Patient Demographics > Age > Adult

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David Fennell Department of Endocrinology, Mater Misericordiae University Hospital, Dublin, Ireland

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Clare Miller Department of Endocrinology, Mater Misericordiae University Hospital, Dublin, Ireland

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Stephen Ludgate Department of Endocrinology, Mater Misericordiae University Hospital, Dublin, Ireland

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John Conneely Department of Surgery, Mater Misericordiae University Hospital, Dublin, Ireland

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Serena O’Brien Department of Critical Care Medicine, Mater Misericordiae University Hospital, Dublin, Ireland

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Ian Conrick-Martin Department of Critical Care Medicine, Mater Misericordiae University Hospital, Dublin, Ireland

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Jennifer Hastings Department of Critical Care Medicine, Mater Misericordiae University Hospital, Dublin, Ireland

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Siobhán E McQuaid Department of Endocrinology, Mater Misericordiae University Hospital, Dublin, Ireland
School of Medicine, University College Dublin, Dublin, Ireland

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Summary

Phaeochromocytoma, a rare neuroendocrine tumour of chromaffin cell origin, is characterised by catecholamine excess. Clinical presentation ranges from asymptomatic disease to life-threatening multiorgan dysfunction. Catecholamine-induced cardiomyopathy is a dreaded complication with high lethality. While there is lack of evidence-based guidelines for use of veno-arterial extracorporeal membrane oxygenation (V-A ECMO) in the management of this condition, limited to case reports and small case series, V-A ECMO has been reported as ‘bridge to recovery’ therapy, providing circulatory support in the initial period of stabilisation prior to surgery. We report on two patients presenting with catecholamine-induced cardiomyopathy and circulatory collapse who were successfully treated with V-A ECMO for 5 and 6 days, respectively, providing initial haemodynamic support. After stabilisation and introduction of alpha-blockade, both cases had favourable outcomes, with successful laparoscopic adrenalectomies on days 62 and 83 of admission, respectively. Our case reports provide further support for the use of V-A ECMO in the treatment of such gravely ill patients.

Learning points

  • Phaeochromocytoma should be considered in the diagnosis of patients presenting with acute cardiomyopathy.

  • Management of catecholamine-induced cardiomyopathy is complex and requires multidisciplinary specialist input.

  • Pre-operative management of phaeochromocytoma involves alpha-blockade; however, haemodynamic instability in the setting of cardiogenic shock can preclude alpha-blockade use.

  • Veno-arterial extracorporeal membrane oxygenation is a life-saving intervention which may be considered in cases of acute catecholamine-induced cardiomyopathy and cardiogenic shock in order to provide the required haemodynamic support in the initial phase of treatment, enabling the administration of traditional pharmacological agents, including alpha-blockade.

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E Pauline Liao Department of Medicine, Division of Endocrinology, Lenox Hill Hospital, New York, New York, USA

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Natalie E Cusano Department of Medicine, Division of Endocrinology, Lenox Hill Hospital, New York, New York, USA

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Summary

We present the first report of use of recombinant human parathyroid hormone (1-84) (rhPTH(1-84)) in a hypoparathyroid patient during early pregnancy and lactation. The patient developed postoperative hypoparathyroidism as a 28-year-old woman following total thyroidectomy for multinodular goiter. She was not well controlled with conventional therapy, and started rhPTH(1-84) in 2015 following its approval in the United States. She became pregnant in 2018 at age 40. She discontinued rhPTH(1-84) therapy at 5 weeks gestation but resumed in the postpartum period while breastfeeding. Her daughter’s serum calcium was borderline elevated at 8 days postpartum but within the normal range at 8 weeks postpartum. The patient stopped nursing at around 6 months postpartum. Her daughter is now at 4 years and 5 months of age and is healthy and meeting developmental milestones. She was again pregnant at 8 months postpartum from her first pregnancy, and she made an informed decision to continue parathyroid hormone. At 15 weeks gestation, rhPTH(1-84) was recalled in the United States due to issues with the delivery device, and she discontinued rhPTH(1-84) treatment and resumed calcium and calcitriol supplements. She gave birth to a baby boy at 39 weeks in January 2020. At 3 years and 2 months of age, he is overall healthy. Further data are needed regarding the safety of rhPTH(1-84) in pregnancy and lactation.

Learning points

  • rhPTH(1-84) is approved for therapy of patients with hypoparathyroidism; however, there are no data regarding the safety of treatment during nursing and pregnancy.

