Abstract
Background
Acquired thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening condition triggered by pregnancy, often in the third trimester, and frequently mimics preeclampsia or HELLP syndrome due to shared features like thrombocytopenia. Refractory cases in twin pregnancies, described in this case, pose unique diagnostic and therapeutic challenges, requiring advanced interventions.
Case Presentation
A 29-year-old woman carrying dichorionic-diamniotic twins presented in the third trimester with palpitations, dyspnea, oral bleeding, numbness, chest heaviness, fatigue, edema, and pelvic pain. Admission showed severe thrombocytopenia (8 × 109/L), microangiopathic hemolytic anemia (schistocytes, elevated LDH), normal blood pressure, and normal liver/kidney function, making preeclampsia/HELLP unlikely. Because of the high bleeding risk posed by the profound thrombocytopenia, and despite a reassuring fetal assessment, an emergency cesarean section was performed and delivered two healthy baby girls with good Apgar scores. ADAMTS13 activity <10% subsequently confirmed acquired TTP. Plasma exchange and corticosteroids were started presumptively on the day of admission; because the platelet response was incomplete, rituximab and caplacizumab were added during the same admission. The patient was discharged after initial hematologic recovery but relapsed with recurrent severe thrombocytopenia three days later, confirming refractory disease; she was readmitted and achieved sustained platelet normalization with continued plasma exchange, rituximab, and caplacizumab. Complications included wound infection with multiple organisms, antibiotic allergy, and superficial venous thrombosis, all managed successfully. Both mother and infants were discharged well, with no further relapse at six-week follow-up. Future pregnancies were discouraged without specialist review.
Conclusions
High suspicion for TTP is essential in pregnant patients with thrombocytopenia and hemolysis, even without hypertension. Rapid ADAMTS13 testing, timely delivery, and combined plasma exchange with rituximab and caplacizumab enabled full recovery in this refractory twin-pregnancy case. Multidisciplinary care is critical to differentiate from obstetric mimics and achieve favorable outcomes.
Keywords: TTP, twin pregnancy, ADAMTS13, caplacizumab, case report
Plain Language Summary
When a rare and dangerous blood disorder appears during pregnancy
Thrombotic thrombocytopenic purpura (TTP) is a rare but very serious blood condition where small blood clots form throughout the body. This can cause dangerously low platelet counts and damage red blood cells. Although TTP is uncommon, it can be triggered by pregnancy and is especially difficult to diagnose because its symptoms can look very similar to common pregnancy complications like preeclampsia or HELLP syndrome.
In this case, a 29-year-old woman pregnant with twins developed TTP in her third trimester. She arrived at the hospital with bleeding gums, shortness of breath, palpitations, and very low platelets. Doctors initially suspected common pregnancy problems, but careful blood tests showed signs of TTP. Because of the high risk to both mother and babies, an emergency caesarean section was performed. After delivery, special blood tests confirmed the diagnosis.
The medical team treated her quickly with plasma exchange, steroids, rituximab, and a newer medication called caplacizumab. Even though she faced complications after surgery (including wound infection), she recovered well. Both the mother and her baby girls were discharged in good health, with no signs of the disease returning after six weeks.
This case shows that with fast recognition, teamwork between obstetricians and blood specialists, and modern treatment, even severe TTP in a twin pregnancy can have a good outcome. It highlights the importance of considering rare conditions when common pregnancy problems do not fully explain a patient’s symptoms.
