Abstract Disclosure: B.K. Bowens: None. C. Godar: None. D. LaChance: None. T.D. Hoang: None. M.K. Shakir: None. Glucose intolerance (GI) is defined as dysglycemia and includes impaired fasting glucose, impaired glucose tolerance, and prediabetes. Early detection of GI could lead to appropriate treatment and delay the progression to diabetes mellitus. The cases below detail two patients with elevated serum alkaline phosphatase (ALP) without other liver-associated enzyme abnormalities as an early indicator of GI. Case 1: A 54-year-old woman with a history of multinodular goiter status post thyroidectomy (2020), adrenal incidentaloma (2016), and asthma was incidentally found to have an elevated HbA1C (A1C) of 6.3% on screening labs in 2015. At that time, her ALP was 73 IU/L (ref 44−121). Her ALP levels slowly rose from 88 to 152 IU/L by September 2020. Work up did not reveal any etiological factors for the elevated ALP. One month later, HbA1C was found to be 7.6%. Metformin was initiated with improvement in A1C to 6.3% with an ALP of 130 IU/L. However, metformin was discontinued due to intolerance. In April 2023, her A1C was 9.3% with an ALP of 134 IU/L. A1C rose to 12.8% in Jun 2023 at which time she was started on insulin glargine, insulin aspart, sitagliptin, and was restarted on metformin. Her A1C decreased to 8.6% in August 2023 with normalization of ALP to 88 IU/L. Case 2: A 53-year-old woman with a history of hypertension, hyperlipidemia, obstructive sleep apnea, and non-ischemic cardiomyopathy in 2004 was found to have an elevated A1C of 5.8% on her screening labs in Jun 2019. Her ALP was notably in the high-normal range until Oct 2021 when it was found to be 138 IU/L. Her most recent A1C was 5.9% with an ALP of 142 IU/L. The patient was started on semaglutide (WegovyTM) briefly but was unable to tolerate the side effects. She was then started on metformin 500mg BID and dulaglutide with normalized ALP level. Discussion: Emerging evidence has shown that serum ALP activity is modestly increased in cardiometabolic diseases such as type 2 diabetes, dyslipidemia, hypertension, and peripheral arterial disease. These are increasingly being considered as inflammatory disorders and it has been shown that serum ALP level was positively and independently associated with metabolic syndrome both in men and women. It is possible that ALP could be an indicator of non-alcoholic fatty liver disease (NAFLD) which is associated with GI. Typically, NAFLD presents with higher ALT and GGT, however, occasionally isolated enzyme elevations or no elevated enzymes at all may occur. Conclusion: These cases suggest that an isolated elevation in ALP could be indicative of GI. Patients incidentally found to have an elevated ALP should be worked up further for possible evidence of GI. Early detection of GI could delay progression to diabetes and decrease morbidity. Presentation: 6/1/2024

Case PresentationA 36-year-old Pakistani phenotypic female patient with a history of prediabetes presented with a new onset type 2 diabetes mellitus, weight gain, and acne. She had unremarkable surgical and family history. She had never been sexually active and denied ever having a normal menstrual cycle but did describe intermittent spotting. Physical examination showed blood pressure of 130/86 mm Hg, body mass index of 29 kg/m2, thin, pale abdominal striae, central obesity, facial acne, mild facial hirsutism, moon facies, and sparse axillary/pubic hairs. The low-dose dexamethasone suppression test result was normal with an undetectable cortisol. Further biochemical assessment included normal results of the thyroid function, prolactin, and dehydroepiandrosterone sulfate tests and a negative human chorionic gonadotropin test result. The total testosterone level increased to 427 ng/dL (normal, 10-55 ng/dL). The dihydrotestosterone (DHT) level was 9.0 ng/dL (normal, 4-22 ng/dL). Karyotyping revealed a 46,XY genotype. The patient did not have clitoromegaly or virilization on examination. Magnetic resonance imaging (Fig. 1) showed an absent uterus, cervix, and ovaries with a blind vaginal pouch posterior to the bladder and anterior to the rectum. Figure 2 shows rudimentary undescended gonads in the proximal inguinal canal bilaterally.Fig. 2View Large Image Figure ViewerDownload Hi-res image Download (PPT)What is the diagnosis?Answer46,XY 5-Alpha-reductase deficiency (5ARD). Differential diagnosis included androgen insensitivity syndrome and gonadal dysgenesis; however, genetic testing revealed a pathogenic variant of SRD5A2 gene confirming the diagnosis of 5ARD. DHT is a main factor in the development of the external male genitalia. Testosterone is important in the development of internal male genitalia and secondary sexual characteristics. 5-Alpha-reductase type 2 enzyme catalyzes the reduction of testosterone to DHT during embryogenesis.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar Generally, 46,XY patients with 5ARD present at birth with female features and a varying degree of hypospadias, normal female genitourinary anatomy, or clitomegaly. 