Adenoma Presenting Research Articles

Endogenous Cushing’s Syndrome Due to Right Adrenal Adenoma Presenting With Bilateral Leg Oedema and Skin Ulceration

Endogenous Cushing’s Syndrome Due to Right Adrenal Adenoma Presenting With Bilateral Leg Oedema and Skin Ulceration

Parathyroid Adenoma Presenting as Femoral Tumor Lesion in a 27-Year-Old Woman.

Metabolic bone diseases should be considered in the differential diagnosis of osteolytic lesions. Here, we describe a case of primary hyperparathyroidism with multiple osteolytic lesions that improved following parathyroidectomy.

A low-grade somatotroph adenoma presenting as a giant pituitary macro-adenoma

A low-grade somatotroph adenoma presenting as a giant pituitary macro-adenoma

An ampullary adenoma presenting with jaundice caused by duodenal intussusception: a case report.

Ampullary adenomas are premalignant lesions. However, biliary obstruction causing jaundice is rare. Duodenal intussusception secondary to an ampullary adenoma rarely occurs because of the fixed position of the duodenum in the retroperitoneum. Herein, we have described a rare case of ampullary adenoma with jaundice caused by duodenal intussusception. A 40-year-old woman presenting with vomiting and yellowish discoloration of the skin was admitted to another hospital. The patient had experienced recurrent epigastric pain and vomiting for the past 18months. Blood test results showed elevated levels of bilirubin (3.9mg/dL), and abdominal computed tomography (CT) showed a 60-mm hypovascular mass in the third part of the duodenum and a left lateral shift of the dilated common bile duct. The patient was referred to our hospital for further evaluation. She recovered from hyperbilirubinemia spontaneously (levels of bilirubin, 1.0mg/dL), and the CT showed a tumor shift from the third part of the duodenum to the second part and improvement of the dilated common bile duct. Hypotonic duodenography revealed a tumor that moved easily from the second to the third portion of the patient's position. Upper gastrointestinal endoscopy revealed a large papillary tumor occupying the second part of the duodenum, which was diagnosed as an adenoma through biopsy. The possibility of malignancy could not be negated owing to the presence of jaundice and an elevated carbohydrate antigen 19-9 level (76.0U/mL). Pancreaticoduodenectomy was performed. The resected specimen showed a 60 × 40 × 40-mm pedunculated ampullary mass with submucosal elongation. The pathological examination indicated that the ampullary tumor was a high-grade intestinal adenoma. The postoperative course was uneventful, and the patient was discharged 26 days postoperatively. This report describes a rare case of a patient with an ampullary adenoma presenting with jaundice resulting from duodenal intussusception. Owing to the possibility of a postoperative cancer diagnosis which may have caused the biliary obstruction and the difficulty in making an accurate preoperative diagnosis, it is imperative to choose the appropriate surgical procedure such as a pancreaticoduodenectomy.