Introduction
Thrombotic thrombocytopenic purpura (TTP) is a rare but life-threatening thrombotic microangiopathy.1,2 It is characterized by severe deficiency of the von Willebrand factor-cleaving protease ADAMTS13, leading to microvascular thrombosis, microangiopathic hemolytic anemia, thrombocytopenia, and potential multi-organ involvement.1,3 In the general population, the annual incidence of TTP is estimated at 2–11 cases per million,4 but pregnancy significantly increases the risk, with pregnancy-associated TTP occurring in approximately 1 in 25,000 to 100,000 pregnancies,5 far higher than non-pregnant rates. Acquired (immune-mediated) TTP, driven by autoantibodies against ADAMTS13, most commonly manifests in the second or third trimester or postpartum period.5 The condition frequently overlaps clinically with more common obstetric conditions such as preeclampsia, HELLP syndrome, and atypical hemolytic uremic syndrome.6 This diagnostic mimicry often delays recognition and treatment, contributing to elevated maternal and fetal morbidity and mortality if untreated.7
Twin pregnancies further complicate the clinical landscape due to heightened physiological demands, including increased plasma volume, enhanced hypercoagulability, and greater hemodynamic stress.8 These changes may amplify thrombotic risk and pose additional therapeutic challenges.9 Twin gestations are inherently associated with higher rates of obstetric complications, such as preterm delivery, hypertensive disorders (including preeclampsia), cesarean sections, and intrauterine growth restriction,10 all of which can compound the management difficulties in TTP and potentially worsen outcomes compared to singleton pregnancies.8
Reports of TTP specifically arising in twin pregnancies remain sparse and are largely confined to isolated case reports rather than systematic series, so the diagnostic approach and expected clinical trajectory in this setting are not well established; this case contributes additional detail on the diagnostic overlap with obstetric emergencies and the relapsing course that can occur in a twin gestation.
The standard first-line management of acquired TTP involves urgent therapeutic plasma exchange combined with corticosteroids.11 Refractory cases, those unresponsive to standard plasma exchange and corticosteroids, require escalated immunosuppression and targeted therapies like caplacizumab (a von Willebrand factor inhibitor) to interrupt microthrombi formation and prevent organ damage.12 Although emerging case reports and series support the safe and effective use of these agents in pregnancy-associated TTP, including in refractory scenarios, documented experiences in twin gestations remain limited,5,13,14 indicating the need for multidisciplinary approaches to optimize maternal and fetal survival.
We present a case of refractory acquired TTP in the third trimester of a twin pregnancy. The case is characterized by diagnostic overlap with obstetric emergencies, profound thrombocytopenia, microangiopathic hemolytic anemia, successful emergency delivery, and confirmation via ADAMTS13 testing. This case indicates the critical importance of early suspicion, rapid diagnostic confirmation, and tailored intervention in high-risk pregnancy scenarios.
Case
Patient History
A 29-year-old Ugandan woman (gravida with one previous live birth via cesarean section due to fetal distress) carrying dichorionic-diamniotic twins presented to the emergency department in the third trimester of her current pregnancy.
Her primary concerns included progressive palpitations, shortness of breath on exertion, bleeding from the mouth (gum bleeding), numbness in the right hand, chest heaviness, generalized fatigue, bilateral pedal edema, and recent pelvic and chest pain. She reported no fever, abdominal pain, headache, visual disturbances, or altered fetal movements. Symptoms had worsened over the preceding weeks, with increasing anxiety and weakness.
Relevant medical history included a prior cesarean section in her first pregnancy, complicated by fetal distress and low pregnancy-related hormones, along with a high body mass index. She had no personal or family history of bleeding disorders, thrombotic events, autoimmune diseases, or genetic conditions (no known thrombophilias or ADAMTS13-related mutations). She was a non-smoker, non-alcoholic consumer, and had no psychosocial stressors reported beyond normal pregnancy concerns. Antenatal care was regular, with frequent visits due to twin gestation and prior history; scans consistently showed normal fetal growth and size, but persistent mild proteinuria was noted on dipstick testing without hypertension.
Relevant past interventions included routine antenatal supplementation (iron, folic acid) and monitoring for gestational complications. No prior blood disorders, transfusions, or immunosuppressive therapies were documented.
Clinical Findings
On admission to the emergency department, the patient was alert, oriented, and hemodynamically stable. Vital signs included normal blood pressure (no hypertension noted), regular pulse, respiratory rate mildly elevated consistent with shortness of breath, and no fever.