5ARD has been described in 46,XX females; these individuals have an increased testosterone-to-DHT ratio, normal female phenotype, and absent arm and leg hair with a decrease in axillary and pubic hair due to low DHT.2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar They have late menarche but normal menstrual function and fertility.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar, 2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar, 3Okeigwe I. Kuohung W. 5-Alpha reductase deficiency: a 40-year retrospective review.Curr Opin Endocrinol Diabetes Obes. 2014; 21: 483-487Crossref PubMed Scopus (32) Google Scholar Management for 5ARD may include initial sex assignment, trial of androgen supplementation, or DHT. This case is atypical because this patient presented with the symptoms at the age of 36 years. This was due to her lack of sexual activity and conservative upbringing. Typically, these patients are identified much earlier as they present with amenorrhea and infertility. This unique case highlights the need for medical providers to consider rare sexual development disorders in the differential for obesity, hirsutism, infertility, and amenorrhea.DisclosureThe authors have no multiplicity of interest to disclose. Case PresentationA 36-year-old Pakistani phenotypic female patient with a history of prediabetes presented with a new onset type 2 diabetes mellitus, weight gain, and acne. She had unremarkable surgical and family history. She had never been sexually active and denied ever having a normal menstrual cycle but did describe intermittent spotting. Physical examination showed blood pressure of 130/86 mm Hg, body mass index of 29 kg/m2, thin, pale abdominal striae, central obesity, facial acne, mild facial hirsutism, moon facies, and sparse axillary/pubic hairs. The low-dose dexamethasone suppression test result was normal with an undetectable cortisol. Further biochemical assessment included normal results of the thyroid function, prolactin, and dehydroepiandrosterone sulfate tests and a negative human chorionic gonadotropin test result. The total testosterone level increased to 427 ng/dL (normal, 10-55 ng/dL). The dihydrotestosterone (DHT) level was 9.0 ng/dL (normal, 4-22 ng/dL). Karyotyping revealed a 46,XY genotype. The patient did not have clitoromegaly or virilization on examination. Magnetic resonance imaging (Fig. 1) showed an absent uterus, cervix, and ovaries with a blind vaginal pouch posterior to the bladder and anterior to the rectum. Figure 2 shows rudimentary undescended gonads in the proximal inguinal canal bilaterally. A 36-year-old Pakistani phenotypic female patient with a history of prediabetes presented with a new onset type 2 diabetes mellitus, weight gain, and acne. She had unremarkable surgical and family history. She had never been sexually active and denied ever having a normal menstrual cycle but did describe intermittent spotting. Physical examination showed blood pressure of 130/86 mm Hg, body mass index of 29 kg/m2, thin, pale abdominal striae, central obesity, facial acne, mild facial hirsutism, moon facies, and sparse axillary/pubic hairs. The low-dose dexamethasone suppression test result was normal with an undetectable cortisol. Further biochemical assessment included normal results of the thyroid function, prolactin, and dehydroepiandrosterone sulfate tests and a negative human chorionic gonadotropin test result. The total testosterone level increased to 427 ng/dL (normal, 10-55 ng/dL). The dihydrotestosterone (DHT) level was 9.0 ng/dL (normal, 4-22 ng/dL). Karyotyping revealed a 46,XY genotype. The patient did not have clitoromegaly or virilization on examination. Magnetic resonance imaging (Fig. 1) showed an absent uterus, cervix, and ovaries with a blind vaginal pouch posterior to the bladder and anterior to the rectum. Figure 2 shows rudimentary undescended gonads in the proximal inguinal canal bilaterally. What is the diagnosis?Answer46,XY 5-Alpha-reductase deficiency (5ARD). Differential diagnosis included androgen insensitivity syndrome and gonadal dysgenesis; however, genetic testing revealed a pathogenic variant of SRD5A2 gene confirming the diagnosis of 5ARD. DHT is a main factor in the development of the external male genitalia. Testosterone is important in the development of internal male genitalia and secondary sexual characteristics. 5-Alpha-reductase type 2 enzyme catalyzes the reduction of testosterone to DHT during embryogenesis.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar Generally, 46,XY patients with 5ARD present at birth with female features and a varying degree of hypospadias, normal female genitourinary anatomy, or clitomegaly. 5ARD has been described in 46,XX females; these individuals have an increased testosterone-to-DHT ratio, normal female phenotype, and absent arm and leg hair with a decrease in axillary and pubic hair due to low DHT.2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar They have late menarche but normal menstrual function and fertility.