Browse

You are looking at 1 - 10 of 24 items

Mawson Wang Department of Endocrinology and Diabetes, Blacktown Hospital, Sydney, Australia
Blacktown Clinical School, School of Medicine, Western Sydney University, Sydney, Australia

Search for other papers by Mawson Wang in
Google Scholar
PubMed
Close
,
Benjamin Jonker Department of Neurosurgery, St. Vincent’s Hospital, Sydney, Australia

Search for other papers by Benjamin Jonker in
Google Scholar
PubMed
Close
,
Louise Killen Department of Pathology, St. Vincent’s Hospital, Sydney, Australia

Search for other papers by Louise Killen in
Google Scholar
PubMed
Close
,
Yvonne Bogum NSW Health Pathology East, Prince of Wales Hospital, Sydney, Australia

Search for other papers by Yvonne Bogum in
Google Scholar
PubMed
Close
,
Ann McCormack Department of Endocrinology, St. Vincent’s Hospital, Sydney, Australia
Garvan Institute of Medical Research, Sydney, Australia
St. Vincent’s Clinical School, Faculty of Medicine, UNSW Sydney, Sydney, Australia

Search for other papers by Ann McCormack in
Google Scholar
PubMed
Close
, and
Ramy H Bishay Department of Endocrinology and Diabetes, Blacktown Hospital, Sydney, Australia
Blacktown Clinical School, School of Medicine, Western Sydney University, Sydney, Australia

Search for other papers by Ramy H Bishay in
Google Scholar
PubMed
Close

Summary

Cushing’s disease is a rare disorder characterised by excessive cortisol production as a consequence of a corticotroph pituitary tumour. While the primary treatment is surgical resection, post-operative radiation therapy may be used in cases of ongoing inadequate hormonal control or residual or progressive structural disease. Despite improved outcomes, radiotherapy for pituitary tumours is associated with hypopituitarism, visual deficits and, rarely, secondary malignancies. We describe an unusual case of a 67-year-old female with presumed Cushing’s disease diagnosed at the age of 37, treated with transsphenoidal resection of a pituitary tumour with post-operative external beam radiotherapy (EBRT), ketoconazole for steroidogenesis inhibition, and finally bilateral adrenalectomy for refractory disease. She presented 30 years after her treatment with a witnessed generalised tonic-clonic seizure. Radiological investigations confirmed an extracranial mass infiltrating through the temporal bone and into brain parenchyma. Due to recurrent generalised seizures, the patient was intubated and commenced on dexamethasone and anti-epileptic therapy. Resection of the tumour revealed a high-grade osteoblastic osteosarcoma. Unfortunately, the patient deteriorated in intensive care and suffered a fatal cardiac arrest following a likely aspiration event. We describe the risk factors, prevalence and treatment of radiation-induced osteosarcoma, an exceedingly rare and late complication of pituitary irradiation. To our knowledge, this is the longest reported latency period between pituitary irradiation and the development of an osteosarcoma of the skull.

Learning points:

  • Cushing’s disease is treated with transsphenoidal resection as first-line therapy, with radiotherapy used in cases of incomplete resection, disease recurrence or persistent hypercortisolism.

  • The most common long-term adverse outcome of pituitary tumour irradiation is hypopituitarism occurring in 30–60% of patients at 10 years, and less commonly, vision loss and oculomotor nerve palsies, radiation-induced brain tumours and sarcomas.

  • Currently proposed characteristics of radiation-induced osteosarcomas include: the finding of a different histological type to the primary tumour, has developed within or adjacent to the path of the radiation beam, and a latency period of at least 3 years.

  • Treatment of osteosarcoma of the skull include complete surgical excision, followed by systemic chemotherapy and/or radiotherapy.

  • Overall prognosis in radiation-induced sarcoma of bone is poor.

  • Newer techniques such as stereotactic radiosurgery may reduce the incidence of radiation-induced malignancies.