General physical examination revealed moderate pallor, mild jaundice of the sclera, bilateral non-pitting pedal edema, with no generalized anasarca or ascites. There were no petechiae, purpura, ecchymoses, or other overt signs of bleeding on skin or mucous membranes. No bruising or red spots were observed on the body.
Cardiovascular examination showed normal heart sounds with no murmurs, rubs, or gallops; however, the patient reported chest heaviness and palpitations, prompting an ECG.
Respiratory examination was unremarkable, with clear lung fields bilaterally, though the patient complained of dyspnea.
Abdominal examination demonstrated a gravid uterus appropriate for third-trimester twin gestation (fundal height and abdominal circumference consistent with gestational age), no tenderness, rebound, or guarding, and normal bowel sounds. Fetal heart tones were present and reassuring, with no reported abnormalities in fetal movements.
Neurological examination was normal: no focal deficits, altered mental status, confusion, headache, visual changes, seizures, or sensory/motor abnormalities.
Other systems were unremarkable.
Diagnostic Assessment
Laboratory Testing
Complete Blood Count
Hemoglobin level was low, platelets profoundly reduced at 8 × 109/L, white blood cell count normal. Figure 1.
Figure 1.
The CBC results during the admissions.
Peripheral Blood Film
Numerous schistocytes (fragmented red blood cells) confirming microangiopathic hemolytic anemia (MAHA). Schistocytes were assessed qualitatively on manual differential; formal grading using a standardized quantitative scoring system, and a representative smear image from the initial admission, were not retained and are not available for inclusion in this report.
Biochemical Markers
Elevated lactate dehydrogenase (LDH, indicating red cell destruction), mildly elevated total bilirubin, normal liver enzymes (ALT/AST), normal renal function (creatinine and urea within reference range initially), normal coagulation profile (prothrombin time, activated partial thromboplastin time, fibrinogen normal, excluding disseminated intravascular coagulation).
Urinalysis
Persistent proteinuria (noted antenatally and on admission), mild hematuria.
ADAMTS13 Activity Assay
Severely reduced (<10% of normal), with subsequent inhibitor assay positive (confirming acquired, immune-mediated TTP).
Imaging and Other Studies
Electrocardiogram (ECG): Minor nonspecific changes (concave ST segments, small QRS notch); no evidence of acute ischemia.
Echocardiogram: Normal cardiac chambers, valves, and function; no pericardial effusion.
Post-delivery imaging (as complications arose): Doppler ultrasound of right arm (superficial vein thrombosis), abdominal ultrasound (minor fluid collection at cesarean wound site), CT pulmonary angiogram (negative for pulmonary embolism).
Diagnostic Challenges
The presentation posed significant diagnostic difficulty due to substantial clinical overlap with pregnancy-specific microangiopathies. Severe thrombocytopenia, proteinuria, and edema raised concern for preeclampsia or HELLP syndrome, both far more common in the third trimester of twin pregnancies. However, the absence of hypertension, normal liver enzymes, and lack of right upper quadrant pain or neurologic symptoms (eg, headache, visual changes) made these less likely. The presence of schistocytes and markedly elevated LDH pointed toward a thrombotic microangiopathy (TMA), but distinguishing TTP from atypical hemolytic uremic syndrome (aHUS) or HELLP-related TMA required ADAMTS13 testing. The twin gestation added complexity, as increased plasma volume and hypercoagulability can mask or exacerbate TMA features. Initial reluctance to perform urgent delivery without a definitive diagnosis risked rapid deterioration in maternal status given the platelet count of 8 × 109/L.
Diagnosis
Acquired (immune-mediated) thrombotic thrombocytopenic purpura (TTP), confirmed by ADAMTS13 activity <10% with evidence of inhibitor.