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar, 2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar, 3Okeigwe I. Kuohung W. 5-Alpha reductase deficiency: a 40-year retrospective review.Curr Opin Endocrinol Diabetes Obes. 2014; 21: 483-487Crossref PubMed Scopus (32) Google Scholar Management for 5ARD may include initial sex assignment, trial of androgen supplementation, or DHT. This case is atypical because this patient presented with the symptoms at the age of 36 years. This was due to her lack of sexual activity and conservative upbringing. Typically, these patients are identified much earlier as they present with amenorrhea and infertility. This unique case highlights the need for medical providers to consider rare sexual development disorders in the differential for obesity, hirsutism, infertility, and amenorrhea. Answer46,XY 5-Alpha-reductase deficiency (5ARD). Differential diagnosis included androgen insensitivity syndrome and gonadal dysgenesis; however, genetic testing revealed a pathogenic variant of SRD5A2 gene confirming the diagnosis of 5ARD. DHT is a main factor in the development of the external male genitalia. Testosterone is important in the development of internal male genitalia and secondary sexual characteristics. 5-Alpha-reductase type 2 enzyme catalyzes the reduction of testosterone to DHT during embryogenesis.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar Generally, 46,XY patients with 5ARD present at birth with female features and a varying degree of hypospadias, normal female genitourinary anatomy, or clitomegaly. 5ARD has been described in 46,XX females; these individuals have an increased testosterone-to-DHT ratio, normal female phenotype, and absent arm and leg hair with a decrease in axillary and pubic hair due to low DHT.2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar They have late menarche but normal menstrual function and fertility.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar, 2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar, 3Okeigwe I. Kuohung W. 5-Alpha reductase deficiency: a 40-year retrospective review.Curr Opin Endocrinol Diabetes Obes. 2014; 21: 483-487Crossref PubMed Scopus (32) Google Scholar Management for 5ARD may include initial sex assignment, trial of androgen supplementation, or DHT. This case is atypical because this patient presented with the symptoms at the age of 36 years. This was due to her lack of sexual activity and conservative upbringing. Typically, these patients are identified much earlier as they present with amenorrhea and infertility. This unique case highlights the need for medical providers to consider rare sexual development disorders in the differential for obesity, hirsutism, infertility, and amenorrhea. 46,XY 5-Alpha-reductase deficiency (5ARD). Differential diagnosis included androgen insensitivity syndrome and gonadal dysgenesis; however, genetic testing revealed a pathogenic variant of SRD5A2 gene confirming the diagnosis of 5ARD. DHT is a main factor in the development of the external male genitalia. Testosterone is important in the development of internal male genitalia and secondary sexual characteristics. 5-Alpha-reductase type 2 enzyme catalyzes the reduction of testosterone to DHT during embryogenesis.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar Generally, 46,XY patients with 5ARD present at birth with female features and a varying degree of hypospadias, normal female genitourinary anatomy, or clitomegaly. 5ARD has been described in 46,XX females; these individuals have an increased testosterone-to-DHT ratio, normal female phenotype, and absent arm and leg hair with a decrease in axillary and pubic hair due to low DHT.2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar They have late menarche but normal menstrual function and fertility.1Kumar G, Barboza-Meca JJ. 5 alpha reductase deficiency. Accessed August 23, 2021. https://www.ncbi.nlm.nih.gov/books/NBK539904/Google Scholar, 2Maimoun L. Philibert P. Cammas B. et al.Phenotypical, biological, and molecular heterogeneity of 5α-reductase deficiency: an extensive international experience of 55 patients.J Clin Endocrinol Metab. 2011; 96: 296-307Crossref PubMed Scopus (145) Google Scholar, 3Okeigwe I. Kuohung W. 5-Alpha reductase deficiency: a 40-year retrospective review.Curr Opin Endocrinol Diabetes Obes. 2014; 21: 483-487Crossref PubMed Scopus (32) Google Scholar Management for 5ARD may include initial sex assignment, trial of androgen supplementation, or DHT. This case is atypical because this patient presented with the symptoms at the age of 36 years. This was due to her lack of sexual activity and conservative upbringing. Typically, these patients are identified much earlier as they present with amenorrhea and infertility. This unique case highlights the need for medical providers to consider rare sexual development disorders in the differential for obesity, hirsutism, infertility, and amenorrhea. DisclosureThe authors have no multiplicity of interest to disclose. The authors have no multiplicity of interest to disclose. The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Army, Department of the Navy, Department of Defense, or U.S. Government.