Open access
Kazuhisa Kusuki Department of Diabetes and Endocrinology, Kanto Central Hospital of the Mutual Aid Association of Public School Teachers, Setagaya-ku, Tokyo, Japan

Search for other papers by Kazuhisa Kusuki in
Google Scholar
PubMed
Close
,
Saya Suzuki Department of Diabetes and Endocrinology, Kanto Central Hospital of the Mutual Aid Association of Public School Teachers, Setagaya-ku, Tokyo, Japan

Search for other papers by Saya Suzuki in
Google Scholar
PubMed
Close
, and
Yuzo Mizuno Department of Diabetes and Endocrinology, Kanto Central Hospital of the Mutual Aid Association of Public School Teachers, Setagaya-ku, Tokyo, Japan

Search for other papers by Yuzo Mizuno in
Google Scholar
PubMed
Close

Summary

A 72-year-old man with no history of diabetes was referred to our department due to hyperglycemia during pembrolizumab treatment for non-small-cell lung carcinoma. His blood glucose level was 209 mg/dL, but he was not in a state of ketosis or ketoacidosis. Serum C-peptide levels persisted at first, but gradually decreased, and 18 days later, he was admitted to our hospital with diabetic ketoacidosis (DKA). The patient was diagnosed with fulminant type 1 diabetes (FT1D) induced by pembrolizumab. According to the literature, the insulin secretion capacity of a patient with type 1 diabetes (T1D) induced by anti-programmed cell death-1 (anti-PD-1) antibody is depleted in approximately 2 to 3 weeks, which is longer than that of typical FT1D. Patients with hyperglycemia and C-peptide persistence should be considered for hospitalization or frequent outpatient visits with insulin treatment because these could indicate the onset of life-threatening FT1D induced by anti-PD-1 antibodies. Based on the clinical course of this patient and the literature, we suggest monitoring anti-PD-1 antibody-related T1D.

Learning points:

  • Immune checkpoint inhibitors, such as anti-PD-1 antibodies, are increasingly used as anticancer drugs. Anti-PD-1 antibodies can cause immune-related adverse events, including T1D.

  • FT1D, a novel subtype of T1D, is characterized by the abrupt onset of hyperglycemia with ketoacidosis, a relatively low glycated hemoglobin level and depletion of C-peptide level at onset.

  • In patients being treated with anti-PD-1 antibody, hyperglycemia with C-peptide level persistence should be monitored through regular blood tests. Because of C-peptide persistence and mild hyperglycemia, it is possible to miss a diagnosis of life-threatening FT1D induced by anti-PD-1 antibody.

  • In particular, in patients who have no history of diabetes, hyperglycemia without DKA is likely to be the very beginning of anti-PD-1 antibody-induced T1D. Therefore, such patients must be considered for either hospitalization or frequent outpatient visits with insulin injections and self-monitoring of blood glucose.

Open access
Frank Gao Department of Endocrinology and Diabetes, The Alfred Hospital, Melbourne, Australia

Search for other papers by Frank Gao in
Google Scholar
PubMed
Close
,
Stephen Hall Department of Medicine, Monash University and Cabrini Health, Melbourne, Australia

Search for other papers by Stephen Hall in
Google Scholar
PubMed
Close
, and
Leon A Bach Department of Endocrinology and Diabetes, The Alfred Hospital, Melbourne, Australia
Department of Medicine (Alfred), Monash University, Melbourne, Australia

Search for other papers by Leon A Bach in
Google Scholar
PubMed
Close

Summary

Sodium/glucose co-transporter 2 (SGLT2) inhibitors are novel oral hypoglycaemic agents that are increasingly used in the management of type 2 diabetes mellitus (T2DM). They are now recommended as second-line pharmacotherapy (in conjunction with metformin) in patients with type 2 diabetes and established atherosclerotic heart disease, heart failure or chronic kidney disease due to their favourable effects on cardiovascular and renal outcomes. We report a case of a 69-year-old man who developed muscle pain, weakness and wasting after commencing the SGLT2 inhibitor empagliflozin. This persisted for 1 year before he underwent resistance testing, which confirmed muscle weakness. His symptoms resolved within weeks of ceasing empagliflozin, with improvement in muscle strength on clinical assessment and resistance testing and reversal of MRI changes. No other cause of myopathy was identified clinically, on biochemical assessment or imaging, suggesting that empagliflozin was the cause of his myopathy.

