Early hypoalbuminemia during zolbetuximab therapy in gastroesophageal adenocarcinoma: a retrospective observational study

Introduction

Treatment strategies of advanced gastroesophageal adenocarcinoma (GEA) have increasingly incorporated biomarker-driven approaches alongside systemic chemotherapy (1). Claudin 18.2 (CLDN18.2) is a tight junction protein physiologically expressed on gastric epithelial cells and contributes to mucosal barrier integrity (2). Although upregulated and exposed in malignant cells, its presence in normal gastric mucosa raises the possibility that targeted therapy may also affect non-malignant epithelium (2).

Zolbetuximab, a monoclonal antibody targeting CLDN18.2, has demonstrated improved progression-free and overall survival when combined with chemotherapy in patients with CLDN18.2-positive advanced GEA in the phase III SPOTLIGHT and GLOW trials (3,4). Nausea and vomiting were among the most common adverse events, often requiring aggressive supportive care (3,4). These gastrointestinal symptoms are believed to reflect a gastritis-like mucosal effect, and consensus management guidelines have been developed to optimize prophylaxis and supportive strategies (5,6). In addition, these trials reported higher rates of hypoalbuminemia and peripheral edema in the zolbetuximab arms compared with chemotherapy alone. However, while hypoalbuminemia was described as an adverse event, the timing, magnitude, and clinical pattern of serum protein decline were not systematically characterized, and a clear mechanistic explanation was not established (3,4).

A recent report by Yanagimoto et al. described two patients with marked hypoalbuminemia during zolbetuximab therapy, in whom liver and renal causes were excluded and protein-losing enteropathy (PLE) was confirmed using technetium-99m-labeled human serum albumin scintigraphy demonstrating gastrointestinal albumin leakage (7). Although limited to two cases, these observations raise the possibility of a treatment-associated protein-losing process, yet it remains unclear whether this represents an isolated phenomenon or a broader and reproducible clinical pattern in routine practice.

In this study, we aimed to characterize longitudinal changes in serum albumin and total protein in patients treated with zolbetuximab in a real-world setting, assess alternative explanations such as renal or hepatic dysfunction and disease progression, and explore available endoscopic correlates to better define the clinical phenotype associated with this toxicity. We present this article in accordance with the STROBE reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0570/rc).

Methods

Study design and endpoints

We conducted a retrospective descriptive cohort study of patients with CLDN18.2 positive GEA who received the combination of chemotherapy plus zolbetuximab across the Mayo Clinic enterprise (Arizona, Florida, and Rochester). Patients were included if they received at least one dose of zolbetuximab and had at least two measurements of serum albumin and/or total protein to allow comparison between baseline and post-treatment values.

The primary endpoint was the percent change in serum albumin from baseline (defined as the last laboratory value prior to zolbetuximab initiation) to the first post-treatment measurement following initiation of therapy. Secondary endpoints included percent change in total protein from baseline to the first post-treatment measurement following treatment initiation, development of new edema on physical examination or ascites on computed tomography (CT) scan not attributable to disease progression, and changes in albumin and total protein after treatment discontinuation. Radiographic disease progression was determined based on treating physician documentation and imaging review during routine clinical care.

Data collection

Collected data included demographics, primary tumor location, and chemotherapy backbone administered with zolbetuximab. Laboratory values collected were serum albumin, total protein, creatinine, estimated glomerular filtration rate (eGFR), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin. Urinalysis to evaluate for any protein in the urine was also collected. Clinical features during treatment, including development of edema or ascites and management with diuretics and/or paracentesis, were documented. When available, esophagogastroduodenoscopy (EGD) findings and corresponding histologic results were reviewed.

Statistical analysis

Analyses were descriptive. Continuous variables were summarized as medians with ranges. Longitudinal trends in serum albumin and total protein were graphed using spider plots to visualize individual trends. Cohort-level median values were plotted across subsequent cycles with error bars representing the standard error.

Ethics

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Mayo Clinic Institutional Review Board (IRB) (IRB No. 24-009377), and informed consent was waived due to its retrospective, low-risk nature.

