Introduction
Hypercalcemia of malignancy (HCM), reported in up to 30% of patients with cancer, is associated with a grave prognosis. Four subtypes with unique pathophysiologic mechanisms have been proposed ( Almuradova and Cicin, 2023 ).
The most common subtype is humoral hypercalcemia of malignancy (HHM), mediated by tumor secretion of parathyroid hormone-related protein (PTHrP). PTHrP shares amino-terminal homology with parathyroid hormone (PTH) and acts like PTH to increase osteoclastic bone resorption and renal tubular calcium reabsorption. HHM is most frequently associated with squamous cell carcinomas of the lung, head and neck, urothelial carcinomas, breast cancers, and renal cell carcinomas, and patients typically have few or no bone metastases ( Almuradova and Cicin, 2023 ).
The second subtype, osteolytic hypercalcemia, results from extensive bone metastases, most commonly from breast cancer or multiple myeloma. Cytokines, interleukins, receptor activator of nuclear factor-κB ligand (RANKL), and PTHrP stimulate osteoclastic bone resorption and suppress osteoblastic bone formation, leading to calcium efflux that exceeds renal clearance capacity ( Almuradova and Cicin, 2023 ).
The third subtype involves ectopic production of 1,25-dihydroxyvitamin D (calcitriol) by tumor cells, which increases intestinal calcium absorption and bone resorption, and is commonly seen in Hodgkin and non-Hodgkin lymphomas ( Almuradova and Cicin, 2023 ).
The rarest subtype, accounting for less than 1% of cases, is ectopic PTH secretion by nonparathyroid tumors. In these cases, elevated serum PTH with normal or low PTHrP mimics primary hyperparathyroidism (PHPT) and frequently leads to misdiagnosis ( Almuradova and Cicin, 2023 ; Wendt et al., 2024 ).
Hypercalcemia in endometrial cancer is rare. In this report, we present two cases of poorly differentiated or dedifferentiated endometrial carcinoma with suspected ectopic PTH production, in which calcium levels closely tracked disease progression. Rapid elevation of calcium preceded clinical deterioration and ultimately fatal outcomes.
Case descriptions
Case 1
A 50-year-old premenopausal woman, gravida 0 para 0 (G0P0), presented with 4–5 months of vaginal bleeding, intermittent abdominal pain, and a 15-lb weight loss. She had no prior medical history. Family history was notable for ovarian cancer in her maternal grandmother (diagnosed at age 80).
Examination revealed an enlarged fibroid uterus (14 weeks in size). Laboratory evaluation revealed severe microcytic iron deficiency anemia with a hemoglobin of 4.6 g/dL. Initial calcium was mildly elevated, ranging from 10.3 to 11.3 mg/dL (normal range: 8.2–10.1). Imaging demonstrated retroperitoneal and pelvic lymphadenopathy, pulmonary metastases, and myometrial invasion of the endometrial tumor. CA-125 was elevated at 106.8 U/mL (normal 0–35), while CEA, CA 19–9, and AFP were normal.
Due to persistent bleeding, she underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH-BSO) and omental biopsy on hospital day 7. Pathology showed FIGO grade 3 endometrioid adenocarcinoma with squamous differentiation, ovarian and tubal involvement, and omental metastasis. Pathologic staging was pT3a, pNx, pM1 (Stage IVB). Immunohistochemistry (IHC) revealed estrogen receptor (ER) and progesterone receptor (PR) positivity, wild-type p53, patchy positivity for p16, and loss of MLH1/PMS2, consistent with mismatch repair (MMR) deficiency.
By day 15, calcium was 10.6 mg/dL and alkaline phosphatase (ALP) was elevated at 836 IU/L (normal range: 36–112). However, CT and MRI performed on day 7 showed no evidence of bone involvement, suggesting that the elevated ALP was unlikely to be due to bone metastases.
By day 30, calcium rose to 16 mg/dL with PTH 167 pg/mL (normal range: 24–85). Symptoms included severe abdominal pain, dyspnea, constipation, and anorexia. Chest imaging performed on the same day showed rapid pulmonary progression, while a CT scan of the abdomen and pelvis demonstrated newly identified spinal lesions consistent with metastatic disease.
Despite aggressive treatment with intravenous (IV) fluids and calcitonin, the calcium level remained elevated. After goals-of-care discussions, she was transitioned to comfort-focused care and died approximately one month after initial presentation.