Differential diagnoses considered:
Preeclampsia with severe features
HELLP syndrome
Immune thrombocytopenic purpura (ITP)
Disseminated intravascular coagulation (DIC)
Atypical hemolytic uremic syndrome (aHUS)
These were excluded based on: normal blood pressure and liver enzymes (against preeclampsia/HELLP), absence of coagulopathy (against DIC), presence of MAHA/schistocytes (against isolated ITP), and ADAMTS13 level (distinguishing TTP from aHUS, where ADAMTS13 is typically normal).
Prognostic Characteristics
Untreated pregnancy-associated TTP carries a high maternal mortality rate and significant fetal risk (prematurity, intrauterine death). Refractory disease (persistent thrombocytopenia or relapse despite plasma exchange) worsens prognosis but responds well to rituximab and caplacizumab in modern series. In this case, early suspicion, emergency delivery, and multimodal therapy, including prompt recognition and treatment of the day 9 relapse that confirmed refractory disease, led to an excellent short-term prognosis with full hematologic recovery and no neurologic/renal sequelae. Long-term relapse risk remains elevated, particularly with future pregnancies, necessitating counseling and specialist follow-up.
Therapeutic Intervention
The therapeutic approach was comprehensive and multidisciplinary, beginning with an emergency cesarean section performed shortly after admission under general anesthesia with rapid-sequence induction to reduce aspiration risk in the context of the patient’s dyspnea and chest symptoms. Fetal assessment on admission was reassuring, and the indication for emergency delivery was therefore maternal rather than fetal: the profound thrombocytopenia (8 × 109/L) posed a high bleeding risk for vaginal delivery, and delivery was undertaken to safeguard the mother while definitive investigation and treatment of the suspected thrombotic microangiopathy proceeded. The procedure resulted in the successful delivery of two healthy baby girls with good Apgar scores, both of whom required only brief neonatal monitoring and had no TTP-related complications.
Specific treatment for acquired TTP commenced presumptively on the day of admission, prior to ADAMTS13 result confirmation, based on strong clinical and laboratory evidence of thrombotic microangiopathy. Daily plasma exchange using 1–1.5 plasma volumes of fresh frozen plasma as replacement fluid was instituted as first-line therapy and continued until platelet recovery and normalization of lactate dehydrogenase, typically spanning 7 days in this case. High-dose corticosteroids were administered concurrently, starting with intravenous dexamethasone 40 mg daily for four days, followed by a transition to oral prednisolone at 1 mg/kg/day with gradual tapering as hematologic parameters improved.
Because platelet response to plasma exchange and corticosteroids alone was incomplete, rituximab was added on day 3 post-delivery at a dose of 375 mg/m2 intravenously weekly for four doses to achieve B-cell depletion and reduce autoantibody production. Caplacizumab was introduced as a further adjunct during this first admission, in view of the persistently incomplete platelet response to plasma exchange, corticosteroids, and rituximab alone, given as an 11 mg subcutaneous injection daily (with the first dose administered intravenously for immediate effect) and continued for 30 days after platelet normalization.
Supportive measures addressed postoperative complications and included weight-adjusted low-molecular-weight heparin (enoxaparin 1 mg/kg subcutaneously twice daily) initiated after ultrasound confirmation of superficial right-arm vein thrombosis and continued for six weeks post-discharge. Intravenous co-amoxiclav was started empirically for wound infection, but the regimen was adjusted based on culture results to target Proteus mirabilis, Enterobacter aerogenes, Peptostreptococcus anaerobius, and Staphylococcus epidermidis; flucloxacillin was discontinued immediately upon development of an acute allergic reaction (manifested as eye pain, watering, and metallic taste) and replaced with meropenem according to sensitivity patterns, followed by oral step-down to complete the course. Daily wound dressings managed minor fluid collection at the cesarean incision site without the need for surgical drainage. Additional supportive care consisted of intravenous fluids, analgesia, packed red cell transfusion, and high-dependency unit monitoring post-delivery.
