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M L Cheneler Department of Internal Medicine, Medical City Weatherford, Weatherford, Texas, USA

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K Qureshi Department of Internal Medicine, Medical City Weatherford, Weatherford, Texas, USA

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C Bahrami Department of Internal Medicine, Medical City Weatherford, Weatherford, Texas, USA

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Summary

Hemichorea–hemiballismus (HCHB) syndrome is a syndrome characterized by choreic movements which are irregular, nonrepetitive, and random movements, and ballismus which are spontaneous and violent movements. HCHB syndrome with a metabolic cause is a rare presentation that can be precipitated by uncontrolled diabetes. Presented here is a case of HCHB syndrome with right-sided neuroimaging findings and contralateral chorea due to uncontrolled type 2 diabetes mellitus. This patient was found to be obtunded with a blood glucose of greater than 500 mg/dL by EMS. After the administration of insulin, she was able to answer clarifying questions of noncompliance with her antihyperglycemic medications. She had a computed tomography without contrast of the head which showed hyperdense lesions in the right caudate nucleus and putamen consistent with HCHB syndrome. She was started on treatment for nonketotic hyperglycemia with insulin. As her mentation improved, she was able to cooperate with physical examination, which revealed irregular and violent movements in the left upper and lower extremities. Her hemichorea and hemiballismus improved with strict glycemic control, and she was able to be discharged to a skilled nursing facility for further rehabilitation. She would later have repeated hospitalizations for poor glycemic control, and repeat neuroimaging would reveal the resolution of hyperdensities after 4 months. HCHB syndrome due to uncontrolled diabetes has been termed diabetic striatopathy and is characterized by poor glycemic control, unilateral striatal hyperdensity on CT imaging, and contralateral choreic movements. Diabetic striatopathy remains a poorly understood disease, and the exact pathophysiologic mechanism has not been definitively elucidated.

Learning points

  • Diabetic striatopathy is a relatively new term for metabolic etiology of hemichorea–hemiballismus syndrome and was coined in 2009.

  • The triad for diabetic striatopathy is poor glycemic control, unilateral striatal hyperdensity on CT imaging, and contralateral choreic movements.

  • Multiple etiologies have been suggested for the cause of diabetic striatopathy including petechial hemorrhage, mineral deposition, myelin destruction, and infarction with reactive astrocytosis; however, the exact mechanism has yet to be determined.

  • Antidopaminergic medications may be used to control the choreic movements of diabetic striatopathy; however, the mainstay of treatment is glycemic control, often with insulin therapy.

Open access
Hakan Ozoran Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
Clinical Medical School, University of Oxford, Oxford, UK
Green Templeton College, University of Oxford, Oxford, UK

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Phoenix Guwa Clinical Medical School, University of Oxford, Oxford, UK
Green Templeton College, University of Oxford, Oxford, UK

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Pam Dyson Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK

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Garry D Tan Oxford Centre for Diabetes, Endocrinology and Metabolism, Oxford University Hospitals Foundation Trust, Oxford, UK
NIHR Biomedical Research Centre, Oxford University Hospitals Foundation Trust, Oxford, UK

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Fredrik Karpe Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
NIHR Biomedical Research Centre, Oxford University Hospitals Foundation Trust, Oxford, UK

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Summary

The use of a low-carbohydrate diet (LCD) reduces insulin requirements in insulinopenic states such as type 1 diabetes mellitus (T1DM). However, the use of potentially ketogenic diets in this clinical setting is contentious and the mechanisms underlying their impact on glycaemic control are poorly understood. We report a case of a patient with a late-onset classic presentation of T1DM who adopted a very low-carbohydrate diet and completely avoided insulin therapy for 18 months, followed by tight glycaemic control on minimal insulin doses. The observations suggest that adherence to an LCD in T1DM, implemented soon after diagnosis, can facilitate an improved and less variable glycaemic profile in conjunction with temporary remission in some individuals. Importantly, these changes occurred in a manner that did not lead to a significant increase in blood ketone (beta-hydroxybutyrate) concentrations. This case highlights the need for further research in the form of randomised controlled trials to assess the long-term safety and sustainability of carbohydrate-reduced diets in T1DM.

Learning points

  • This case highlights the potential of low-carbohydrate diets (LCDs) in type 1 diabetes mellitus (T1DM) to mediate improved diabetes control and possible remission soon after diagnosis.

  • Could carbohydrate-reduced diets implemented early in the course of T1DM delay the decline in endogenous insulin production?

  • Adherence to an LCD in T1DM can facilitate an improved and less variable glycaemic profile.

  • This case suggests that LCDs in T1DM may not be associated with a concerning supraphysiological ketonaemia.

