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Evangelos Karvounis Department of Endocrine Surgery, ‘Euroclinic’ Hospital, Athens, Greece

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Ioannis Zoupas Department of Endocrine Surgery, ‘Euroclinic’ Hospital, Athens, Greece

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Dimitra Bantouna Private Practice, Patras, Greece

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Rodis D Paparodis Private Practice, Patras, Greece
Center for Diabetes and Endocrine Research, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA

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Roxani Efthymiadou PET-CT Department, Hygeia Hospital, Athens, Greece

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Christina Ioakimidou Department of Pathology

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Christos Panopoulos Department of Medical Oncology, ‘Euroclinic’ Hospital, Athens, Greece

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Summary

Large-cell neuroendocrine carcinoma (LCNEC) is a rare neuroendocrine prostatic malignancy. It usually arises after androgen deprivation therapy (ADT), while de novo cases are even more infrequent, with only six cases described. The patient was a 78-year-old man with no history of ADT who presented with cervical lymphadenopathy. Diagnostic approaches included PET/CT, MRI, CT scans, ultrasonography, biopsies, and cytological and immunohistochemical evaluations. Results showed a poorly differentiated carcinoma in the thyroid gland accompanied by cervical lymph node enlargement. Thyroid surgery revealed LCNEC metastasis to the thyroid gland. Additional metastases were identified in both the adrenal glands. Despite appropriate treatment, the patient died of the disease. De novo LCNEC of the prostate is a rare, highly aggressive tumor with a poor prognosis. It is resistant to most therapeutic agents, has a high metastatic potential, and is usually diagnosed at an advanced stage. Further studies are required to characterize this tumor.

Learning points

  • De novo LCNECs of the prostate gland can metastasize almost anywhere in the body, including the thyroid and adrenal glands.

  • LCNECs of the prostate are usually associated with androgen-depriving therapy, but de novo cases are also notable and should be accounted for.

  • Further studies are required to fully understand and treat LCNECs more effectively.

Open access
Omayma Elshafie Department of Endocrinology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Sultanate of Oman

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Samir Hussein Department of Radiology, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

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Moza Al Kalbani Department of Gynaecology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Sultanate of Oman

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Aisha Al Hamadani Department of Pathology

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Abir Bou Khalil Department of Endocrinology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Sultanate of Oman

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Nicholas Woodhouse Department of Endocrinology, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

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Summary

A 33-year-old female presented in 2013 with left flank pain. Ultrasound and MRI pelvis showed a complex mass 9 × 7 cm arising from the left ovary suggestive of ovarian torsion. She underwent a laparoscopic cystectomy, but the patient was lost to follow-up. Three years later, she presented with abdominal distension. Ultrasound and CT scan revealed a solid left ovarian mass with ascites and multiple peritoneal metastasis. Investigations showed elevated CA 125, CA 19-9. Ovarian malignancy was suspected. She underwent total abdominal hysterectomy and bilateral salpingo-oophorectomy on November 2016. The histopathology confirmed a well-differentiated thyroid cancer of ovarian origin with features of a papillary follicular variant without evidence of ovarian cancer and the thyroglobulin (Tg) level was elevated, more than 400 consistent with the diagnosis of malignant struma ovarii. The follow-up post-surgery showed normalization of CA 125, CA 19-9 and Tg. The patient underwent total thyroidectomy on January 2017. The histology was benign excluding thyroid cancer metastases to the ovary. She was started on thyroxine suppression, following which she received two ablation doses 131iodine (131I) each 5.3 GBq. The Tg remains slightly elevated at less than 10. 131I WBS showed no residual neck uptake and no distant avid metastasis. She was planned for molecular analysis which may indicate disease severity. We describe a case of malignant struma ovarii with widespread metastatic dissemination and a good response to surgery and 131I treatment without recurrence after 5 years of follow-up. The Tg remains slightly elevated indicating minimal stable residual disease.

Learning points

  • Malignant struma ovarii is a rare disease; diagnosis is difficult and management is not well defined.

