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Abstract

Clinical Neuropathology, Vol. 45 – No. 4/2026 (130-136)

Human bornavirus encephalitis: Neuropathological insights from a rare but lethal disease

Nicola Jungbäck¹#², Przemyslaw Grochowski², Patrick Adam³#⁴, Anja Osterloh¹, and Friederike Liesche-Starnecker¹

¹Institute of Neuropathology, Ulm University Hospital, Faculty of Medicine, Ulm University, Ulm, ²Pathology, Medical Faculty, University of Augsburg, ³Pathology, Ingolstadt, and ⁴Institute of Pathology, School of Medicine and Health, Technical University of Munich, Germany
Aims: This work aims at supporting structured neuropathological assessment and early case identification for human bornavirus encephalitis. It summarizes current neuropathological and immunopathogenic findings of infection with Borna disease virus 1 (BoDV-1) in humans, complemented by comparative data from animal dead-end hosts.
Materials and methods: This narrative review is based on a targeted literature search in PubMed and Google Scholar. Of 114 identified records (PubMed: 62; Google Scholar: 52), 40 remained after duplicate removal. Following abstract and full-text screening, 16 studies, published between 1999 and 2025, were included.
Results: BoDV-1 encephalitis displays a largely uniform histopathological pattern, typically presenting as lymphocytic, sclerosing panencephalomyelitis with astroglial and microglial activation, and detection of intranuclear inclusions. In animals olfactory and limbic structures are predominantly affected, whereas in humans, the disease frequently extends to additional regions, particularly the basal ganglia.
Conclusion: In both human and animal dead-end hosts, BoDV-1 encephalitis shows a consistent histomorphological profile that allows reliable recognition based on characteristic neuropathological features and distribution. Definitive diagnosis requires specific detection of BoDV-1, most commonly facilitated by immunohistochemistry.Correspondence to:
Univ.-Prof. Dr. med. Friederike Liesche-Starnecker
Institute of Neuropathology
Ulm University Hospital, Medical Faculty
Ulm University
Albert-Einstein-Allee 23, 89081 Ulm, Germany
Email: [email protected]

Abstract

Eiji Kose¹,², Mizuki Kawashima³, and Toshimi Kimura¹,²

¹Graduate School of Pharmacy and Pharmaceutical Science, ²Laboratory of Clinical Pharmacology, Faculty of Pharmacy, and ³Department of Pharmacy, Teikyo University School of Medicine University Hospital, Tokyo, Japan
Objectives: To investigate differences in drug-induced dysphagia profiles among causative drugs, with a focus on reporting risk, patient age, and time to onset. Background: Drug-induced dysphagia is one of several causes of dysphagia. However, its detailed profile, including differences among drugs and age groups, has not yet been thoroughly examined. Materials and methods: Data were obtained from the Japanese Adverse Drug Event Report Database. Reports submitted between April 2004 and October 2021 were analyzed. The 10 drugs with the highest number of reports of drug-induced dysphagia were selected as the target drugs. Reporting odds ratios were calculated to evaluate the association between each drug and dysphagia. The primary endpoint was the reporting odds ratio, while age distribution and time to onset were secondary outcomes. Results: A total of 756,965 reports were analyzed. All target drugs were associated with drug-induced dysphagia. Cevimeline was identified as a novel finding because dysphagia was not observed during clinical trials. For most drugs, dysphagia occurred within approximately 25 days of administration. In contrast, paroxetine and milnacipran were associated with dysphagia even after long-term use. The age distribution of reported cases differed by drug, suggesting drug-specific differences in susceptible age groups. Conclusion: Drug-induced dysphagia profiles differ among drugs, particularly in terms of timing of onset and patient age distribution. Therefore, clinicians should consider both the causative drug and the patient’s age when monitoring for dysphagia. Correspondence to:
Eiji Kose, Pharm PhD, Graduate School of Pharmacy and Pharmaceutical Science/Faculty of Pharmacy, Laboratory of Clinical Pharmacology, Juntendo University, 6-8-1 Hinode, Urayasu City, Chiba 279-0013, Japan
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 64 – No. 10/2026 (555-558)

Acquired apparent mineralocorticoid excess induced by compound glycyrrhizin tablets: A case report and literature review 

Yu Li¹#², Juan Du¹, and Guojie Ma²

¹Institute of Pharmaceutical Research and School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, and ²Department of Pharmacy,Anyang Third People’s Hospital, Anyang, China
Compound glycyrrhizin tablets, derived from licorice root, are widely used for their anti-inflammatory and hepatoprotective properties. However, their active metabolite, glycyrrhetinic acid, can induce acquired apparent mineralocorticoid excess (AME) – a clinical syndrome where cortisol abnormally activates mineralocorticoid receptors due to the inhibition of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), mimicking primary aldosteronism. We report a case of a 57-year-old male who developed severe hypertension and hypokalemia after 30 days of treatment with compound glycyrrhizin (150 mg, t.i.d.). Laboratory investigations revealed profound hypokalemia (2.03 mmol/L) and metabolic alkalosis. Critically, both plasma renin activity (< 0.5 μIU/mL) and aldosterone levels (2.4 – 2.7 ng/dL) were significantly suppressed, effectively ruling out primary and secondary hyperaldosteronism. A diagnosis of acquired AME was established based on the temporal relationship with glycyrrhizin intake, the “double-low” hormonal profile, and the exclusion of Cushing’s syndrome. Following treatment with amlodipine and potassium supplementation, the patient’s symptoms resolved. At the 2-week post-discharge follow-up, after discontinuing all medications, his blood pressure remained stable (< 140/90 mmHg) and serum potassium normalized to 4.55 mmol/L, confirming the reversible nature of acquired AME.Correspondence to:
Du Juan, Associate Professor
Institute of Pharmaceutical Research and School of Pharmaceutical Sciences
Zhengzhou University
Zhengzhou 450001, China
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 64 – No. 10/2026 (526-536)