Open access
Omayma Elshafie Department of Endocrinology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Anjali Jain Department of Nuclear Medicine, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Summit Bichpuria Department of Radiology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Yamina Rassou Department of Pathology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Syed Furqan Hashmi Department of Radiation Oncology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Abir Bou Khalil Department of Endocrinology, Sultan Qaboos Comprehensive Cancer Care and Research Centre, Muscat, Oman

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Summary

A 60-year-old woman presented to our clinic with an acute onset 3 months history of right ankle pain. The patient had a history of poorly differentiated thyroid cancer, which was treated with total thyroidectomy, left lateral neck dissection levels II–V and central neck dissection levels VI–VII followed by postoperative I-131 radioactive iodine (131I) ablation therapy 3.7 GBq 6 months ago. The post-131I WBS showed residual iodine-avid thyroid tissue with no other iodine-avid disease or metastasis. SPECT/CT of the neck and chest showed nonavid bilateral pulmonary nodules, discrete nodal masses in mediastinum and nonavid bone lesions. FDG-PET CT scan showed FDG-avid mediastinal lymph nodes (LN), innumerable non-FDG-avid subcentimetric pulmonary nodules and few FDG-avid lytic lesions in the skeleton. X-ray and MRI of the right ankle showed a well-marginated lytic lesion in the posterior body of calcaneus and 5 × 6 cm soft tissue mass lesion, respectively. The histopathology of the calcaneus mass confirmed a positive immunostaining for thyroid origin which includes thyroglobulin and TTF-1 with PAX-8. Endobronchial mediastinal and bronchial LN biopsy confirmed thyroid cancer metastasis. Gene mutation showed HRAS and GNA13 with a high tumor mutational burden. We describe a rare case of poorly differentiated thyroid cancer in a patient who presented with right ankle pain; we confirmed the cause to be a calcaneus metastasis from the thyroid cancer, with calcaneus being an extremely rare site for bone metastases. Gene mutations points toward treatment with immune checkpoint inhibitors.

Learning points

  • Poorly differentiated thyroid carcinoma (PDTC) usually metastasizes to lung and bone but can rarely occur in the calcaneus.

  • Patients with distant metastases have significantly worse long-term prognosis.

  • Radiotherapy is effective in reducing the metastatic pains as well as reducing the size of the metastasis.

  • PAX-8 staining can be used to differentiate thyroid carcinomas from lung adenocarcinomas.

  • The importance of searching for gene mutations to decide the treatment of PDTC.

Open access
Sandra Martens Ghent University Hospital, Ghent, Belgium

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Bruno Lapauw Ghent University Hospital, Ghent, Belgium
Ghent University, Ghent, Belgium

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Summary

Mitotane is used for treatment of advanced adrenocortical carcinoma. It is administered when the carcinoma is unresectable, metastasized, or at high-risk of recurrence after resection. In addition, mitotane is considered to have direct adrenolytic effects. Because of its narrow therapeutic–toxic range, therapeutic drug monitoring (TDM) is warranted. In 2020, a left-sided adrenal gland tumor was found (5.8 cm) in a 38-year-old man. Considering the size of this lesion and inability to exclude an adrenocortical carcinoma on imaging, a laparoscopic adrenalectomy was performed. Histopathologic examination determined presence of an adrenocortical carcinoma (pT2N0M0 ENSAT stadium II; ki67 10–15%). There was no evidence for residual or metastatic disease but given the high risk of recurrence, adjuvant therapy with mitotane was initiated. During TDM, a sudden and spuriously high level of mitotane was observed but without signs or symptoms of toxicity. After exploration, it was found that this high concentration was completely due to uncontrolled hypertriglyceridemia. After correction thereof, mitotane levels were again in the therapeutic range. This observation underscores the importance of TDM sampling in a fasting state with concurrent control of prevalent or incident dyslipidemia.

Learning points

  • TDM of mitotane is advocated to achieve therapeutic levels while avoiding toxicity. For correct TDM, sampling should be done at least 12 h after last intake of mitotane.

  • Although sampling in fasting conditions in not explicitly mentioned in the guidelines, fasting state should be considered as elevated serum triglyceride levels might cause spuriously high mitotane levels.

  • In patients undergoing treatment with mitotane and presenting with too high or unexplained fluctuating mitotane levels without signs or symptoms of toxicity, hypertriglyceridemia as a possible cause should be investigated.

  • If dyslipidemia occurs in patients under mitotane treatment, other causes than mitotane (e.g. alcohol abuse and diabetes) should be considered and appropriate treatment should be initiated.

Open access
Anne Cathrine Parelius Wammer Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway

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Ingrid Nermoen Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway
Institute of Clinical Medicine, University of Oslo, Oslo, Norway

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Per Medbøe Thorsby Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Hormone Laboratory, Department of Medical Biochemistry and Biochemical Endocrinology and Metabolism Research Group, Oslo University Hospital, Aker, Norway

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Nils Bolstad Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway

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Kari Lima Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway

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Hoa Tran Department of Haematology, Akershus University Hospital, Lørenskog, Norway

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Ivar Følling Department of Endocrinology, Akershus University Hospital, Lørenskog, Norway
Institute of Clinical Medicine, University of Oslo, Oslo, Norway

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Summary

We present a young woman with treatment resistant insulin autoimmune syndrome (IAS) with a protracted course. Her serum insulin level was 6945 pmol/l (<160), C-peptide 4042 pmol/L (<1480), anti-insulin antibodies 5305 U/mL (<0.4) were monoclonal IgG kappa. After 12 h of fasting, her blood glucose fell to 1.2 mmol/L. Post-meal blood glucose peaked at 12.2 mmol/L with reactive hypoglycaemia below 2 mmol/L. Frequent meals and continuous blood glucose monitoring were helpful, but further treatments advocated in the literature with prednisolone, rituximab, plasmapheresis, cyclophosphamide and ciclosporin were without beneficial effect.