  • Presentation may mimic advanced carcinoma of the ovary.

  • Predominant sites of metastasis are adjacent pelvic structures.

  • Thyroidectomy and 131iodine therapy should be considered. The management should be similar to that of metastatic thyroid cancer.

Open access
Caoimhe Casey University Hospital Kerry, Tralee, Co. Kerry, Ireland

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Tom Higgins University Hospital Kerry, Tralee, Co. Kerry, Ireland

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Summary

Subacute thyroiditis is an inflammatory disorder of the thyroid gland that has previously been described following viral illnesses and occasionally post vaccination such as influenza vaccine. 2021 was a revolutionary year for the development of SARS-CoV-2 vaccinations with multiple different vaccines now available. There are increasing numbers of case reports of thyroiditis following these vaccinations. We report a case of a 50-year-old female who developed subacute thyroiditis 6 days post ChAdOx1 nCoV-19 vaccine (AZD1222 produced by AstraZeneca Vaxzevria). The initial thyrotoxic phase was followed by overt hypothyroidism. This resolved spontaneously within 5 months without levothyroxine replacement. We hope that our case will add to the growing literature of cases of thyroiditis occurring after multiple different types of SARS-CoV-2 vaccination and create awareness of this rare but treatable adverse effect. We also review the literature on the proposed mechanisms behind this adverse effect.

Learning points

  • Subacute thyroiditis is an inflammatory disorder of the thyroid gland that can occur after a viral illness or vaccination against certain infections.

  • Subacute thyroiditis is a rare adverse effect that has been reported to occur after different types of SARS-CoV-2 vaccinations.

  • Subacute thyroiditis post vaccination is relatively straightforward to manage, with some patients requiring non-steroidal anti-inflammatory drugs and beta-blockers, while more severe cases may require corticosteroid therapy. This adverse effect should not dissuade vaccination use at a population level.

  • There are many postulated mechanisms for the development of subacute thyroiditis following vaccination including the presence of the ACE-2 receptor for SARS-CoV-2 on the thyroid gland, an inflammatory/immune response as is seen in COVID-19 infection itself and molecular mimicry between SARS-CoV-2 spike protein and healthy thyroid antigen.

Open access
Adam I Kaplan Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Department of Endocrinology, Royal North Shore Hospital, Sydney, Australia

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Catherine Luxford Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Cancer Genetics Laboratory, Kolling Institute, Royal North Shore Hospital, Sydney, Australia

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Roderick J Clifton-Bligh Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
Department of Endocrinology, Royal North Shore Hospital, Sydney, Australia
Cancer Genetics Laboratory, Kolling Institute, Royal North Shore Hospital, Sydney, Australia

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Summary

Biallelic pathological variants in the thyroid stimulating hormone (TSH) subunit β gene (TSHB) result in isolated TSH deficiency and secondary hypothyroidism, a rare form of central congenital hypothyroidism (CCH), with an estimated incidence of 1 in 65 000 births. It is characterised by low levels of free thyroxine and inappropriately low serum TSH and may therefore be missed on routine neonatal screening for hypothyroidism, which relies on elevated TSH. We describe a patient with CCH who developed recurrence of pituitary hyperplasia and symptomatic hypothyroidism due to poor compliance with thyroxine replacement. She was diagnosed with CCH as a neonate and had previously required trans-sphenoidal hypophysectomy surgery for pituitary hyperplasia associated with threatened chiasmal compression at 17 years of age due to variable adherence to thyroxine replacement. Genetic testing of TSHB identified compound heterozygosity with novel variant c.217A>C, p.(Thr73Pro), and a previously reported variant c.373delT, p.(Cys125Valfs*10). Continued variable adherence to treatment as an adult resulted in recurrence of significant pituitary hyperplasia, which subsequently resolved with improved compliance without the need for additional medications or repeat surgery. This case describes a novel TSHB variant associated with CCH and demonstrates the importance of consistent compliance with thyroxine replacement to treat hypothyroidism and prevent pituitary hyperplasia in central hypothyroidism.