SAT203 Parathyroid Adenoma Masquerading As Parathyroid Carcinoma

Abstract Disclosure: M. Fariduddin: None. A. Lupieri: None. H.L. Calero: None. A. Rubenfeld: None. Y. Eisenberg: None. Case: 22 y/o pregnant female (5 weeks gestation) presented to the endocrinology clinic after a hospital admission for nausea, vomiting, constipation, fatigue and joint pain with labs showing calcium (corrected) of 14 mg/dL and PTH of 1200 pg/ml. Labs in the clinic showed calcium at 16 mg/dL and PTH 1500 pg/ml. She was re-admitted for IV fluids, calcitonin and zoledronic acid. Severe hypercalcemia, young age, and extremely high PTH levels were highly suggestive of parathyroid cancer. CT of neck showed a 2 cm right inferior parathyroid mass abutting the esophagus with concern for esophageal invasion with no evident plane between the mass and the esophagus. No cervical adenopathy was noted. Patient in conjunction with her obstetrician made an informed decision to terminate the pregnancy as this was an undesired pregnancy. She underwent an urgent right inferior gland parathyroidectomy. The mass was not fixed to underlying structures and was resected in-toto. Pathology showed chief cells with clear cytoplasm, and homogeneously round nuclei. There were no atypical mitoses, lymphovascular invasion, perineural invasion, or other invasive features concluding the final pathology as parathyroid adenoma. Discussion: Primary hyperparathyroidism predominantly affects postmenopausal women. Most common cause is parathyroid adenoma (80-85%). Parathyroid carcinoma is a rare cause of primary hyperparathyroidism (1-2%).80% people with parathyroid adenoma and primary hyperparathyroidism are diagnosed incidentally with mildly elevated calcium. PTH elevation is around 1.5-2 times the upper limit of normal. Symptoms are mild sequelae of hypercalcemia. PTH levels 5-10 times upper limit of normal, severe hypercalcemia (Ca > 14 mg/dl) or a hypercalcemia crisis are highly suspicious for parathyroid cancer. Surgical resection is the mainstay of treatment. Clinical criteria play a key role in early identification of parathyroid carcinoma in order to get these patients to surgery before tumor spread and improve long term survival. Our patient with significantly elevated calcium and parathyroid hormone had an atypical presentation of a parathyroid adenoma thus uncovering the limitations of clinical criteria in identifying a parathyroid carcinoma. Most of the patients with a parathyroid adenoma will eventually require surgery, however the technique, extent and urgency of surgery is affected based on clinical situations like these. The timing of the surgery could be detrimental when coupled with a scenario like our patient’s pregnancy wherein you could delay the surgery until the second trimester had the patient wanted to continue the pregnancy. This case highlights the importance of awareness of atypical presentations of parathyroid adenomas and to have a cautious approach in patients with clinical concern for parathyroid carcinoma especially if there is a potential benefit to delay surgery. Presentation: Saturday, June 17, 2023

Giant parathyroid adenoma presenting with multiple pathologic fractures: A case report

Key Clinical MessageHyperparathyroidism is a common endocrine disorder, which must be suspected in patients presenting with fatigue, history of pathologic fracture and the diagnosis can be confirmed by elevated calcium and PTH levels, and the preferred treatment option.AbstractPrimary hyperparathyroidism (PHPT), a common endocrine condition, with elevated parathormone production causes increased blood calcium levels. Parathyroid adenomas cause the majority of PHPT cases. Significant hypercalcemia can result from giant parathyroid adenomas. A calcium crisis may not always arise in these individuals, despite enormous parathyroid adenomas and high parathyroid hormone levels, and the masses may first be mistaken for a thyroid mass. In this article, we discuss the case of a 57‐year‐old Iranian man who suffered from PHPT due to a massive parathyroid adenoma and had a history of extreme fatigue and several traumatic fractures. As specialists, we should have a strong clinical suspicion of giant parathyroid adenoma as reason of hyperparathyroidism. In patients with multiple bone problems such as pain and multiple pathological fractures and elevated levels of calcium and PTH, the diagnosis of GPA must be considered and their preferred treatment is surgery.

Oncocytic parathyroid adenoma presenting with refractory hypercalcaemia and multiple incidental Brown tumours

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Abstract #1406558: Severe Renal Compromise Associated with Hypercalcemic Crisis Due to Giant Parathyroid Adenoma in a Woman with Bilateral Adrenal Incidentalomas

