmune glomerulonephritis (GN) is rare. If during IFN-treatment a relevant decline of GFR, hematuria, proteinuria, nephritic/nephrotic syndrome, or newly occurring arterial hypertension is documented the patient has to be referred to a nephrologist and therapy with IFN has to be stopped. After a renal biopsy, therapy of autoimmune GN is dependent on the risk and type.¹⁵

Multidisciplinary clinical practice recommendations will not be a substitute for the generation of evidence. In this respect, this might be a limitation of these recommendations. However, hematologists are confronted with autoimmune-related disorders during treatment with pegylated IFNα for MPN in daily clinical practice and have to manage those patients despite scarce evidence.

Conclusion

Although pegylated IFNα-treatment in patients with MPN induces high rates of CHR and molecular responses and is therefore increasingly used in clinical practice, IFN-mediated autoimmune diseases can occur, either exacerbating preexisting or inducing new autoimmune phenomena. Before starting a patient on pegylated IFNα-treatment it is therefore important to take a comprehensive personal and familial medical history and to perform a thorough physical examination. There is, however, little evidence on the management of those autoimmune diseases developing during pegylated IFN-α-treatment. And although our multidisciplinary proposal is not a substitute for evidence-based recommendations it might presently still be the basis for the management of such MPN-patients with a suggestion of clinical evaluation and laboratory parameters before and during pegylated IFNα-treatment. Knowledge on diagnostic and therapeutic approaches of IFN-related autoimmune phenomena in patients with MPN is essential to optimize treatment outcome.

Supplemental Material

sj-docx-1-tah-10.1177_20406207251338942 – Supplemental material for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations

Supplemental material, sj-docx-1-tah-10.1177_20406207251338942 for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations by Axel Rüfer, Christoph Brand, Andrea de Gottardi, Stefan Fischli, Ralph Melzer, Urs Odermatt, Walter A. Wuillemin and Sacha S. Zeerleder in Therapeutic Advances in Hematology

Supplemental Material

sj-docx-2-tah-10.1177_20406207251338942 – Supplemental material for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations

Supplemental material, sj-docx-2-tah-10.1177_20406207251338942 for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations by Axel Rüfer, Christoph Brand, Andrea de Gottardi, Stefan Fischli, Ralph Melzer, Urs Odermatt, Walter A. Wuillemin and Sacha S. Zeerleder in Therapeutic Advances in Hematology

Footnotes

Acknowledgements

We would like to thank the two patients described in the case reports allowing us to report their case, stimulating us to write the manuscript, and propose multidisciplinary clinical practice recommendations after reviewing the available literature.

Correction (June 2025):

Article has been updated to remove the phrase “in the middle of the column” from the headings of Tables 1 and 2. This correction addresses the errors that were introduced during the publication process.

Declarations

ORCID iDs

Axel Rüfer

Urs Odermatt

Supplemental material

Supplemental material for this article is available online.

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Supplementary Material

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Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report,review of the literature and multidisciplinary clinical practice recommendations

Abstract

Keywords

Case report

Case report 1

Case report 2

Review of the literature and multidisciplinary clinical practice recommendations

Psoriasis

Rheumatological diseases

Thyroid

Liver

Diabetes mellitus

Sarcoidosis

Antiphospholipid antibodies

Renal

Conclusion

Supplemental Material

sj-docx-1-tah-10.1177_20406207251338942 – Supplemental material for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations

Supplemental Material

sj-docx-2-tah-10.1177_20406207251338942 – Supplemental material for Management of common autoimmune diseases in patients with myeloproliferative neoplasms treated with pegylated interferon alfa—case report, review of the literature and multidisciplinary clinical practice recommendations

Footnotes

Acknowledgements

Correction (June 2025):

Declarations

ORCID iDs

Supplemental material

References

Supplementary Material