  • There are multiple alterations in mineral metabolism during normal pregnancy and lactation.

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Prishila Fookeerah Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, Australia
School of Medicine, Western Sydney University, Sydney, Australia

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Mark McLean Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, Australia
School of Medicine, Western Sydney University, Sydney, Australia

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Summary

The anatomy of the pituitary fossa is complex. The wall of the fossa can vary, resulting in inconsistencies in the nature and integrity of the sella barrier. Cerebrospinal fluid is generally confined to the subarachnoid space and does not circulate freely in the pituitary fossa. Spontaneous haemorrhage in the fossa typically occurs in the context of pre-existing intrasellar pathology such as a pituitary adenoma. Extravasation of blood into the subarachnoid space can rarely be observed following pituitary apoplexy. We describe the unique occurrence of subarachnoid haemorrhage in a largely empty pituitary fossa after the rupture of a cerebral aneurysm.

Learning points

  • Pituitary apoplexy and subarachnoid haemorrhage (SAH) are both high in the differential diagnosis of sudden onset severe headaches.

  • Haemorrhagic pituitary apoplexy may result in extravasation into the subarachnoid space, resulting in typical SAH symptoms and signs.

  • This is the first reported case of primary SAH resulting in blood pooling in an empty sella arising from previous surgical resection of a large macroadenoma.

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

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Summary

A 40-year-old Japanese woman presented to the outpatient clinic with fever and palpitations 2 days after receiving the influenza vaccine (Influenza HA Vaccine ‘KMB’®) following the second dose of coronavirus disease 2019 (COVID-19) vaccine (COVID-19 vaccine Moderna intramuscular injection®). At the first visit, the patient presented with a swollen thyroid gland with mild tenderness, and she was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free T3: 5.42 pg/mL; free T4: 2.34 ng/dL; and thyroid-stimulating hormone (TSH): <0.01 μIU/mL), a high C-reactive protein level (5.77 mg/dL), a negative TSH receptor antibody, and characteristic ultrasound findings. The patient’s human leukocyte antigen types were A2, A11, B35, B51, DR4, and DR1403. Prednisolone (15 mg/day) was given as an initial dose, after which the fever subsided, and the dose was tapered and discontinued after 6 weeks. The patient was thought to have developed SAT due to influenza vaccination. SAT after influenza vaccination may be overlooked. For patients with SAT, it is necessary to obtain information regarding their vaccination history.

Learning points

  • After influenza vaccination, subacute thyroiditis (SAT) may develop.

  • If persistent fever, anterior neck pain, swelling, tenderness of the thyroid gland, and symptoms of thyrotoxicosis are observed immediately after vaccination for several viruses, including influenza, an examination to rule out the onset of SAT is recommended.

  • Human leukocyte antigen type A2 (HLA-A2) and HLA-B35 may be linked to the development of SAT following influenza vaccination.

  • The two doses of the coronavirus disease 2019 (COVID-19) vaccine given before the influenza vaccine may affect the onset of SAT.

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Paula Condé Lamparelli Elias Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Marcelo Volpon Department of Surgery and Anatomy, Ribeirão Preto Medical School, University of São Paulo

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Giovana de Gobbi Azevedo Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Helio Machado Department of Surgery and Anatomy, Ribeirão Preto Medical School, University of São Paulo

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Gabriel Henrique Marques Gonçalves Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Antonio Carlos Santos Department of Radiology, Hematology and Oncology, Ribeirão Preto Medical School, University of São Paulo

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Livia M Mermejo Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Margaret de Castro Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Ayrton C Moreira Department of Internal Medicine, Division of Endocrinology, Ribeirão Preto Medical School, University of São Paulo