Case 2
A 47-year-old postmenopausal woman, G0P0, presented with two months of vaginal spotting and acute pelvic pain. Her history included type 2 diabetes, hypertension, obesity, and fibromyalgia.
Imaging revealed a heterogeneous low-density uterine mass with endometrial thickening. An endometrial biopsy confirmed endometrioid carcinoma. At presentation, calcium ranged from 9.3 to 11.7 mg/dL, with PTH 310 pg/mL.
One day prior to planned hysterectomy, she developed chest pain and dyspnea. CT angiography demonstrated pulmonary nodules concerning for metastases, and her calcium increased to 15 mg/dL. PTHrP was normal. 25-hydroxyvitamin D was mildly elevated at 74.4 ng/mL (normal 20–50), while 1,25-dihydroxyvitamin D was normal.
She was treated with IV fluids, calcitonin, and cinacalcet. After six doses of calcitonin, calcium decreased to 12 mg/dL, and she continued cinacalcet.
Lung biopsy on day 38 confirmed poorly differentiated adenocarcinoma. Immunostaining was positive for AE1/3 and CDX2, partially positive for CK7, and negative for PAX8, ER, TTF-1, p40, GATA-3, GCDFP, mammaglobin, and synaptophysin.
On day 48, she presented with recurrent severe hypercalcemia (up to 15.6 mg/dL), complicated by acute pancreatitis. She was managed with bisphosphonates and cinacalcet. Endocrinology initially suspected primary hyperparathyroidism due to persistently elevated PTH levels. Neck ultrasound showed no parathyroid adenoma.
Following multidisciplinary review, it was concluded that she had metastatic endometrial cancer, with the lung biopsy representing a dedifferentiated component. On day 56, she started chemotherapy with carboplatin and paclitaxel, resulting in marked regression of lung and uterine disease and normalization of calcium and PTH levels. Four months after diagnosis, she developed brain metastases, treated with Gamma Knife radiosurgery.
On day 141, after four cycles of chemotherapy, she underwent palliative TAH-BSO to reduce bleeding risk. Pathology revealed FIGO grade 3 endometrioid carcinoma, ypT1b ypM1 (Stage IVB). IHC showed patchy CK7 positivity, CDX2 positivity, and negativity for CK20, PAX8, and Desmin. It also showed wild-type p53, heterogeneous p16, and loss of MSH6. In contrast to IHC, next-generation sequencing (NGS) revealed no MSI-high status, and germline testing was negative for MSH6 mutations and for all other 47 known pathogenic variants.
Nine months after diagnosis, she developed recurrent vaginal and pulmonary disease and started pembrolizumab with lenvatinib. Hypercalcemia recurred intermittently with rising PTH, requiring repeated cinacalcet, bisphosphonates, and hydration. Disease progression ultimately involved bone, brain, and lymph nodes. She transitioned to hospice care and died approximately 16 months after initial presentation.
Regarding the use of cinacalcet, it was initially used after one dose of bisphosphonate with good results. Its use was interrupted while her calcium level was normal and reinitiated for hypercalcemia episodes on day 48 (in combination with bisphosphonates) and during disease progression from months 9 through 16.
Discussion
In this report, we presented two cases of hypercalcemia in patients with endometrial cancer, highlighting two key observations.
First, the degree of hypercalcemia closely correlated with tumor burden and disease progression. This was evident in Case 1, in which calcium levels markedly decreased following debulking surgery and subsequently rose with rapid progression of pulmonary metastases ( Fig. 1 ). Similarly, in Case 2, calcium levels remained normal during periods of response to chemotherapy, with or without cinacalcet, but showed marked elevation as the disease progressed with involvement of the pelvis, bones, and brain near the end of life ( Fig. 2 ). Fig. 1 Calcium trends (A) and PTH level (B) and disease progression (Case 1). Normal reference ranges: calcium 8.2–10.1 mg/dL; PTH 24–85 pg/mL (upper limits represented by orange dashed lines). Fig. 1 Fig. 2 Correlation between calcium (A) and PTH (B) levels with disease activity (Case 2). The x-axis represents months from diagnosis. Key clinical events are annotated with vertical connector lines. The green bar indicates periods of cinacalcet administration. The horizontal bracket denotes the duration of carboplatin/paclitaxel chemotherapy (6 cycles). Normal reference ranges: calcium 8.2–10.1 mg/dL; PTH 24–85 pg/mL (upper limits represented by orange dashed lines). Fig. 2
Both cases demonstrated elevated PTH with normal PTHrP. In Case 2, the initial elevated PTH level led to consideration of primary hyperparathyroidism, reflecting limited awareness of the association between endometrial cancer and ectopic PTH production. In both patients, PTH levels paralleled tumor burden and disease activity. Collectively, these observations support the notion that ectopic production of PTH by tumor tissue was the primary mechanism of hypercalcemia in these two cases. Notably, during periods of rapid disease progression, both patients developed bone metastases, suggesting that osteolytic hypercalcemia likely contributed as a concurrent mechanism.
