Patient Demographics > Ethnicity > Black - other
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Institute of Radiology, University of Padova, Padova, Italy
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Endocrine Disease Unit, University of Padova, Padova, Italy
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Nuclear Medicine Unit, University-Hospital of Padova, Padova, Italy
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Endocrine Disease Unit, University of Padova, Padova, Italy
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Summary
A 61-year-old man went to the Emergency Department with left upper abdominal quadrant pain and low-grade fever, as well as a loss of weight (3 kg in 6 weeks). A solid-cystic lesion in the left adrenal lodge was discovered by abdominal ultrasonography. A slight increase in the serum amylase with normal lipase was observed, but there were no signs or symptoms of pancreatitis. A contrast-enhanced CT revealed a tumor that was suspected of adrenocortical cancer. Therefore, he was referred to the endocrine unit. The hormonal evaluation revealed no signs of excessive or inadequate adrenal secretion. To characterize the mass, an MRI was performed; the lesion showed an inhomogeneous fluid collection with peripheral wall contrast-enhancement, as well as a minor 18-fluorodeoxyglucose uptake at PET/CT images. The risk of primary adrenal cancer was minimal after the multidisciplinary discussion. An acute necrotic collection after focal pancreatitis was suspected, according to the characteristics of imaging. Both CT-guided drainage of the necrotic accumulation and laboratory analysis of the aspirated fluid confirmed the diagnosis.
Learning points
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Different types of expansive processes can mimic adrenal incidentalomas.
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Necrotic collection after acute focal pancreatitis could be misdiagnosed as an adrenal mass, since its CT characteristics could be equivocal.
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MRI has stronger capacities than CT in differentiating complex lesions of the adrenal lodge.
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A multidisciplinary approach is fundamental in the management of patients with a newly discovered adrenal incidentaloma and equivocal/suspicious imaging features (low lipid content and size >4 cm).
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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
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Symptoms of increased intracranial pressure (ICP) include headache, vomiting, transient visual changes, and tinnitus.
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Secondary causes of increased ICP should be considered in males, young children, older patients, and those not overweight.
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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.
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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
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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.
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Most reports of TSHR I568T mutation have been detected in patients with benign thyroid conditions.
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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.
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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.
Banner University Medical Center – Phoenix, Phoenix, Arizona, USA
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Division of Endocrinology, Diabetes and Metabolism, University of Arizona College of Medicine – Phoenix, Phoenix, Arizona, USA
Carl T Hayden Phoenix VA Medical Center, Phoenix, Arizona, USA
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Division of Endocrinology, Diabetes and Metabolism, University of Arizona College of Medicine – Phoenix, Phoenix, Arizona, USA
Carl T Hayden Phoenix VA Medical Center, Phoenix, Arizona, USA
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Division of Endocrinology, Diabetes and Metabolism, University of Arizona College of Medicine – Phoenix, Phoenix, Arizona, USA
Carl T Hayden Phoenix VA Medical Center, Phoenix, Arizona, USA
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Division of Endocrinology, Diabetes and Metabolism, University of Arizona College of Medicine – Phoenix, Phoenix, Arizona, USA
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Summary
Immobilization-induced hypercalcemia is an uncommon cause of elevated calcium which is usually diagnosed following extensive systemic workup and exclusion of more common etiologies. Previously reported cases have largely described this phenomenon in adolescents and young adults a few weeks to months after the initial onset of immobilization. Metabolic workup tends to demonstrate hypercalcemia, hypercalciuria, and eventual osteoporosis. While the exact mechanism remains largely unclear, a dysregulation between bone resorption and formation is central to the pathogenesis of this disease. Decreased mechanical loading from prolonged bedrest tends to increase osteoclast induced bone resorption while promoting osteocytes to secrete proteins such as sclerostin to reduce osteoblast mediated bone formation. We describe the case of an 18-year-old male who was admitted following intraabdominal trauma. He underwent extensive abdominal surgery including nephrectomy resulting in initiation of dialysis. After 6 months of hospitalization, the patient gradually began developing uptrending calcium levels. Imaging and laboratory workup were unremarkable for any PTH-mediated process, malignancy, thyroid disorder, adrenal disorder, or infection. Workup did reveal significant elevated bone turnover markers which in combination with the clinical history led the physicians to arrive at the diagnosis of immobilization induced hypercalcemia. In order to prevent decreased rates of bone loss, the patient was administered denosumab for treatment. Hypocalcemia followed treatment expectedly and was repleted with supplementation via the patient’s total parenteral nutrition.
Learning points
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Immobilization-induced hypercalcemia should remain as a differential diagnosis of patients with prolonged hospitalizations with hypercalcemia.
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Extensive workup of common etiologies of hypercalcemia should be considered prior to arriving at this diagnosis.
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Denosumab, while off-label for this usage, offers an effective treatment option for immobilization-induced hypercalcemia though it carries a risk of hypocalcemia especially among patients with renal disease.