Learning points:

  • Empagliflozin, a commonly used SGLT2 inhibitor, was associated with myopathy.

  • A high degree of suspicion is required to diagnose drug-induced myopathy, with a temporal relationship between starting the medication and symptom onset being the main indicator.

  • Recognition of drug-induced myopathy is essential, as discontinuation of the offending drug typically improves symptoms.

Open access
Maria Tomkins Department of Endocrinology and Diabetes, Beaumont Hospital Dublin, Dublin, Ireland

Search for other papers by Maria Tomkins in
Google Scholar
PubMed
Close
,
Roxana Maria Tudor Department of Endocrinology and Diabetes, Beaumont Hospital Dublin, Dublin, Ireland

Search for other papers by Roxana Maria Tudor in
Google Scholar
PubMed
Close
,
Diarmuid Smith Department of Endocrinology and Diabetes, Beaumont Hospital Dublin, Dublin, Ireland

Search for other papers by Diarmuid Smith in
Google Scholar
PubMed
Close
, and
Amar Agha Department of Endocrinology and Diabetes, Beaumont Hospital Dublin, Dublin, Ireland

Search for other papers by Amar Agha in
Google Scholar
PubMed
Close

Summary

This case is the first to describe a patient who experienced concomitant agranulocytosis and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis as an adverse effect of propylthiouracil treatment for Graves’ disease. A 42-year-old female with Graves’ disease presented to the emergency department (ED) with a 2-week history of fevers, night sweats, transient lower limb rash, arthralgia, myalgia and fatigue. She had been taking propylthiouracil for 18 months prior to presentation. On admission, agranulocytosis was evident with a neutrophil count of 0.36 × 109/L and immediately propylthiouracil was stopped. There was no evidence of active infection and the patient was treated with broad-spectrum antibodies and one dose of granulocyte colony-stimulation factor, resulting in a satisfactory response. On further investigation, ANCAs were positive with dual positivity for proteinase 3 and myeloperoxidase. There was no evidence of end-organ damage secondary to vasculitis, and the patient’s constitutional symptoms resolved completely on discontinuation of the drug precluding the need for immunosuppressive therapy.

Learning points:

  • Continued vigilance and patient education regarding the risk of antithyroid drug-induced agranulocytosis is vital throughout the course of treatment.

  • ANCA-associated vasculitis is a rare adverse effect of antithyroid drug use.

  • Timely discontinuation of the offending drug is vital in reducing end-organ damage and the need for immunosuppressive therapy in drug-induced ANCA-associated vasculitis.

  • Similarities in the pathogenesis of agranulocytosis and drug-induced ANCA-associated vasculitis may offer insight into an improved understanding of vasculitis and agranulocytosis.

Open access
Florence Gunawan Barwon Health, Geelong University Hospital, Geelong, Victoria, Australia

Search for other papers by Florence Gunawan in
Google Scholar
PubMed
Close
,
Elizabeth George Barwon Health, Geelong University Hospital, Geelong, Victoria, Australia

Search for other papers by Elizabeth George in
Google Scholar
PubMed
Close
, and
Mark Kotowicz Barwon Health, Geelong University Hospital, Geelong, Victoria, Australia

Search for other papers by Mark Kotowicz in
Google Scholar
PubMed
Close

Summary

Denosumab is a fully human MAB that acts as a potent anti-resorptive by inhibiting activation of osteoclasts by inhibiting the receptor activator of nuclear factor-kappa B (RANK) ligand. Hypocalcaemia has been reported as one of the serious adverse sequelae of use of denosumab. We present a case of refractory hypocalcaemia following administration of a single dose of denosumab in a patient with metastatic castrate-resistant prostate cancer. The patient’s serum calcium and vitamin D concentrations and renal function were normal prior to denosumab administration. Serum alkaline phosphatase (ALP) level was however elevated pre-morbidly consistent with known bone metastases. The patient was treated with high-dose oral and IV calcium without any appreciable response in serum calcium. During his 30-day hospital admission, he demonstrated disease progression with development of new liver metastases and bone marrow involvement. Normocalcaemia was not achieved despite 1 month of aggressive therapy. Given the patient was asymptomatic and prognosis guarded, he was eventually discharged for ongoing supportive care under the palliative care team.

