We present an interesting scenario of dual pathology found within the thyrothymic tract of a patient with primary hyperparathyroidism. Pre-operatively, Tc-99 m sestamibi and 4-D parathyroid CT were concordant for a solitary adenoma adjacent to the lower pole of the right thyroid lobe. CT also reported an indeterminate 'vascular lesion' adjacent to the adenoma. At surgery, a 690 mg fat deplete parathyroid adenoma was identified at the cranial end of the thyrothymic tract (Fig. 1). Macroscopically, an incidental second lesion was noted. This appeared as a well-defined 8 mm ovoid pinkish lesion with a feeding vessel from the inferior thyroid artery. This was larger than a normal parathyroid gland but smaller than expected for a second adenoma. Colouration was not typical of either a normal parathyroid ('London tan') or an adenomatous/hyperplastic one ('brick red'). Sharp edges and a 'feeding vessel' are shared attributes of parathyroid glands. Histology reported a thymic hamartoma composed of mature fat, malformed vessels, and thymic elements—a 'thymoangiolipoma' (Fig. 2). Thymic neoplasms are rare tumours that account for less than 1% of all adult malignancies.1 There are only two prior reports of a thymoangiolipoma in the literature. We present this finding to raise awareness amongst surgeons of thymic lesions to avoid misidentification and potentially non-curative parathyroid surgery. Whilst the risk of this occurring is low with the benefit of positive pre-operative localizing studies, it is possible in cases of non-localisation or multi-gland hyperplasia where 4 gland (bilateral neck) exploration is required. The thymus is a specialized lymphoid organ found in the anterior mediastinum that plays an important role in the development of the cellular immune system.2, 3 The thymus and inferior parathyroid glands share an embryological origin from the third pharyngeal pouch. Both disconnect from the pharyngeal wall and descend; the thymus to the mediastinum and the inferior parathyroids coming to rest in a more cranial location posterior to the thyroid.4 Up to 16% of parathyroid glands are ectopic and found along the path of embryological descent.5 Thymic tumours may be of epithelial or non-epithelial cell origin.6 First described by Hall in 1949,7 thymoangiolipomas are a rare subtype of epithelial derived thymolipomas. Diagnosis is histological, and it is thought that the lesions are either hamartomas or neoplastic lesions arising from thymic fat.8-10 To our knowledge this is the third ever reported case of a thymoangiolipoma; the first reported in Australia and during parathyroidectomy. Focal thymic lesions can mimic enlarged parathyroid glands and this should be kept in mind when evaluating inferior glands. In cases where abnormal parathyroids are localized on pre-operative imaging and these are correlated with macroscopic operative findings, the risk of mis-identification is low. When localizing studies are discordant or negative (multi gland hyperplasia) and bilateral neck exploration is undertaken, lesions that do not meet all the criteria of a pathological parathyroid gland should be viewed with a degree of caution. Adjuncts to aid in the correct diagnosis macroscopically include size around 10 mm, bean shape, brick red colour, sharp edges and a polar vessel. Thymic lesions, thyroid rests and lymph nodes tend towards shades of pink. Where doubt persists, confirmation can be sought by frozen section analysis or intra-operative PTH level. Open access publishing facilitated by The University of Notre Dame Australia, as part of the Wiley - The University of Notre Dame Australia agreement via the Council of Australian University Librarians. Samuel Thompson: Investigation; resources; visualization; writing – original draft. Elan Novis: Project administration; writing – original draft; writing – review and editing. Julia Low: Investigation; resources; writing – review and editing. Tamara Preda: Conceptualization; resources; supervision; validation; writing – review and editing. Patient consent was obtained for presentation of this clinical case. Institutional ethics approval not required due to single case presentation.

Context The recent WHO 2022 Classification of pituitary tumours identified a novel group of ‘plurihormonal tumours without distinct lineage differentiation (WDLD)’. By definition, these express multiple combinations of lineage commitment transcription factors, in a monomorphous population of cells. Objectives To determine the expression of stem cell markers (SOX2, Nestin, CD133) within tumours WDLD, immature PIT-1 lineage and acidophil stem cell tumours, compared with committed cell lineage tumours. Methods Retrospective evaluation of surgically resected pituitary tumours from St Vincent’s Hospital, Sydney. Patients were selected to cover a range of tumour types, based on transcription factor and hormone immunohistochemistry. Clinical data was collected from patient files. Radiology reports were reviewed for size and invasion. Samples were analysed by immunohistochemistry and RT-qPCR for SF-1, PIT-1, T-PIT, SOX2, Nestin and CD133. Stem cell markers were compared between tumours WDLD and those with classically “mature” types. Results On immunohistochemistry, SOX2 was positive in a higher proportion of tumours WDLD compared with those meeting WHO lineage criteria, 7/10 v 10/42 (70 v 23.4%, p = 0.005). CD133 was positive in 2/10 tumours WDLD but 0/41 meeting lineage criteria, P = 0.003. On RT-qPCR, there was no significant difference in relative expression of stem cell markers (SOX2, CD133, Nestin) between tumours with and WDLD. Conclusions Our study is the first to biologically characterise pituitary tumours WDLD. We demonstrate that these tumours exhibit a higher expression of the stem cell marker SOX2 compared with other lineage-differentiated tumours, suggesting possible involvement of stem cells in their development.

