Browse

You are looking at 1 - 8 of 8 items

Diana Catarino Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitário de Coimbra EPE, Coimbra, Portugal

Search for other papers by Diana Catarino in
Google Scholar
PubMed
Close
,
Cristina Ribeiro Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitário de Coimbra EPE, Coimbra, Portugal

Search for other papers by Cristina Ribeiro in
Google Scholar
PubMed
Close
,
Leonor Gomes Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitário de Coimbra EPE, Coimbra, Portugal

Search for other papers by Leonor Gomes in
Google Scholar
PubMed
Close
, and
Isabel Paiva Endocrinology, Diabetes and Metabolism Department, Centro Hospitalar e Universitário de Coimbra EPE, Coimbra, Portugal

Search for other papers by Isabel Paiva in
Google Scholar
PubMed
Close

Summary

Pituitary infections, particularly with fungus, are rare disorders that usually occur in immunocompromised patients. Cushing’s syndrome predisposes patients to infectious diseases due to their immunosuppression status. We report the case of a 55-year-old woman, working as a poultry farmer, who developed intense headache, palpebral ptosis, anisocoria, prostration and psychomotor agitation 9 months after initial diabetes mellitus diagnosis. Cranioencephalic CT scan showed a pituitary lesion with bleeding, suggesting pituitary apoplexy. Patient underwent transsphenoidal surgery and the neuropathologic study indicated a corticotroph adenoma with apoplexy and fungal infection. Patient had no preoperative Cushing’s syndrome diagnosis. She was evaluated by a multidisciplinary team who decided not to administer anti-fungal treatment. The reported case shows a rare association between a corticotroph adenoma and a pituitary fungal infection. The possible contributing factors were hypercortisolism, uncontrolled diabetes and professional activity. Transsphenoidal surgery is advocated in these infections; however, anti-fungal therapy is still controversial.

Learning points:

  • Pituitary infections are rare disorders caused by bacterial, viral, fungal and parasitic infections.

  • Pituitary fungal infections usually occur in immunocompromised patients.

  • Cushing’s syndrome, as immunosuppression factor, predisposes patients to infectious diseases, including fungal infections.

  • Diagnosis of pituitary fungal infection is often achieved during histopathological investigation.

  • Treatment with systemic anti-fungal drugs is controversial.

  • Endocrine evaluation is recommended at the time of initial presentation of pituitary manifestations.

Open access
N Siddique Departments of Diabetes and Endocrinology, Connolly Hospital Blanchardstown, Royal College of Surgeons in Ireland, Dublin, Ireland

Search for other papers by N Siddique in
Google Scholar
PubMed
Close
,
R Durcan Departments of Diabetes and Endocrinology, Connolly Hospital Blanchardstown, Royal College of Surgeons in Ireland, Dublin, Ireland

Search for other papers by R Durcan in
Google Scholar
PubMed
Close
,
S Smyth Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland

Search for other papers by S Smyth in
Google Scholar
PubMed
Close
,
T Kyaw Tun Departments of Diabetes and Endocrinology, Connolly Hospital Blanchardstown, Royal College of Surgeons in Ireland, Dublin, Ireland

Search for other papers by T Kyaw Tun in
Google Scholar
PubMed
Close
,
S Sreenan Departments of Diabetes and Endocrinology, Connolly Hospital Blanchardstown, Royal College of Surgeons in Ireland, Dublin, Ireland

Search for other papers by S Sreenan in
Google Scholar
PubMed
Close
, and
J H McDermott Departments of Diabetes and Endocrinology, Connolly Hospital Blanchardstown, Royal College of Surgeons in Ireland, Dublin, Ireland

