APTT dynamics after susoctocog alfa for early diagnostic support in suspected acquired hemophilia A: a case report

Introduction

Clinical recognition of acquired hemophilia A (AHA) is often challenging, particularly in elderly patients. Bleeding manifestations are frequently atypical, involving subcutaneous, muscular, gastrointestinal, or genitourinary sites rather than hemarthrosis, and many patients have multiple comorbidities or receive antiplatelet or anticoagulant therapy. These factors may lead clinicians to attribute bleeding to more common causes, resulting in frequent diagnostic delays associated with adverse clinical outcomes (1,2).

The diagnosis of AHA is suggested by unexplained or disproportionate bleeding with isolated prolongation of activated partial thromboplastin time (APTT) and is confirmed by reduced factor VIII (FVIII) activity with detectable FVIII inhibitors (3,4). Although cross-mixing studies can support early suspicion of an inhibitor, definitive diagnosis requires quantitative FVIII activity and inhibitor assays. Outside specialized hemophilia centers, these assays are often unavailable on an urgent basis and must be outsourced, requiring clinicians in resource-limited settings to make therapeutic decisions before laboratory confirmation is obtained.

Management during this diagnostic interval presents a clinical dilemma. Prompt initiation of hemostatic therapy is essential, yet commonly used bypassing agents do not permit routine laboratory monitoring of intrinsic coagulation activity, leaving treatment response to be assessed primarily by clinical observation alone.

Susoctocog alfa, a recombinant porcine FVIII product, differs from bypassing agents in that its hemostatic effect is reflected in APTT measurements, allowing indirect assessment of intrinsic pathway activity. We reasoned that serial observation of APTT dynamics following susoctocog alfa administration might provide supplementary diagnostic information during the diagnostic interval in patients with suspected AHA.

Here, we report a case of an elderly patient treated in a Japanese community hospital in whom APTT-guided observation after susoctocog alfa administration contributed to early disease-specific management prior to definitive laboratory confirmation, illustrating a pragmatic diagnostic adjunct for resource-limited clinical environments. We present this article in accordance with the CARE reporting checklist (available at https://aob.amegroups.com/article/view/10.21037/aob-2026-1-0003/rc).

Case presentation

Patient background

An 84-year-old woman weighing 35 kg was admitted to Yokosuka General Medical Center with gross hematuria and severe anemia. Her medical history was significant for surgical aortic valve replacement and an ischemic stroke resulting in left-sided hemiparesis. Her regular medications included aspirin, which had been intermittently withheld due to previous bleeding episodes and had already been discontinued at the time of the current admission. There was no personal or family history of congenital bleeding disorders.

Prior clinical course and recurrent bleeding

Approximately seven months before the current admission, the patient was hospitalized for severe anemia (hemoglobin 3.0 g/dL) and melena. Upper gastrointestinal endoscopy revealed a large hiatal hernia with reflux esophagitis, and the anemia was attributed to chronic gastrointestinal blood loss. At that time, coagulation testing revealed a prolonged APTT of 61.7 seconds; however, this abnormality was not further investigated because the bleeding was considered to be gastrointestinal in origin.

During that hospitalization, she developed recurrent soft tissue bleeding, including a progressive subcutaneous hematoma of the right forearm after a fall and spontaneous bleeding from the contralateral forearm. These episodes were attributed to minor trauma and antiplatelet therapy, and no underlying coagulation disorder was suspected.

Index bleeding event and laboratory findings

The patient recently presented with new-onset gross hematuria and worsening anemia. No sheet-like subcutaneous bruising or other cutaneous bleeding manifestations typically seen in AHA were observed. Initial laboratory evaluation was remarkable for a profound, isolated prolongation of APTT at 105.0 seconds. APTT was measured using the HemosIL^® SynthASil reagent (Instrumentation Laboratory, Bedford, MA, USA), with an institutional reference interval of 25.1–36.5 seconds. As detailed in Figure 1, other coagulation parameters were all within normal limits, and the platelet count showed no abnormalities. Other causes of isolated APTT prolongation were also considered. Lupus anticoagulant testing using a dilute Russell viper venom assay showed no evidence of lupus anticoagulant (ratio 1.1). In addition, factor IX activity was preserved (76.3%), making deficiency of other intrinsic pathway factors unlikely as an explanation for the marked APTT prolongation. Heparin contamination was considered unlikely because the patient was not receiving heparin therapy and blood samples were obtained by direct venipuncture.

