Browse

You are looking at 1 - 10 of 12 items

Baris Akinci Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA
Division of Endocrinology and Metabolism, Dokuz Eylul University, Izmir, Turkey

Search for other papers by Baris Akinci in
Google Scholar
PubMed
Close
,
Rasimcan Meral Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Rasimcan Meral in
Google Scholar
PubMed
Close
,
Diana Rus Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Diana Rus in
Google Scholar
PubMed
Close
,
Rita Hench Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Rita Hench in
Google Scholar
PubMed
Close
,
Adam H Neidert Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Adam H Neidert in
Google Scholar
PubMed
Close
,
Frank DiPaola Division of Pediatric Gastroenterology, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Frank DiPaola in
Google Scholar
PubMed
Close
,
Maria Westerhoff Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Maria Westerhoff in
Google Scholar
PubMed
Close
,
Simeon I Taylor Division of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Baltimore, Maryland, USA

Search for other papers by Simeon I Taylor in
Google Scholar
PubMed
Close
, and
Elif A Oral Brehm Center for Diabetes Research and Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, Michigan, USA

Search for other papers by Elif A Oral in
Google Scholar
PubMed
Close

Summary

A patient with atypical partial lipodystrophy who had a transient initial response to metreleptin experienced acute worsening of her metabolic state when neutralizing antibodies against metreleptin appeared. Because her metabolic status continued to deteriorate, a therapeutic trial with melanocortin-4 receptor agonist setmelanotide, that is believed to function downstream from leptin receptor in the leptin signaling system, was undertaken in an effort to improve her metabolic status for the first time in a patient with lipodystrophy. To achieve this, a compassionate use (investigational new drug application; IND) was initiated (NCT03262610). Glucose control, body fat by dual-energy X-ray absorptiometry and MRI, and liver fat by proton density fat fraction were monitored. Daily hunger scores were assessed by patient filled questionnaires. Although there was a slight decrease in hunger scales and visceral fat, stimulating melanocortin-4 receptor by setmelanotide did not result in any other metabolic benefit such as improvement of hypertriglyceridemia or diabetes control as desired. Targeting melanocortin-4 receptor to regulate energy metabolism in this setting was not sufficient to obtain a significant metabolic benefit. However, complex features of our case make it difficult to generalize these observations to all cases of lipodystrophy. It is still possible that melanocortin-4 receptor agonistic action may offer some therapeutic benefits in leptin-deficient patients.

Learning points:

  • A patient with atypical lipodystrophy with an initial benefit with metreleptin therapy developed neutralizing antibodies to metreleptin (Nab-leptin), which led to substantial worsening in metabolic control. The neutralizing activity in her serum persisted for longer than 3 years.

  • Whether the worsening in her metabolic state was truly caused by the development of Nab-leptin cannot be fully ascertained, but there was a temporal relationship. The experience noted in our patient at least raises the possibility for concern for substantial metabolic worsening upon emergence and persistence of Nab-leptin. Further studies of cases where Nab-leptin is detected and better assay systems to detect and characterize Nab-leptin are needed.

  • The use of setmelanotide, a selective MC4R agonist targeting specific neurons downstream from the leptin receptor activation, was not effective in restoring metabolic control in this complex patient with presumed diminished leptin action due to Nab-leptin.

  • Although stimulating the MC4R pathway was not sufficient to obtain a significant metabolic benefit in lowering triglycerides and helping with her insulin resistance as was noted with metreleptin earlier, there was a mild reduction in reported food intake and appetite.

  • Complex features of our case make it difficult to generalize our observation to all leptin-deficient patients. It is possible that some leptin-deficient patients (especially those who need primarily control of food intake) may still theoretically benefit from MC4R agonistic action, and further studies in carefully selected patients may help to tease out the differential pathways of metabolic regulation by the complex network of leptin signaling system.