Parathyroid or hypercalcaemic crisis is a rare presenting manifestation of primary hyperparathyroidism (PHPT). We present a woman with severe hypercalcaemia due to giant parathyroid adenoma presenting as exacerbated chronic kidney disease, who was also found to have non-functioning bilateral adrenal adenomas. A 74-year-old woman, a history of arterial hypertension 10 years ago and lumbar spine scoliosis, usual medication irbersartan 150 mg/day, was admitted by emergency with a 1-week illness time characterized by lower limb weakness, severe low back pain, nausea and vomiting, which intensified the day of admission. Examination revealed BP 120/60 mmHg, heart rate 89 beats/min, weight 75kg, height 1.72cm, dry oral mucosa, no lymphadenopathy or nodules palpable at neck level. Laboratory tests: Arterial gases pH: 7.3, HCO3: 17mmol/L, Calcium: 3.8meq/L; hemoglobin: 10.1g/dl, creatinine: 7.32mg/dl, urea: 181mg/dl, sodium: 140mmol/L, potassium: 5mmol/L, calcium: 14.1mg/dl, phosphorus: 5.6mg/dl, magnesium: 2.18mg/dl. Renal ultrasound showed: signs of bilateral chronic kidney disease. Given the suspicion of malignancy and awaiting the result of parathormone (PTH), the body CT in the emergency room showed a solid lesion at the neck level, located posteriorly and in contact with the left thyroid lobe, measuring 39 x 14 x 30 mm, contacted the trachea and partially displaced the esophagus to the right without infiltrating them, it maintained interface with the left carotid and jugular, suggesting parathyroid dependence; and incidentally, both adrenal glands were diffusely thickened, the left showed a nodular formation of 20 x 15 mm, with an attenuation of -10 HU. She was hospitalized, received hydration, furosemide and pamidronate, did not require renal replacement therapy. Intact PTH was 1114 pg/mL; it was possible to normalize the levels of calcium, phosphorus, magnesium, creatinine decreased to 2.53mg/dl. Sestamibi scintigraphy showed an image compatible with lower left parathyroid adenoma and bone densitometry showed osteoporosis with a high risk of fracture (left forearm (1/3): bdm= 0.475g/cm2, Tscore= -5.3, hip: bdm= 0.435g /cm2, tscore= -4.5). The patient underwent a lower left parathyroidectomy, where a 5x3.5cm parathyroid tumor was reported with an increased consistency of brown coloration; the pathology reported giant adenoma of the parathyroid gland with apoplexy. In the postoperative period, the intact PTH was 57 pg/ml, at the same time the functionality of the adrenal adenoma was ruled out. She developed hungry bone syndrome for which she receives calcium and calcitriol to this day. Some studies provided an unclear definition of hypercalcemic crisis as a serum calcium concentration >3.5 mmol/L, accompanied by signs and symptoms. A hypercalcemic crisis was first described in 1939 by Hanes, and is considered as an endocrine emergency and fatal in the absence of optimal treatment. The acute effects of PHPT on renal function are not well understood. Furthermore, non-oliguric acute kidney injury caused by refractory hypercalcemia requires emergent hemodialysis, which was not necessary in our patient.

Differential Diagnosis of Lateral Neck Masses

Introduction: The neck and parapharyngeal space are one of the most vital regions in the body, encompassing multiple major blood vessels, nerves, spine and the airway itself. Lateral neck masses that present to an ENT practitioner may not only include a wide variety of differentials, but may present as emergencies in case of an airway compromise. In such situations, decision making and arriving at the diagnosis becomes important not only from a curative perspective but also from a lifesaving one. Here we discuss a few cases of lateral neck masses that had presented to us with unusual presentation or had a rare diagnosis, along with the line of management that was followed.
 Cases: We present a case of a giant pleomorphic adenoma presenting with stridor, an adult onset cystic hygroma, a schwannoma presenting with dyspnea, an isolated infiltrating lipoma and 2 other cases of schwannoma.
 Conclusion: Tumours of the neck and parapharyngeal region have a wide variety as this region contains almost every kind of tissue. Diagnosis of any lesion should be done with caution, using the appropriate history, examination and investigative tools available. Not only the common presentation, but also outliers and uncommon presentations of common tumours should be kept in mind.

Parathyroid adenoma presenting as dysphagia and nephrogenic diabetes insipidus

This case describes a patient with a parathyroid adenoma presenting with dysphagia and nephrogenic diabetes insipidus without demonstrating a parathyroid lesion on imaging. The parathyroid adenoma was detected during surgical exploration and excised which resulted in the normalization of calcium and sodium levels and led to symptomatic relief from dysphagia.