Figure 1 Laboratory findings on admission. Detailed clinical laboratory data at the time of admission. Underlined values indicate results outside the institutional reference range (the values in parentheses indicate the reference ranges of our institution). Specialized coagulation assays were performed at an external laboratory; therefore, these results were not available on the day of admission. ALP, alkaline phosphatase; ALT, alanine transaminase; APTT, activated partial thromboplastin time; AST, aspartate transaminase; AT-III, antithrombin III; BUN, blood urea nitrogen; CRE, creatinine; CRP, C-reactive protein; Fbg, fibrinogen; FDP, fibrin/fibrinogen degradation products; FVIII, factor VIII; FIX, factor IX; Hb, hemoglobin; Hct, hematocrit; LDH, lactate dehydrogenase; Plt, platelet; PT-INR, prothrombin time-international normalized ratio; RBC, red blood cell; T-Bil, total bilirubin; UA, uric acid; vWF, von Willebrand Factor; WBC, white blood cell.

A cross-mixing study demonstrated a time-dependent, incomplete correction of the APTT. The study was performed using patient and normal plasma mixed at ratios of 4:0, 3:1, 2:2, 1:3, and 0:4. APTT was measured using the HemosIL^® SynthASil reagent (Instrumentation Laboratory, Bedford, MA, USA). One set of mixtures was measured immediately, and a second set was incubated at 37 ℃ for 2 hours before measurement. This pattern was highly suggestive of a coagulation inhibitor rather than a factor deficiency (Figure 2). The Rosner index calculated from the immediate 1:1 mixture was 22.3, exceeding the commonly used threshold of 15 (5) and supporting the presence of a coagulation inhibitor. Based on these findings, acquired AHA was strongly suspected. While samples for factor VIII activity and inhibitor assays were dispatched to an external laboratory, the results were not expected to be available for approximately one to two weeks.

Figure 2 Cross-mixing study of APTT. The study was conducted using various normal: patient plasma ratios. The immediate reaction is represented by the solid line with square markers, while the delayed reaction (following a two-hour incubation at 37 ℃) is indicated by the dashed line with circular markers. A characteristic convex (inhibitor) pattern is observed in both reactions, particularly after incubation, demonstrating a time-dependent, incomplete correction of the APTT. The Rosner index calculated from the immediate 1:1 mixture was 22.3 (threshold for inhibitor pattern: >15) (5). This finding is highly suggestive of a factor VIII inhibitor rather than a factor deficiency. APTT, activated partial thromboplastin time.

Hemostatic intervention and diagnostic confirmation

Given the clinically significant bleeding and profound anemia, hemostatic treatment was initiated prior to definitive laboratory confirmation. Susoctocog alfa (recombinant porcine factor VIII) was administered as a single intravenous dose of 200 U/kg (total dose, 7,000 U) on Day 0.

Following administration, the patient’s coagulation profile was closely monitored. Frequent short-interval blood sampling (e.g., 1, 2, 4, and 8 hours) for pharmacokinetic assessment was not performed because the patient presented with severe bleeding and profound anemia, and repeated blood sampling solely for detailed pharmacokinetic evaluation was considered clinically inappropriate. The APTT shortened from 105.0 seconds at baseline to 80.8 seconds 12 hours after infusion. However, at 36 hours post-administration, the APTT re-prolonged to 111.2 seconds. Clinically, the gross hematuria gradually resolved without the need for additional bypassing agents, and hemoglobin levels improved from 3.3 to 8.6 g/dL with transfusion support (Figure 3). Due to this rapid hemostatic response, the actual treatment cost was limited to 3.76 million JPY in this patient. Table 1 provides illustrative projected cumulative cost ranges based on typical dosing regimens; however, cross-agent cost comparisons should be interpreted cautiously given substantial variability in clinical response.

Figure 3 Clinical course and treatment response. Timeline of APTT (left y-axis, s) and Hb (right y-axis, g/dL) following admission. Susoctocog alfa (200 U/kg) was administered on Day 0 (indicated by the arrow). APTT shortened from 105 to 80.8 s at 12 hours after infusion and subsequently reprolonged to 111.2 s at 36 hours. PSL (1 mg/kg/day) was initiated on Day 0. Emicizumab (Hemlibra) prophylaxis was initiated with a loading dose of 6 mg/kg on Day 15, followed by 3 mg/kg on Day 16. This dosing approach follows the AGEHA study protocol for acquired hemophilia A (6). Starting on Day 22, the maintenance regimen was transitioned to 1.5 mg/kg once weekly via subcutaneous injection. Factor VIII activity and inhibitor titers at selected time points (Days 0, 7, and 15) are shown below the graph. Hemoglobin improved from 3.3 to 7.8 g/dL with transfusion support, with no recurrence of major bleeding. AGEHA study, Study of Emicizumab Prophylaxis for Acquired Hemophilia A; APTT, activated partial thromboplastin time; Hb, hemoglobin; PSL, prednisolone; RBC, red blood cell.