Learning points

  • Pathogenic variants in the TSH subunit β gene (TSHB) are rare causes of central congenital hypothyroidism (CCH).

  • c.217A>C, p.(Thr73Pro), is a novel TSHB variant, presented in association with CCH in this case report.

  • Thyroxine replacement is critical to prevent clinical hypothyroidism and pituitary hyperplasia.

  • Pituitary hyperplasia can recur post-surgery if adherence to thyroxine replacement is not maintained.

  • Pituitary hyperplasia can dramatically reverse if compliance with thyroxine replacement is improved to maintain free thyroxine (FT4) levels in the middle-to-upper normal range, without the need for additional medications or surgeries.

Open access
Caroline Schulmeister Pediatric Endocrinology, University of California at San Francisco, San Francisco, California, USA
Pediatric Endocrinology, University of California at Davis, Sacramento, California, USA

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Jason Lee Pediatric Nephrology, University of California at San Francisco, San Francisco, California, USA
Pediatric Nephrology, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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Farzana Perwad Pediatric Nephrology, University of California at San Francisco, San Francisco, California, USA

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Roger Long Pediatric Endocrinology, University of California at San Francisco, San Francisco, California, USA

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Shylaja Srinivasan Pediatric Endocrinology, University of California at San Francisco, San Francisco, California, USA

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Summary

Skeletal abnormalities with delayed bone age and decreased linear bone growth are commonly found in children with prolonged juvenile hypothyroidism. However, rachitic bone abnormalities have not been previously reported in children with acquired hypothyroidism. Here, we present a case of newly found rickets in an 8-year-old female with untreated acquired hypothyroidism secondary to Hashimoto’s thyroiditis. Laboratory finding for abnormalities in calcium/phosphorus homeostasis and hormones that regulate skeletal health was normal. Her radiographic anomalies resolved with levothyroxine treatment alone, suggesting that hypothyroidism was the etiology of the rickets. To our knowledge, this is the first case report of rickets associated with long-standing severe acquired hypothyroidism that resolved exclusively with thyroid repletion.

Learning points

  • Thyroid hormone plays an important role in bone mineralization.

  • Prolonged hypothyroidism can result in rachitic bone abnormalities noted on radiographs.

  • Hypothyroidism should be considered in the evaluation of a child with rickets.

Open access
Tamaryn Fox Department of Internal Medicine, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA

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Hamza Akhtar Department of Cardiology, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA

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Nissa Blocher Department of Endocrinology and Metabolism, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA

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Catherine Anastasopoulou Department of Endocrinology and Metabolism, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA

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Summary

Graves’ disease can have multiple cardiac manifestations. A rare complication is that of severe mitral regurgitation secondary to mitral valve chordae rupture, due to both compromise of valve integrity by deposition of glycosaminoglycans and the hemodynamic stresses of thyrotoxicosis. Pregnancy, with its related hemodynamic changes, is another setting in which mitral valve chordae rupture has occasionally been documented. We present a unique case of a 36-year-old female with uncontrolled Graves’ disease who presented during pregnancy at 13 weeks gestation with atrial flutter and features of congestive heart failure. Echocardiogram found severe mitral regurgitation secondary to a ruptured mitral chord. She was treated conservatively with diuresis and ultimately delivered her baby without complication at 28 weeks when she had preterm premature rupture of membranes. She is currently on methimazole and propranolol and pending definitive management of her Graves’ disease. This represents not only a rare cardiac complication in a patient with Graves’ disease but also is the first in the literature, to our knowledge, which describes this complication in a pregnant patient with Graves’ disease.

Learning points

  • Thyroid disease can have multiple effects on the heart through hemodynamic and structural changes and can result in heart failure, arrhythmias, valvular disease, and pulmonary hypertension.

  • Graves’ disease can cause glycosaminoglycan deposition in valvular tissue resulting in fragile leaflets that can rupture with little stress.

