Multiple recurrences of Talaromyces marneffei infection with HLH in an HIV-negative patient: a case report

Abstract

Background

Talaromycosis complicated by hemophagocytic lymphohistiocytosis (HLH) is a life-threatening condition associated with high mortality, yet the management of recurrent disease in HIV-negative patients is not well defined.

Case presentation

We report a 49-year-old man who presented with fever, lymphadenopathy, and an uncommon ulcerative scalp lesion that has been poorly documented in HIV-negative talaromycosis. Talaromyces marneffei (T. marneffei) infection was confirmed by blood culture, and HLH was subsequently diagnosed. Initial induction therapy with amphotericin B deoxycholate (AmB-D) followed by itraconazole (ITZ) maintenance resulted in clinical improvement; however, the patient experienced multiple recurrences over three years, including a recurrence while on ITZ. Immunological evaluation later revealed positive anti-interferon-γ autoantibodies (AIGA). Re-induction with liposomal amphotericin B (L-AmB) followed by maintenance posaconazole (PCZ) resulted in short-term remission, with no recurrence during three months of follow-up.

Conclusions

This case demonstrates the successful management of recurrent talaromycosis with L-AmB induction followed by PCZ maintenance in an HIV-negative patient with AIGA-associated immunodeficiency presenting with initial HLH, highlighting the importance of early diagnosis, individualized antifungal strategies, and the potential utility of PCZ as maintenance therapy in high-risk patients.

Introduction

Talaromyces marneffei (T. marneffei) is a thermally dimorphic fungus endemic in Southeast Asia and southern China [1]. Infection has historically been associated with advanced HIV but is increasingly recognized in non-HIV immunocompromised individuals [2]. The clinical presentation is often non-specific and may mimic tuberculosis or lymphoma, leading to frequent misdiagnosis and delayed treatment [3–5]. Characteristic skin lesions are present in only 21% of HIV-negative cases and poorly documented in the literature [2, 3].

Hemophagocytic lymphohistiocytosis (HLH) as a complication of talaromycosis in HIV-negative patients is rare but associated with markedly high mortality in limited reports [6, 7]. Treatment strategies in HIV-negative patients are often extrapolated from regimens established for HIV-associated talaromycosis, in which amphotericin B induction followed by itraconazole (ITZ) consolidation or maintenance remains the core approach [8]. However, optimal treatment duration and discontinuation criteria remain poorly defined in HIV-negative patients [5, 8, 9]. Recurrence has been reported in a subset of patients, yet detailed reports on their clinical course and management are scarce [10]. Moreover, reliable biomarkers and data on antifungal selection after relapse remain limited [8].

Herein, we report an HIV-negative patient with talaromycosis complicated by HLH who, despite multiple recurrences, ultimately achieved remission following re-induction with liposomal amphotericin B (L-AmB) and maintenance with posaconazole (PCZ), and remained recurrence-free during three months of follow-up. At initial presentation, the patient exhibited a rarely documented characteristic cutaneous manifestation.

Case report

A 49-year-old man presented to our department with a one-month history of recurrent sore throat and fever (maximum 39 °C). The patient had a history of hypertension but no other significant medical, family, or psychosocial history, and reported no specific dietary or lifestyle factors relevant to the present illness. Initial evaluation at a local hospital revealed leukocytosis with neutrophilia. Oropharyngeal magnetic resonance imaging demonstrated inflammatory lesions in the left oropharyngeal and nasopharyngeal soft tissues, with multiple enlarged lymph nodes in bilateral parapharyngeal spaces and neck. ¹⁸F-FDG PET/CT performed at a local hospital revealed extensive hypermetabolic lymphadenopathy (cervical, supraclavicular, mediastinal, retroperitoneal, and pelvic regions) and hypermetabolic thickening of the left pharyngeal wall and left iliac fossa intestinal wall, with findings highly suggestive of lymphoma (Fig. 1). However, pathological examination of the left tonsil and oral mucosa revealed only chronic inflammation, and empirical anti-inflammatory and antipyretic therapies yielded no significant improvement.

Fig. 1.