Diagnostic confirmation and long-term management

On Day 7, definitive laboratory results confirmed the diagnosis, showing factor VIII activity of less than 1.0% and a factor VIII inhibitor titer of 155.4 Bethesda units. Immunosuppressive therapy with prednisolone (1 mg/kg/day) had been initiated on Day 0 based on strong clinical suspicion.

For secondary prophylaxis against recurrent bleeding, emicizumab was introduced on Day 15 with a loading dose of 6 mg/kg, followed by 3 mg/kg on Day 16, and subsequently transitioned to weekly maintenance therapy starting on Day 22 (1.5 mg/kg once weekly), consistent with the AGEHA study protocol (6). During follow-up, the inhibitor titer gradually decreased, and no further major bleeding episodes occurred. All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of Yokosuka General Medical Center (No. 20250067), and written informed consent was obtained from the patient for the publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

This case illustrates a pragmatic approach to the diagnostic and therapeutic challenges of AHA in a resource-limited setting. To our knowledge, this is one of the few reports describing the intentional observation of APTT dynamics after susoctocog alfa administration as a supportive diagnostic clue before definitive FVIII inhibitor confirmation. While tertiary facilities in Japan and other developed countries can provide immediate FVIII activity and inhibitor testing, the majority of patients with suspected AHA initially present to community hospitals, regional facilities, or emergency departments where such specialized assays require outsourcing and may take 7–14 days to complete (1,7). This diagnostic interval creates a clinical dilemma: clinicians must balance the risks of ongoing bleeding against the costs and potential complications of empiric hemostatic therapy, all while lacking definitive laboratory confirmation.

In this context, our case demonstrates two interrelated clinical lessons: first, the potential utility of APTT-guided observation following susoctocog alfa administration as a supportive diagnostic adjunct; and second, the persistent vulnerability of elderly patients to delayed recognition of AHA when bleeding is attributed to more common causes.

AHA is an uncommon disorder, with an estimated annual incidence of approximately 0.8–1.2 cases per million population in Japan, comparable to Western countries, predominantly affecting elderly individuals and associated with an in-hospital mortality rate of approximately 15–20%, with diagnostic delay being a major contributing factor (2,7,8). The disease predominantly affects elderly individuals, with a median age at diagnosis of 75–80 years. Registry and cohort studies have reported similar mortality rates (7,9). These epidemiologic features underscore the clinical importance of timely recognition and early disease-specific intervention, particularly in older patients.

Diagnostic challenges in acquired AHA

AHA is a rare but potentially life-threatening bleeding disorder characterized by autoantibody-mediated inhibition of FVIII, most commonly affecting elderly individuals without a prior personal or family history of bleeding (3). The diagnosis typically requires unexplained bleeding, isolated prolongation of APTT, reduced FVIII activity, and detection of FVIII inhibitors using the Bethesda assay (4,10). Prompt diagnosis is crucial, because delayed recognition has been associated with persistent bleeding, increased transfusion requirements, and higher mortality rates (1). In clinical practice, a systematic differential diagnosis for isolated APTT prolongation—including lupus anticoagulant, heparin contamination, and intrinsic pathway factor deficiencies—is essential before concluding that AHA is the most likely cause.

However, in real-world clinical practice, especially outside specialized hemophilia centers, definitive FVIII activity and inhibitor assays are frequently unavailable on the day of presentation. In Japan, as in many other countries, these tests are often outsourced, resulting in delays of several days to over a week before confirmation (7). During this diagnostic gap, clinicians must make critical decisions regarding hemostatic management based on incomplete information, balancing the risks of ongoing bleeding against the costs and potential complications of empiric therapy (1).