Results

Cohort characteristics

A total of 24 patients with GEA received at least one dose of zolbetuximab during the study period and met inclusion criteria. The median age was 67 years (range, 33–89 years), and most patients were male (17/24; 70.8%). Primary tumor location was gastric in 10/24 (41.7%) patients and esophageal/gastroesophageal junction (GEJ) in 14/24 (58.3%) patients. Five of 24 patients (20.8%) had undergone prior surgery, all of which were esophagectomies performed before initiation of zolbetuximab therapy. Zolbetuximab was most commonly administered with FOLFOX (fluorouracil, leucovorin, and oxaliplatin) (19/24; 79.2%) followed by FOLFIRI (fluorouracil, leucovorin, and irinotecan) (5/24; 20.8%) and the median number of zolbetuximab cycles was 5 (range, 1–13). One patient had baseline edema, and no patients had underlying cirrhosis. Most importantly, most patients (20/24; 83.3%) had a normal baseline albumin (baseline albumin ≥3.5 g/dL). Baseline demographic and clinical characteristics are summarized in Table 1.

Longitudinal albumin and total protein trends

Prior to therapy initiation, the median baseline albumin and total protein were 3.8 g/dL (range, 2.9–4.5 g/dL; normal range, 3.5–5.0 g/dL), and 6.2 g/dL (range, 5.1–7.5 g/dL; normal range 6.3–7.9 g/dL), respectively. Baseline laboratory values were obtained a median of 1 day (range, 0–5 days) before the start of zolbetuximab therapy. Following cycle 1 of zolbetuximab infusion and immediately prior to cycle 2, median albumin and total protein were 2.8 (range, 2.3–3.4) and 4.6 (range, 3.5–5.7) g/dL, respectively (Figures 1,2). At the patient level, albumin declined by a median of 0.9 g/dL (range, 0.1–2.1 g/dL; 22.5%) and protein by median of 1.5 g/dL (range, 0.3–3.1 g/dL; 24.2%) from baseline (Figure 3). Furthermore, 13/24 (54.2%) had albumin level less than 3 g/dL after the first zolbetuximab cycle compared to zero before starting treatment. The median values for albumin and total protein remained lower than baseline for the remainder of the treatment period (range 70–94% of baseline value). In patients who had discontinued therapy and had at least one laboratory test of albumin and total protein (n=14), the first post-treatment laboratory assessment occurred at a median of 14 days (range, 11–26 days) after the last zolbetuximab dose, with median albumin 3 g/dL (range, 1.7–4.1 g/dL) and median total protein 4.7 g/dL (range, 3.1–6.4 g/dL).

Figure 1 Longitudinal serum albumin trajectories during zolbetuximab treatment. Spider plot showing individual patient trajectories of serum albumin (g/dL) across zolbetuximab treatment cycles. Each colored line represents a single patient. Black open circles denote the cycle at which zolbetuximab was discontinued for that patient. A consistent decline in serum albumin is observed following treatment initiation in most patients, with variable degrees of recovery or stabilization over subsequent cycles. Z, zolbetuximab.

Figure 2 Longitudinal serum total protein trajectories during zolbetuximab treatment. Spider plot showing individual patient trajectories of serum total protein (g/dL) across zolbetuximab treatment cycles. Each colored line represents a single patient. Black open circles denote the cycle at which zolbetuximab was discontinued for that patient. A consistent decline in serum total protein is observed following treatment initiation in most patients, with variable degrees of recovery or stabilization over subsequent cycles. Z, zolbetuximab.

Figure 3 Change from baseline in serum albumin and total protein during zolbetuximab therapy. Line plot showing median percent change from baseline in serum albumin and total protein across zolbetuximab treatment cycles. Error bars represent the IQR. Both parameters demonstrate an early decline following treatment initiation with relative stabilization over subsequent cycles. IQR, interquartile range; Z, zolbetuximab.

Among 10 patients with available laboratory data at baseline, during therapy, and following treatment discontinuation, median albumin declined from 3.65 g/dL (range, 3.1–4.5 g/dL) at baseline to 2.9 g/dL (range, 2.3–3.4 g/dL) after the first zolbetuximab cycle and subsequently increased to 3.15 g/dL (range, 1.7–4.1 g/dL) following treatment discontinuation. The last available albumin measurement, obtained at a median of 128 days (range, 28–185 days) after the final zolbetuximab dose, further improved to 3.5 g/dL (range, 2.0–3.9 g/dL) (Figure S1). A similar pattern was observed for total protein, which declined from a median of 6.2 g/dL (range, 5.5–7.2 g/dL) at baseline to 4.7 g/dL (range, 3.5–5.7 g/dL) after the first zolbetuximab cycle, and subsequently remained stable at 4.65 g/dL (range, 3.1–6.4 g/dL) following treatment discontinuation. The last available total protein measurement, obtained at a median of 128 days after the final zolbetuximab dose, further improved to 5.75 g/dL (range, 4.1–6.7 g/dL) (Figure S2). Overall, both albumin and total protein demonstrated gradual recovery toward baseline values following treatment discontinuation, although complete normalization was not observed in all patients during the available follow-up (Figure S3).