Representative PET/CT fusion images showing diffusely elevated ¹⁸F-FDG metabolism in widespread lesions. (A) Sagittal PET/CT and coronal PET views. (B) Axial neck PET/CT slices. The solid red arrowhead (▷) indicates thickening of the left lateral pharyngeal wall with intense ¹⁸F-FDG uptake; red arrows (→) mark multiple hypermetabolic cervical lymph nodes. (C) Axial pelvic PET/CT slices. Asterisks (*) denote thickening of the intestinal wall in the left iliac fossa with elevated ¹⁸F-FDG metabolism. (D) Axial abdominal PET/CT slices. Red arrows (→) indicate hypermetabolic retroperitoneal and abdominal lymph nodes

On admission, physical examination revealed the patient was febrile (38.8 °C), with white plaques on the posterior pharyngeal wall, enlarged tonsils, palpable cervical and submandibular lymphadenopathy, and an ulcerative scalp rash (Fig. 2A). Laboratory evaluation revealed leukocytosis, elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), elevated liver enzymes, hyperferritinemia, and elevated serum (1,3)-β-D-glucan (G-test); immunological workup showed decreased immunoglobulins and T-cell subsets (Table 1). Autoimmune workup revealed negative antinuclear antibody (ANA), with normal anti-streptolysin O (ASO) and antiphospholipid antibodies. Cytokine profiling demonstrated elevated interleukin-6, interleukin-10, interferon-γ, and interleukin-17 A. Imaging studies, including B-mode ultrasound and chest computed tomography, confirmed extensive lymphadenopathy, hepatosplenomegaly, ascites, bilateral pleural effusion, and pulmonary inflammation—suspicious for lymphoma. Clinically, the patient presented with recurrent high fever (> 38.5 °C, peak 39.5 °C) and cough. Empirical antibacterial and voriconazole antifungal therapy, along with liver protection and symptomatic support, was initiated.

Fig. 2.

Serial scalp photographs and clinical treatment timeline. (A) Evolution of scalp lesions during the initial episode (first treatment course), before, during, and after AmB‑D treatment. Serial photographs were obtained on hospital day 3, hospital day 7, hospital day 19, hospital day 30, and on day 94 from initial presentation. (B) Clinical course timeline showing antifungal regimens, key clinical events, and serial serum (1,3)-β-D-glucan (G-test) levels. The dotted horizontal line indicates the normal reference threshold (< 60 pg/mL). Abbreviations: AmB‑D, Amphotericin B deoxycholate; L‑AmB, Liposomal amphotericin B; ITZ, Itraconazole; PCZ, Posaconazole

Table 1.

Laboratory findings at admission

Characteristic	Result	Reference range
Complete blood count
WBC	10.06 × 10⁹/L	4–10
Neutrophil count	9.36 × 10⁹/L	2–7
Hemoglobin	118 g/L	131–172
Platelets	177 × 10⁹/L	83–303
CRP	85 mg/L	0–6
ESR	38 mm/h	0–15
Liver function
ALT	172 U/L	9–50
AST	122 U/L	15–40
ALP	261 U/L	45–125
GGT	331 U/L	10–60
Tbil	14.6 µmol/L	0–26
Dbil	12 µmol/L	0–8
HLH-related parameters
Ferritin	5146.53 ng/mL	11.2-488.8
Triglycerides	1.25 mmol/L	0.3–1.7
Fibrinogen	4.6 g/L	2.0–4.0
sCD25	27,820 pg/mL	< 6400
NK cell activity	12.29%	≥ 15.11
Immunoglobulins
IgG	540 mg/dL	860–1740
IgA	129 mg/dL	100–420
IgM	39.6 mg/dL	30–220
Lymphocyte subsets
CD3⁺ T cells	47.7%	50–84
CD4⁺ T cells	20%	27–51
CD8⁺ T cells	24.6%	15–44
NK cells	6.2%	7–40
Serum 1,3-β-D-glucan test (G-test)	166.21 pg/ml	1–60
HIV p24 antigen/antibody	Negative	S/CO < 1.0
CMV DNA	Below detection limit	0-200 IU/mL
EBV DNA	Below detection limit	0-200 IU/mL
T-SPOT	Negative