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
Jose León Mengíbar Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Jose León Mengíbar in
Google Scholar
PubMed
Close
,
Ismael Capel Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Ismael Capel in
Google Scholar
PubMed
Close
,
Teresa Bonfill Medical Oncology Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Teresa Bonfill in
Google Scholar
PubMed
Close
,
Isabel Mazarico Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Isabel Mazarico in
Google Scholar
PubMed
Close
,
Laia Casamitjana Espuña Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Laia Casamitjana Espuña in
Google Scholar
PubMed
Close
,
Assumpta Caixàs Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Assumpta Caixàs in
Google Scholar
PubMed
Close
, and
Mercedes Rigla Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

Search for other papers by Mercedes Rigla in
Google Scholar
PubMed
Close

Summary

Durvalumab, a human immunoglobulin G1 kappa monoclonal antibody that blocks the interaction of programmed cell death ligand 1 (PD-L1) with the PD-1 and CD80 (B7.1) molecules, is increasingly used in advanced neoplasias. Durvalumab use is associated with increased immune-related adverse events. We report a case of a 55-year-old man who presented to our emergency room with hyperglycaemia after receiving durvalumab for urothelial high-grade non-muscle-invasive bladder cancer. On presentation, he had polyuria, polyphagia, nausea and vomiting, and laboratory test revealed diabetic ketoacidosis (DKA). Other than durvalumab, no precipitating factors were identified. Pre-durvalumab blood glucose was normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. Simultaneously, he presented a thyroid hormone pattern that evolved in 10 weeks from subclinical hyperthyroidism (initially attributed to iodinated contrast used in a previous computerised tomography) to overt hyperthyroidism and then to severe primary hypothyroidism (TSH: 34.40 µU/mL, free thyroxine (FT4): <0.23 ng/dL and free tri-iodothyronine (FT3): 0.57 pg/mL). Replacement therapy with levothyroxine was initiated. Finally, he was tested positive for anti-glutamic acid decarboxylase (GAD65), anti-thyroglobulin (Tg) and antithyroid peroxidase (TPO) antibodies (Abs) and diagnosed with type 1 diabetes mellitus (DM) and silent thyroiditis caused by durvalumab. When durvalumab was stopped, he maintained the treatment of multiple daily insulin doses and levothyroxine. Clinicians need to be alerted about the development of endocrinopathies, such as DM, DKA and primary hypothyroidism in the patients receiving durvalumab.

Learning points:

  • Patients treated with anti-PD-L1 should be screened for the most common immune-related adverse events (irAEs).

  • Glucose levels and thyroid function should be monitored before and during the treatment.

  • Durvalumab is mainly associated with thyroid and endocrine pancreas dysfunction.

  • In the patients with significant autoimmune background, risk–benefit balance of antineoplastic immunotherapy should be accurately assessed.

Open access
Miriam Hinaa Ahmad
Search for other papers by Miriam Hinaa Ahmad in
Google Scholar
PubMed
Close
and
Ismat Shafiq Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Rochester, Rochester, New York, USA

Search for other papers by Ismat Shafiq in
Google Scholar
PubMed
Close

Summary

We report a case of a 21-year-old African American female with history of pre-diabetes, and a diagnosis of a rare leukemia, blastic-plasmacytoid dendritic neoplasm (BPDCN), who developed diabetic ketoacidosis (DKA) after the third dose of PEG-asparaginase infusion. She was successfully treated with insulin. Asparaginase is a vital part of treatment protocols for acute lymphoblastic leukemia (ALL) in combination with other chemotherapeutic drugs. Asparaginase therapy has been reported to cause hyperglycemia especially when used in conjunction with glucocorticoids for the treatment of ALL in the pediatric population. Multiple mechanisms for hyperglycemia have been hypothesized which include decreased insulin secretion, impaired insulin receptor function and excess glucagon formation. Hyperglycemia is usually self-limiting but can deteriorate to diabetic ketoacidosis. DKA is a rare adverse effect with asparaginase therapy with an incidence rate of about 0.8%.

Learning points:

  • DKA is a rare finding following asparaginase therapy.

  • Hyperglycemia is most commonly seen with asparaginase treatment when used along with glucocorticoid.

  • Frequent blood glucose monitoring and prompt initiation of insulin treatment with hyperglycemia can prevent severe complications.

  • Patients and physician education on this complication can reduce morbidity due to DKA.