Abstract Disclosure: B.K. Bowens: None. D. LaChance: None. M.K. Shakir: None. T.D. Hoang: None. Background: Primary hyperparathyroidism (PHPT) is a relatively common condition which affects 1-7 people per 1000. However, intrathyroidal parathyroid adenomas (ITPA) have a prevalence of 1.3% to 6.7%. In this case series, we report 3 cases of ITPA. Case 1: 66-year-old male with a history of PHTP without intervention at initial diagnosis presented to Endocrinology several years after initial diagnosis due to an incidental thyroid nodule on routine CT lung cancer screening. Parathyroid hormone (PTH) level found to be 109.3 from a previous level of 80 (ref 10-55pg/mL) in the setting of mild hypercalcemia and osteopenia. Initial bedside thyroid ultrasound was suggestive of a right ITPA. Parathyroid scan, formal thyroid US and CT gated scan revealed a 1.5cm parathyroid adenoma (PA) posterior to the right superior aspect of the thyroid gland. Fine Needle Aspiration (FNA) was completed with PTH washout of 399.40 pg/mL. Right superior parathyroidectomy confirmed ITPA due to an intrathyroidal parathyroid adenoma Case 2: 44-year-old female presented with 9 months of fatigue and was diagnosed with PHPT. Her PTH level was 167 with a serum calcium of 10.9 (ref 8.5-10.4 mg/dL). CT SPECT with tech-99M sestamibi was positive for a right parathyroid adenoma. Explorative surgery did not localize parathyroid adenoma. Thyroid ultrasound revealed a 9mm hypoechoic lesion in the right inferior lobe with polar artery. FNA of this lesion was completed with PTH washout of 4737 pg/mL. Right hemi-thyroidectomy was completed with resolution of PHTP. Case 3: 54-year-old male with history of PHPT and carcinoma of the right kidney s/p nephrectomy presented with persistent hypercalcemia. Serum calcium of 10.2-11.0 mg/dL and PTH of 160-186 pg/mL. Thyroid US showed a 1.1cm hyperechoic, cystic nodule in the left inferior thyroid lobe. Sestamibi was consistent with ITPA. FNA of left thyroid mass with PTH washout of 2602 pg/mL. Parathyroidectomy with left thyroid lobectomy was completed with resolution of hypercalcemia. Discussion: PHPT is a common endocrinopathy with 85% of cases due to PAs, 15% due to parathyroid hyperplasia, and <1% due to carcinoma. ITPAs have an incidence of 1.3% to 6.7% and are due to improper embryologic migration. Sestamibi parathyroid scan allows for localization of PA and for minimally invasive procedures. Other imaging modalities include SPECT, US, SPECT-CT, and MRI. PTH washout with more than 101 pg/mL confirms the presence of parathyroid tissue or adenoma. Conclusion: This is a rare presentation of a common endocrinopathy. These patients were noted to have PHTP. Initial exploratory neck dissections did not localize. FNA and US were able to confirm IPTAs and hemi-thyroidectomy was needed for definitive management with resolution of PHTP. Presentation: Saturday, June 17, 2023

Abstract Introduction Approximately 60-80% of all hyperthyroid cases are caused by Graves’ disease, which is mediated by thyroid receptor antibodies. The prevalence of Graves Ophthalmopathy (GO) and pretibial myxedema is 0.15/10,000 and occurs in less than 5% of patients with Graves’ disease. We report a rare case of Graves disease with development of GO and pretibial myxedema post-thyroidectomy. Case Report A 51-year-old African American female with no medical history presented with tachycardia, palpitations, heat intolerance, weight loss, anxiety, and panic attacks. She was found to have an undetectable TSH, free T4 6.1 ng/dL (0.93-1.7 ng/dL), total T3 332.4 ng/dL (80-200 ng/dL), thyroid stimulating immunoglobulin (TSI) 19.50 IU/L (0.00-0.55 IU/L) and thyrotropin receptor antibody (TRAb) 27 U/L (<1.0 U/L). She denied vision changes, eye irritation or pain. Her initial exam revealed no exophthalmos, chemosis or reduced ocular range of motion. Thyroid ultrasound revealed an enlarged, heterogeneous, hypervascular thyroid. Treatment was initiated with atenolol and methimazole to achieve euthyroidism. Patient elected for total thyroidectomy. Within 3 months after thyroidectomy, she developed hyperpigmentation of bilateral anterior lower extremities with firm, compressible papules and scattered coalescent plaques. These lesions worsened and progressed over time. Skin biopsy revealed increased mucin in the papillary and reticular dermis and the subcutaneous soft tissue, consistent with pretibial myxedema. She also developed GO with exophthalmos, spontaneous orbital