Abbreviations: WBC, White blood cell count; CRP, C-reactive protein; ESR, Erythrocyte sedimentation rate; ALT, Alanine aminotransferase; AST, Aspartate aminotransferase; ALP, Alkaline phosphatase; GGT, Gamma-glutamyl transferase; TBil, Total bilirubin; DBil, Direct bilirubin; HLH, Hemophagocytic lymphohistiocytosis; sCD25, Soluble CD25; NK, Natural killer; Ig, Immunoglobulin; CD, Cluster of differentiation; HIV, Human immunodeficiency virus; CMV, Cytomegalovirus; EBV, Epstein–Barr virus; DNA, Deoxyribonucleic acid; G-test, Serum 1,3-β-D-glucan test; T-SPOT, Tuberculosis-specific interferon-gamma release assay

Because of the lack of response to empirical anti-infective therapy, an excisional biopsy of a left cervical lymph node was performed on hospital day 4 to further exclude lymphoma. The oropharyngeal biopsy slides from the local hospital were also re-reviewed by our pathologists. Notably, a blood culture collected on admission grew T. marneffei on hospital day 7. Following infectious disease consultation, antifungal therapy was promptly switched to amphotericin B deoxycholate (AmB-D) at 0.5 mg/kg/day (35 mg/day). On hospital day 8, the cervical lymph node biopsy result confirmed T. marneffei infection and showed no malignant cells. Concurrently, a diagnosis of HLH was made (5 of 8 HLH-2004 criteria met; Table 2), supported by reduced NK cell activity (12.29%; normal range ≥ 15.11%, measured by flow cytometry using K562-GEP target cells, performed in duplicate by KingMed Diagnostics) and markedly elevated soluble CD25 levels (27820 pg/mL; normal range < 6400), in conjunction with other clinical findings. The reviewed oropharyngeal biopsy (result available on hospital day 10) also confirmed T. marneffei infection and showed no malignant cells. Bone marrow (BM) examination, including aspiration, biopsy, immunophenotyping, and cytogenetic analysis, showed no evidence of hemophagocytosis or lymphoma cells. Thus, no evidence of lymphoma was identified based on histopathological and immunophenotypic findings. Respiratory and dermatological consultations further attributed the pulmonary lesions and scalp rash to disseminated talaromycosis.

Table 2.

Diagnostic evaluation of HLH based on the HLH-2004 criteria and HScore

HLH-2004 criteria1	Patient’s finding	Fulfilled
Fever (≥ 38.5 °C)	> 39.4 °C	Yes
Splenomegaly	Present	Yes
Cytopenias affecting ≥ 2/3 lineages in the peripheral blood	Hb 118 g/L; platelets 177 × 10⁹/L; neutrophils 9.36 × 10⁹/L	No
Hypertriglyceridemia and/or hypofibrinogenemia: fasting triglycerides ≥ 3.0 mmol/L; fibrinogen ≤ 1.5 g/L	TG 1.25 mmol/L, Fibrinogen 4.6 g/L	No
Hemophagocytosis	Not observed on bone marrow aspiration	No
Low or absent NK-cell activity	12.29%, below the reference range	Yes
Ferritin ≥ 500 ng/mL	5146.53 ng/m	Yes
Elevated sCD25	27,820 pg/mL, above the reference range	Yes
Total criteria met		5/8
HScore2		125

Note: HLH was evaluated according to the HLH-2004 criteria. HScore was calculated separately and was not counted as one of the HLH-2004 criteria

Abbreviations: Hb, Hemoglobin; HLH, Hemophagocytic lymphohistiocytosis; NK, Natural killer; Plt, Platelet; sCD25, Soluble CD25; sIL-2R, Soluble interleukin-2 receptor; TG, Triglyceride

¹Fardet, L., Galicier, L., Lambotte, O., Marzac, C., Aumont, C., Chahwan, D., Coppo, P. and Hejblum, G. (2014), Development and Validation of the HScore, a Score for the Diagnosis of Reactive Hemophagocytic Syndrome. Arthritis & Rheumatology, 66: 2613-2620. https://doi.org/10.1002/art.38690

²Fardet L, Galicier L, Lambotte O, et al. Development and validation of the HScore, a score for the diagnosis of reactive hemophagocytic syndrome. Arthritis Rheumatol. 2014;66(9):2613-2620. doi:10.1002/art.38690

After targeted treatment with AmB-D (1 month) and cefoperazone–sulbactam, the patient’s fever, ascites, inflammatory markers, and oropharyngeal lesions improved. The characteristic skin lesions of talaromycosis gradually evolved and eventually resolved (Fig. 2A). The patient received oral ITZ at 200 mg twice daily for 2 months, then 200 mg once daily for 4 months (Fig. 2B), before the patient voluntarily discontinued the medication.