Predictors of early discontinuation and therapeutic response to anamorelin in patients with cancer cachexia: A retrospective study 

Katsuyuki Takahashi¹, Minami Abe¹, Hirotake Yamase², Hideki Yoshino², Kayo Tsujii², Yuika Komatsu¹, Toru Otori¹, and Masahiko Kobayashi²

¹Division of Social Pharmacy, Faculty of Pharmacy, Kindai University, and ²Department of Pharmacy, Japanese Red Cross Osaka Hospital, Osaka, Japan
Objective: Cancer cachexia is associated with poor tolerance to anticancer therapies and reduced survival rates. Anamorelin, a ghrelin receptor agonist, has been introduced for the management of cachexia; however, early discontinuation and variable therapeutic responses are frequently observed in clinical practice. We aimed to identify the real-world predictors of early discontinuation and therapeutic response to anamorelin.
Materials and methods: We conducted a retrospective cohort study of 90 patients with cancer cachexia who received anamorelin therapy. Early discontinuation was defined as the cessation of treatment within 3 weeks. Therapeutic response was evaluated using changes in the modified Glasgow Prognostic Score (mGPS) in patients who continued treatment and had evaluable laboratory data. Nutritional and inflammatory indices, including the prognostic nutritional index (PNI), were assessed. Multivariate logistic regression analyses were performed to identify independent predictors.
Results: 43 (47.8%) patients discontinued anamorelin treatment within 3 weeks. Multivariate analysis showed that high baseline white blood cell count, low baseline PNI, and gastrointestinal tumor type were independently associated with early discontinuation. Among 38 evaluable patients in the continuation group, 14 (36.8%) demonstrated improvement or stabilization of the mGPS. A high baseline PNI and the absence of concomitant nonsteroidal anti-inflammatory drug use were independently associated with a therapeutic response.
Conclusion: Baseline nutritional and inflammatory statuses strongly influence both treatment continuation and response to anamorelin. The PNI is a practical predictor for identifying patients who are likely to benefit from therapy. Early intervention before severe nutritional deterioration may optimize the outcomes of patients with cancer cachexia.Correspondence to:
Katsuyuki Takahashi, PhD
Division of Social Pharmacy, Faculty of Pharmacy
Kindai University Osaka
3-4-1 Kowakae Higashi-Osaka,
Osaka, 577-8502, Japan
Email: [email protected]

Abstract

International Journal of Clinical Pharmacology and Therapeutics, Vol. 64 – No. 10/2026 (537-547)

Safety profile of sintilimab and establishment of a risk prediction model based on medical records of 337 cases 

Chengting Rong¹*, Hong Zhang²*, Ling Hu¹, Yingning Li¹, Jianjuan Xin¹, and Xinan Wu¹

¹Department of Pharmacy, Hefei BOE Hospital, Anhui, Hefei, and ²Department of Pharmacy, Fuyang People’s Hospital, Anhui, Fuyang, China
Objective: To retrospectively analyze the clinical safety and adverse drug reactions (ADRs) of sintilimab, to evaluate risk factors for ADR occurrence, and to develop a predictive model to support individualized treatment strategies.
Materials and methods: Medical records of patients who received sintilimab treatment in the period January 2021 to December 2022 were examined. Clinical data, including demographic characteristics, medication details, and ADRs were recorded and evaluated using univariate and multivariate logistic regression analyses to identify independent risk factors for sintilimab-induced ADRs. Variables such as gender, age, comorbidities, and treatment regimens were included. Receiver operating characteristic (ROC) curve analysis was performed to assess the predictive accuracy of individual and combined risk factors, enabling the safety profile of sintilimab to be established.
Results: A total of 337 cases were retrieved of which 208 (61.72%) referred to patients who experienced ADRs. Multivariate analysis identified combination drug therapy (OR = 25.670, 95% CI: 11.319 – 58.218, p < 0.001) and pretreatment baseline assessment (OR = 0.388, 95% CI: 0.191 – 0.789, p = 0.009) as two independent risk factors. The logistic model indicated that the combined prediction ability of these factors gave an area under the curve (AUC) of 0.800 (p < 0.001), which indicated prediction superiority compared to using the factors alone. Cross-validation using 115 cases demonstrated an accuracy of ~ 80.87% for the model.
Conclusion: Combination therapy and pretreatment baseline assessment are independent risk factors for ADRs occurring during therapy with sintilimab. The combined predictive model derived shows high accuracy and may have value in predicting treatment risks and managing personalized medication.

*Co-first authors.Correspondence to:
Xinan Wu
Department of Pharmacy
Hefei BOE Hospital Co., Ltd., China
Anhui, Hefei 230013, China
Email: [email protected]

Abstract

Trace Elements and Electrolytes, Vol. 43 – No. 3/2026 (97-106)

Sodium and mineral contents of solids and broth in ready-to-cook products: To eat the broth or not?