The second observation is that both cases showed poorly differentiated or dedifferentiated histology, known to be aggressive tumor subtypes with ultimately aggressive clinical behavior. Additionally, both cases showed some level of mismatch repair deficiency. Of note, mismatch repair deficiency has been found in approximately half of the cases of poorly differentiated tumors vs 9% in well to moderately differentiated tumors ( Fiumicino et al., 2001 ). Hypercalcemia and ectopic PTH production may be preferentially associated with the poorly differentiated component, which is also more commonly associated with dMMR status; yet whether and how dMMR status facilitates aberrant ectopic PTH production remains to be studied.
Both PTHrP and PTH bind to and activate the same PTH1 receptor, producing similar downstream effects on bone resorption and renal calcium handling. Standard immunoassays can differentiate the two molecules ( Walker and Shane, 2022 ). In the vast majority of cancer-associated hypercalcemia, PTHrP is elevated while PTH is suppressed. When PTH is found to be elevated, one should consider the possibility of ectopic PTH production, as shown in these cases and other reported cases ( Table 1 ). A parathyroid ultrasound should also be performed to rule out concurrent primary hyperparathyroidism. Table 1 Summary of cases of endometrial carcinoma associated with PTH-mediated hypercalcemia. Case Pathology Site Calcium, Highest (mg/dL), NR: 8.5–10.5 PTH, Highest (pg/mL), NR: 24–85 Tumor DNA mismatch repair status Treatment Survival Case 1 FIGO G3 (poorly differentiated) carcinoma Endometrial 16.2 167 Deficient in MLH1 and PMS2 TAH-BSO 1 month after initial presentation Case 2 FIGO grade 3 (poorly differentiated) adenocarcinoma Endometrial 15.4 843 Deficient in MSH6 Chemotherapy (paclitaxel and carboplatin), TAH-BSO, RT, pembrolizumab and lenvatinib, doxorubicin 16 months after initial presentation Literature 1 (Batarseh N et al.) ( Batarseh et al., 2019 ) De-differentiated Endometrial 12.8 135 No data TAH-BSO Few weeks after diagnosis Literature 2 (Liu H et al.) ( Liu et al., 2023 ) Poorly differentiated carcinoma Endometrial 14.16 2586 Deficient in MLH-1 and PMS-2 CRS (including TAH-BSO, bilateral ovarian artery ligation, bilateral internal iliac artery ligation, appendectomy, omentectomy, pelvic and para-aortic lymph node dissection); chemotherapy (3 courses Paclitaxel + Cisplatin, 1 course Paclitaxel + Carboplatin); immunotherapy (3 courses sintilimab) 5 months later after CRS Literature 3 (Yang L et al.) ( Yang et al., 2021 ) Poorly differentiated Endometrial 18.92 366.90 No data CRS; neoadjuvant chemotherapy (3 cycles carboplatin and paclitaxel) Alive at time of publication Literature 4 (Buller R et al.) ( Buller et al., 1991 ) Poorly differentiated Endometrial 14.9 345 No data TAH-BSO No data Literature 5 (Ogino T et al) ( Ogino et al., 2025 ) Dedifferentiated Endometrial 15.9 312 No data TAH-BSO, partial omentectomy; whole-brain irradiation; chemotherapy (carboplatin and paclitaxel) 3 months after surgery Literature 6 (Hocker et al.) ( Hocker et al., 2021 ) Endometroid carcinoma, pathology not mentioned. CT-guided lung biopsy revealed poorly differentiated carcinoma (suspected to be of pancreatic origin) Endometrial and lung metastasis (unknown primary site) 18.4 3593 No mismatch repair defects in endometrioid carcinoma No cancer-directed treatment Approximately 1 month since initial presentation Abbreviations: NR – Normal range; PTH – Parathyroid hormone; TAH-BSO – Total abdominal hysterectomy and bilateral salpingo-oophorectomy; RT – Radiotherapy; CRS – Cytoreductive surgery.