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Summary

Postoperative (PO) complications after transsphenoidal surgery (TSS) are rare when performed in pituitary referral centers. Partial hypopituitarism is more frequent and somewhat expected. Meningitis, cerebrospinal fluid leaks, and visual deficits are unusual. Cerebrovascular complications, including cerebral vasospasm are rare, usually under-appreciated and not mentioned to the patient prior to the surgery. This is a report of a 51-year-old male with a non-functioning pituitary macroadenoma presenting with partial hypopituitarism and visual field loss. The patient was submitted to an uneventful TSS. On the first PO day, he developed a left palpebral ptosis with unequal pupils and impaired consciousness (12 points on Glasgow Coma Scale). CT scan revealed a perimesencephalic subarachnoid hemorrhage (SAH) grade 1 according to the modified Fisher scale. High-dose dexamethasone (16 mg/day) was initiated and the patient became more alert (Glasgow 14). On the fifth PO day, due to progression of the neurological deficits (left III, IV, and VI cranial nerves palsy, ataxia, dysdiadochokinesia, right dysmetria, and dysarthria), a magnetic resonance angiography was obtained and revealed a recent mesencephalic infarct without evident vasospasm. Nevertheless, nimodipine 60 mg 4/4 h was initiated. No improvement was seen after 3 days of treatment. The patient was discharged and put on rehabilitation, returning to normal gait and balance after 7 months. This, therefore, is a case of an unexpected mesencephalic infarct probably due to vasospasm induced by minor SAH. Although exceptionally rare, informing the patient about this event prior to TSS is important due to its significant neurological impact. More data are needed considering preventive treatment with nimodipine as soon as SAH is detected after TSS and whether it would improve neurological outcomes.

Learning points

  • Whenever neurological deficits arise after transsphenoidal surgery (TSS), systemic infection, meningitis, electrolyte imbalance, and evident hemorrhage must be promptly investigated.

  • Although rare, cerebral vasospasm (CVS) after TSS is associated with high morbidity and high mortality rates.

  • Vigilance for vasospasm is necessary for patients undergoing TSS for pituitary adenoma, especially those with significant suprasellar extension.

  • Informing this event to the patient prior to TSS is essential due to its significant morbidity and mortality.

  • Post-TSS subarachnoid hemorrhage and hemiparesis may be important clues indicating CVS and infarction.

  • There is limited evidence in the literature regarding post-TSS CVS surveillance and treatment strategies which could have an impact on clinical decisions.

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Beryl Lin Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, NSW, Australia

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Stephen M Twigg Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, NSW, Australia
Sydney Medical School (Central), University of Sydney, Sydney, NSW, Australia

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Summary

Functional hypogonadotropic hypogonadism is a relatively common condition in middle-aged to elderly men that can significantly impair quality of life. Besides lifestyle optimisation, androgen replacement remains the mainstay of treatment; however, its adverse effects on spermatogenesis and testicular atrophy are undesirable. Clomiphene citrate is a selective oestrogen receptor modulator that acts centrally to increase endogenous testosterone without affecting fertility. Although it has demonstrated effectiveness in shorter-duration studies, its longer-term outcomes are less well-documented. In this study, we report the case of a 42-year-old male with functional hypogonadotropic hypogonadism who sustained an excellent dose-dependent, titratable clinical and biochemical response to clomiphene citrate with no known adverse effects for 7 years to date. This case highlights that clomiphene citrate has potential as a safe and titratable longer-term treatment option, and the need for further randomised control trials in therapy options to normalise androgen status.

Learning points

  • Functional hypogonadotropic hypogonadism is a relatively common, but likely underdiagnosed, condition in middle-aged to older males.

  • Testosterone replacement is the current mainstay of endocrine therapy but can cause sub-fertility and testicular atrophy.

  • Clomiphene citrate is a serum oestrogen receptor modulator that acts centrally to increase endogenous testosterone production without affecting fertility.

  • It has potential as a safe and efficacious longer-term treatment option that can be titrated to increase testosterone and relieve clinical symptoms in a dose-dependent manner.

  • Longitudinal prospective studies as randomised control trials evaluating alternatives to exogenous testosterone are required.

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Chelsea Tan Bendigo Health, Victoria, Australia

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Jessica Triay Bendigo Health, Victoria, Australia

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Summary

A 64-year-old man with progressive metastatic castrate-resistant prostate adenocarcinoma presented with recurrent fluid overload, severe hypokalaemia with metabolic alkalosis and loss of glycaemic control. Clinical features were facial plethora, skin bruising and proximal myopathy. Plasma adrenocorticotrophic hormone (ACTH), serum cortisol and 24-h urinary cortisol levels were elevated. Low-dose dexamethasone failed to suppress cortisol. Pituitary MRI was normal and 68Gallium-DOTATATE PET–CT scan showed only features of metastatic prostate cancer. He was diagnosed with ectopic ACTH syndrome secondary to treatment-related neuroendocrine prostate cancer differentiation. Medical management was limited by clinical deterioration, accessibility of medications and cancer progression. Ketoconazole and cabergoline were utilised, but cortisol remained uncontrolled. He succumbed 5 months following diagnosis. Treatment-related neuroendocrine differentiation of prostate adenocarcinoma is a rare cause of ectopic ACTH syndrome.