  • Pregnancy and thyrotoxicosis have similar hemodynamic consequences with increased cardiac output and reduced systemic vascular resistance.

  • Be vigilant in those with hyperthyroidism with a new murmur or features of acute heart failure, as a ruptured valve chord can result in increased morbidity and mortality if not recognized and addressed quickly.

Open access
Yudi Camacho Department of Endocrinology, Diabetes and Metabolism

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Yusra Jamal Department of Endocrinology, Diabetes and Metabolism

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Andy Wang Department of Internal Medicine, Westchester Medical Center, Valhalla, New York, USA

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Patrick Chiarolanzio Department of Radiology, Westchester Medical Center, Valhalla, New York, USA

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Gayotri Goswami Department of Endocrinology, Diabetes and Metabolism

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Summary

Mass effect from a goiter is a serious complication with potentially life-threatening consequences. In rare instances, a goiter can compress nearby vessels, compromising cerebral blood flow, which can lead to an ischemic stroke. Ischemic strokes generally occur due to atherogenic or embolic phenomenon, albeit a rare etiology can be due to a mechanical obstruction of great vessels of the neck that provide blood supply to the brain. An unusual example of a similar obstruction is the mass effect of an expansive goiter on the carotid artery (CA) in the neck. We present a rare case of a 90-year-old female who had a historically untreated goiter for 13 years. She presented with symptoms of acute stroke, including right-sided weakness and dysarthria. CT angiogram of the neck revealed a massively enlarged thyroid gland causing compression and intermittent obstruction of the blood flow in the left common CA. Subsequently, the patient underwent a total thyroidectomy. Postoperatively, she had a remarkable recovery of her symptoms of right-sided weakness and dysarthria. Acknowledging stroke as a grave mechanical complication of a large multinodular goiter is crucial for timely and appropriate management to avoid serious consequences.

Learning points

  • The natural history of euthyroid multinodular goiters include abnormal enlargement of the thyroid gland, which results in local compression of structures in the neck causing neurovascular injury.

  • Timely diagnosis and surgical management of an enlarging goiter compressing the CA can reduce morbidity from an ischemic stroke.

  • Ischemic stroke is a rare and dangerous complication of a giant multinodular goiter.

Open access
Mone Murashita Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Norio Wada Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Shuhei Baba Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Hajime Sugawara Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Arina Miyoshi Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Shinji Obara Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan

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Summary

We report a 26-year-old Japanese man who visited our outpatient clinic presenting fever immediately after i.m. injection of the second dose of a coronavirus disease 2019 (COVID-19) vaccine (Moderna®). At the first visit, the patient had a fever of 37.7°C and a swollen thyroid gland with mild tenderness. He was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free tri-iodothyronine, 32.3 pg/mL; free thyroxine, >7.77 ng/dL; and thyroid-stimulating hormone (TSH) < 0.01 μIU/mL), high C-reactive protein level (7.40 mg/dL), negative TSH receptor antibody, and characteristic ultrasound findings. His HLA types were A*02:01/24:02, B*15:11/35:01, Cw*03:03, DRB1*09:01/12:01, DQB1*03:03, and DPB1*05: 01/41:01. He was initially administered prednisolone 15 mg/day, following which the fever subsided. After 10 days, he developed limb weakness and could not walk. The serum potassium level decreased to 1.8 mEq/L, which confirmed the diagnosis of thyrotoxic periodic paralysis (TPP). Potassium supplementation was initiated. The muscle weakness gradually decreased. Prednisolone therapy was terminated 6 weeks after the first visit. His thyroid function returned to normal 5 months after the first visit, through a hypothyroid state. To our knowledge, this is the first reported case of TPP-associated SAT following COVID-19 vaccination. Persistent fever following vaccination should be suspected of SAT. Additionally, TPP may be associated with SAT in Asian male patients.

Learning points

  • Following coronavirus disease 2019 (COVID-19) vaccination, subacute thyroiditis may develop regardless of the vaccine type.