Open access
Sebastian Hörber Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany

Search for other papers by Sebastian Hörber in
Google Scholar
PubMed
Close
,
Sarah Hudak Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany

Search for other papers by Sarah Hudak in
Google Scholar
PubMed
Close
,
Martin Kächele Department of Internal Medicine, Medical Intensive Care Unit, University of Tübingen, Tübingen, Germany

Search for other papers by Martin Kächele in
Google Scholar
PubMed
Close
,
Dietrich Overkamp Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany

Search for other papers by Dietrich Overkamp in
Google Scholar
PubMed
Close
,
Andreas Fritsche Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany

Search for other papers by Andreas Fritsche in
Google Scholar
PubMed
Close
,
Hans-Ulrich Häring Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany

Search for other papers by Hans-Ulrich Häring in
Google Scholar
PubMed
Close
,
Andreas Peter Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany

Search for other papers by Andreas Peter in
Google Scholar
PubMed
Close
, and
Martin Heni Division of Endocrinology, Diabetology, Vascular Medicine, Nephrology and Clinical Chemistry, Department of Internal Medicine, University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany

Search for other papers by Martin Heni in
Google Scholar
PubMed
Close

Summary

Diabetic ketoacidosis is a life-threatening complication of diabetes mellitus. It usually occurs in patients with type 1 diabetes where it is typically associated with only moderately increased blood glucose. Here, we report the case of a 52-year-old female patient who was admitted to the emergency unit with severely altered mental status but stable vital signs. Laboratory results on admission revealed very high blood glucose (1687 mg/dL/93.6 mmol/L) and severe acidosis (pH <7) with proof of ketone bodies in serum and urine. Past history revealed a paranoid schizophrenia diagnosed 10 years ago and for which the patient was treated with risperidone for many years. Acute treatment with intravenous fluids, intravenous insulin infusion and sodium bicarbonate improved the symptoms. Further laboratory investigations confirmed diagnosis of autoimmune type 1 diabetes. After normalization of blood glucose levels, the patient could soon be discharged with a subcutaneous insulin therapy.

Learning points:

  • Diabetic ketoacidosis as first manifestation of type 1 diabetes can occur with markedly elevated blood glucose concentrations in elder patients.

  • Atypical antipsychotics are associated with hyperglycemia and an increased risk of new-onset diabetes.

  • First report of risperidone-associated diabetic ketoacidosis in new-onset type 1 diabetes.

  • Patients treated with atypical antipsychotics require special care and regular laboratory examinations to detect hyperglycemia and diabetic ketoacidosis.

  • In cases when the diagnosis is in doubt, blood gas analysis as well as determination of C-peptide and islet autoantibodies can help to establish the definite diabetes type.

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
Prashanth Rawla Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA

Search for other papers by Prashanth Rawla in
Google Scholar
PubMed
Close
,
Anantha R Vellipuram Texas Tech University Health Sciences Center, El Paso, Texas, USA

Search for other papers by Anantha R Vellipuram in
Google Scholar
PubMed
Close
,
Sathyajit S Bandaru Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA

Search for other papers by Sathyajit S Bandaru in
Google Scholar
PubMed
Close
, and
Jeffrey Pradeep Raj Department of Pharmacology, St John’s Medical College, Bangalore, India

Search for other papers by Jeffrey Pradeep Raj in
Google Scholar
PubMed
Close

Summary

Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA.

Learning points:

  • Euglycemic diabetic ketoacidosis is rare.

  • Consider ketosis in patients with DKA even if their serum glucose levels are normal.

  • High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma.

  • Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels.

Open access
Gordon Sloan Department of Diabetes and Endocrinology, Sheffield Teaching Hospital, Sheffield, UK

Search for other papers by Gordon Sloan in
Google Scholar
PubMed
Close
,
Amjad Ali Department of Diabetes and Endocrinology, Sheffield Teaching Hospital, Sheffield, UK

Search for other papers by Amjad Ali in
Google Scholar
PubMed
Close
, and
Jonathan Webster Department of Diabetes and Endocrinology, Sheffield Teaching Hospital, Sheffield, UK

Search for other papers by Jonathan Webster in
Google Scholar
PubMed
Close

Summary

Ketoacidosis occurring during lactation has been described infrequently. The condition is incompletely understood, but it appears to be associated with a combination of increased metabolic demands during lactation, reduction in carbohydrate intake and acute illness. We present a case of a 27-year-old woman, 8 weeks post-partum, who was exclusively breastfeeding her child whilst following a low carbohydrate diet. She developed gastroenteritis and was unable to tolerate an oral diet for several days. She presented with severe metabolic acidosis on admission with a blood 3-hydroxybutyrate of 5.4 mmol/L. She was treated with intravenous dextrose and intravenous sodium bicarbonate, and given dietary advice to increase her carbohydrate intake. She made a rapid and full recovery. We provide a summary of the common causes of ketoacidosis and compare our case with other presentations of lactation ketoacidosis.