Minseo Choi*, Su-Ryeon Han*, Jihye Hong, and Mi-Kyeong Choi

Department of Food and Nutrition, Kongju National University, Yesan, Korea
Objective: Limiting broth consumption is commonly recommended to reduce sodium intake; however, this practice may also decrease the intake of essential minerals. This study aimed to investigate the sodium and mineral contents of solids and broth in ready-to-cook products and to propose dietary guidelines for soup-based processed foods that balance sodium reduction with the maintenance of mineral intake.
Materials and methods: A total of 1,449 soup-based products were surveyed on the basis of data from the Korean Ministry of Food and Drug Safety processed food database. Five representative products from each category – packaged instant noodles, cup noodles, and cup rice soup – were selected and cooked according to the package instructions. Sodium and 13 mineral contents in the broth and solids were analyzed using inductively coupled plasma mass spectrometry.
Results: The average serving sizes of packaged instant noodles, cup noodles, and cup rice soup were 191.44, 183.24, and 247.42 g, respectively (p < 0.001). The corresponding energy contents were 381.96, 448.05, and 331.51 kcal per serving, respectively, while the sodium contents were 1,696.23, 1,672.63, and 1,323.74 mg, respectively (p < 0.001). After cooking, the sodium leaching rates into the broth were 45.11% for packaged instant noodles, 59.48% for cup noodles, and 43.56% for cup rice soup (p < 0.01). The average leaching rate of the 13 minerals was ~ 25%, with no significant differences among product types.
Conclusion: Avoiding broth consumption can effectively reduce sodium intake; however, it may also lead to a reduction in the intake of essential minerals.

*These authors contributed equally to this work.Correspondence to:
Mi-Kyeong Choi, PhD
Department of Food and Nutrition
Kongju National University
54 Daehak-ro, Yesan 32439, Korea
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 45 – No. 4/2026 (137-147)

Medial accessory olivary nucleus asymmetry and its selective degeneration in Parkinson’s disease: A human neuropathological study

Tahreem Fatima¹ and Shahzad Shams²

¹Cooperative Trials Group for Neuro-Oncology (COGNO), Sydney, Australia; formerly Computational Neurosurgery Fellow, Macquarie University Hospital, Sydney, Australia, formerly affiliated with Mayo Hospital Lahore, and ²Omar Hospital Lahore and Mayo Hospital Lahore, Lahore, Pakistan
Objective: The medial accessory olivary nucleus (MAO), a distinct but inconsistently present subnucleus of the human inferior olivary complex, is poorly characterized despite its proposed role in cerebellar motor circuitry. We aimed to investigate its structural asymmetry, functional correlates, and pathological vulnerability in humans.
Materials and methods: We performed high-resolution histological analysis (Nissl and immunohistochemistry) in 35 neurologically normal brains to quantify MAO volume and neuronal numerical density and relate these to handedness and lifetime manual dexterity. In a separate cohort of 20 Parkinson’s disease (PD) brains (Braak stages 4 – 6), we compared MAO neuronal numerical density and α-synuclein pathology to age-matched controls.
Results: The MAO was identifiable in 74% (26/35) of neurologically normal cases. A significant volumetric asymmetry was present (p < 0.01), with larger MAO volume contralateral to the dominant hand, and the asymmetry index correlated with lifetime manual dexterity scores (r = 0.54, p = 0.002). PD brains showed a 43% reduction in MAO neuronal numerical density versus controls (p < 0.001) and more severe α-synuclein pathology (median grade 3 vs. 0, p < 0.001).
Conclusion: The MAO may be a neuroanatomically variable but functionally lateralized structure that appears linked to fine motor control and may exhibit selective vulnerability in PD.Correspondence to:
Tahreem Fatima, MD
5 Lachlan Avenue
Macquarie Park, NSW 2113, Australia
Email: [email protected]

Abstract

Mari Shimoda¹, Yoshito Gando², Saori Aizawa³, Takeo Yasu¹,², and Masao Tsukada⁴

¹Department of Pharmacy, Tokyo Metropolitan Tama Medical Center, ²Department of Clinical Pharmacodynamics and Toxicology Analytics, Meiji Pharmaceutical University, ³Department of Clinical Laboratory, and ⁴Department of Otolaryngology-Head and Neck Surgery, Tokyo Metropolitan Tama Medical Center, Tokyo, Japan
Objective: To characterize intra-patient variability in belumosudil exposure during coadministration of two azole antifungals that differ in cytochrome P450 3A4 (CYP3A4) inhibition strength – voriconazole (strong) vs. isavuconazole (moderate) – in a patient with steroid-refractory chronic graft-versus-host disease (cGVHD), and to discuss the subsequent implications for therapeutic drug monitoring (TDM). Case history: A man in his 50s with pulmonary cGVHD was initiated on belumosudil 200 mg once daily after cord blood transplantation, which was later increased to 200 mg twice daily (400 mg/day). Concomitant voriconazole was switched to isavuconazole due to elevated galactomannan levels and Common terminology criteria for adverse events (CTCAE) grade 2 hepatotoxicity. A single plasma sample was collected at 2 hours post-dose (C2) to approximate the peak exposure, based on a reported median time to maximum concentration of ~ 2 hours in healthy Japanese adults. Results: Over the clinical course, 28 C2 samples were analyzed (18 with voriconazole and 10 with isavuconazole). The overall median C2 was 857.04 ng/mL (range, 173.59 – 2,749.19). The median C2 was significantly higher with voriconazole (889.88 ng/mL) than with isavuconazole (395.96 ng/mL) according to the exact Wilcoxon signed-rank test (p < 0.001). Median plasma concentrations of coadministered azoles were 1.94 µg/mL (voriconazole) and 7.04 µg/mL (isavuconazole). Conclusion: Belumosudil exposure varied according to the degree of CYP3A4 inhibition (voriconazole > isavuconazole). These intra-patient data, together with clinical factors affecting absorption and hepatic function, support consideration of TDM and careful antifungal selection when combining belumosudil with azoles, particularly in pulmonary cGVHD where treatment responses are often limited. Correspondence to:
Takeo Yasu, PhD, Department of Clinical Pharmacodynamics and Toxicology Analytics, Meiji Pharmaceutical University; 2-522-1, Noshio, Kiyose, Tokyo 204-8588, Japan
Email: [email protected]