During therapy, 9/24 (37.5%) patients developed edema and 6/24 (25%) developed ascites without evidence of disease progression. One additional patient had pre-existing edema that worsened after initiation of zolbetuximab. 8/24 (33.3%) required diuretics and/or paracentesis. These were new symptoms in all but one patient, who had baseline edema that was noted to worsen after starting zolbetuximab. Among the eight patients who received treatment, 7 (87.5%) demonstrated improvement in edema and/or ascites after treatment. Three patients (12.5%) received intravenous albumin during therapy; however, none demonstrated sustained correction of hypoalbuminemia following infusion.

Transthoracic echocardiography (TTE) was available in 6 of the 10 patients among this group. Left ventricular ejection fraction was >55% in five patients and 39% in one patient. All studies demonstrated normal right ventricular chamber size and normal cardiac chamber dimensions, including in the patient with reduced ejection fraction. As an exploratory analysis, CLDN18.2 expression was compared between patients who developed edema/ascites and those who did not to assess whether tumor expression level differed between groups. No meaningful difference was observed. The median CLDN18.2 expression was 90% in patients who developed edema/ascites and 95% in those who did not. The minimum and maximum expression values were similar in both groups (75% and 100%, respectively).

Renal and hepatic laboratory trends

Overall, there was no biochemical evidence of clinically relevant renal dysfunction, hepatocellular injury, or cholestasis during zolbetuximab therapy. Renal and hepatic laboratory parameters were evaluated to assess alternative explanations for serum protein decline (Table 2). Median baseline creatinine was 0.88 mg/dL (range, 0.54–1.56 mg/dL), and eGFR was 71.5 mL/min/1.73 m² (range, 42–90 mL/min/1.73 m²). Urine protein testing was available in 15/24 (62.5%) patients. Baseline urine protein was available in nine patients; five had negative or trace protein levels and four had protein levels less than 30 mg/dL, with no patient having nephrotic-range proteinuria at baseline. On-treatment, urine protein measurements were available in six patients and demonstrated only negative, trace, or protein levels less than 30 mg/dL without progressive proteinuria. Post-treatment urine protein testing in 10 patients showed negative, trace (grade 1), or protein level less than 30 mg/dL in all.

Liver-associated laboratory parameters remained stable throughout treatment. Median baseline AST and ALT were 25 (range, 16–44) and 23.5 (range, 11–70) U/L, respectively, with no consistent pattern of transaminase elevation across the cohort. Isolated peak AST and ALT elevations were observed in a small number of patients but did not reflect a uniform trend. Total bilirubin remained within normal limits at baseline [0.4 mg/dL (0.2–0.9)] with the same trend observed during zolbetuximab therapy. Lab parameters for each patient are documented in Table S1.

Endoscopic findings

EGD was performed during zolbetuximab therapy in four patients for the following indications: dysphagia with acute-on-chronic worsening of solid food intolerance, melena, reassessment of a previously placed palliative gastric stent for a stenosing tumor, and routine surveillance. Two patients underwent EGD after the first cycle and demonstrated diffuse gastric mucosal friability with contact bleeding (one with nodularity), with normal-appearing duodenum in both. A third patient (after four cycles) had erythematous gastric mucosa without ulceration, and a fourth (after one cycle) had a normal-appearing stomach and jejunum. In all cases, serum albumin and total protein had declined from baseline at the time of endoscopy. No biopsies were obtained during on-treatment procedures.

Pre-treatment endoscopy was available in two patients and was either limited by stenosis or showed non-inflammatory findings. Among four patients with EGD before and after completion of therapy, one developed new chronic gastritis with reactive gastropathy following 13 cycles, while the remaining cases showed either unchanged findings or limited evaluation.

Discussion

In this real-world cohort of patients with GEA treated with zolbetuximab in combination with systemic chemotherapy, we observed a consistent decline in serum albumin and total protein after treatment initiation, with recovery toward baseline after treatment discontinuation among patients who had ended therapy. A significant subset of patients developed edema or ascites requiring supportive care, without imaging findings of disease progression. Renal and hepatic laboratory parameters remained stable, suggesting that protein loss was most likely not driven by kidney or liver dysfunction. Endoscopic evaluation in selected patients revealed heterogeneous gastric mucosal findings during therapy, ranging from mucosal abnormalities to preserved mucosal integrity. These observations suggest that declines in serum protein and albumin levels during zolbetuximab treatment are common in clinical practice and may, in some patients, be consistent with a gastrointestinal protein-losing process, although this mechanism cannot be confirmed based on the current study.