Search for other papers by J H McDermott in
Google Scholar
PubMed
Close

Summary

We present three cases of acute diabetic neuropathy and highlight a potentially underappreciated link between tightening of glycaemic control and acute neuropathies in patients with diabetes. Case 1: A 56-year-old male with poorly controlled type 2 diabetes (T2DM) was commenced on basal-bolus insulin. He presented 6 weeks later with a diffuse painful sensory neuropathy and postural hypotension. He was diagnosed with treatment-induced neuropathy (TIN, insulin neuritis) and obtained symptomatic relief from pregabalin. Case 2: A 67-year-old male with T2DM and chronic hyperglycaemia presented with left lower limb pain, weakness and weight loss shortly after achieving target glycaemia with oral anti-hyperglycaemics. Neurological examination and neuro-electrophysiological studies suggested diabetic lumbosacral radiculo-plexus neuropathy (DLPRN, diabetic amyotrophy). Pain and weakness resolved over time. Case 3: A 58-year-old male was admitted with blurred vision diplopia and complete ptosis of the right eye, with intact pupillary reflexes, shortly after intensification of glucose-lowering treatment with an SGLT2 inhibitor as adjunct to metformin. He was diagnosed with a pupil-sparing third nerve palsy secondary to diabetic mononeuritis which improved over time. While all three acute neuropathies have been previously well described, all are rare and require a high index of clinical suspicion as they are essentially a diagnosis of exclusion. Interestingly, all three of our cases are linked by the development of acute neuropathy following a significant improvement in glycaemic control. This phenomenon is well described in TIN, but not previously highlighted in other acute neuropathies.

Learning points:

  • A link between acute tightening of glycaemic control and acute neuropathies has not been well described in literature.

  • Clinicians caring for patients with diabetes who develop otherwise unexplained neurologic symptoms following a tightening of glycaemic control should consider the possibility of an acute diabetic neuropathy.

  • Early recognition of these neuropathies can obviate the need for detailed and expensive investigations and allow for early institution of appropriate pain-relieving medications.

Open access
Mohammed Faraz Rafey Galway University Hospitals, Galway, Ireland
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland

Search for other papers by Mohammed Faraz Rafey in
Google Scholar
PubMed
Close
,
Arslan Butt Galway University Hospitals, Galway, Ireland

Search for other papers by Arslan Butt in
Google Scholar
PubMed
Close
,
Barry Coffey Galway University Hospitals, Galway, Ireland

Search for other papers by Barry Coffey in
Google Scholar
PubMed
Close
,
Lisa Reddington Galway University Hospitals, Galway, Ireland

Search for other papers by Lisa Reddington in
Google Scholar
PubMed
Close
,
Aiden Devitt Galway University Hospitals, Galway, Ireland

Search for other papers by Aiden Devitt in
Google Scholar
PubMed
Close
,
David Lappin Galway University Hospitals, Galway, Ireland

Search for other papers by David Lappin in
Google Scholar
PubMed
Close
, and
Francis M Finucane Galway University Hospitals, Galway, Ireland
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland

Search for other papers by Francis M Finucane in
Google Scholar
PubMed
Close

Summary

We describe two cases of SGLT2i-induced euglycaemic diabetic ketoacidosis, which took longer than we anticipated to treat despite initiation of our DKA protocol. Both patients had an unequivocal diagnosis of type 2 diabetes, had poor glycaemic control with a history of metformin intolerance and presented with relatively vague symptoms post-operatively. Neither patient had stopped their SGLT2i pre-operatively, but ought to have by current treatment guidelines.

Learning points:

  • SGLT2i-induced EDKA is a more protracted and prolonged metabolic derangement and takes approximately twice as long to treat as hyperglycaemic ketoacidosis.

  • Surgical patients ought to stop SGLT2i medications routinely pre-operatively and only resume them after they have made a full recovery from the operation.

  • While the mechanistic basis for EDKA remains unclear, our observation of marked ketonuria in both patients suggests that impaired ketone excretion may not be the predominant metabolic lesion in every case.

  • Measurement of insulin, C-Peptide, blood and urine ketones as well as glucagon and renal function at the time of initial presentation with EDKA may help to establish why this problem occurs in specific patients.