Rationale for APTT-guided observation following susoctocog alfa

Susoctocog alfa, a recombinant porcine FVIII concentrate, has a unique pharmacologic profile among hemostatic agents used in AHA. Clinical studies have demonstrated its efficacy in controlling bleeding in patients with AHA (11). Unlike bypassing agents such as recombinant activated factor VII (rFVIIa) or activated prothrombin complex concentrate (aPCC), susoctocog alfa directly supplements FVIII activity, allowing its effect to be reflected in conventional coagulation assays, including APTT and FVIII activity measurements (11). This characteristic allows indirect assessment of treatment response through serial APTT monitoring. The decision to prioritize susoctocog alfa over conventional bypassing agents was based on the patient’s critical condition, characterized by profound anemia and the urgent need for a definitive hemostatic effect. Furthermore, in an elderly patient with multiple cardiovascular comorbidities, restoring intrinsic FVIII activity was considered a more physiologically targeted approach than the use of bypassing agents, which carry a higher inherent risk of thromboembolic complications. Cross-reactive inhibitors to porcine FVIII have been reported in up to approximately half of patients with AHA, potentially compromising rpFVIII efficacy (3,4,12).

In the present case, a porcine FVIII inhibitor assay was not performed. Notably, the patient’s gross hematuria visibly improved and the urine color became markedly lighter shortly after administration of a single dose of susoctocog alfa, suggesting a clinically meaningful hemostatic response. Based on this rapid improvement, no additional doses were administered and further testing for porcine FVIII inhibitors was not pursued. Nevertheless, the potential presence of cross-reactive inhibitors should be considered when empirically using porcine FVIII products in suspected AHA.

The reported terminal half-life of susoctocog alfa is approximately 10 hours (11), suggesting that its hemostatic effect should be transient in the presence of high-titer inhibitors. In this context, a characteristic temporal pattern of APTT shortening following administration, followed by re-prolongation as the infused FVIII is neutralized or cleared, may provide indirect but biologically plausible support for the presence of FVIII inhibition (10,11). In the present case, von Willebrand factor activity was markedly elevated (≥200%), likely reflecting an acute phase response associated with active bleeding and inflammation; however, the observed APTT dynamics remained consistent with transient FVIII replacement followed by inhibitor-mediated neutralization.

In the present case, serial APTT monitoring demonstrated such a shortening-re-prolongation pattern, temporally consistent with the expected pharmacokinetics of susoctocog alfa. Similar temporal APTT changes following recombinant porcine FVIII administration have been reported in clinical cases. Hayden et al. described that APTT initially shortened after rpFVIII administration and subsequently attenuated as rpFVIII trough levels declined or were neutralized by inhibitors (13).

In our patient, the bleeding manifestation was gross hematuria, allowing direct clinical observation of bleeding status. The visible improvement in urine color after susoctocog alfa administration suggested a meaningful hemostatic response. The concordance between this clinical improvement and the temporal pattern of APTT shortening followed by re-prolongation strengthened our clinical suspicion of FVIII inhibition prior to laboratory confirmation.

Importantly, this observation was made prior to the availability of definitive FVIII and inhibitor assay results, which were later found to confirm severe FVIII deficiency and a high inhibitor titer. Transient fluctuations in APTT may also occur due to acute-phase changes in coagulation factors, laboratory variability, or pharmacokinetic differences in factor replacement therapy. However, such APTT dynamics are not specific for AHA and should therefore be interpreted only as a supportive clinical observation rather than a diagnostic criterion.

Comparison with existing literature

Previous reports and clinical trials have described the use of APTT or FVIII activity monitoring to assess the hemostatic efficacy of susoctocog alfa after AHA diagnosis has been established (11). To our knowledge, few reports have described the intentional observation of APTT dynamics following susoctocog alfa administration as a supportive clinical observation before laboratory confirmation.

This scarcity of prior reports likely reflects differences in healthcare delivery systems rather than lack of clinical relevance. In many European and North American countries, patients with suspected AHA are promptly referred to specialized hemophilia centers where FVIII activity and inhibitor titers can be measured on the same day. In contrast, in community hospitals and regional facilities in Japan and other resource-limited settings, FVIII assays are frequently outsourced to reference laboratories, resulting in turnaround times of several days to more than one week (7,10).

Patient blood management (PBM) and cost considerations

Hemostatic therapy for AHA is associated with substantial healthcare costs. Bypassing agents such as rFVIIa and aPCC typically require frequent dosing over several days until bleeding control is achieved, resulting in high cumulative costs (14). Susoctocog alfa is similarly expensive and is generally administered repeatedly until FVIII activity stabilizes and bleeding resolves (11,13).

In this case, clinically meaningful hemostasis was achieved with a single dose of susoctocog alfa, without the need for additional bypassing agents. Although this outcome may not be representative, it highlights an important PBM principle: early recognition, targeted therapy, and careful clinical monitoring may help avoid unnecessary drug exposure and transfusion in selected cases (15). The favorable cost observed in this case resulted from an atypical single-dose response and should not be interpreted as evidence of cost-effectiveness. Importantly, all hemostatic agents for AHA are intended to be continued until bleeding control is achieved, and this report does not imply superiority of single-dose therapy.