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Summary
We report a rare case of posterior reversible encephalopathy syndrome (PRES), precipitated by ectopic Cushing’s syndrome, in a patient with a metastatic pancreatic neuroendocrine tumour. A 55-year-old female presented as a hypertensive emergency with seizures and severe biochemical disturbance, including alkalosis, hypokalaemia and hyperglycaemia. MRI showed vasogenic oedema in the parieto-occipital region, consistent with a diagnosis of PRES. She had a significantly raised serum cortisol (>6000 nmol/L) which did not suppress with dexamethasone. Plasma adrenocorticotropic hormone (ACTH) concentrations were neither suppressed nor raised but were consistently within the normal reference range. The unexpected finding of a normal ACTH may be explained by either tumour secretion of unmeasured ACTH-related peptides, immunoassay antibody interference or episodic ACTH secretion. PRES is usually reversible with prompt and appropriate treatment. Hypercortisolism associated PRES is rare and may be associated with a worse outcome.
Learning points
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PRES secondary to ectopic Cushing’s syndrome is very rare.
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PRES in this context may indicate a worse prognosis.
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In ectopic Cushing’s syndrome, if the serum ACTH level is normal, consider testing for ACTH-related peptides or interfering antibodies.
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Further research is required to establish the best treatment approach and to improve patients’ outcomes.
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Summary
Pituitary adenomas can be classified as functioning or non-functioning adenomas. Approximately 64% of clinically non-functioning pituitary adenomas are found to be gonadotroph adenomas on immunohistochemistry. There are reported cases of gonadotroph adenomas causing clinical symptoms, but this is unusual. We present the case of a 36-year-old female with abdominal pain. Multiple large ovarian cysts were identified on ultrasound requiring bilateral cystectomy. Despite this, the cysts recurred resulting in further abdominal pain, ovarian torsion and right oophorectomy and salpingectomy. On her 3rd admission with abdominal pain, she was found to have a rectus sheath mass which was resected and histologically confirmed to be fibromatosis. Endocrine investigations revealed elevated oestradiol, follicle-stimulating hormone (FSH) at the upper limit of the normal range and a suppressed luteinising hormone (LH). Prolactin was mildly elevated. A diagnosis of an FSH-secreting pituitary adenoma was considered and a pituitary MRI revealed a 1.5 cm macroadenoma. She underwent transphenoidal surgery which led to resolution of her symptoms and normalisation of her biochemistry. Subsequent pelvic ultrasound showed normal ovarian follicular development. Clinically functioning gonadotroph adenomas are rare, but should be considered in women presenting with menstrual irregularities, large or recurrent ovarian cysts, ovarian hyperstimulation syndrome and fibromatosis. Transphenoidal surgery is the first-line treatment with the aim of achieving complete remission.
Learning points:
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Pituitary gonadotroph adenomas are usually clinically non-functioning, but in rare cases can cause clinical symptoms.
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A diagnosis of a functioning gonadotroph adenoma should be considered in women presenting with un-explained ovarian hyperstimulation and/or fibromatosis.
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In women with functioning gonadotroph adenomas, the main biochemical finding is elevated oestradiol levels. Serum FSH levels can be normal or mildly elevated. Serum LH levels are usually suppressed.
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Transphenoidal surgery is the first-line treatment for patients with functioning gonadotroph adenomas, with the aim of achieving complete remission.
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Elizabeth Glaser Pediatric AIDS Foundation, Washington, District of Columbia, USA
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Summary
An 11-year-old male with perinatally acquired human immune deficiency virus (HIV) infection on antiretroviral regimen, which included abacavir plus lamivudine (Epzicom), didanosine, ritonavir and atazanavir presented with bilateral axillary striae, increased appetite, fatigue, facial swelling and acute weight gain. Two months prior to presentation, the patient had received a diagnostic and therapeutic intra-articular triamcinolone injection in the knee for pain relief and subsequently became progressively swollen in the face, developed striae bilaterally at the axillae, experienced increased appetite, fatigue and an 8 pound weight gain. During the endocrine workup, suspicion for adrenal insufficiency prompted 24-h urine collection for free cortisol, which was found to be undetectable (below LLQ of 1.0 µg/L). This prompted further evaluation of the hypothalamic–pituitary axis (HPA) by standard dose adrenocorticotropic hormone (ACTH) stimulation test. A 250 µg cosyntropin stimulation test was performed and confirmed HPA axis suppression. Baseline cortisol level was <1 µg/dL and stimulated cortisol level at 30 min was 3.8 µg/dL. The patient was diagnosed with iatrogenic Cushing syndrome and suppression of HPA axis secondary to the drug interaction between ritonavir (RTV) and intra-articular triamcinolone injection. Following endocrine evaluation and workup, the patient was admitted for planned orthopaedic procedure including elective left hamstring lengthening, distal femoral osteotomy and patellar tendon advancement. Taking into consideration the diagnosis of iatrogenic Cushing syndrome, at the start of the surgical procedure, 100 mg IV stress dose of hydrocortisone followed by 50 mg hydrocortisone every 8 h for 24 h was administered. Stress dosing was discontinued 24 h after the procedure. Throughout the hospitalization and upon discharge, the patient continued his ART. From initial presentation, patient has remained clinically stable throughout surgery and postoperative period.