Table 1
Summary of cases of endometrial carcinoma associated with PTH-mediated hypercalcemia.
Abbreviations: NR – Normal range; PTH – Parathyroid hormone; TAH-BSO – Total abdominal hysterectomy and bilateral salpingo-oophorectomy; RT – Radiotherapy; CRS – Cytoreductive surgery.
| Case | Pathology | Site | Calcium, Highest (mg/dL), NR: 8.5–10.5 | PTH, Highest (pg/mL), NR: 24–85 | Tumor DNA mismatch repair status | Treatment | Survival |
| Case 1 | FIGO G3 (poorly differentiated) carcinoma | Endometrial | 16.2 | 167 | Deficient in MLH1 and PMS2 | TAH-BSO | 1 month after initial presentation |
| Case 2 | FIGO grade 3 (poorly differentiated) adenocarcinoma | Endometrial | 15.4 | 843 | Deficient in MSH6 | Chemotherapy (paclitaxel and carboplatin), TAH-BSO, RT, pembrolizumab and lenvatinib, doxorubicin | 16 months after initial presentation |
| Literature 1 (Batarseh N et al.) ( Batarseh et al., 2019 ) | De-differentiated | Endometrial | 12.8 | 135 | No data | TAH-BSO | Few weeks after diagnosis |
| Literature 2 (Liu H et al.) ( Liu et al., 2023 ) | Poorly differentiated carcinoma | Endometrial | 14.16 | 2586 | Deficient in MLH-1 and PMS-2 | CRS (including TAH-BSO, bilateral ovarian artery ligation, bilateral internal iliac artery ligation, appendectomy, omentectomy, pelvic and para-aortic lymph node dissection); chemotherapy (3 courses Paclitaxel + Cisplatin, 1 course Paclitaxel + Carboplatin); immunotherapy (3 courses sintilimab) | 5 months later after CRS |
| Literature 3 (Yang L et al.) ( Yang et al., 2021 ) | Poorly differentiated | Endometrial | 18.92 | 366.90 | No data | CRS; neoadjuvant chemotherapy (3 cycles carboplatin and paclitaxel) | Alive at time of publication |
| Literature 4 (Buller R et al.) ( Buller et al., 1991 ) | Poorly differentiated | Endometrial | 14.9 | 345 | No data | TAH-BSO | No data |
| Literature 5 (Ogino T et al) ( Ogino et al., 2025 ) | Dedifferentiated | Endometrial | 15.9 | 312 | No data | TAH-BSO, partial omentectomy; whole-brain irradiation; chemotherapy (carboplatin and paclitaxel) | 3 months after surgery |
| Literature 6 (Hocker et al.) ( Hocker et al., 2021 ) | Endometroid carcinoma, pathology not mentioned. CT-guided lung biopsy revealed poorly differentiated carcinoma (suspected to be of pancreatic origin) | Endometrial and lung metastasis (unknown primary site) | 18.4 | 3593 | No mismatch repair defects in endometrioid carcinoma | No cancer-directed treatment | Approximately 1 month since initial presentation |
Ectopic PTH secretion is exceedingly rare but has been reported in various cancers, including endometrial cancers ( Table 1 ). Although PTHrP is the most common mediator of malignancy-associated hypercalcemia and responds well to bisphosphonates, hypercalcemia due to PTH overproduction may respond better to cinacalcet. This report illustrates the possibility of elevated PTH as a rare mechanism for hypercalcemia, which should be considered and tested for in cases where PTHrP is normal and the clinical pattern does not fit bone metastases or a lymphoma diagnosis.