pain and edema and erythema of her eyelids and conjunctiva. Current plan of care is treatment with teprotumumab infusions with possibility of orbital decompression surgery. Conclusion The occurrence of GO and pretibial myxedema in a patient with Graves’ disease status post thyroidectomy is very uncommon, occurring in less than 5% of patients with Graves’ disease, especially since the source of the antigen for GO has been eliminated. Pretibial myxedema occurs as a result of the deposition of glycosaminoglycans (GAG) secreted by fibroblasts which have been found to express thyroid stimulating hormone receptor (TSHR) leading to deposition of mucin in the papillary and reticular dermis. In a similar manner, orbital accumulation of GAG and subsequent expansion of retrobulbar tissue leads to the clinical manifestation of exophthalmos. Despite thyroidectomy, the thyroid antibodies themselves may lead to the accumulation of GAG which may lead to the development of GO in the absence of a thyroid. Pretibial myxedema management depends on the symptomatology, as it may be asymptomatic or associated with pruritus and irritation. Topical or intralesional glucocorticoids are used to treat symptomatic cases, though there is a 30% chance of recurrence. Teprotumumab has been approved to treat GO and only case reports of teprotumumab leading to improvement of pretibial myxedema have been described. More data is needed to determine its efficacy as a treatment option for pretibial myxedema. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

We report a 51-year-old woman with thyroid eye disease and biopsy-proven pretibial myxedema that was subsequently treated with teprotumumab with improvement.

Described is an atypical presentation of a rare condition. It highlights the importance of thorough algorithm of medical and family history, physical examination, appropriate investigations, and perioperative workup and for surgery. The report demonstrates how even such very rare nonsecreting paragangliomas can be secondary to mass effects.

Abstract SDHD Mutation: Nonfunctional paragangliomas presenting as bilateral carotid body tumors with syncope Background: A mutation of the SDHD gene is associated with hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes which most commonly originate in the head and neck region, and usually form in the carotid body. Paragangliomas (PGL) can be secretory or non-secretory with about 95% of head and neck PGL being non-secretory. They can rarely present with symptoms due to compression, however, as in this case of a 29 year-old female presenting with syncope. Clinical Case: A 29 year-old female presented for evaluation after syncope. She had a syncopal event and fell down while walking in her home. Syncope was preceded by about 15 minutes of flushing, nausea and palpitations. She reported similar episodes once weekly in the preceding months, which generally lasted an hour. Initial workup included normal vital signs at presentation, normal ECG and echocardiogram, normal TFT, CBC, complete metabolic panel. Subsequent head/neck CT revealed bilateral masses in the carotid bifurcations consistent with carotid body tumors. Further history revealed a family history of bilateral carotid body tumors in her father which had never been evaluated. Plasma and urine metanephrines were normal. She underwent carotid body tumor excision. The left carotid body tumor was successfully excised and pathology revealed a paraganglioma with positive synaptophysin and chromogranin stains. Genetic testing revealed an SDHD (succinate dehydrogenase complex subunit D) gene mutation. Repeat biochemical assessment 4 months later was again negative and patient remained asymptomatic postoperatively. Conclusion: Paragangliomas can be secretory or non-secretory with about 95% of head and neck paragangliomas being non-secretory, as in this case. Symptoms can arise from catecholamine hypersecretion, which generally presents as hypertension, headaches, diaphoresis, flushing, anxiety or palpitations, and can be episodic or sustained, or mass effect. Syncope as a presenting symptom is rare, however, and has not been quantified but only reported in case reports. The exact etiology of syncope in our patient is not clear. Hereditary PGL/PCC syndromes should be suspected in any individual with multiple, recurrent, early-onset (age less than 45 years) or family history of PGL/PCC, as these syndromes are inherited in an autosomal dominant manner.