Abstract

Allergien gegen asiatische Hornisse – Präventive SLIT bei sensibilisierten Vorschulkindern – IgG4-Antworten auf dominante Hymenopterengiftallergene bei Venom-Immuntherapie und natürlicher Exposition – Allergenverkapselte Nanopa

Abstract

Allergologie, Jahrgang 49, Nr. 8/2026, S. 385-404

Auswahl und Wechsel von Biologika bei Patienten mit schwerem Asthma – Real- World-Daten aus dem German Asthma Net (GAN)

A. Lenoir¹, R. Buhl², C. Muemmler¹#¹⁶, J. Behr¹, R. Ehmann³, E. Hamelmann⁴, A. Holtdirk⁵, M. Idzko⁶, M. Jandl⁷, F. Kaessner⁸, O. Schmidt⁹, C. Schulz¹⁰, D. Skowasch¹¹, H. Suhling¹², C. Taube¹³, S. Korn¹⁴, K. Milger¹#¹⁵; sowie GAN-Forscher

¹Klinik für Innere Medizin V, Universitätsklinikum der LMU, LMU München, Comprehensive Pneumology Center (CPC), Mitglied des Deutschen Zentrums für Lungenforschung (DZL), LMU München, München, ²Universitätsklinikum Mainz, Abteilung für Pneumologie, Mainz, ³Ambulante Pneumologie mit Allergiezentrum, Stuttgart, ⁴Kinderzentrum Bethel, Evangelisches Klinikum Bethel, Universität Bielefeld, Bielefeld, ⁵RQMplus Germany, Ahlen, ⁶Abteilung für Pneumologie, Universitätsklinikum Wien AKH, Medizinische Universität Wien, Wien, Österreich, ⁷Hamburger Institut für Therapieforschung GmbH, Hamburg, ⁸Ambulantes Zentrum für Lungenkrankheiten und Schlafmedizin, Cottbus, ⁹Pneumologie Mittelrhein und Studienzentrum KPPK, Bendorf am Rhein, ¹⁰Klinik und Poliklinik für Innere Medizin, Abteilung für Pneumologie, Universitätsklinikum Regensburg, Universität Regensburg, Regensburg, ¹¹Klinik für Innere Medizin II – Pneumologie, Universitätsklinikum Bonn, Bonn, ¹²Pneumologicum Hannover, Hannover, ¹³Klinik für Lungenheilkunde, Universitätsklinikum Essen-Ruhrlandklinik, Essen, ¹⁴IKF Pneumologie Mainz und Thoraxklinik Heidelberg, Mainz und Heidelberg, ¹⁵Abteilung für Pneumologie, Klinik für Innere Medizin, Medizinische Universität Graz, Graz, Österreich, ¹⁶Institute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz München, Mitglied des Deutschen Zentrums für Lungenforschung (DZL), München
Da bis 2025 sechs zugelassene Biologika zur Behandlung von schwerem Asthma zur Verfügung stehen, stellt die Wahl der optimalen Ersttherapie und die Entscheidung, auf welches andere Biologikum bei unzureichendem Nutzen umgestellt werden soll, eine Herausforderung dar. Um die Patientencharakteristika in Abhängigkeit vom gewählten Biologikum und die Umstellungsmuster besser zu verstehen, haben wir erwachsene Patienten mit schwerem Asthma aus dem GAN-Register ausgewertet, die vor Aufnahme in das Register keine Behandlung mit einem Biologikum erhalten hatten („Biologika-naive“ Patienten). Zwischen 2011 und 2024 erhielten 2.649 Patienten mit schwerem Asthma erstmals ein Biologikum, hiervon: 26% einen Anti-Interleukin-5-Rezeptor-Antikörper (Anti-IL5R), 25% einen Anti-IL5-Antikörper, 16% einen Anti-IL4R-Antikörper, 24% einen Anti-Immunglobulin-E-Antikörper (Anti-IgE) und 9% einen Anti-Thymic-Stromal-Lymphopoietin-Antikörper (Anti-TSLP). Die Häufigkeiten der jeweils eingesetzten Biologika variierten zwischen den Zeiträumen, was deren Verfügbarkeit im Laufe der Zeit widerspiegelte. Patienten, die mit Anti-IgE behandelt wurden, waren zum Zeitpunkt der Asthmadiagnose am jüngsten (Mittelwert 26 Jahre) und wiesen die höchsten Raten an allergischen Begleiterkrankungen auf (80%). Die Eosinophilenzahl im Blut war bei Patienten, die einen Anti-IL5R-Antikörper erhielten, am höchsten (Median 433/µL) und bei denen, die Anti-TSLP erhielten, am niedrigsten (Median 159/µl), während der FeNO-Wert bei Patienten, die mit Anti-IL5, Anti-IL5R oder Anti-IL4R behandelt wurden, am höchsten war (Median 39, 38 bzw. 35 ppb). Bei 14,3% (n = 378) der Patienten erfolgte ein Wechsel vom ersten Biologikum zu einem anderen. Die häufigsten Wechselkonstellationen waren von Anti-IL5 zu Anti-IL5R, von Anti-IL5R zu Anti-IL4R und von Anti-IL5 zu Anti-IL4R. Nach einem Wechsel erreichten je nach Konstellation bis zu 46% der Patienten eine Remission. Die Phänotypisierung von Patienten mit schwerem Asthma bestimmt die Wahl der biologischen Therapie in der klinischen Praxis. Die Wahl und der Wechsel des Biologikums haben sich im Laufe der Zeit unter dem Einfluss der Verfügbarkeit verschiedener Medikamente weiterentwickelt. Unsere Analyse unterstützt die Praxis, bei unzureichendem Ansprechen auf die Ersttherapie auf ein anderes Biologikum umzustellen.