  • If persistent fever, anterior neck pain, swelling and tenderness of thyroid gland, and symptoms of thyrotoxicosis are observed immediately after the COVID-19 vaccination, examination in consideration of the onset of subacute thyroiditis is recommended.

  • HLA-B35 may be associated with the onset of subacute thyroiditis after the COVID-19 vaccination.

  • Although rare, subacute thyroiditis can be associated with thyrotoxic periodic paralysis, especially in Asian men.

  • Glucocorticoid therapy for subacute thyroiditis may induce thyrotoxic periodic paralysis through hypokalemia.

Open access
Jay Nguyen Lincoln Memorial University-DeBusk College of Osteopathic Medicine, Harrogate, Tennessee, USA

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Dennis Joseph Endocrinology Center of Lake Cumberland, Somerset, Kentucky, USA

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Summary

Increased intracranial pressure (ICP) can present with symptoms of headache, vomiting, visual changes, and tinnitus. Papilledema may be seen on physical exam. Thyroid disease has been a rare secondary cause of increased ICP. We present a 16-year-old female who had a worsening headache for 6 months. She was found to have signs, symptoms, physical exam findings, and diagnostic studies consistent with both increased ICP and previously undiagnosed Graves’ disease. The patient was treated with a 19-month course of methimazole 40 mg daily. Her headache and papilledema resolved shortly after medication initiation. The timeline of symptoms and resolution of her increased ICP symptoms with treatment of Graves’ disease suggests that hyperthyroidism was the underlying cause of her increased ICP. Clinicians should consider Graves’ disease as the etiology in pediatric patients presenting with signs and symptoms of increased ICP with papilledema.

Learning points

  • Symptoms of increased intracranial pressure (ICP) include headache, vomiting, transient visual changes, and tinnitus.

  • Secondary causes of increased ICP should be considered in males, young children, older patients, and those not overweight.

  • Clinicians should consider Graves’ disease as the etiology in pediatric patients presenting with signs and symptoms of increased ICP with papilledema. They should assess for orbitopathy and thyromegaly and inquire about symptoms that would be indicative of hyperthyroidism.

Open access
Jay Nguyen Lincoln Memorial University-DeBusk College of Osteopathic Medicine, Harrogate, Tennessee, USA

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Dennis Joseph Endocrinology Center of Lake Cumberland, Somerset, Kentucky, USA

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Summary

Autonomous thyroid adenomas are caused by activating mutations in the genes encoding the thyroid-stimulating hormone receptor (TSHR) or mutations in the Gas subunit of the TSHR. Nodules with suspicious sonographic features should be submitted to fine-needle aspiration. Additional molecular testing may be performed to characterize the thyroid nodule’s malignant potential further. We present a patient who underwent whole-transcriptome RNA-sequencing that indicated a TSHR I568T mutation after an ultrasound showed suspicious sonographic features and fine-needle aspiration was ‘suspicious for malignancy’. The patient underwent thyroid resection and was found to have a locally invasive classical papillary thyroid carcinoma. Most reports of TSHR I568T mutation have been seen in patients with benign thyroid conditions. While there is insufficient data to suggest that the TSHR I568T mutation causes aggressive thyroid malignancy, we believe clinicians who identify the presence of this mutation on genome sequencing should be cautious about the possibility of locally invasive thyroid malignancy, especially when associated with Bethesda V cytopathology.

Learning points

  • Germline and somatic activating mutations in the genes coding for the thyroid-stimulating hormone receptor (TSHR) have been frequently reported in familial and sporadic autonomous thyroid adenomas and non-autoimmune hyperthyroidism.

  • Most reports of TSHR I568T mutation have been detected in patients with benign thyroid conditions.

  • We present a patient who underwent whole-transcriptome RNA-sequencing that indicated a TSHR I568T mutation and subsequently underwent thyroid resection and was found to have a locally invasive classical papillary thyroid carcinoma.

  • Clinicians who identify the presence of TSHR I568T mutation on genome sequencing should be cautious about the possibility of locally invasive thyroid malignancy, especially when associated with Bethesda V cytopathology.

Open access