Previous reports have used various methods to confirm ectopic PTH production by tumors, including venous sampling, IHC, and molecular analyses. Ectopic PTH secretion has been demonstrated in hepatocellular carcinoma and small cell lung cancer through biochemical localization and tumor-specific PTH expression, with exclusion of parathyroid disease ( Koyama et al., 1999 ; Yoshimoto et al., 1989 ). Similar findings have been reported in other solid tumors, including penile squamous cell carcinoma, where elevated intact PTH, normal PTHrP, and positive PTH immunostaining supported a paraneoplastic etiology ( Sardiñas et al., 2018 ). More recently, Ogino et al. confirmed ectopic PTH production in dedifferentiated endometrial carcinoma using IHC and reverse transcription polymerase chain reaction (RT-PCR), with hormone levels normalizing after tumor resection and recurring with metastatic disease ( Ogino et al., 2025 ).
In Case 1, tumor IHC staining showed loss of expression of MLH1/PMS2, which is a common pattern seen for MLH1 deficiency, either due to MLH1 promoter hypermethylation, which accounts for up to 85% of cases, or a hereditary germline mutation associated with hereditary nonpolyposis colorectal cancer (HNPCC) syndrome ( Kurpiel et al., 2022 ). Interestingly, in Case 2, MSH6 was initially found to be deficient in IHC, but was not confirmed by subsequent NGS testing and was not shown on IHC of the subsequent surgical specimen. The most likely explanation involves somatic changes associated with tumor heterogeneity. Of note, discordance between IHC and microsatellite testing exists in a very small percentage of cases, while discordance in MSH6 loss is more prevalent due to functional compensation by MSH3 ( Xi et al., 2026 ).
The management of patients with hypercalcemia starts with IV hydration with isotonic saline, targeting urine output of 100–150 mL/h. For severe HCM (calcium >14 mg/dL), calcitonin (4–8 IU/kg every 8–12 h) combined with an antiresorptive agent, either a bisphosphonate or denosumab, can be used in the first 48–72 h, as prolonged use of calcitonin can lead to tachyphylaxis. Bisphosphonates are the cornerstone of treatment for malignancy-related hypercalcemia and act by inhibiting osteoclastic bone resorption. Cinacalcet is a calcimimetic agent that modulates the calcium-sensing receptor and suppresses PTH secretion. It is the primary treatment for primary hyperparathyroidism when parathyroidectomy is not feasible. The 2023 Endocrine Society guideline recommends a calcimimetic or antiresorptive for PTH-mediated hypercalcemia of malignancy, and cinacalcet may be initiated first for mild hypercalcemia ( El-Hajj Fuleihan et al., 2023 ). Table 2 summarizes the four subtypes of hypercalcemia of malignancy, their distinguishing biochemical profiles, and recommended diagnostic and therapeutic approaches. Table 2 Differential diagnosis, diagnostic workup, and treatment of cancer-associated hypercalcemia. Feature Humoral (PTHrP-mediated) Local Osteolytic 1,25-(OH)₂D-Mediated Ectopic PTH Frequency ∼60–80% of cases ∼20% of cases 1% of cases <1% of cases Common tumor types Squamous (lung, head and neck), breast, renal, urothelial Breast, multiple myeloma Hodgkin and non-Hodgkin lymphomas Ovarian, lung, thyroid, pancreatic, endometrial (rare) Bone metastases None or few Extensive None or few None or few (may develop later) Serum PTH Suppressed (20 pg/mL) Suppressed Suppressed Elevated or inappropriately normal Serum PTHrP Elevated Low Low Low 25-OH Vitamin D Normal Normal Normal or low Normal 1,25-(OH)₂ Vitamin D Variable (usually low-normal) Variable Elevated Elevated (PTH-driven conversion) Serum phosphorus Low Variable High Low Key diagnostic test PTHrP level Skeletal imaging 1,25-(OH)₂D level PTH level; parathyroid localization (negative); tumor PTH IHC Distinguishing from PHPT PTH suppressed (unlike PHPT) PTH suppressed PTH suppressed PTH elevated; must exclude PHPT with imaging (sestamibi, US, 4D-CT); PTH tracks tumor burden First-line treatment IV hydration + IV bisphosphonate or denosumab IV hydration + IV bisphosphonate or denosumab Glucocorticoids ± IV bisphosphonate or denosumab IV hydration + cinacalcet and/or IV bisphosphonate or denosumab Adjunctive treatment Calcitonin (48–72 h) for severe HCM (Ca >14) Calcitonin for severe HCM Calcitonin for severe HCM Calcitonin for severe HCM; cinacalcet for PTH suppression Definitive treatment Treatment of underlying malignancy Treatment of underlying malignancy Treatment of underlying malignancy Treatment of underlying malignancy; surgical resection if feasible Abbreviations: PTHrP, parathyroid hormone-related protein; PTH, parathyroid hormone; PHPT, primary hyperparathyroidism; IHC, immunohistochemistry; HCM, hypercalcemia of malignancy; US, ultrasound; 4D-CT, four-dimensional computed tomography. Adapted from references.