Over the following years, the patient experienced multiple febrile recurrences of talaromycosis, with elevated G-test levels in most episodes (Table 3). The first recurrence (at 11 months) was confirmed by blood metagenomic next-generation sequencing (mNGS). This recurrence was managed with AmB-D re-induction (35 mg/day for 30 days), followed by ITZ at 200 mg twice daily for 2 months, then 200 mg once daily for 4 months, for a total of 6 months. Subsequent episodes occurred at 22 months (intestinal obstruction with CT findings of small bowel obstruction (Fig. 3); emergency resection at a local hospital; pathology confirmed T. marneffei infection after expert pathological consultation), for which the patient took ITZ only intermittently due to poor adherence; at 29 months (high fever with abdominal lymphadenopathy), which was managed with AmB-D (25 mg/day for 15 days), followed by ITZ maintenance for 5 months; and at 34 months (recurrence while on ITZ), with positive blood culture, positive BM NGS, and anti-interferon-γ autoantibodies (AIGA) detected by ELISA (positive, titer 1:8000). For the episode at 34 months, the patient received L-AmB at 150 mg/day for 30 days, followed by PCZ maintenance at 300 mg once daily for 8 months, with normalization of serum G-test and BM NGS findings at the time of treatment discontinuation. Treatment was then stopped. PCZ trough levels measured at 3, 4, and 8 months after initiation of maintenance therapy were 1.86 mg/L, 2.09 mg/L, and 1.52 mg/L, respectively, all above the recommended therapeutic threshold (> 1.0 mg/L). As of the last follow-up, the patient had been recurrence-free for three months.

Table 3.

Timeline of initial and recurrent disseminated talaromycosis episodes and antifungal treatment

Episode	Time point	Clinical presentation	Microbiological/pathological confirmation	Serum 1,3-β-D-glucan, pg/mL	Imaging findings	Antifungal treatment	Maintenance and duration	Outcome
Initial episode	Month 0	Fever, cough, sore throat, and ulcerative scalp lesions	Blood culture and pathological examination confirmed T. marneffei infection	166.21	PET/CT showed extensive hypermetabolic lymphadenopathy involving cervical, supraclavicular, mediastinal, abdominal, and pelvic regions, with hypermetabolic lesions in the pharyngeal/intestinal wall; chest CT showed bilateral pulmonary inflammatory lesions and pleural effusion.	AmB-D, 35 mg/day for 30 days	ITZ for 6 months	Improved
Recurrence 1	Month 11	Fever	Blood mNGS detected T. marneffei	21	Chest CT showed decreased supraclavicular/mediastinal lymphadenopathy and partially absorbed pulmonary inflammatory lesions; abdominal CT showed small bowel wall thickening, mesenteric lymphadenopathy, peritoneal thickening, and enlarged abdominal lymph nodes.	AmB-D, 35 mg/day for 30 days	ITZ for 6 months	Improved
Recurrence 2	Month 22	Abdominal pain, vomiting, and intestinal obstruction	Pathological examination of the resected small bowel confirmed T. marneffei infection	Not measured	Chest CT showed scattered tiny nodules in both lungs. Abdominal CT showed marked thickening of the small bowel wall with surrounding exudates, suspicious for a mass, and incomplete small bowel obstruction.	No re-induction; ITZ alone	Intermittent ITZ for 5 months	Improved after surgery
Recurrence 3	Month 29	Fever and abdominal lymphadenopathy	Not microbiologically or pathologically confirmed; clinical recurrence was suspected based on symptoms, imaging findings, elevated 1,3-β-D-glucan, and treatment response	640	Abdominal CT showed postoperative small bowel changes and multiple enlarged lymph nodes in the porta hepatis and retroperitoneal regions.	AmB-D, 25 mg/day for 15 days	ITZ for 5 months	Improved
Recurrence 4	Month 34	Fever, abdominal distension, and fatigue	Blood culture was positive for T. marneffei; bone marrow NGS also detected T. marneffei	893	Chest CT showed bilateral pulmonary inflammatory lesions, focal consolidation, and bilateral pleural effusion; abdominal CT/MRI showed hepatosplenomegaly, splenic lesions, intra-abdominal exudation, and small-volume ascites.	L-AmB, 150 mg/day for 1 month	PCZ for 8 months	No recurrence during the available follow-up period

Note: Serum 1,3-β-D-glucan is a nonspecific fungal biomarker and was interpreted together with clinical manifestations, microbiological/pathological evidence, imaging findings, and treatment response.