Rather, this case highlights that, in selected circumstances, early disease recognition combined with careful clinical and laboratory observation may allow more individualized and potentially resource-sparing management without compromising patient safety.

Delayed recognition of AHA in elderly patients

The second major lesson from this case concerns the diagnostic delay commonly observed in elderly patients with AHA. Multiple studies and reviews have emphasized that AHA in older adults is frequently underdiagnosed or misattributed to more common conditions, such as trauma, antiplatelet or anticoagulant therapy, disseminated intravascular coagulation, or age-related skin fragility (16).

In elderly patients, bleeding manifestations of AHA are often atypical and may involve subcutaneous, muscular, gastrointestinal, or genitourinary sites rather than hemarthrosis. Moreover, the frequent presence of multiple comorbidities, age-related skin fragility, recurrent falls, and concomitant use of antiplatelet or anticoagulant agents commonly leads clinicians to attribute bleeding to more prevalent etiologies. Consequently, AHA in older adults is frequently underrecognized or misdiagnosed, a phenomenon repeatedly documented in observational studies and registry-based analyses (16,17).

In this patient, recurrent bleeding episodes at different anatomical sites were initially interpreted as trauma-related events in the context of frequent falls, antiplatelet therapy, and poor functional status. Similar patterns have been reported in observational studies and registry data, which show that a substantial proportion of patients experience diagnostic delays of more than one week, and in some cases more than one month (17). Such delays have been associated with prolonged bleeding, increased use of hemostatic agents, and worse clinical outcomes (1).

These findings underscore the importance of maintaining a high index of suspicion for AHA in elderly patients presenting with unexplained or disproportionate bleeding and isolated APTT prolongation, regardless of concurrent antithrombotic therapy or apparent traumatic triggers.

Limitations and ethical considerations

This report has several limitations. First, it describes a single patient, and the observed APTT pattern may not be reproducible in all cases of AHA, particularly in those with lower inhibitor titers or differing pharmacokinetics. Second, the use of susoctocog alfa prior to definitive laboratory confirmation raises ethical and reimbursement considerations, as its approved indication is bleeding in patients with confirmed AHA (11).

In the present case, the decision was made based on life-threatening anemia, strong clinical suspicion supported by mixing studies, and the absence of immediate diagnostic alternatives. Nonetheless, this approach should be considered cautiously on a case-by-case basis. Prospective studies are needed to evaluate the reproducibility, clinical utility, and cost-effectiveness of APTT-guided observation strategies in suspected AHA. Importantly, this observation should not be interpreted as evidence that susoctocog alfa should be administered for diagnostic purposes, but rather as a clinical observation that may incidentally provide supportive information when the drug is used for hemostatic treatment.

Conclusions

This case demonstrates a pragmatic approach to the diagnosis and management of AHA in a resource-limited clinical setting. By leveraging the unique ability of susoctocog alfa to influence APTT, serial APTT monitoring provided supportive diagnostic information prior to definitive factor VIII and inhibitor confirmation. Observation of a transient APTT shortening followed by re-prolongation strengthened clinical confidence in the suspected diagnosis and facilitated timely disease-specific management while minimizing unnecessary exposure to hemostatic agents.

Beyond its diagnostic implications, this case underscores the persistent risk of delayed recognition of AHA in elderly patients, in whom bleeding is frequently attributed to trauma, antiplatelet therapy, or age-related factors. Heightened awareness of isolated APTT prolongation in the setting of unexplained or disproportionate bleeding remains essential for early diagnosis.

While APTT-guided observation cannot replace definitive laboratory testing, it may serve as a practical supplementary tool in environments where specialized coagulation assays are not immediately available. Further studies are warranted to evaluate the reproducibility and clinical utility of this observation. The observations described in this report should be interpreted cautiously, as they are derived from a single clinical case.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://aob.amegroups.com/article/view/10.21037/aob-2026-1-0003/rc

Peer Review File: Available at https://aob.amegroups.com/article/view/10.21037/aob-2026-1-0003/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aob.amegroups.com/article/view/10.21037/aob-2026-1-0003/coif). T.S. serves as a special appointed director of the Japanese Society of Transfusion Medicine and Cell Therapy. 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. All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of Yokosuka General Medical Center (No. 20250067), and written informed consent was obtained from the patient for the publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.

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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