Learning points:

  • Denosumab is a potent anti-resorptive therapy and hypocalcaemia is one of the known adverse effects.

  • Serum calcium and vitamin D concentrations must be replete prior to administration of denosumab to reduce the risk of hypocalcaemia.

  • Denosumab has been proven to be more effective than zoledronic acid in preventing skeletal-related adverse effects in patients with metastatic castrate-resistant prostate cancer.

Open access
Misaki Aoshima Departments of Endocrinology Diabetes and Metabolism, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Misaki Aoshima in
Google Scholar
PubMed
Close
,
Koji Nagayama Departments of Endocrinology Diabetes and Metabolism, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Koji Nagayama in
Google Scholar
PubMed
Close
,
Kei Takeshita Departments of Endocrinology Diabetes and Metabolism, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Kei Takeshita in
Google Scholar
PubMed
Close
,
Hiroshi Ajima Departments of Endocrinology Diabetes and Metabolism, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Hiroshi Ajima in
Google Scholar
PubMed
Close
,
Sakurako Orikasa Departments of Endocrinology Diabetes and Metabolism, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Sakurako Orikasa in
Google Scholar
PubMed
Close
,
Ayana Iwazaki ²Departments of Endocrinology Diabetes and Metabolism, Seirei Hamamatsu General Hospital, Hamamatsu, Shizuoka, Japan

Search for other papers by Ayana Iwazaki in
Google Scholar
PubMed
Close
,
Hiroaki Takatori Department of Rheumatology, Hamamatsu Medical Center, Hamamatsu, Shizuoka, Japan

Search for other papers by Hiroaki Takatori in
Google Scholar
PubMed
Close
, and
Yutaka Oki Department of Family and Community Medicine, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan

Search for other papers by Yutaka Oki in
Google Scholar
PubMed
Close

Summary

Patients treated with immunosuppressive drugs, especially methotrexate (MTX), rarely develop lymphoproliferative disorders (LPDs), known as MTX-related LPD (MTX–LPD). The primary site of MTX–LPD is often extranodal. This is the first reported case of MTX–LPD in the pituitary. A 65-year-old woman was admitted to our hospital with symptoms of oculomotor nerve palsy and multiple subcutaneous nodules. She had been treated with MTX for 11 years for rheumatoid arthritis. Computed tomography showed multiple masses in the orbit, sinuses, lung fields, anterior mediastinum, kidney, and subcutaneous tissue. Brain magnetic resonance imaging revealed a sellar mass. She was diagnosed with hypopituitarism and central diabetes insipidus based on endocrine examination. Although pituitary biopsy could not be performed, we concluded that the pituitary lesion was from MTX–LPD, similar to the lesions in the sinuses, anterior mediastinum, and subcutaneous tissue, which showed polymorphic LPD on biopsy. MTX was discontinued, and methylprednisolone was administered to improve the neurologic symptoms. After several weeks, there was marked improvement of all lesions, including the pituitary lesion, but the pituitary function did not improve. When pituitary lesions are caused by MTX–LPD, the possibility of anterior hypopituitarism and central diabetes insipidus needs to be considered. Further studies are needed to investigate the effectiveness of early diagnosis and treatment of MTX–LPD in restoring pituitary dysfunction.

Learning points

  • Pituitary lesions from MTX–LPD may cause hypopituitarism and central diabetes insipidus.

  • Pituitary metastasis of malignant lymphoma and primary pituitary lymphoma, which have the same tissue types with MTX–LPD, have poor prognosis, but the lesions of MTX–LPD can regress only after MTX discontinuation.