Phase III trials of zolbetuximab in CLDN18.2-positive GEA reported hypoalbuminemia in approximately 15–22% of treated patients (3,4). However, these estimates were derived from CTCAE-coded adverse event reporting rather than a systematic longitudinal assessment of within-patient changes. In contrast, our analysis evaluated percent change in serum albumin from baseline in all treated patients, capturing early declines that may not have met formal CTCAE grading thresholds or been recorded as adverse events. In our cohort, the median albumin decline after the first treatment cycle was 0.9 g/dL, and 13 of 24 patients (54.2%) developed albumin levels <3 g/dL after the first cycle despite normal baseline levels in most patients. This methodological difference likely accounts for the higher frequency of albumin decline observed in our cohort and suggests that the magnitude and early timing of serum protein decline may be underrepresented in clinical trial adverse-event tables.

While these trials did not define a mechanistic explanation for hypoalbuminemia, a recent case report by Yanagimoto et al. described two patients who developed marked hypoalbuminemia during zolbetuximab therapy, in whom endoscopy demonstrated diffuse gastric mucosal erythema and edema and technetium-99m-labeled albumin scintigraphy confirmed gastrointestinal protein leakage, establishing a diagnosis of PLE (7). Furthermore, Yamamoto et al. showed that zolbetuximab use was linked to early-onset transient gastritis which was significantly associated with hypoalbuminemia (6). In our cohort, we similarly observed a near-universal decline in serum albumin and total protein following initiation of zolbetuximab, in the absence of biochemical evidence of renal or hepatic dysfunction or disease progression. Zolbetuximab is commonly associated with early nausea and vomiting, which may reduce oral intake and contribute to hypoalbuminemia in some patients (8). However, the rapid and near-universal decline in albumin and total protein observed shortly after treatment initiation suggests that decreased intake alone is unlikely to fully explain the pattern seen in our cohort. Given the approximately 20-day half-life of serum albumin, the early decline observed after a single treatment cycle appears more rapid than would be expected from reduced nutritional intake alone, raising the possibility that the observed changes could be attributed to zolbetuximab treatment.

CLDN18.2 is physiologically expressed on normal gastric epithelial cells in addition to malignant tissue (2). Binding of zolbetuximab to CLDN18.2-expressing gastric mucosa has been shown to cause antibody-dependent cellular cytotoxicity and local inflammatory injury (2). It is therefore plausible that treatment-related damage to normal gastric epithelium may increase mucosal permeability and promote loss of serum proteins into the gastrointestinal lumen. This proposed mechanism is supported by endoscopic and histologic gastric mucosal injury observed in reported cases of zolbetuximab-associated PLE and by similar mucosal findings in a subset of patients in our cohort (7). Nonetheless, the heterogeneous observations highlight the need for further study to clarify the mechanisms underlying these effects. Our findings suggest that serum albumin and total protein should be monitored during zolbetuximab therapy, especially in patients who develop edema, ascites, or gastrointestinal symptoms. Recognition of this potential toxicity may help guide supportive care strategies, including early optimization of nutritional status, assessment of caloric and protein intake, and involvement of nutrition specialists when appropriate.

This study has several limitations. The retrospective design meant that laboratory measurements and endoscopic evaluations were not performed at standardized timepoints. Confirmatory testing for PLE was not obtained, so a definitive diagnosis could not be established in the patients. The cohort size was relatively small and drawn from a single healthcare system, which may limit broader generalizability. Albumin levels may be influenced by disease burden, systemic inflammation, or nutritional status, which cannot be fully controlled in this design. An additional limitation is the uneven distribution of chemotherapy backbones, with most patients receiving FOLFOX rather than FOLFIRI. Although descriptive analyses demonstrated similar early albumin declines across both regimens, the potential contribution of oxaliplatin-containing chemotherapy to hypoalbuminemia cannot be excluded and should be considered when interpreting these findings. Furthermore, the study lacked a comparator arm. Despite these limitations, the consistency of the observed laboratory trends across patients raises the possibility of the signal described.