Abbreviations: AmB-D, amphotericin B deoxycholate; CT, computed tomography; ITZ, itraconazole; L-AmB, liposomal amphotericin B; mNGS, metagenomic next-generation sequencing; NGS, next-generation sequencing; PCZ, posaconazole; PET/CT, positron emission tomography/computed tomography.

Fig. 3.

Axial slices of contrast-enhanced whole-abdominal CT demonstrating incomplete small bowel obstruction. (A) Low pelvic axial slice. The red arrow marks segmental small bowel in the right lower abdomen and pelvic cavity with mural thickening and surrounding peritoneal exudation. (B) Upper abdominal axial slice. The left red arrow points to small bowel with mural thickening; the right red arrow indicates dilated proximal small intestinal loops with gas and fluid retention

Of note, radiographically, pulmonary lesions had largely cleared by the time of the second recurrence, whereas abdominal lymphadenopathy slightly enlarged after the intestinal obstruction and did not resolve until the fourth episode was controlled.

Discussion

We report an HIV-negative patient with disseminated talaromycosis complicated by HLH who survived multiple recurrences over three years. This case demonstrates the successful management of recurrent talaromycosis with L-AmB induction followed by PCZ maintenance in a patient with AIGA-associated immunodeficiency presenting with initial HLH, an area with limited published evidence.

Early diagnosis and management

Talaromycosis-associated HLH confers high mortality in non-HIV populations, with early death and fatal outcomes persisting despite antifungal therapy [6, 7]. Our patient’s survival reflects early diagnosis and timely treatment: blood culture grew T. marneffei within seven days, enabling targeted AmB-D within one month of symptom onset—within the critical therapeutic window associated with improved survival. Diagnostic challenges in this case included the non-specific presentation and the difficulty in distinguishing talaromycosis from lymphoma, which required repeated biopsies.

Cutaneous manifestations

The characteristic rash provided a diagnostic clue. Our patient presented with an ulcerative scalp rash, a morphology that is recognized but poorly documented in HIV-negative patients with talaromycosis [2, 3]. Although T. marneffei-associated skin manifestations are more frequently documented in HIV-positive patients, particularly in the context of immune reconstitution inflammatory syndrome [11], the scalp lesion in our patient evolved and resolved in parallel with antifungal therapy (Fig. 2A), further supporting its association with disseminated talaromycosis and underscoring its potential diagnostic value.

Recurrences, treatment duration, and maintenance therapy

The multiple recurrences raise questions about optimal antifungal duration. The first three recurrences occurred after the patient self-discontinued ITZ following 5–6 months of maintenance therapy. Although this exceeds the recommended 10–12 week consolidation period, the optimal treatment duration in HIV-negative patients with AIGA-associated immunodeficiency remains undefined [8]. The fourth recurrence occurred despite ITZ adherence, prompting a switch to L-AmB re-induction followed by PCZ maintenance. The 2025 updated guidelines recommend L-AmB as the preferred induction therapy for talaromycosis, with PCZ serving as a potential alternative for recurrence while receiving ITZ based on its favorable in vitro antifungal activity [8, 12], and with its successful use documented in HIV-negative patients [13].

We acknowledge that antifungal susceptibility testing and ITZ therapeutic drug monitoring were not performed. Adherence to ITZ was based on patient report without drug level confirmation, and intermittent adherence following intestinal obstruction, along with potential issues with drug absorption, may have contributed to recurrence.

Role of AIGA and immunological features

AIGA detected during the fourth recurrence likely contributed to the relapsing course. AIGA-mediated adult-onset immunodeficiency is a well-recognized predisposing factor in HIV-negative individuals, particularly among Asian populations, and is strongly associated with relapse risk [14, 15]. Longitudinal immunological analysis revealed that while immunoglobulins partially recovered after antifungal therapy, lymphocyte subsets (including CD4⁺ and CD8⁺ T cells, NK cells, and B cells) remained persistently low (Table 4). This pattern of generalized lymphopenia, despite improvement in humoral immunity, may have contributed to the patient’s continued susceptibility to relapse. Genetic testing for inborn errors of immunity and HLH-related genes was not performed, which is a limitation of this report.