  • In cases of pituitary lesions alone, a diagnosis of MTX–LPD may be difficult, unless pituitary biopsy is performed. This possibility should be considered in patients treated with immunosuppressive drugs.

  • Pituitary hypofunction and diabetes insipidus may persist, even after regression of the lesions on imaging due to MTX discontinuation.

Open access
Xin Chen Division of Internal Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

Search for other papers by Xin Chen in
Google Scholar
PubMed
Close
,
Dina Kamel Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

Search for other papers by Dina Kamel in
Google Scholar
PubMed
Close
,
Braden Barnett Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

Search for other papers by Braden Barnett in
Google Scholar
PubMed
Close
,
Evan Yung Division of Pathology, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

Search for other papers by Evan Yung in
Google Scholar
PubMed
Close
,
Adrienne Quinn Keck School of Medicine, University of Southern California, Los Angeles, California, USA

Search for other papers by Adrienne Quinn in
Google Scholar
PubMed
Close
, and
Caroline Nguyen Division of Endocrinology, Diabetes, and Metabolism, Keck School of Medicine, LAC+USC Medical Center, University of Southern California, Los Angeles, California, USA

Search for other papers by Caroline Nguyen in
Google Scholar
PubMed
Close

Summary

There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH). Histopathologic findings from such patients who underwent partial/total pancreatomy, however, can vary widely from minimal changes to classic nesidioblastosis, making the pathologic diagnosis challenging. PGBH typically presents as postprandial hypoglycemia, as opposed to insulinoma, which presents as fasting hypoglycemia. Herein, we describe an unusual case of a patient with PGBH who initially presented with postprandial hypoglycemia three years after surgery, but later developed fasting hyperinsulinemic hypoglycemia as the disease progressed. Our hypothesis for this phenomenon is that this disease is progressive, and later in its course, the insulin release becomes dissociated from food stimulation and is increased at baseline. Future studies are needed to investigate the prevalence as well as etiology of this progression from postprandial to fasting hypoglycemia.

Learning points:

  • There has been an increasing awareness of post gastric bypass hypoglycemia (PGBH).

  • Histopathologically, PGBH can vary from minimal changes to nesidioblastosis.

  • Although uncommon, patients with PGBH after Roux-en-Y gastric bypass may present with both postprandial and fasting hyperinsulinemic hypoglycemia as disease progresses.

  • Our hypothesis for this phenomenon is that the insulin release becomes dissociated from food stimulation and is increased at baseline with disease progression.

Open access
Benedetta Zampetti Endocrinology Niguarda Hospital, Galeazzi Institute IRCCS, Milan, Italy

Search for other papers by Benedetta Zampetti in
Google Scholar
PubMed
Close
,
Roberto Attanasio Endocrinology, Galeazzi Institute IRCCS, Milan, Italy

Search for other papers by Roberto Attanasio in
Google Scholar
PubMed
Close
, and
Renato Cozzi Endocrinology Niguarda Hospital, Galeazzi Institute IRCCS, Milan, Italy

Search for other papers by Renato Cozzi in
Google Scholar
PubMed
Close

Summary

A 69-year-old male was admitted for severe hyponatremia disclosed after an accidental fall. He was anticoagulated from 2 months after the implantation of a biologic aortic valve prosthesis. The work-up disclosed adrenal failure and MRI showed bilateral adrenal hemorrhage. Clinical picture and lab parameters normalized quickly after the appropriate replacement treatment. Anticoagulation excess should be added to the list of drugs potentially causing hyponatremia.

Learning points:

  • Hyponatremia requires a complete and timely workup in order to start an appropriate treatment for the improvement of clinical conditions.

  • History is crucial: a detailed list of drugs potentially causing hyponatremia should be collected. Anticoagulants should be added to the list, mostly in the event of excessive anticoagulation.

  • Intra-adrenal hemorrhage is a rare cause of hyponatremia and adrenal failure.

  • The ACTH test is still the gold standard for the diagnosis of hypoadrenalism.