Open access
Khaled Aljenaee Department of Endocrinology, St James Hospital, Dublin, Ireland

Search for other papers by Khaled Aljenaee in
Google Scholar
PubMed
Close
,
Osamah Hakami Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital Blanchardstown, Dublin, Ireland

Search for other papers by Osamah Hakami in
Google Scholar
PubMed
Close
,
Colin Davenport Department of Endocrinology, St Columcille’s Hospital, Dublin, Ireland

Search for other papers by Colin Davenport in
Google Scholar
PubMed
Close
,
Gemma Farrell Department of Clinical Biochemistry, Connolly Hospital, Blanchardstown, Dublin, Ireland

Search for other papers by Gemma Farrell in
Google Scholar
PubMed
Close
,
Tommy Kyaw Tun Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital Blanchardstown, Dublin, Ireland

Search for other papers by Tommy Kyaw Tun in
Google Scholar
PubMed
Close
,
Agnieszka Pazderska Department of Endocrinology, St James Hospital, Dublin, Ireland

Search for other papers by Agnieszka Pazderska in
Google Scholar
PubMed
Close
,
Niamh Phelan Department of Endocrinology, St James Hospital, Dublin, Ireland

Search for other papers by Niamh Phelan in
Google Scholar
PubMed
Close
,
Marie-Louise Healy Department of Endocrinology, St James Hospital, Dublin, Ireland

Search for other papers by Marie-Louise Healy in
Google Scholar
PubMed
Close
,
Seamus Sreenan Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital Blanchardstown, Dublin, Ireland

Search for other papers by Seamus Sreenan in
Google Scholar
PubMed
Close
, and
John H McDermott Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital Blanchardstown, Dublin, Ireland

Search for other papers by John H McDermott in
Google Scholar
PubMed
Close

Summary

Measurement of glycated haemoglobin (HbA1c) has been utilised in assessing long-term control of blood glucose in patients with diabetes, as well as diagnosing diabetes and identifying patients at increased risk of developing diabetes in the future. HbA1c reflects the level of blood glucose to which the erythrocyte has been exposed during its lifespan, and there are a number of clinical situations affecting the erythrocyte life span in which HbA1c values may be spuriously high or low and therefore not reflective of the true level of glucose control. In the present case series, we describe the particulars of three patients with diabetes who had spuriously low HbA1c levels as a result of dapsone usage. Furthermore, we discuss the limitations of HbA1c testing and the mechanisms by which it may be affected by dapsone in particular.

Learning points:

  • Various conditions and medications can result in falsely low HbA1c.

  • Dapsone can lead to falsely low HbA1c by inducing haemolysis and by forming methaemoglobin.

  • Capillary glucose measurement, urine glucose measurements and fructosamine levels should be used as alternatives to HbA1c for monitoring glycaemic control if it was falsely low or high.

Open access
Michal Barabas Wolfson Diabetes & Endocrine Clinic, Cambridge University Hospitals NHS Foundation Trust

Search for other papers by Michal Barabas in
Google Scholar
PubMed
Close
,
Isabel Huang-Doran Wellcome-MRC Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge, UK

Search for other papers by Isabel Huang-Doran in
Google Scholar
PubMed
Close
,
Debbie Pitfield Wolfson Diabetes & Endocrine Clinic, Cambridge University Hospitals NHS Foundation Trust

Search for other papers by Debbie Pitfield in
Google Scholar
PubMed
Close
,
Hazel Philips Department of Cardiology, Bedford Hospital NHS Trust, Bedford, UK

Search for other papers by Hazel Philips in
Google Scholar
PubMed
Close
,
Manoj Goonewardene Department of Cardiology, Bedford Hospital NHS Trust, Bedford, UK

Search for other papers by Manoj Goonewardene in
Google Scholar
PubMed
Close
,
Ruth T Casey Wolfson Diabetes & Endocrine Clinic, Cambridge University Hospitals NHS Foundation Trust

Search for other papers by Ruth T Casey in
Google Scholar
PubMed
Close
, and
Benjamin G Challis Wolfson Diabetes & Endocrine Clinic, Cambridge University Hospitals NHS Foundation Trust
IMED Biotech Unit, Clinical Discovery Unit, AstraZeneca, Cambridge, UK