Giant Pituitary Adenoma Presenting as Nasal Mass.

Giant Pituitary Adenoma Presenting as Nasal Mass.

CASE REPORT ON NON-FUNCTIONING PITUITARY ADENOMA PRESENTING WITH SHORT STATURE, DELAYED PUBERTY AND PRIMARY AMENORRHEA

Delayed puberty in girls is dened as lack of secondary sexual characteristics by the age of 13 years and absence of menarche by the age of 16 years or 5 years after onset of puberty indicates pubertal delay. Constitutional delay of growth and puberty (CDGP) is the most commonly encountered cause of delayed puberty in girls. Pituitary tumors are not very common in childhood and adolescence, and prevalence of up to 1 per million children has been reported. Non-functioning pituitary adenomas (NFPAs) are benign adenohypophyseal tumors not associated with clinical evidence of hormonal hypersecretion. Patients with NFPAs usually come to medical attention as a result of “mass effects” symptoms like headaches, visual disturbances, and/or cranial nerve dysfunction caused by lesions large enough to mechanically compress and damage surrounding structures. Other manifestations are hypopituitarism as a result of mass effect by the compression of the normal anterior pituitary, and hyperprolactinemia due to pituitary stalk deviation can also be present. Here is a case of 16 year old female adolescent with pituitary adenoma presenting with delayed puberty and primary amenorrhea with short stature.

Primary hyperparathyroidism presenting as acute hypercalcemic crisis: a case report

BackgroundHyperparathyroid crisis, or “parathyroid storm” is a rare manifestation of primary hyperparathyroidism, characterized by sudden onset of symptomatic, severe hypercalcemia (> 3.5 mmol/L). Hemorrhage into a parathyroid adenoma has rarely been reported as an inciting or associated event. We present a case of hemorrhage into a longstanding adenoma presenting with acute onset of profound hypercalcemia and associated complications.Case presentationA 60-year-old male presented to hospital with sudden onset of confusion, muscle weakness, and ataxia. Initial labs showed serum calcium 4.79 mmol/L, parathyroid hormone 2043 ng/L; creatinine 364 μmol/L. Review of the patient’s medical history indicated a 4-year history of recurrent nephrolithiasis, but no prior documented calcium levels. The hypercalcemia did not respond to 5 days of aggressive medical management with fluid resuscitation, denosumab and calcitonin, and later pamidronate and cinacalcet. He continued to deteriorate, requiring intubation and continuous renal replacement therapy. Imaging demonstrated 4.8 cm cystic right paratracheal mass; Technetium (Tc99m) Sestamibi scintigraphy was non-localizing. Urgent parathyroidectomy was completed, revealing a 5 × 3.3 × 1.8 cm hemorrhagic, atypical hypercellular parathyroid. Unfortunately, the patient died from complications from anticoagulation therapy for treatment of deep vein thrombosis 4 weeks after admission. His renal function had not recovered at the time of his death.ConclusionThis case gives potential insight into the etiology of hyperparathyroid crisis, and the difficulty in achieving control of hypercalcemia with medical means. Surgical intervention is the definitive management in these cases and should be considered urgently.Graphical