Table 2
Differential diagnosis, diagnostic workup, and treatment of cancer-associated hypercalcemia.
Abbreviations: PTHrP, parathyroid hormone-related protein; PTH, parathyroid hormone; PHPT, primary hyperparathyroidism; IHC, immunohistochemistry; HCM, hypercalcemia of malignancy; US, ultrasound; 4D-CT, four-dimensional computed tomography. Adapted from references.
| Feature | Humoral (PTHrP-mediated) | Local Osteolytic | 1,25-(OH)₂D-Mediated | Ectopic PTH |
| Frequency | ∼60–80% of cases | ∼20% of cases | 1% of cases | <1% of cases |
| Common tumor types | Squamous (lung, head and neck), breast, renal, urothelial | Breast, multiple myeloma | Hodgkin and non-Hodgkin lymphomas | Ovarian, lung, thyroid, pancreatic, endometrial (rare) |
| Bone metastases | None or few | Extensive | None or few | None or few (may develop later) |
| Serum PTH | Suppressed (20 pg/mL) | Suppressed | Suppressed | Elevated or inappropriately normal |
| Serum PTHrP | Elevated | Low | Low | Low |
| 25-OH Vitamin D | Normal | Normal | Normal or low | Normal |
| 1,25-(OH)₂ Vitamin D | Variable (usually low-normal) | Variable | Elevated | Elevated (PTH-driven conversion) |
| Serum phosphorus | Low | Variable | High | Low |
| Key diagnostic test | PTHrP level | Skeletal imaging | 1,25-(OH)₂D level | PTH level; parathyroid localization (negative); tumor PTH IHC |
| Distinguishing from PHPT | PTH suppressed (unlike PHPT) | PTH suppressed | PTH suppressed | PTH elevated; must exclude PHPT with imaging (sestamibi, US, 4D-CT); PTH tracks tumor burden |
| First-line treatment | IV hydration + IV bisphosphonate or denosumab | IV hydration + IV bisphosphonate or denosumab | Glucocorticoids ± IV bisphosphonate or denosumab | IV hydration + cinacalcet and/or IV bisphosphonate or denosumab |
| Adjunctive treatment | Calcitonin (48–72 h) for severe HCM (Ca >14) | Calcitonin for severe HCM | Calcitonin for severe HCM | Calcitonin for severe HCM; cinacalcet for PTH suppression |
| Definitive treatment | Treatment of underlying malignancy | Treatment of underlying malignancy | Treatment of underlying malignancy | Treatment of underlying malignancy; surgical resection if feasible |
Conclusions
Hypercalcemia due to ectopic PTH secretion is rare and may be misdiagnosed as primary hyperparathyroidism. It can occur in poorly differentiated or dedifferentiated endometrioid carcinomas and closely reflects disease activity. The two cases described here demonstrated close correlation of calcium and PTH levels with disease progression and tumor burden, suggestive of ectopic PTH production.
Recognition of this entity is important, as calcium and PTH levels may serve as biomarkers of tumor burden. In addition to bisphosphonates, cinacalcet, the calcimimetic drug, may be effective adjunctive therapy.
CRediT authorship contribution statement
Alina Zatsepina: Writing – review & editing, Writing – original draft, Visualization. Uliana Cheliadinova: Writing – review & editing, Conceptualization. Kripa Tiwari: Writing – review & editing, Visualization. Hao Li: Writing – original draft, Visualization. Vipluv Singh: Writing – review & editing, Visualization, Conceptualization. Rafi Mohamed Shaji: Writing – original draft, Visualization. Christine Resta: Supervision, Methodology. Yiqing Xu: Writing – review & editing, Supervision, Methodology, Data curation, Conceptualization.
Informed consent
Written informed consent was obtained from the patient for publication of this case report and accompanying images.
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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