Follow-Up and Outcomes
Following initiation of plasma exchange, corticosteroids, rituximab, and caplacizumab during the first admission, the patient demonstrated an initial hematologic response. Platelet counts began to rise within 48–72 hours of starting plasma exchange and, together with declining lactate dehydrogenase and a progressively resolving peripheral smear, reached normal levels (242 × 109/L) by day 6, at which point she was discharged home with complete resolution of her presenting symptoms (fatigue, dyspnea, chest heaviness, oral bleeding, and numbness), on continued outpatient rituximab and caplacizumab.
Three days after this initial discharge (day 9 of the overall clinical course), the patient was readmitted with recurrence of profound thrombocytopenia (platelet count 11 × 109/L) despite ongoing rituximab and caplacizumab therapy. This relapse, occurring after an initial adequate hematologic response to plasma exchange, corticosteroids, rituximab, and caplacizumab, confirmed the diagnosis of refractory acquired TTP. She was managed with reinstitution of plasma exchange alongside continued rituximab and caplacizumab, and was monitored in a high-dependency unit before transfer to a general ward as her condition stabilized. Platelet counts normalized again (376 × 109/L) and she was discharged in good condition on day 18 overall, with both mother and her twin daughters well. Both infants required only routine neonatal care and exhibited normal growth and development at discharge, with no evidence of TTP-related sequelae. Details in Table 1.
Table 1.
Summary of Key Biochemical Findings on Admission and Their Trend During the Treatment Course
| Parameter | Admission (Day 1) | Trend During Treatment Course | Reference/Interpretation |
|---|---|---|---|
| Lactate dehydrogenase (LDH) | Markedly elevated | Progressive normalization with plasma exchange | Elevated indicates active hemolysis |
| Total bilirubin | Mildly elevated | Normalized | – |
| ALT/AST (liver enzymes) | Normal | Remained normal throughout | – |
| Creatinine and urea (renal function) | Normal | Remained normal throughout | – |
| Coagulation profile (PT, aPTT, fibrinogen) | Normal | Remained normal (argued against DIC) | – |
| Platelet count | Severely reduced (8 × 109/L) | Biphasic course – see Figure 1 for serial values | 150–450 × 109/L |
| ADAMTS13 activity | Severely reduced (<10%) | Not reassessed after treatment | Severe deficiency defined as <10% |
Notes: Exact numeric laboratory values for LDH, bilirubin, and renal/liver function were not retained in the patient’s local records beyond the qualitative trends summarized above; this is acknowledged as a limitation in the Discussion. Serial platelet and complete blood count values are provided in Figure 1.
At six-week outpatient follow-up, measured from the second and final hospital discharge, the patient remained asymptomatic with normal platelet counts, hemoglobin, LDH, and renal/liver function tests, and no further relapse. Repeat ADAMTS13 activity was not rechecked per local protocol, which we acknowledge as a limitation in confirming durable biochemical remission. No neurologic, renal, or cardiac complications developed. Low-molecular-weight heparin was continued for the full six weeks post-thrombosis diagnosis and then discontinued without recurrence of venous events. Immunosuppressive therapy (prednisolone) was tapered and stopped without rebound thrombocytopenia, and rituximab effects were well-tolerated with no infectious sequelae attributable to B-cell depletion during the follow-up period.
Adherence to the prescribed regimen was excellent, as assessed through direct patient questioning, review of inpatient medication administration records, and confirmation of outpatient prescription fulfillment and attendance at follow-up visits. The patient reported good tolerability of plasma exchange (no major procedural complications), rituximab (infusions completed without infusion reactions), and caplacizumab (daily subcutaneous injections self-administered post-education without significant injection-site reactions or bleeding). Corticosteroids were well-tolerated at the doses used, with no hyperglycemia, hypertension exacerbation, or other common adverse effects noted.