Table 4.

Longitudinal immunological findings during the disease course and follow-up

Episode/Time point	IgG (860–1740 mg/dL)	IgA (100–490 mg/dL)	IgM (30–220 mg/dL)	NK cells (136–880 cells/µL)	CD3 + T cells (834–2216 cells/µL)	CD8 + T cells (269–1059 cells/µL)	B cells (91–498 cells/µL)	CD4 + T cells (395–1264 cells/µL)		CD4/CD8 ratio (0.6–2.88)	NK-cell activity (≥ 15.11%)	AIGA
At diagnosis Month 0	540↓	129	39.6	—	—	—	—	—		—	12.29↓	—
Recurrence 1 Month 11	550↓	135	59.6	—	—	—	—		—	—	—	—
Recurrence 2 Month 22	473↓	121	38.8	—	—	—	—		—	—	—	—
Recurrence 3 Month 29	716↓	174	81.2	—	—	—	—		—	—	—	—
Recurrence 4 Month 34	—	—	—	76.8↓	309↓	132↓	99		171↓	1.29	—	Positive; titer, 1:8000
After recurrence 4 Month 36	1050	164	83	96↓	344↓	181↓	15.7↓		153↓	0.85	—	—
Last follow-up Month 44	679↓	171	115	97↓	393↓	193↓	59↓		181↓	0.94	—	—

Note: ↓ indicates a value below the corresponding reference range. The dash indicates that the test was not performed at that time point. Reference ranges were based on the corresponding laboratory reports.

Abbreviations: AIGA, Anti-interferon-γ autoantibody; CD, Cluster of differentiation; IgA, Immunoglobulin A; IgG, Immunoglobulin G; IgM, Immunoglobulin M; NK, Natural killer

Biomarkers and heterogeneous disease response

Serial G-test measurements appeared to partly parallel disease activity in this patient, with elevated levels during the initial episode and several subsequent recurrences and a decline after effective antifungal treatment. However, the G-test was not consistently elevated at every clinically relevant episode and was not measured during one recurrence, highlighting its limitations as a solitary marker of relapse. In clinical practice, suspected recurrence of talaromycosis should therefore not be judged by the G-test alone, but should be assessed in combination with the patient’s systemic condition, fever pattern, inflammatory markers, microbiological or pathological evidence when available, and longitudinal imaging findings. This case also illustrates heterogeneous disease responses across anatomical sites, as pulmonary lesions improved whereas abdominal lymphadenopathy and intestinal involvement became more prominent during later episodes. Comprehensive clinical, laboratory, and radiographic monitoring is therefore essential, particularly in high-risk patients with underlying immune abnormalities. The G-test may serve as a useful adjunctive and trackable biomarker, but it is non-specific and should not be interpreted as a stand-alone diagnostic or recurrence marker for talaromycosis.

Conclusions

This case demonstrates that early diagnosis and timely antifungal therapy can be critical in HIV-negative patients with talaromycosis-associated HLH. The recurrence while on ITZ and the subsequent disease control on PCZ highlight the need for individualized strategies, particularly in patients with AIGA-associated immunodeficiency. For such high-risk patients requiring re-induction, L-AmB is a rational choice given its favorable safety profile and guideline recommendation. Nevertheless, given the single-patient nature of this report and the limited post-treatment follow-up (3 months), further observation is needed to confirm the long-term durability of this remission.

Author contributions

LZ collected data and wrote the main manuscript. YL performed the figure. RT and LZ managed the patient, LSY reviewed the manuscript. All authors participated in the drafting of the manuscript and approved its final version.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

All data generated or analysed during this study are included in this published article. No additional data are available.

Declarations

Ethics approval

This study was approved by the Research Ethics Committee of The First Affiliated Hospital of Zhejiang University School of Medicine (approval number: [2006B] IIT Ethics Approval No.0525) and complied with the principles of the Declaration of Helsinki.

Consent to participate

Written informed consent to participate in the study was obtained from the patient.

Consent for publication

Written informed consent was obtained from the patient for publication of the case details.

Competing interests

The authors declare no competing interests.