Open access
Gordon Sloan Diabetes and Endocrinology Department, Barnsley District General Hospital, Barnsley, UK

Search for other papers by Gordon Sloan in
Google Scholar
PubMed
Close
,
Tania Kakoudaki Diabetes and Endocrinology Department, Barnsley District General Hospital, Barnsley, UK

Search for other papers by Tania Kakoudaki in
Google Scholar
PubMed
Close
, and
Nishant Ranjan Diabetes and Endocrinology Department, Barnsley District General Hospital, Barnsley, UK

Search for other papers by Nishant Ranjan in
Google Scholar
PubMed
Close

Summary

We report a case of a 63-year-old man who developed diabetic ketoacidosis (DKA) associated with canagliflozin, a sodium glucose co-transporter 2 (SGLT-2) inhibitor. He presented acutely unwell with a silent myocardial infarction, diverticulitis and DKA with a minimally raised blood glucose level. Standard therapy for DKA was initiated. Despite this, ketonaemia persisted for a total of 12 days after discontinuation of canagliflozin. Glucosuria lasting for several days despite discontinuation of the medications is a recognised phenomenon. However, this is the longest duration of ketonaemia to be reported. The cause of prolonged SGLT-2 inhibition remains uncertain. Deviation from the normal DKA treatment protocol and use of personalised regimens may be required in order to prevent relapse into ketoacidosis while avoiding hypoglycaemia in those that develop this condition.

Learning points:

  • Diabetic ketoacidosis (DKA) may develop in the presence of lower-than-expected blood glucose levels in patients treated with a sodium glucose co-transporter 2 (SGLT-2) inhibitor.

  • Certain individuals prescribed with SGLT-2 inhibitors may be more at risk of DKA, for example, those with a low beta cell function reserve, excessive alcohol consumption and a low carbohydrate diet.

  • In order to reduce the risk of SGLT-2 inhibitor-associated DKA, all patients must be carefully selected before prescription of the medication and appropriately educated.

  • Increased serum ketone levels and glucosuria have been reported to persist for several days despite discontinuation of their SGLT-2 inhibitor.

  • Physicians should consider individualised treatment regimens for subjects with prolonged DKA in the presence of SGLT-2 inhibition.

Open access
Senhong Lee of Endocrinology, Monash Health, Clayton, Victoria, Australia

Search for other papers by Senhong Lee in
Google Scholar
PubMed
Close
,
Aparna Morgan of Endocrinology, Monash Health, Clayton, Victoria, Australia

Search for other papers by Aparna Morgan in
Google Scholar
PubMed
Close
,
Sonali Shah of Endocrinology, Monash Health, Clayton, Victoria, Australia

Search for other papers by Sonali Shah in
Google Scholar
PubMed
Close
, and
Peter R Ebeling of Endocrinology, Monash Health, Clayton, Victoria, Australia
Department of Medicine, School of Clinical Sciences, Monash University, Clayton, Victoria, Australia

Search for other papers by Peter R Ebeling in
Google Scholar
PubMed
Close

Summary

We report a case of a 67-year-old man with type 2 diabetes presented with diabetic ketoacidosis, two weeks after his first dose of nivolumab therapy for non–small-cell lung carcinoma. He was started on empagliflozin two days prior in the setting of hyperglycaemia after the initiation of nivolumab therapy. Laboratory evaluation revealed an undetectable C-peptide and a positive anti-glutamic acid decarboxylase (GAD) antibody. He was treated with intravenous fluids and insulin infusion and was subsequently transitioned to subcutaneous insulin and discharged home. He subsequently has developed likely autoimmune thyroiditis and autoimmune encephalitis.

Learning points:

  • Glycemic surveillance in patients receiving immune checkpoint inhibitors is recommended.

  • Early glycemic surveillance after commencement of anti-programmed cell death-1 (PD-1) inhibitors may be indicated in selected populations, including patients with underlying type 2 diabetes mellitus and positive anti-glutamic acid decarboxylase (GAD) antibody.

  • Sodium-glucose co transporter-2 (SGLT2) inhibitors should be used with caution in patients on immunotherapy.

Open access