Adverse and unanticipated events included postoperative wound infection with polymicrobial organisms (Proteus mirabilis, Enterobacter aerogenes, Peptostreptococcus anaerobius from wound swabs and Staphylococcus epidermidis bacteremia likely line-related), which required prolonged intravenous antibiotics and temporary regimen changes due to an acute allergic reaction to flucloxacillin (manifested as periorbital pain, lacrimation, and metallic taste within minutes of infusion). This was promptly recognized, the drug was discontinued, and substituted with an alternative agent based on sensitivity results, with resolution of infection. A superficial right-arm vein thrombosis was detected on ultrasound after cannula-site swelling and pain, treated successfully with anticoagulation without progression to deep vein thrombosis or pulmonary embolism (CT pulmonary angiogram negative). Minor subcutaneous fluid collection at the cesarean wound site resolved with conservative dressing management and did not require drainage or re-intervention.
Overall, the maternal and neonatal outcomes were excellent, with complete clinical and hematologic remission, no long-term sequelae, and return to normal daily activities by the six-week review. The patient was counseled regarding the high risk of TTP relapse in future pregnancies and advised to avoid conception without preconception hematology and high-risk obstetrics consultation, including potential prophylactic plasma exchange in any subsequent gestation.
Discussion
This case report describes the successful management of refractory acquired thrombotic thrombocytopenic purpura (TTP) in the third trimester of a twin pregnancy. The medical literature on pregnancy-associated TTP highlights its rarity and diagnostic pitfalls, with acquired immune-mediated TTP comprising most cases triggered in the second or third trimester. Scully et al15 reported that pregnancy-associated TTP often overlaps with preeclampsia/HELLP, leading to diagnostic delays and historically high mortality though plasma exchange has reduced this to 10–20% in modern cohorts.16,17 Twin pregnancies appear underrepresented but carry heightened risks due to increased hypercoagulability and hemodynamic demands.9,10 Jacob et al18 described a refractory first-trimester twin case requiring plasma exchange, rituximab, and caplacizumab after initial failure, resulting in fetal loss but maternal recovery. Similarly, reviews emphasize that refractory TTP (persistent thrombocytopenia despite plasma exchange and corticosteroids) benefits from adjunctive rituximab for B-cell depletion and caplacizumab to inhibit von Willebrand factor-platelet interactions, with emerging reports supporting their use in pregnancy despite limited safety data.5,19
Outcomes in treated cases are generally excellent when prompt, with complete hematologic remission in 80–90% and low relapse during the index pregnancy, though subsequent pregnancies carry 30–50% relapse risk in acquired TTP.20,21 Placental pathology often shows maternal vascular underperfusion, but prophylactic plasma in known cases improves fetal survival.22 Our case aligns with these trends, demonstrating effective multimodal therapy in a late twin gestation despite complications.
A major strength was the rapid recognition of thrombotic microangiopathy based on clinical features (severe thrombocytopenia, microangiopathic hemolytic anemia with schistocytes, elevated lactate dehydrogenase) despite diagnostic overlap with preeclampsia and HELLP syndrome. The absence of hypertension, normal liver enzymes, and prompt peripheral blood smear examination facilitated early suspicion of TTP, enabling presumptive initiation of plasma exchange before ADAMTS13 results were available. The multidisciplinary collaboration among obstetrics, hematology, critical care, and neonatology teams ensured coordinated care. These included timely emergency cesarean delivery to mitigate maternal bleeding risk and fetal compromise, and escalation to rituximab and caplacizumab for refractory disease. Postoperative complications (polymicrobial wound infection, antibiotic allergy, superficial thrombosis) were managed effectively with culture-guided antibiotics, prompt allergy substitution, and anticoagulation, contributing to full recovery without long-term sequelae.