Search for other papers by Benjamin G Challis in
Google Scholar
PubMed
Close

Summary

A 67-year-old woman presented with a generalised rash associated with weight loss and resting tachycardia. She had a recent diagnosis of diabetes mellitus. Biochemical evaluation revealed elevated levels of circulating glucagon and chromogranin B. Cross-sectional imaging demonstrated a pancreatic lesion and liver metastases, which were octreotide-avid. Biopsy of the liver lesion confirmed a diagnosis of well-differentiated grade 2 pancreatic neuroendocrine tumour, consistent with metastatic glucagonoma. Serial echocardiography commenced 4 years before this diagnosis demonstrated a progressive left ventricular dilatation and dysfunction in the absence of ischaemia, suggestive of glucagonoma-associated dilated cardiomyopathy. Given the severity of the cardiac impairment, surgical management was considered inappropriate and somatostatin analogue therapy was initiated, affecting clinical and biochemical improvement. Serial cross-sectional imaging demonstrated stable disease 2 years after diagnosis. Left ventricular dysfunction persisted, however, despite somatostatin analogue therapy and optimal medical management of cardiac failure. In contrast to previous reports, the case we describe demonstrates that chronic hyperglucagonaemia may lead to irreversible left ventricular compromise. Management of glucagonoma therefore requires careful and serial evaluation of cardiac status.

Learning points:

  • In rare cases, glucagonoma may present with cardiac failure as the dominant feature. Significant cardiac impairment may occur in the absence of other features of glucagonoma syndrome due to subclinical chronic hyperglucagonaemia.

  • A diagnosis of glucagonoma should be considered in patients with non-ischaemic cardiomyopathy, particularly those with other features of glucagonoma syndrome.

  • Cardiac impairment due to glucagonoma may not respond to somatostatin analogue therapy, even in the context of biochemical improvement.

  • All patients with a new diagnosis of glucagonoma should be assessed clinically for evidence of cardiac failure and, if present, a baseline transthoracic echocardiogram should be performed. In the presence of cardiac impairment these patients should be managed by an experienced cardiologist.

Open access
Aoife Garrahy Department of Diabetes and Endocrinology, Mater Misericordiae University Hospital, Dublin 7, Ireland

Search for other papers by Aoife Garrahy in
Google Scholar
PubMed
Close
,
Matilde Bettina Mijares Zamuner Department of Diabetes and Endocrinology, Mater Misericordiae University Hospital, Dublin 7, Ireland

Search for other papers by Matilde Bettina Mijares Zamuner in
Google Scholar
PubMed
Close
, and
Maria M Byrne Department of Diabetes and Endocrinology, Mater Misericordiae University Hospital, Dublin 7, Ireland

Search for other papers by Maria M Byrne in
Google Scholar
PubMed
Close

Summary

Coexistence of autoimmune diabetes and maturity-onset diabetes of the young (MODY) is rare. We report the first case of coexisting latent autoimmune diabetes of adulthood (LADA) and glucokinase (GCK) MODY. A 32-year-old woman was treated with insulin for gestational diabetes at age 32 years; post-partum, her fasting blood glucose was 6.0 mmol/L and 2-h glucose was 11.8 mmol/L following an oral glucose tolerance test, and she was maintained on diet alone. Five years later, a diagnosis of LADA was made when she presented with fasting blood glucose of 20.3 mmol/L and HbA1C 125 mmol/mol (13.6%). GCK-MODY was identified 14 years later when genetic testing was prompted by identification of a mutation in her cousin. Despite multiple daily insulin injections her glycaemic control remained above target and her clinical course has been complicated by multiple episodes of hypoglycaemia with unawareness. Although rare, coexistence of latent autoimmune diabetes of adulthood and monogenic diabetes should be considered if there is a strong clinical suspicion, for example, family history. Hypoglycaemic unawareness developed secondary to frequent episodes of hypoglycaemia using standard glycaemic targets for LADA. This case highlights the importance of setting fasting glucose targets within the expected range for GCK-MODY in subjects with coexisting LADA.