S-22-1: GENETIC MECHANISMS OF HYPERTENSION IN DIFFERENT FORMS OF PRIMARY ALDOSTERONISM

Primary aldosteronism is the most common form of secondary arterial hypertension, affecting up to 10% of hypertensive patients. It is responsible for treatment resistance and increased risk of cardiovascular complications. Due to the difficulty of its diagnosis, PA is frequently missed, and as a result, treatment of the condition is either delayed by many years after the onset of hypertension, or is not initiated at all. Over the past 10 years, important discoveries have been made regarding the genetic basis of aldosterone producing adenoma and familial forms of primary aldosteronism. In most cases, genetic abnormalities are found in genes coding for ion channels (KCNJ5, CACNA1D, CACNA1H, CLCN2) as well as ion pumps (ATP1A1, ATP2B3). They occur as somatic mutations in aldosterone producing adenoma and as germline mutations in familial forms of the disease. Mutations in these genes affect intracellular ion homeostasis and/or cell membrane potential, leading to increased intracellular calcium concentrations and activation of calcium signalling, which is the main regulator of aldosterone biosynthesis. In addition, double mutations in CTNNB1 and GNAQ/GNA11 have been identified in aldosterone producing adenoma presenting in puberty, pregnancy and menopause. Genetic studies have opened interesting diagnostic and treatment opportunities. While surrogate biomarkers of the mutation status may facilitate diagnosis and subtype identification in primary aldosteronism, innovative therapies are currently studied targeting mutated proteins. Finally, recent evidence suggests a continuum between unilateral and bilateral forms of primary aldosteronism, with somatic mutations being found in aldosterone producing cell clusters and aldosterone producing adenoma in patients with bilateral forms. We have recently identified genetic risk loci for primary aldosteronism through genome wide association studies, which may explain shared susceptibility and reveal new mechanisms involved in adrenal gland function and the development of aldosterone producing adenoma and bilateral adrenal hyperplasia.

Pituitary macro adenoma presenting as severe hyponatremia: A case report

Hyponatremia in panhypopituitarism is multifactorial, it can be explained by the corticotropic deficit observed in pituitary insufficiency which is responsible for a lifting of inhibition on the anti-diuretic hormone with a consequent net reduction of water excretion, Hypothyroidism is also cited as a contributing mechanism for the development of acute hyponatremia in pituitary insufficiency through reduced free water excretion. Hyponatremia as a mode of revelation remains rare, we report a case of severe hyponatremia revealing pituitary insufficiency on pituitary macroadenoma.

Pituitary macro adenoma presenting as severe hyponatremia: A case report

Pituitary macro adenoma presenting as severe hyponatremia: A case report

174. Intraductal carcinoma of the parotid gland – a rare salivary malignancy accompanied by a pleomorphic adenoma: case report and review of the literature

Low-grade intraductal carcinoma (LGIC) is an extremely rare salivary ductal malignancy. We present a case of an LGIC and pleomorphic adenoma presenting within the same parotid gland, and the potential challenges this uncommon situation poses.

Left adrenal aldosteronism coexisting with left paraaortic paraganglioma presenting as bilateral adrenal and left paraaortic tumors– comprehensive adrenal evaluation aiding perfect management: a case report

BackgroundCoexistence of a catecholamine-secreting tumor and an adrenal cortical tumor is quite rare which makes both diagnosis and management challenging. The purpose of this article is to describe the presence of this condition, share a stepwise approach for preoperative evaluation, and review the related literature.Case presentationA 44-year-old male patient had a history of hypertension and aggravating hypokalemia for years. Abdominal computed tomography incidentally found concomitant bilateral adrenal and left para-aortic tumors. Comprehensive adrenal hormone tests revealed a high aldosterone renin ratio and mildly elevated 24-h urine vanillylmandelic acid and norepinephrine levels. Subsequently, a metaiodobenzylguanidine scan showed uptake over the left para-aortic tumor, and NP-59 adrenal scintigraphy showed uptake over the left adrenal tumor. Further confirmatory tests, including captopril suppression, irbesartan suppression, and saline infusion, all confirmed the diagnosis of hyperaldosteronism. Adrenal venous sampling following 2 months of preparation with an alpha blocker demonstrated a left aldosterone-producing adrenal adenoma. Combining hormonal analysis, imaging studies, and adrenal venous sampling, the patient was diagnosed with left adrenal aldosteronoma, right adrenal nonfunctional tumor, and left para-aortic paraganglioma (PGL). Accordingly, laparoscopic left adrenalectomy and left PGL excision were performed smoothly under alpha blocker maintenance. The pathology report confirmed left adrenal cortical adenoma and left para-aortic PGL. Postoperatively, the blood pressure, biochemical tests, and adrenal hormone assays returned to normal, and related symptoms disappeared and were relatively stable during the follow-up period of two years.ConclusionsThis is the first case of left para-aortic PGL coexisting with an ipsilateral aldosterone-producing adenoma presenting as a left para-aortic tumor associated with bilateral adrenal tumors. Awareness of the rarity of this coexistence can avoid unexpected disasters during the process of evaluation and management.