Learning points

  • Neuroendocrine differentiation following prostate adenocarcinoma treatment with androgen deprivation has been described.

  • Ectopic adrenocorticotrophic hormone (ACTH) syndrome should be considered where patients with metastatic prostate cancer develop acute electrolyte disturbance or fluid overload.

  • Ketoconazole interferes with adrenal and gonadal steroidogenesis and can be used in ectopic ACTH syndrome, but the impact may be insufficient. Inhibition of gonadal steroidogenesis is favourable in prostate cancer.

  • More data are required to evaluate the use of cabergoline in ectopic ACTH syndrome.

  • Ectopic ACTH syndrome requires prompt management and is challenging in the face of metastatic cancer.

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Azusa Morishita Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Yasuo Hozumi Department of Breast and Endocrine Surgery, Ibaraki Prefectural Central Hospital, Koibuchi, Kasama, Ibaraki, Japan

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Hiroaki Ishii Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Yukio Hokazono Department of Pathology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Clovis Manuel Yosei Kikuchi Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Megumi Shimasaki Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Mikiko Itaya Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Masaharu Oura Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Ken Kuriki Department of Pathology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Akira Hishida Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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George Seki Department of Nephrology, Yaizu City Hospital, Dobara, Yaizu, Shizuoka, Japan

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Summary

Hypercalcemia due to parathyroid carcinoma (PC) is safely and quickly controlled with rapidly increasing evocalcet doses. Most parathyroid carcinomas are detected because of hypercalcemia due to primary hyperparathyroidism (PHPT). Hypercalcemia becomes more severe in patients with PC than those with parathyroid adenoma or hyperplasia. Hypercalcemia often causes renal dysfunction, gastrointestinal symptoms, and psychiatric symptoms. Consequently, the serum calcium level needs to be promptly corrected. Here, we report a case of PC with remarkably persistent hypercalcemia, which we safely and quickly controlled with rapidly increasing evocalcet doses. A 77-year-old female presented with renal dysfunction. Her serum calcium (Ca) and intact parathyroid hormone serum levels were 13.9 mg/dL and 1.074 pg/mL, respectively. Her renal function worsened because of hypercalcemia due to PHPT. Technetium-99 m methoxy-isobutyl-isonitrile parathyroid scintigraphic examination revealed an accumulation below the right thyroid lobe. CT examination showed a 35-mm mass. Hypercalcemia needed to be immediately corrected because of the patient’s worsening renal function. Evocalcet treatment at a gradually increasing dose of up to 20 mg over 3 weeks allowed her serum Ca level to be maintained below 11 mg/dL. Only mild nausea was observed at the beginning of the treatment. The mass was suspected as PC because the hypercalcemia was refractory to high-dose evocalcet. The patient was treated with parathyroidectomy and ipsilateral thyroidectomy. PC was diagnosed based on the pathological findings of capsular and venous invasion. The patient’s renal function improved and surgery could be safely performed by promptly correcting hypercalcemia.

Learning points

  • Hypercalcemia due to parathyroid carcinoma (PC) is often more severe than that caused by parathyroid adenoma or hyperplasia.

  • PC is a rare disease, but it should be considered if the patient has intractable hypercalcemia due to primary hyperparathyroidism (PHPT).

  • Evocalcet, which is used to treat hypercalcemia due to PHPT, does not interact with P450 (CYP) and causes few side effects.

  • Complications, including renal dysfunction, were improved and the surgery could be safely performed by promptly correcting hypercalcemia.

  • PC has a high recurrence rate. En-block excision is necessary when PC is suspected.

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Erika Sugito Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Akiyo Tanabe Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Koji Maruyama Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Kyoko Nohara Department of Surgery, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Naoki Enomoto Department of Surgery, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Ryotaro Bouchi Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan
Diabetes and Metabolism Information Center, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan

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Mitsuru Ohsugi Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan
Diabetes and Metabolism Information Center, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan

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Kohjiro Ueki Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan
Department of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan

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Kazuhiko Yamada Department of Surgery, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Hiroshi Kajio Department of Diabetes, Endocrinology, and Metabolism, Center Hospital, National Center for Global Health and Medicine, Tokyo, Japan