Erstpublikation in Allergologie select, mit freundlicher Genehmigung der Autoren

Lenoir A, Buhl R, Muemmler C, Behr J, Ehmann R, Hamelmann E, Holtdirk A, Idzko M, Jandl M, Kaessner F, Schmidt O, Schulz C, Skowasch D, Suhling H, Taube C, Korn S, Milger K; GAN investigators. Choosing and switching biologics for patients with severe asthma: Real-world data from the German Asthma Net (GAN). Allergol Select. 2026; 10: 158-169.
DOI 10.5414/ALX02636ECorrespondence to:
Ass.-Prof. Priv.-Doz. Dr. med. Katrin Milger-Kneidinger
Klinische Abteilung für Pneumologie
Universitätsklinik für Innere Medizin (UKIM)
Medizinische Universität Graz
Auenbruggerplatz 15, 8036 Graz, Österreich
und
Dr. med. Alexandra Lenoir
Klinik für Innere Medizin V
Universitätsklinikum der LMU, LMU München
Comprehensive Pneumology Center (CPC)
Mitglied des Deutschen Zentrums für Lungenforschung (DZL)
Marchioninistr. 15, 80377 München
Email: [email protected]; [email protected]

Abstract

Allergologie, Jahrgang 49, Nr. 8/2026, S. 406-418

Der MRGPRX2-Paradigmenwechsel: Neudefinition der Mastzellaktivierungswege bei chronischer Urtikaria

K. Wu und J. Liu

Department of Dermatology and Venereology, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China
Die chronische Urtikaria (CU) ist gekennzeichnet durch wiederkehrende Episoden von Gefäßerweiterung und erhöhter Permeabilität der kutanen und mukosalen Mikrovaskulatur. Obwohl weiterhin Antihistaminika die Erstlinientherapie und Omalizumab die Zweitlinientherapie darstellen, entwickelt ein signifikanter Anteil der Patienten therapierefraktäre Krankheitsphänotypen. Innovative Therapieansätze sind also dringend vonnöten. In den letzten Jahren haben neue Erkenntnisse zu MRGPRX2 (Mas-related G protein-coupled receptor X2) neue Perspektiven für das Verständnis der Pathobiologie der refraktären CU eröffnet. Als G-Protein-gekoppelter Rezeptor (GPCR) der Klasse A, der vorwiegend in Mastzellen lokalisiert ist, steuert MRGPRX2 die nicht-IgE-vermittelte Mastzelldegranulation durch seine pluripotente Fähigkeit zur Erkennung von Liganden, indem er verschiedene exogene kationische Verbindungen, Neuropeptide und bestimmte pharmakologische Wirkstoffe einbindet. Diese umfassende Übersichtsarbeit bewertet die jüngsten Fortschritte beim Verständnis der Rolle von MRGPRX2 in der Pathogenese der CU mit dem Ziel, die Entwicklung präziser Diagnose- und Therapieansätze für das Management der CU zu unterstützen.

Erstpublikation in Allergologie select, mit freundlicher Genehmigung der Autoren

Wu K, Liu J. The MRGPRX2 paradigm shift: Redefining mast cell activation pathways in chronic urticaria. Allergol Select. 2026; 10: 52-62.
DOI 10.5414/ALX02618ECorrespondence to:
Prof. Dr. Junlin Liu
Department of Dermatology and Venereology
The Second Affiliated Hospital of Hainan Medical University
Haikou, Hainan, China
Email: [email protected]

Abstract

Allergologie, Jahrgang 49, Nr. 8/2026, S. 419-421

Lässt sich anhand des Teicoplanin-Hauttests eine IgE-vermittelte Überempfindlichkeit vorhersagen?