Conclusions

In this real-world cohort of patients treated with zolbetuximab, we observed a consistent decline in serum albumin and total protein that was not explained by renal or hepatic dysfunction or disease progression. These findings may reflect a treatment-associated gastrointestinal protein-losing process, given the temporal relation between treatment initiation and the observed decline in total protein and albumin levels. However, this mechanism could not be definitively confirmed in this present study. Prospective studies are warranted to further define the mechanism and clinical implications of this phenomenon.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0570/rc

Data Sharing Statement: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0570/dss

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0570/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0570/coif). Tanios Bekaii-Saab reports research funding to the institution from Agios, Arys, Arcus, Atreca, Boston Biomedical, Bayer, Eisai, Celgene, Lilly, Ipsen, Clovis, Seattle Genetics, Genentech, Novartis, Mirati, Merus, Abgenomics, Incyte, Pfizer, BMS and Revolution Medicine; and reports consulting fees to the institution from Servier, Ipsen, Arcus, Pfizer, Seattle Genetics, Bayer, Genentech, Incyte, Eisai, Merus, Merck KGaA, Revolution Medicines and Merck and received consulting fees from Stemline, AbbVie, Blueprint Medicines, Boehringer Ingelheim, Janssen, Daiichi Sankyo, Natera, Takeda, TreosBio, Celularity, Caladrius Biosciences, Exact Science, Sobi, Beigene, Kanaph, Astra Zeneca, Deciphera, Zai Labs, Exelixis, MJH Life Sciences, Aptitude Health, Illumina, Foundation Medicine and Sanofi. Glaxo SmithKline, Arsenal Bio, Xilio and RYGHT AI. He served as a data safety monitoring board member of The Valley Hospital, Fibrogen, Suzhou Kintor, Astra Zeneca, Exelixis, Merck/Eisai, PanCan and 1Globe and served as a scientific advisory board of Imugene, Immuneering, Xilis, Replimune, Artiva and Sun Biopharma. Tanios Bekaii-Saab also reports royalties from Uptodate and is an inventior on the following patents: WO/2018/183488: HUMAN PD1 PEPTIDE VACCINES AND USES THEREOF-Licensed to Imugene, and WO/2019/055687: METHODS AND COMPOSITIONS FOR THE TREATMENT OF CANCER CACHEXIA-Licensed to Recursion. H.X. reports consulting or Advisory Role with Cardiff Oncology (Inst), Xilio Therapeutics (Inst), and received research funding from Xilio Therapeutics (Inst), SparX Biopharmaceutical Corp (Inst), Cardiff Oncology (Inst), DynamiCure Biotechnology (Inst), BioNTech SE (Inst), Qurient Therapeutics (Inst), Xilis (Inst), Pfizer (Inst), AstraZeneca (Inst), BeiGene (Inst), Innovent Biologics (Inst), he also owns patents, royalties, other intellectual property: Patent application entitled “DEGRADERS OF SON OF SEVENLESS HOMOLOG 1” was filed with the United States Patent and Trademark Office on 8/11/2023. J.S.S. is a consultant for Boehringer-Ingelheim, Novartis, Jazz Pharmaceuticals, Exexilis and received research support to the institution from Boehringer-Ingelheim, Amgen, Viewpoint Molecular Therapeutics, Novartis, AstraZeneca, RayzeBio, Kyowa Therapeutics, Arcus Biosciences. N.H.T. is a consultant on advisory boards, received research funding, or paid presentations from the following entities (all paid directly to the Mayo Clinic Foundation): AstraZeneca, Exelixis, DAVA Oncology, Elevar Therapeutics, EXACT SCIENCES, Genentech, Ipsen, MD Outlook, QED/Helsinn Therapeutics. B.G. is a consultant for Foundation Medicine, Taiho Oncology, BTG (Boston Scientific), Roche/Genentech, Astra Zeneca, Pfizer, Astellas, Amgen and received research support from Roche/Genentech (Inst), Hoffman La-Roche (Inst), Taiho Oncology (Inst), Toray (Inst), Hutchison Medipharma (Inst), Mirati Therapeutics (Inst), CARsgen (Inst), Glyconex (Inst), Helix Biopharma (Inst), Pfizer (Inst), Tvardi Therapeutics (Inst), Faeth Therapeutics (Inst), BionTech (Inst), Transcenta (Inst), Legend Biotech (Inst), Elicio Therapeutics (Inst), Obsidian(Inst). C.D.J.O. served as an advisory board member for Incyte. H.H.Y. reports receiving grant and/or contract funding from Amgen, Bristol Myers Squibb, CARsgen Therapeutics, Macrogenics, and Merck, and consulting fees from ALX Oncology, Amgen, Astellas, AstraZeneca, and BeiGene, and travel fees from BeiGene. M.B.S. reports personal consulting fees from Novartis, consulting paid to institution from Bayer, Boehringer Ingelheim and research support to the institution from Taiho and Eli Lilly. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Mayo Clinic Institutional Review Board (IRB No. 24-009377).Informed consent was waived due to retrospective nature of the study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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