Background: cIMPACT-NOW guidelines state optimal assessment of WHO grade II/III gliomas requires analysis of copy number variations (CNVs). SydPath has pioneered a referral pathway for affordable, validated comparative genomic hybridisation single nucleotide polymorphism (CGH-SNP) array for CNV analysis of gliomas. Aim: To optimise the referral pathway of gliomas for CGH-SNP array, enabling scalability to external centres. Methods: Consecutive adult patients with glial neoplasms received at SydPath over two years to June 2019 were retrospectively analysed. Referral processes and outcomes of CGH-SNP array were recorded. Results: Of 77 patients with glial neoplasms, six IDH-wildtype gliomas with grade II/III morphology were upgraded to grade IV following CNV analysis as per cIMPACT-NOW guidelines. Identification of high-grade morphology on subsequent histological examination enabled timely cancellation of four tests. Ten cases with available tissue were not referred, all prior to cIMPACT-NOW guideline publication. Thirteen cases lacked tissue for referral; only four tests failed due to insufficient tissue. Discussion: Referral for CGH-SNP array provided clinically relevant CNV analysis of gliomas. Improved efficiency can be achieved with our optimised tissue and case selection criteria, including complete morphological and IDH status assessment prior to testing. This will enable referral from external centres, allowing widespread adoption of cIMPACT-NOW guidelines using an affordable, validated test. References1.Brat DJ, Aldape K, Colman H, et al. cIMPACT-NOW update 3: recommended diagnostic criteria for "Diffuse astrocytic glioma, IDH-wildtype, with molecular features of glioblastoma, WHO grade IV". Acta Neuropathol 2018; 136: 805–10.2.Wood MD, Halfpenny AM, Moore SR. Applications of molecular neuro-oncology - a review of diffuse glioma integrated diagnosis and emerging molecular entities. Diagn Pathol 2019; 14: 29–44.

To the Editor: We would like to inform the readers about Sarcina sp, an organism that has been predominantly reported in adults and is often thought to be a benign commensal. We evaluated a 14-year-old girl with repaired long-gap esophageal atresia (EA) with a gastric pull up. Her growth was normal (above the 50th percentile) with no gastrostomy. She underwent laparoscopic fundoplication and hiatal hernia repair following recurrent distal esophageal strictures secondary to gastroesophageal reflux disease. The difficult fundoplication surgery may have contributed to an area with relative ischemia in the distal esophagus. The stricture recurred 6 months after fundoplication with 5 cm of inflammation below the stricture (Fig. 1). Biopsies revealed Sarcina-like organisms (Fig. 2). These findings persisted on follow-up gastroscopy, so the patient was treated with ciprofloxacin and metronidazole. Follow-up gastroscopy revealed resolution of inflammation and Sarcina-like organisms.FIGURE 1: Surveillance gastroscopy in late 2017, area on inflammation below the esophageal anastomotic site.FIGURE 2: Photomicrographs demonstrating the presence of Sarcina-like organisms adjacent to gastric mucosa, and inflammation within the lamina propria on routine hematoxylin and eosin staining of biopsies from the anastomotic site (original magnification 400×).Of the 9 cases of S ventriculi previously reported in children, only 1 had a repaired EA making ours the second to be reported (1). Presentations with Sarcina in the stomach are often seen in those with gastroparesis, and range from asymptomatic carriers to those with emphysematous gastritis and gastric perforation (2,3). Whether the presence of S ventriculi with associated inflammation in patients with EA worsens the already impaired motility of the EA cohort or whether they exist as a commensal organism in patients with inherently impaired motility is unclear. Interestingly this organism has not been reported in other conditions predisposing to poor esophageal clearance such as achalasia, pre- or postcorrective procedures such as dilation or myotomy. It is possible that the recurrent gastroesophageal reflux in conjunction with impaired esophageal motility created a predisposing environment for the overgrowth of S ventriculi resulting in active inflammation, supported by the observation that the distal inflammation resolved only after treatment of the Sarcina with ciprofloxacin and metronidazole (2). In most cases, S ventriculi is benign and does not warrant treatment unless overgrowth is suspected. In patients with coexisting conditions that contribute to dysmotility such as EA, treatment should, however, be considered, especially in the presence of mucosal inflammation (4).