Learning points:

  • We report the first case of coexisting latent autoimmune diabetes of adulthood (LADA) and GCK-MODY.

  • It has been suggested that mutations in GCK may lead to altered counter-regulation and recognition of hypoglycaemia at higher blood glucose levels than patients without such mutation. However, in our case, hypoglycaemic unawareness developed secondary to frequent episodes of hypoglycaemia using standard glycaemic targets for LADA.

  • This case highlights the importance of setting fasting glucose targets within the expected range for GCK-MODY in subjects with coexisting LADA to avoid hypoglycaemia.

Open access
Akihiko Ando Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan

Search for other papers by Akihiko Ando in
Google Scholar
PubMed
Close
,
Shoichiro Nagasaka Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan
Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, Showa University Fujigaoka Hospital, Kanagawa Japan

Search for other papers by Shoichiro Nagasaka in
Google Scholar
PubMed
Close
, and
Shun Ishibashi Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan

Search for other papers by Shun Ishibashi in
Google Scholar
PubMed
Close

Summary

We report a case of a woman with diabetes mellitus caused by a genetic defect in ABCC8-coding sulfonylurea receptor 1 (SUR1), a subunit of the ATP-sensitive potassium (KATP) channel protein. She was diagnosed with diabetes at 7 days after birth. After intravenous insulin drip for 1 month, her hyperglycaemia remitted. At the age of 13 years, her diabetes relapsed, and after that she had been treated by intensive insulin therapy for 25 years with relatively poor glycaemic control. She was switched to oral sulfonylurea therapy and attained euglycaemia. In addition, her insulin secretory capacity was ameliorated gradually.

Learning points:

  • Genetic testing should be considered in any individuals or family with diabetes that occurred within the first year or so of life.

  • Sulfonylurea can achieve good glycaemic control in patients with KATP channel mutations by restoring endogenous insulin secretion, even if they were treated with insulin for decades.

  • Early screening and genetic testing are important to improve the prognosis of patients with neonatal diabetes mellitus arising from ABCC8 or KCNJ11 mutation.

Open access
E Rapti Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by E Rapti in
Google Scholar
PubMed
Close
,
S Karras Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by S Karras in
Google Scholar
PubMed
Close
,
M Grammatiki Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by M Grammatiki in
Google Scholar
PubMed
Close
,
A Mousiolis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by A Mousiolis in
Google Scholar
PubMed
Close
,
X Tsekmekidou Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by X Tsekmekidou in
Google Scholar
PubMed
Close
,
E Potolidis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by E Potolidis in
Google Scholar
PubMed
Close
,
P Zebekakis Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by P Zebekakis in
Google Scholar
PubMed
Close
,
M Daniilidis 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by M Daniilidis in
Google Scholar
PubMed
Close
, and
K Kotsa Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by K Kotsa in
Google Scholar
PubMed
Close

Summary

Latent autoimmune diabetes in adults (LADA) is a relatively new type of diabetes with a clinical phenotype of type 2 diabetes (T2D) and an immunological milieu characterized by high titers of islet autoantibodies, resembling the immunological profile of type 1 diabetes (T1D). Herein, we report a case of a young male, diagnosed with LADA based on both clinical presentation and positive anti-glutamic acid decarboxylase antibodies (GAD-abs), which were normalized after combined treatment with a dipeptidyl peptidase-4 inhibitor (DPP-4) (sitagliptin) and cholecalciferol.

Learning points

  • Anti-glutamic acid decarboxylase antibodies (GAD-abs) titers in young patients being previously diagnosed as type 2 diabetes (T2D) may help establish the diagnosis of latent autoimmune diabetes in adults (LADA).

  • Sitagliptin administration in patients with LADA might prolong the insulin-free period.

  • Vitamin D administration in patients with LADA might have a protective effect on the progression of the disease.

Open access