A limitation was the reliance on a reference laboratory for ADAMTS13 testing, which delayed confirmatory results post-delivery; in resource-limited settings, this could prolong diagnostic uncertainty. Additionally, while caplacizumab was used successfully, its application in pregnancy remains off-label with limited prospective data, reflecting the challenge of balancing maternal benefit against potential fetal risks in rare conditions. The twin gestation added complexity due to amplified physiological stress, but outcomes were favorable compared to reported higher fetal loss rates in untreated or delayed cases. As with any single case report, these findings cannot be generalized. The six-week follow-up period, timed from the second and final hospital discharge, is relatively short and cannot exclude late relapse, and ADAMTS13 activity was not reassessed after treatment, so durable biochemical remission could not be confirmed; longer, ADAMTS13-guided follow-up would strengthen confidence in this favorable short-term outcome.
Conclusion
This case adds to the small body of literature on refractory acquired TTP in twin pregnancy by illustrating two specific clinical lessons. First, an initial hematologic response to plasma exchange, corticosteroids, rituximab, and caplacizumab does not exclude subsequent relapse: our patient’s disease recurred three days after apparent recovery and was confirmed refractory only at that point, underscoring the need for close monitoring even after platelet counts normalize and the patient is discharged. Second, unlike a previously reported first-trimester refractory twin case that ended in fetal loss, both twins in our later-gestation case survived, suggesting that gestational age at presentation and prompt delivery may meaningfully influence fetal outcome in this setting. We should maintain a low threshold for TTP in pregnant women with thrombocytopenia and hemolytic signs even without hypertension, anticipate the possibility of relapse after an initial response before escalation to rituximab and caplacizumab is considered complete, and ensure close postpartum monitoring, ADAMTS13-guided follow-up, and preconception counseling to mitigate relapse risks in future gestations. Broader recommendations for the general management of TTP in pregnancy should continue to rely on larger case series rather than this single report.
Acknowledgments
The authors express their sincere gratitude to the multidisciplinary team at Mulago National Referral Hospital and affiliated facilities, including the hematology, obstetrics, critical care, neonatology, infectious diseases, microbiology, and nursing teams, for their collaborative and dedicated care of the patient. We also thank the patient and her family for their cooperation, trust, and written consent to share this clinical experience for educational and scientific purposes.
Funding Statement
This case report received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Declaration on the Use of Artificial Intelligence
The authors declare that Artificial Intelligence tools were used in the preparation of this manuscript in accordance with the Taylor & Francis AI Policy. Grammarly (Grammarly Inc.) was used for grammar checking, spelling correction, sentence clarity, and language polishing throughout the manuscript. As a continuously updated, cloud-based service, Grammarly does not issue a discrete, citable version number; the free/web version was used during manuscript preparation in 2026. All suggestions generated by Grammarly were carefully reviewed, critically evaluated, and edited by the authors. The final content, clinical interpretations, diagnostic reasoning, scientific conclusions, and intellectual responsibility remain entirely with the authors.
Data Sharing Statement
All relevant de-identified data supporting the findings of this case report are available from the corresponding author (Morrish Obol Okello) upon reasonable request, subject to institutional approval and compliance with data protection regulations.
Ethics Approval and Consent to Participate
This case report was prepared in accordance with ethical principles for medical case reporting. No separate formal ethical approval was required for publication of a single anonymized case report at our institutions, as it does not constitute human subjects research involving systematic investigation designed to develop or contribute to generalizable knowledge. Written informed consent for publication was obtained as described above, in full compliance with institutional guidelines and CARE reporting standards. Patient confidentiality was strictly maintained throughout, and all data were handled in accordance with applicable data protection principles.
Consent for Publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. The patient was informed that all personally identifiable information would be de-identified, that the report would be submitted to a peer-reviewed medical journal, and that she retained the right to withdraw consent at any time before publication. A signed consent form is retained in the patient’s medical file and is available from the corresponding author upon reasonable request.
Author Contributions
All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Disclosure
The authors declare that they have no competing interests, financial or otherwise, related to this case report.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All relevant de-identified data supporting the findings of this case report are available from the corresponding author (Morrish Obol Okello) upon reasonable request, subject to institutional approval and compliance with data protection regulations.