Learning points:

  • Ketoacidosis in the lactating woman is a rare cause of raised anion gap metabolic acidosis.

  • Low carbohydrate intake, starvation, intercurrent illness or a combination of these factors could put breastfeeding women at risk of ketoacidosis.

  • Ketoacidosis in the lactating woman has been shown to resolve rapidly with sufficient carbohydrate intake and intravenous dextrose.

  • Early diagnosis and prompt treatment are essential because the condition is reported to be reversible with a low chance of recurrence with appropriate dietary advice.

Open access
Anil Piya Laboratory of Biochemistry, Mercer University School of Medicine, Savannah, Georgia, USA
Division of Pediatric Endocrinology, Memorial University Medical Center, Savannah, Georgia, USA

Search for other papers by Anil Piya in
Google Scholar
PubMed
Close
,
Jasmeet Kaur Laboratory of Biochemistry, Mercer University School of Medicine, Savannah, Georgia, USA
Anderson Cancer Institute, Memorial University Medical Center, Savannah, Georgia, USA

Search for other papers by Jasmeet Kaur in
Google Scholar
PubMed
Close
,
Alan M Rice Division of Pediatric Endocrinology, Memorial University Medical Center, Savannah, Georgia, USA
Augusta University School of Medicine, Augusta, Georgia, USA

Search for other papers by Alan M Rice in
Google Scholar
PubMed
Close
, and
Himangshu S Bose Laboratory of Biochemistry, Mercer University School of Medicine, Savannah, Georgia, USA
Anderson Cancer Institute, Memorial University Medical Center, Savannah, Georgia, USA

Search for other papers by Himangshu S Bose in
Google Scholar
PubMed
Close

Summary

Cholesterol transport into the mitochondria is required for synthesis of the first steroid, pregnenolone. Cholesterol is transported by the steroidogenic acute regulatory protein (STAR), which acts at the outer mitochondrial membrane prior to its import. Mutations in the STAR protein result in lipoid congenital adrenal hyperplasia (CAH). Although the STAR protein consists of seven exons, biochemical analysis in nonsteroidogenic COS-1 cells showed that the first two were not essential for pregnenolone synthesis. Here, we present a patient with ambiguous genitalia, salt-lossing crisis within two weeks after birth and low cortisol levels. Sequence analysis of the STAR, including the exon–intron boundaries, showed the complete deletion of exon 1 as well as more than 50 nucleotides upstream of STAR promoter. Mitochondrial protein import with the translated protein through synthesis cassette of the mutant STAR lacking exon 1 showed protein translation, but it is less likely to have synthesized without a promoter in our patient. Thus, a full-length STAR gene is necessary for physiological mitochondrial cholesterol transport in vivo.

Learning points:

  • STAR exon 1 deletion caused lipoid CAH.

  • Exon 1 substitution does not affect biochemical activity.

  • StAR promoter is responsible for gonadal development.

Open access
Runa Acharya University of Pittsburgh Medical Center-Endocrinology, Diabetes and Metabolism Fellowship Program, Pittsburgh, Pennsylvania, USA

Search for other papers by Runa Acharya in
Google Scholar
PubMed
Close
and
Udaya M Kabadi Veteran Affairs Medical Center and Broadlawns Medical Center, Des Moines University of Osteopathic Medicine, Des Moines, Iowa, USA
University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
Medicine and Endocrinology, University of Iowa, Iowa City, Iowa, USA
Des Moines University, Des Moines, Iowa, USA

Search for other papers by Udaya M Kabadi in
Google Scholar
PubMed
Close

Summary

Diabetic ketoacidosis (DKA) is commonly encountered in clinical practice. The current case is a unique and rare presentation of DKA as the initial manifestation of Cushing’s disease secondary to ACTH-secreting pituitary adenoma. Appropriate management as elaborated in the article led to total remission of diabetes as well as the Cushing’s disease.

Learning points:

  • DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus.

  • Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness.

  • In a patient presenting with DKA, the presence of a mixed acid–base disorder warrants further evaluation for precipitants of DKA.

  • We present a rare case of DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma.

Open access