Learning points:
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Drug–drug interaction between ritonavir and triamcinolone can cause Cushing syndrome.
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Although triamcinolone has a half-life of 3 h, an intra-articular injection may be systematically absorbed for 3 weeks after injection, and adrenal suppression may last as long as 30 days.
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Co-administration of ritonavir and corticosteroids may result in an increase of plasma levels of corticosteroids levels, as they are both eliminated by CYP3A metabolism, and this interaction has the potential to prolong the half-life of triamcinolone several fold.
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No specific guidelines are available for the management of iatrogenic Cushing syndrome secondary to ritonavir and corticosteroids.
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One treatment option includes replacing ritonavir with a non-protease inhibitor-based regimen.
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Initiating hydrocortisone replacement therapy to prevent an adrenal crisis is also an alternate option.
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Summary
Adrenacarcinomas are rare, and hypoglycemic syndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by these tumors have been described infrequently. This study describes the case of a young woman with severe persistent hypoglycemia and a large adrenal tumor and discusses the physiopathological mechanisms involved in hypoglycemia. The case is described as a 21-year-old woman who presented with 8 months of general symptoms and, in the preceding 3 months, with episodes of mental confusion and visual blurring secondary to hypoglycemia. A functional assessment of the adrenal cortex revealed ACTH-independent hypercortisolism and hyperandrogenism. Hypoglycemia, hypoinsulinemia, low C-peptide and no ketones were also detected. An evaluation of the GH–IGF axis revealed GH blockade (0.03; reference: up to 4.4 ng/mL), greatly reduced IGF-I levels (9.0 ng/mL; reference: 180–780 ng/mL), slightly reduced IGF-II levels (197 ng/mL; reference: 267–616 ng/mL) and an elevated IGF-II/IGF-I ratio (21.9; reference: ~3). CT scan revealed a large expansive mass in the right adrenal gland and pulmonary and liver metastases. During hospitalization, the patient experienced frequent difficult-to-control hypoglycemia and hypokalemia episodes. Octreotide was ineffective in controlling hypoglycemia. Due to unresectability, chemotherapy was tried, but after 3 months, the patient’s condition worsened and progressed to death. In conclusion, our patient presented with a functional adrenal cortical carcinoma, with hyperandrogenism associated with hypoinsulinemic hypoglycemia and blockage of the GH–IGF-I axis. Patient’s data suggested a diagnosis of hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor (low levels of GH, greatly decreased IGF-I, slightly decreased IGF-II and an elevated IGF-II/IGF-I ratio).
Learning points:
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Hypoglycemyndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by adrenal tumors is a rare condition.
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Hypoinsulinemic hypoglycemia associated with hyperandrogenism and blockage of the GH–IGF-I axis suggests hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor.
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Hypoglycemia in cases of NICTH should be treated with glucocorticoids, glucagon, somatostatin analogs and hGH.
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Summary
Solitary sellar plasmacytomas are exceedingly rare and difficult to distinguish from other pituitary tumors. We report a case of a 62-year-old woman presenting with blurred vision of the right eye and tenderness of the right temporal region, which was interpreted as temporal arteritis. MRI revealed a pituitary mass lesion (20mm×14mm×17mm) without compression of the optic chiasm and her pituitary function was normal. Pituitary surgery was undertaken due to growth of the lesion, and histopathological examination showed a highly cellular neoplasm composed of mature monoclonal plasma cells. Subsequent examinations revealed no evidence of extrasellar myeloma. The patient received pituitary irradiation and has remained well and free of symptoms apart from iatrogenic central diabetes insipidus. Until now, only eight cases of solitary sellar plasmacytoma have been reported. Most frequent symptoms stem from compression of the cranial nerves in the cavernous sinus (III, IV, V), whereas the anterior pituitary function is mostly intact.
Learning points
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A solitary plasmacytoma is a rare cause of a sellar mass lesion.
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The radiological and clinical features are nonspecific, but cranial nerve affection and intact pituitary function are usually present.
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The diagnosis is made histologically and has important therapeutic implications.
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Summary
Cerebral vascular accidents are caused by vasospasm when induced by preeclampsia or by dopamine agonists. However, six arteries nourish the pituitary and prevent against vasospasm-induced damage, which up until now has not been thought to occur. Bromocriptine was used to arrest lactation in a 31-year-old with secondary amenorrhea following preeclampsia and fetal demise at 28 weeks gestation. Tests and history revealed panhypopituitarism not associated with hemorrhage or mass infarction but instead caused by vasospasm. The present study is the first report of pituitary damage from a non-hemorrhagic, vaso-occlusive event in the literature. In keeping with Sheehan's and Simon's syndromes, we have named pituitary damage resulting from vaso-occlusion as Dahan's syndrome, and a literature review suggests that it may be a common and previously overlooked disorder.
Learning points
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Vasospasm can cause damage to the pituitary gland, although it was not previously believed to do so.
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Preeclampsia and the use of a dopamine agonist, particularly in the peripartum state, may trigger vasospasm.
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Vasospasm resulting from dopamine agonists may be a common cause of injury to the pituitary gland, and it may have been overlooked in the past.