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Summary

A 47-year-old man was diagnosed with a left adrenal incidentaloma at 40 years of age. The tumor had irregular margins and grew from 18 mm to 30 mm in maximum diameter over 7 years. On computed tomography scan, the mass appeared to localize within the tip of the lateral limb of the left adrenal gland, and between the left adrenal gland and the posterior wall of the stomach. The plasma corticotropin and cortisol concentrations and the 24-h urine fractionated metanephrine levels were normal. 123I-metaiodobenzylguanidine scintigraphy showed tumor avidity consistent with a hormonally inactive pheochromocytoma. A laparoscopic left adrenalectomy was performed; however, no tumor was present in the resected specimen. Abdominal computed tomography postoperatively showed that the tumor remained intact and appeared to connect to the posterior wall of the stomach. A laparotomy was performed and the tumor was removed. The tumor was localized to the intraperitoneal space and isolated from the posterior wall of the stomach. The pathological diagnosis was a gastrointestinal stromal tumor. Clinicians need to be aware of the limitations of diagnostic imaging studies in diagnosing non-functioning adrenal incidentalomas, which require a pathological analysis for the final diagnosis. Moreover, clinicians need to provide patients with sufficient informed consent when deciding on treatment strategies.

Learning points

  • Anatomic structures and tumors that develop in neighboring tissues to the adrenal glands may be confused with primary adrenal tumors.

  • 123I- metaiodobenzylguanidine (MIBG) scintigraphy is specific for diagnosing pheochromocytomas and paragangliomas; however, it has been reported that 123I-MIBG may accumulate in neuroendocrine tumors as well as other tumors.

  • Clinicians should recognize the limitations of imaging studies and the uncertainty of an imaging-based preoperative diagnosis.

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Valerie Lai Department of Medicine, University of Alberta, Edmonton, AB, Canada

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Mariam Shahidi Department of Medicine, University of Alberta, Edmonton, AB, Canada
Division of Endocrinology and Metabolism, University of Alberta, Edmonton, AB, Canada

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Alicia Chan Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada

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Shailly Jain-Ghai Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada

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Summary

3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lyase deficiency is an inborn error of metabolism resulting in a lack of ketogenesis and leucine catabolism. Hallmarks of decompensation include hypoglycemia without ketosis (or hypoketosis), metabolic acidosis, and hyperammonemia. Management includes avoiding fasting and restricting dietary protein and fat. Conversely, type 2 diabetes mellitus (T2DM) requires carbohydrate restriction and/or anti-hyperglycemic agents; thus, managing these co-existing disorders is challenging. A 36-year-old male with HMG-CoA lyase deficiency and T2DM (Hemoglobin A1c (HbA1c): 7.9%) presented with confusion and shock. Blood work revealed metabolic acidosis, hyperammonemia, hyperglycemia, and hypoketosis. The patient was diagnosed with hyperosmolar non-ketotic hyperglycemia and hyperammonemia secondary to HMG-CoA lyase metabolic decompensation requiring intensive care unit admission. Hyperammonemia management was challenging because alternative calories with i.v. dextrose (due to hyperglycemia) and i.v. lipids (due to HMG-CoA lyase deficiency) could not be provided as usual. The patient was started on hemodialysis and i.v. insulin with marked improvement. Once stabilized, metformin and insulin were initiated. T2DM impaired cellular glucose uptake and produced a state similar to hypoglycemia, despite the patient being profoundly hyperglycemic, which led to metabolic decompensation of HMG-CoA lyase deficiency. Managing T2DM and HMG-CoA lyase deficiency warrants special considerations due to the potential for metabolic decompensation with both hyperglycemia and hypoglycemia.

Learning points

  • In a patient with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) lyase deficiency and type 2 diabetes mellitus (T2DM), management principles include avoiding hypoglycemia to prevent metabolic decompensation, providing insulin for proper glucose utilization, and moderation of carbohydrate intake to prevent consequences of chronic hyperglycemia.

  • The development of insulin resistance in the form of T2DM in HMG-CoA lyase deficiency likely triggered a state similar to hypoglycemia, leading to cellular energy deficiency and subsequently metabolic decompensation.

  • It is important to avoid hypoglycemia in patients with HMG-CoA lyase deficiency and T2DM, as the risk of metabolic decompensation is increased due to the lack of ketogenesis in HMG-CoA lyase deficiency.

  • Selection of antidiabetic agents in this patient population requires careful consideration, and agents that have a higher risk of hypoglycemia should be avoided.

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