N.B. Baştuğ İnan, Ö. Göktürk, Y. Karahan und K. Aksu

Division of Immunology and Allergy, Department of Chest Diseases, Ankara Atatürk Sanatoryum Training and Research Hospital, University of Health Sciences, Ankara, Türkiye
Lässt sich anhand des Teicoplanin-Hauttests eine IgE-vermittelte Überempfindlichkeit vorhersagen? 
Nach der Verabreichung von Teicoplanin wurden verschiedene Typ-IV-Überempfindlichkeitsreaktionen berichtet, darunter das DRESS-Syndrom (Drug Rash with Eosinophilia and Systemic Symptoms) und die akute generalisierte exanthematische Pustulose (AGEP). Bis vor kurzem galten IgE-vermittelte Überempfindlichkeitsreaktionen auf Teicoplanin als selten. In den letzten Jahren haben die Berichte über solche Reaktionen jedoch zugenommen. Diese Fallberichte deuten auch darauf hin, dass der Teicoplanin-Hauttest IgE-vermittelte Überempfindlichkeitsreaktionen vorhersagen kann. Im vorliegenden Fall waren der Teicoplanin-Pricktest und der Intrakutantest negativ, dennoch trat während der Provokation eine sofortige Hautreaktion auf.

Erstpublikation in Allergologie select, mit freundlicher Genehmigung der Autoren

Baştuğ İnan NB, Göktürk Ö, Karahan Y, Aksu K. Does the teicoplanin skin test predict IgE-mediated hypersensitivity? Allergol Select. 2026; 10: 98-100.
DOI 10.5414/ALX02632ECorrespondence to:
Kurtuluş Aksu, MD, Professor in Allergy and Pulmonology
Ankara Atatürk Sanatoryum Eğitim ve Araştırma Hastanesi
06280, Keçiören, Ankara, Türkiye
Email: [email protected]

Abstract

Allergologie, Jahrgang 49, Nr. 8/2026, S. 422-430

Arzneimittelüberempfindlichkeiten

K. Brockow†, R. Treudler¹ und I. Neustädter²

¹Institut für Allergieforschung IFA, Charité – Universitätsmedizin, Campus Benjamin, Franklin, Berlin, ²Abteilung Allergologie, Pädiatrische Intensivmedizin, Neonatologie, Dikoneo KdöR, Hallerwiese – Cnopfsche Kinderklinik Nürnberg, Nürnberg
Nachdruck aus der 5. Auflage des „Weißbuch Allergie in Deutschland“. Kapitel 3.12.Correspondence to:
Prof. Dr. Regina Treudler
Institut für Allergieforschung IFA
Charité – Universitätsmedizin
Campus Benjamin Franklin
Hindenburgdamm 30, 12203 Berlin
Email: [email protected]

Abstract

Xiyue Tian¹, Rangyue Han², Xiaojiao Gu³, Yuqing Li³, Honglian Wang³,⁴, Qiongdan Hu¹,⁵, and Li Wang³

¹Department of Nephrology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Sichuan, ²Department of Nephrology, Jiangjin Hospital, Chongqing University of Chinese Medicine, Chongqing, ³Research Center of Integrated Traditional Chinese and Western Medicine, Department of Nephrology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Sichuan, ⁴School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, and ⁵Department of Nephrology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China
Background: Podocyte injury is a pivotal driver of chronic kidney disease (CKD) progression in focal segmental glomerulosclerosis (FSGS). Although hederagenin (HDG) has shown promise in the treatment of CKD, its specific protective effects against podocyte injury in FSGS, along with its underlying pharmacological mechanisms, remain to be fully elucidated. Materials and methods: Potential protein targets of HDG and FSGS-related genes were retrieved from the Genecards database. Molecular docking was performed to validate binding interactions between HDG and key targets. Building on findings from adriamycin (ADR)-induced FSGS mouse and MPC5 cell line studies, HDG’s inhibitory effect on podocyte injury in FSGS was further confirmed. Results: A total of 103 potential HDG targets and 2378 FSGS-related targets were identified. Integrated drug–disease network and protein–protein interaction (PPI) analyses suggested potential mechanisms for HDG in FSGS treatment. Molecular docking pinpointed IL-6 and NOS2 as therapeutic targets, indicating their involvement in HDG’s inhibitory effects. In vivo and in vitro experiments demonstrated that HDG alleviated renal injury in ADR-induced FSGS in mice and attenuated TGF-β1-induced damage in MPC5 cells. Furthermore, HDG significantly reduced both mRNA and protein expression levels of IL-6 and NOS2. Conclusion: HDG protects podocytes from injury by inhibiting IL-6 and NOS2 in FSGS, which is consistent with the results predicted by network pharmacological analysis. These findings support HDG as a promising therapeutic candidate for FSGS treatment. Correspondence to:
Dr. Qiongdan Hu, Department of Nephrology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, No.182 Chunhui Road, Longmatan District 646000, Sichuan, China, or Prof. Li Wang, Research Center of Integrated Traditional Chinese and Western Medicine, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, No.182 Chunhui Road, Longmatan District 646000, Sichuan, China
Email: [email protected]

Abstract

Merve Oruc¹, İsmail Baloglu¹, Mehmet Burak Erçin¹, Yasin Öztürk¹, Harun Aydemir², Hakan Ozer³, İbrahim Kilinc⁴, Recep Tunc², and Kültigin Türkmen¹