Based on this case and a review of the literature, we propose that IAS is not one but two different diseases with different therapeutic strategies. The first disease, polyclonal IAS, predominates in Asia and is characterized by polyclonal anti-insulin antibodies, association with certain HLA genotypes and other autoimmune conditions, medications and viral infections possibly triggering the disease, a possible female predominance among young patients and a tendency towards spontaneous remission. The other disease, monoclonal IAS, predominates in Caucasians. Typical features are monoclonal anti-insulin antibodies, only weak HLA association, no drug predisposition, no sex difference, rare remission and conventional therapy often being without any clinical effect. We suggest that monoclonal IAS with IgG or IgA anti-insulin antibodies should receive therapy targeting plasma cells rather than lymphocytes.

Learning points

  • IAS may be considered as two separate diseases, polyclonal and monoclonal.

  • The presence of either polyclonal or monoclonal antibodies should determine the choice of treatment for IAS.

  • In polyclonal IAS, discontinuation of a triggering medication and treatment of triggering conditions should be the backbone of therapy.

  • Monoclonal IAS should receive treatment targeting plasma cells.

Open access
Dave Duggan Waikato Regional Diabetes Service, Te Whatu Ora Health New Zealand, Hamilton, New Zealand

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Cinthia Minatel Riguetto Waikato Regional Diabetes Service, Te Whatu Ora Health New Zealand, Hamilton, New Zealand

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Summary

There is a scarcity of literature relating to post-bariatric hypoglycaemia (PBH) in pregnancy. Recurrent hyperglycaemia and hypoglycaemia can have significant consequences for both the mother and the developing fetus. We describe a case of a young pregnant woman who was diagnosed with symptomatic PBH in the second trimester of pregnancy using continuous glucose monitoring (CGM) 3 years after Roux-en-Y gastric bypass (RYGB) surgery. Instigating a low glycaemic index and complex carbohydrate diet significantly improved the patient’s glycaemic excursions. Given that this condition is likely underdiagnosed as a complication of RYGB surgery, a greater awareness of this complication is needed. Patients should be adequately consented pre-operatively for this relatively frequent late surgical complication to enable patients to identify symptoms of this condition at an early stage and seek medical treatment.

Learning points

  • PBH is an important diagnosis in patients post-RYGB surgery, particularly in women of childbearing age when consequences of both hyperglycaemia and hypoglycaemia during pregnancy can adversely affect both mother and the fetus.

  • Adverse outcomes of recurrent hypoglycaemia to the fetus can include small for gestational age, intrauterine growth restriction and possible impairment of beta cell function.

  • Providing adequate carbohydrate intake to allow growth of the fetus during pregnancy while also attempting to resolve both hyperglycaemia and hypoglycaemia associated with PBH by reducing the intake of simple carbohydrates and high glycaemic index foods can prove challenging.

  • Patients should be adequately consented for late complications of RYGB surgery such as PBH in order to allow early recognition of symptoms and enable prompt treatment.

Open access
Ishara Ranathunga Department of Diabetes and Endocrinology, North Cumbria Integrated Care NHS Foundation Trust, Whitehaven, UK

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Chandima Idampitiya Department of Diabetes and Endocrinology, North Cumbria Integrated Care NHS Foundation Trust, Whitehaven, UK

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Summary

Type 1 diabetes mellitus (T1DM) is an autoimmune disorder caused by the destruction of the pancreatic beta cells, which produce insulin. Individuals with T1DM usually require at least 3-5 years to develop microvascular complications in comparison to people with type 2 diabetes (T2DM), who may develop complications even before the diagnosis of diabetes. We discuss a patient who presented with proliferative diabetic retinopathy subsequently diagnosed with T1DM and diabetic neuropathy following investigations. Diabetic retinopathy or other microvascular complications as the presenting feature of T1DM is rarely known or reported in the literature. A 33-year-old healthcare worker had been seen by the opticians due to 1-week history of blurred vision. The ophthalmology assessment had confirmed proliferative retinopathy in the right eye and severe non-proliferative retinopathy in the left eye with bilateral clinically significant macular oedema. His BMI was 24.9 kg/m2. The nervous system examination revealed bilateral stocking type peripheral neuropathy. The random venous glucose was 24.9 mmol/L. Plasma ketones were 0.7 mmol/L and HbA1c was 137 mmol/mol. On further evaluation, the anti-glutamic acid decarboxylase (GAD) antibody was positive, confirming the diagnosis of T1DM. He was started on aflibercept injections in both eyes, followed by panretinal photocoagulation. Subsequent nerve conduction studies confirmed the presence of symmetrical polyneuropathy. The pathogenesis of the development of microvascu