ODP091 Giant Parathyroid Adenoma Presenting with Pseudoclubbing - A Case Report

Abstract Giant parathyroid adenoma is a rare type of parathyroid adenoma defined as weighing >3.5 grams. Although it presents with primary hyperparathyroidism,the clinical and laboratory findings are more profound. Bone changes are common in long standing hyperparathyroidism but presentation with clubbing is rare. Here,we report a case of 60 year male with history of finger deformities and swelling in neck,who on evaluation had hypercalcemia with high PTH levels. He underwent parathyroidectomy for the gaint parathyroid adenoma but had eventful postoperative period with prolonged hypocalcemia. This emphasizes the importance of timely management of hyperparathyroidism to prevent untoward consequences. Presentation: No date and time listed

ODP286 A Case of Synchronous Growth Hormone and Adrenocorticotrophic Hormone Secretion in a Patient with an Incidental Pituitary Adenoma.

Abstract The most common type of co-secreting functional pituitary adenoma is a tumor-producing growth hormone and prolactin. Other types of co-existing functioning adenomas are extremely rare. We present a 68-year-old male patient with a pituitary adenoma presenting with acromegaly and Cushing's disease (CD). A 68-year-old male was referred for an incidental pituitary macroadenoma found on magnetic resonance imaging (MRI) for his chronic nasal congestion. He denied headaches or blurry vision. He reported an increase in shoe size, worsening hypertension and diabetes, and a 40-pounds weight gain over several years. Past medical history included arthritis, type two diabetes mellitus, hypertension, sleep apnea, hypogonadism, chronic kidney disease, and coronary artery disease. Physical exam was notable for BMI of 51 kg/m2 and enlarged hands and feet. No stigmata of Cushing's syndrome were present. MRI showed a 2. 0×2.5 cm sellar mass involving the right cavernous sinus without a mass effect on the optic chiasm. Laboratory workup showed an elevated IGF-1 level of 703 ng/mL and 678 on repeat, growth hormone (GH) 1.1 ng/mL, adrenocorticotropic hormone (ACTH) 41 pg/mL, and am cortisol 15 mcg/dL. Am cortisol after 1 mg of dexamethasone was 6.2 mcg/dL with an appropriate dexamethasone level. His and 24-hour urine-free cortisol was elevated at 87.1 mcg/24h, HgbA1C was 8.3%, testosterone level was low, and PRL and thyroid levels were normal. He underwent transsphenoidal surgery (TSS). Postoperative morning cortisol day 1 was 18.9 mcg/dL. Pathology showed a sparsely granulated somatotroph adenoma. Seven days post-surgery, he presented with diplopia, ophthalmoplegia, and ptosis. MRI showed enlargement of the right cavernous sinus with possible residual tumor and blood products. He underwent a second TSS with evacuation of a hematoma. The patient's nadir postoperative serum cortisol was 14.4 mcg/dL and IGF-1 level 513 ng/mL one month after his initial surgery. Pathology showed organizing hemorrhage and necrotic pituitary adenoma. His ophthalmoplegia resolved, and diplopia partially improved. The synchronous occurrence of CD and acromegaly is an extremely rare condition. It can be secondary to either a plurihormonal adenoma or two functional adenomas. In our case, the pathology findings suggest double adenomas. Surgical resection is first-line therapy for acromegaly and CD. Stereotactic radiosurgery and medical therapy are second-line options in persistent disease. The 5-year remission rates with Gamma Knife radiosurgery are higher in CD (81%) as compared to acromegaly. 1 Pasireotide, a somatostatin receptor ligand approved for both CD and acromegaly. Worsening glycemic control is a significant challenging aspect of its use. Presentation: No date and time listed