¹Department of Nephrology, ²Department of Rheumatology, Meram School of Medicine, Necmettin Erbakan University, ³Department of Nephrology, Konya City Hospital, University of Health Sciences, and ⁴Department of Biochemistry, Meram School of Medicine, Necmettin Erbakan University Konya, Turkey
Background: Dickkopf-3 (DKK3) is a stress-induced glycoprotein involved in Wnt/β-catenin signaling and has emerged as a marker of renal tubular injury and fibrosis. Although urinary DKK3 has been associated with kidney disease progression independent of albuminuria, its relationship with vascular dysfunction in diabetic kidney disease (DKD) remains unclear. This study aimed to investigate the association between urinary DKK3, albuminuria, and arterial stiffness in patients with DKD. Materials and methods: In this cross-sectional study, 45 patients with DKD and 30 age- and sex-matched healthy controls were enrolled. Urinary DKK3 levels were measured using enzyme-linked immunosorbent assay and normalized to urinary creatinine. Arterial stiffness was assessed by pulse wave velocity (PWV) using an oscillometric device. Correlation and multivariable linear regression analyses were performed to evaluate independent associations among urinary DKK3, albuminuria, and PWV. Results: Urinary DKK3/creatinine ratios were significantly higher in patients with DKD compared to controls (p < 0.001). In DKD patients, urinary DKK3 showed strong positive correlations with albuminuria (r = 0.785, p < 0.001) and PWV (r = 0.454, p = 0.023). Albuminuria was also significantly correlated with PWV (r = 0.543, p = 0.005). In multivariable regression analysis, urinary DKK3 independently predicted albuminuria (β = 0.546, p = 0.004), whereas albuminuria was the only independent predictor of PWV (β = 0.443, p = 0.026). Conclusion: Urinary DKK3 is significantly associated with albuminuria and arterial stiffness in DKD. While DKK3 primarily reflects renal tubular stress and fibrotic activation, albuminuria represents systemic endothelial dysfunction and vascular damage. These findings suggest that urinary DKK3 provides complementary information by capturing tubular injury within the cardiorenal axis. If validated in prospective studies, DKK3 may serve as a noninvasive biomarker for early risk stratification of cardiorenal progression. Correspondence to:
Merve Oruc, MD, Meram School of Medicine, Department of Nephrology, Necmettin Erbakan University, 42090 Konya, Turkey
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 45 – No. 4/2026 (155-161)

Clinicopathologic mismatch in young-onset parkinsonism: Multiple system atrophy masquerading as a neurotransmitter synthesis disorder

John Michael Newman¹, Jin Kyung Kim², Jeff Nirschl¹, Jacinda Sampson², and Hannes Vogel¹

¹Department of Pathology, Division of Neuropathology, and ²Department of Neurology, Stanford Health Care, Stanford, CA, USA
Background: Multiple system atrophy (MSA) is a progressive adult-onset synucleinopathy that remains difficult to diagnose clinically, particularly in younger patients and during early disease stages. Brainstem nuclei degeneration resulting in reduced monoamines in cerebrospinal fluid (CSF) analysis may further complicate diagnostic interpretation. Objectives: To describe a clinicopathologic case of early-onset MSA found to have decreased CSF monoamines suggestive of a primary neurotransmitter synthesis disorder.
Materials and methods: Clinical records, neuroimaging findings, CSF neurotransmitter analysis, and postmortem neuropathologic examination were reviewed.
Results: A 41-year-old woman developed rapidly progressive parkinsonism, dystonia, dysphagia, and speech impairment. Broad CSF analysis was significant for reduced homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and tetrahydrobiopterin, raising concern for a monoamine synthesis defect and prompting treatment for sepiapterin reductase deficiency (SRD). Despite directed therapy, neurologic decline continued. Postmortem examination demonstrated neuropathologic findings consistent with MSA, parkinsonian subtype (MSA-P). Early cortical and allocortical amyloid-β deposition corresponding to Thal phase 2 was also identified. No additional proteinopathies were present.
Conclusion: Degeneration of dopaminergic and serotonergic nuclei in MSA can reduce CSF monoamine metabolite levels and mimic disorders of neurotransmitter biosynthesis despite correlation with tetrahydrobiopterin levels. This case highlights a potential diagnostic pitfall when interpreting CSF neurotransmitter studies in adults with parkinsonism.Correspondence to:
Dr. John Michael Newman
920 Beach Park Blvd
Foster City, CA 94404, USA
Email: [email protected]

Abstract

Rückblick auf die 5. Sitzung des DGfI-Arbeitskreises für Allergologie und Immunologie