Cranial fasciitis (CF) is a rare, rapid-growing, but benign fibroblastic tumour of the skull, which occurs in young children. It was first described by Lauer and Enzinger in 1980. Cranial fasciitis is closely related to nodular fasciitis (NF).1 A subset of CF has been found to be associated with the WNT/B-catenin pathway.2

cial detachable embolization coils are available and there is no evidence of superiority among the coils. The main principle applicable regardless of the embolization coil device is that it is imperative for the aneurysm to be packed as tightly as possible in order to facilitate thrombosis and occlusion of the aneurysm. In our case, there was successful exclusion of the aneurysmal sac with no significant flow noted at the efferent branches. Placement of a stent-graft was considered for complete occlusion of the feeding vessel. This was however not performed given the satisfactory angiographic result, and placement of a stent at this point would have been excessive. Additional stent graft placement at the thoracic aorta would also increase the risk of spinal ischaemia. It is also of the authors’ opinion that a stent-graft would have negated future possibilities of endovascular therapy in this patient. It may be more prudent to follow-up the patient and to place a stent-graft in the future if the need arises. In summary, we report a case of a large mediastinal BAA with short vascular neck that was successfully treated with coil embolization. Endovascular therapy is being increasingly used as it is effective, less invasive and is associated with lesser morbidity and shorter hospital stays as compared to surgical treatment.

Description: Melanotic neuroectodermal tumour of infancy (MNTI) is a rare, locally aggressive but usually benign tumour typically arising in the bones of the head and neck in infants and young children. Histologically, MNTI is a biphasic tumour of neural crest origin, composed of neuroblastic and pigmented epithelial components. Findings: We present a case arising from the skull of an 18-month-old boy requiring extensive neurosurgical resection. Histological examination confirmed MNTI but with unusual features, viz: (a) the 'small-round-blue-cell' neuroblastic component, usually bland with rare mitoses, showed morphological features suggestive of malignancy, including abundant mitoses (up to 67/10 hpf) and karyorrhexis, foci of necrosis, and a high Ki67 proliferative index (∼40%); and (b) the neuroblastic component, in addition to showing typical 'small-round-blue-cell' morphology, included large areas of neuropil containing neuroblastic cells showing varying degrees of ganglionic differentiation. Discussion: Less than 500 MNTIs are reported in the published literature; only 7% are malignant, the latter based on the presence of metastatic disease.1 There are currently no defined histological criteria for malignant MNTI,2 and there was no evidence of metastatic disease in our patient. Ganglionic differentiation is described in MNTI3,4 but, to our knowledge, this usually constitutes a minor component. References1.Fowler DJ, Chisholm J, Roebuck D, et al. Melanotic neuroectodermal tumor of infancy: clinical, radiological, and pathological features. Fetal Pediatr Pathol 2006; 25: 59–72.2.Kapadia SB, Frisman DM, Hitchcock CL, et al. Melanotic neuroectodermal tumor of infancy: clinicopathological, immunohistochemical, and flow cytometric study. Am J Pathol 1993; 17: 566–73.3.Reddy ER, Kumar MS, Aduri R, et al. Melanotic neuroectodermal tumor of infancy: A rare case report. Contemp Clin Dent 2013; 4: 559–62.4.Shah RV, Jambhekar NA, Rana DN, et al. Melanotic neuroectodermal tumor of infancy: report of a case with ganglionic differentiation. J Surg Oncol 1994; 55: 65–8.

Placenta creta (including placenta accreta, increta and percreta) is an uncommon indication for emergency caesarean section requiring emergency hysterectomy. It is defined as abnormally adherent placenta to the uterine wall, and occurs in approximately 1 in 2500 pregnancies. Risk factors include previous caesarean delivery, advanced maternal age, high gravidity, multiparity, previous curettage and placenta previa. The underlying pathophysiology is thought to be due to abnormal or absent decidualization of endometrium. There are also theories that excessive trophoblast invasion contributes to more morbid invasive placenta creatas (ie, placenta increta and percreta). This is postulated to be due to dehiscence of uterine scars or splaying of thin myometrium, rather than true trophoblastic invasion. We present a case series of eight women who were diagnosed with placenta percreta, over the last 10 years, at the Royal Hospital for Women, a tertiary obstetric referral centre in Sydney, Australia. We compare risk factors and clinical outcome, as well as histological diagnosis in relation to the pathophysiological theories of placenta creta. Placenta creta (including placenta accreta, increta and percreta) is an uncommon indication for emergency caesarean section requiring emergency hysterectomy. It is defined as abnormally adherent placenta to the uterine wall, and occurs in approximately 1 in 2500 pregnancies. Risk factors include previous caesarean delivery, advanced maternal age, high gravidity, multiparity, previous curettage and placenta previa. The underlying pathophysiology is thought to be due to abnormal or absent decidualization of endometrium. There are also theories that excessive trophoblast invasion contributes to more morbid invasive placenta creatas (ie, placenta increta and percreta). This is postulated to be due to dehiscence of uterine scars or splaying of thin myometrium, rather than true trophoblastic invasion. We present a case series of eight women who were diagnosed with placenta percreta, over the last 10 years, at the Royal Hospital for Women, a tertiary obstetric referral centre in Sydney, Australia. We compare risk factors and clinical outcome, as well as histological diagnosis in relation to the pathophysiological theories of placenta creta.