Abstract

Tiantian Zhou¹, Shangchao Liu¹, Hao Zhang³, Yongqiang Ji², and Wei Lv⁴

¹School of Clinical Medicine, Shandong Second Medical University, Weifang, ²Department of Nephrology, Yantai Yuhuangding Hospital Affiliated to Qingdao University, ³Yantaishan Hospital, and ⁴Physical Examination Center, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong, China
Background: IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, with ~ 30% of patients progressing to end-stage kidney disease (ESKD) within 20 years of diagnosis, imposing a significant disease burden. Objective: To systematically review the progression of IgAN from its pathogenesis to ESKD and explore modern management strategies based on precise risk stratification. Materials and methods: A systematic review of existing literature was conducted to integrate key evidence in the fields of IgAN pathogenesis, risk assessment, and treatment. Results: The progression of IgAN is driven by the “four-hit” theory, with abnormal activation of the complement system being a key amplifier of injury. Persistent proteinuria, hypertension, and tubular atrophy/interstitial fibrosis (T lesion) on renal biopsy are the strongest predictors of disease progression. Modern management emphasizes precise risk stratification integrating clinical and pathological indicators. In terms of treatment, renin-angiotensin system inhibitors (RASi) and SGLT2 inhibitors are the cornerstone of supportive therapy for all patients with proteinuria. For those with rapid progression and remaining at high risk despite optimized supportive treatment, glucocorticoids or novel targeted drugs may be considered as appropriate. Conclusion: The management of IgAN has entered the era of precision medicine, with the integration of mechanism research, risk prediction, and diversified treatment strategies being the core for delaying disease progression. Correspondence to:
Wei Lv, Physical Examination Center, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong, China
Email: [email protected]

Abstract

Savas Ozturk

Department of Nephrology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Türkiye
Aim: C3 glomerulopathy (C3G) is a rare, complement-mediated kidney disease with significant diagnostic and therapeutic challenges. Despite a growing number of publications, no study has comprehensively mapped the global research landscape. This bibliometric analysis aimed to evaluate publication trends, influential contributors, thematic evolution, and collaboration networks in C3G research from 1980 to 2025. Materials and methods: A systematic bibliometric analysis was conducted using PubMed-indexed publications from 1980 – 2025 retrieved with predefined Boolean queries. Eligible articles included original research and reviews addressing the pathophysiology, diagnosis, and management of C3G. Bibliometric parameters were analyzed using the Bibliometrix package in R (v4.3) and VOSviewer (v1.6.20). Citation data were verified via Google Scholar. Results: A total of 967 publications across 273 journals were identified. Research output increased exponentially after 2013, coinciding with the C3G Consensus Report and the rise of complement-targeted therapies. Pediatric Nephrology, Kidney International, and JASN were the leading publication venues. The United States, United Kingdom, and Italy were the most productive countries, with emerging contributions from China, India, and Türkiye. S. Sethi was the most prolific author (24 papers). Keyword co-occurrence and citation network analyses demonstrated a thematic shift from morphologic classification (“dense deposit disease”) toward molecular and therapeutic paradigms (“complement inhibition,” “iptacopan,” “pegcetacoplan”). Collaboration networks remained modest and regionally clustered. Conclusion: Global research on C3G has evolved from descriptive pathology toward precision complement therapeutics. However, significant geographical disparities persist, emphasizing the need for stronger international collaboration and equitable access to emerging complement inhibitors. Correspondence to:
Prof. Dr. Savas Ozturk, Department of Nephrology, Istanbul University, Istanbul Faculty of Medicine, Istanbul, Türkiye
Email: [email protected]

Abstract

Clinical Nephrology, Vol. 106 – No. 4/2026 (276-285)

An observational study of patients receiving delayed-release budesonide (Nefecon) for immunoglobulin A nephropathy in the United States: A case series of Asian-American patients 

Wei Sun¹, Terri Madison², Li Yang¹, Elizabeth Liang¹, Giancarlo Pesce³, Sarah Zaidi⁴, Vishnudas Sarda⁵, Ramin Tolouian⁶, and Christopher Ngai⁶

¹Chinatown Kidney Care, New York, NY, ²Madison Epi Solutions, LLC, Ann Arbor, MI, USA, ³Evidence and Access, Certara, Milan, Italy, ⁴Evidence and Access, Certara, Québec, Canada, ⁵Evidence and Access, Certara, Hyderabad, India, and ⁶Calliditas Therapeutics, New York, NY, USA
Introduction: IgA nephropathy (IgAN) is a leading cause of glomerulonephritis worldwide with variability by race and ethnicity. This study aimed to provide insights on the treatment journey and clinical outcomes in Asian-American patients with IgAN treated with delayed-release budesonide (Nefecon) in a real-world setting.
Materials and methods: In this observational cohort study, a total of 45 consecutive patients with IgAN treated with Nefecon at Chinatown Kidney Care (CKC) (New York, NY, USA) were included. Study outcomes included treatment patterns and clinical outcomes (time to kidney failure, estimated glomerular filtration rate (eGFR), and urine protein-to-creatinine ratio (UPCR)). All variables were summarized descriptively. Subgroup analyses were performed among patients who were treated for ≥ 9 months vs. those treated for < 9 months.
Results: Overall, after 9 months of treatment, eGFR remained stable and UPCR decreased by an average of 19%. Improved clinical outcomes were reported among those who were treated for ≥ 9 months (preservation of eGFR and 26% reduction in UPCR) compared with those treated for < 9 months (decline in eGFR and ~ 3% reduction in UPCR). Nefecon was well tolerated with no severe or unexpected adverse events reported.
Conclusion: Real-world IgA nephropathy treatment-associated outcomes with Nefecon in Asian-American patients for proteinuria and kidney function were consistent with those observed in the NefIgArd clinical trial. The reduction in proteinuria and improvement in kidney function was greater in patients who completed the 9-month course of therapy. These findings reveal an opportunity for further education among nephrologists regarding the recommended duration of treatment with Nefecon.Correspondence to:
Giancarlo Pesce, PhD
Evidence and Access, Certara
Via Melchiorre Gioia 8
20124 Milan, Italy
Email: [email protected]

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