A case of newly diagnosed autoimmune diabetes in pregnancy presenting after acute onset of diabetic ketoacidosis

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Charissa DiNobile ◽  
Anna Fuchs ◽  
Kimberly Herrera

Abstract Objectives We present a case of immune-mediated diabetes mellitus, diagnosed in pregnancy upon presentation with diabetic ketoacidosis, found to have normal glucose control postpartum. Case presentation A 28-year-old medically uncomplicated G1P0 presented in diabetic ketoacidosis at 28.2 weeks gestation. Workup for pancreatic autoantibodies revealed indeterminate anti-islet cell antibodies and positive anti-glutamic acid antibodies. She was stabilized with intravenous fluids and insulin, and transitioned to long and short acting subcutaneous insulin. Her insulin requirements decreased over the course of her pregnancy. Spontaneous vaginal delivery occurred at 37 weeks. Her postpartum glucose control was normal without re-initiation of insulin. Conclusions The diagnosis of diabetic ketoacidosis during pregnancy should prompt further investigation into an underlying diagnosis of immune mediated diabetes. These patients should be followed closely in the postpartum period.

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Nabila Chekhlabi ◽  
Amal Haoudar ◽  
Nadia Echcharii ◽  
Said Ettair ◽  
Nezha Dini

Background and Aims. There is growing evidence that the 2019 coronavirus disease (COVID-19) is emerging as a potential trigger virus for the development of diabetes mellitus in children. This can occur even in patients without factors predisposing to impaired glucose metabolism. Here, we report two rare cases of diabetic ketoacidosis revealing new-onset diabetes and precipitated by COVID-19. These cases are reported in view of their rarity and originality. The relationship between type 1 diabetes mellitus and COVID-19 is discussed. Results. Two children developed symptoms suggestive of diabetic ketoacidosis preceded by polyuria, polydipsia, and asbestos. There is a documented COVID-19 infection in the parents of the 2 children. An asymptomatic infection was detected in the 2 patients on the basis of a reverse transcription polymerase chain reaction (RT-PCR) test. Thoracic imaging and inflammatory workup were negative in both cases. Both patients responded well to treatment, including rehydration regimens and intravenous insulin. On the 2nd day of their hospitalization, they were transferred to several injections of subcutaneous insulin with therapeutic and nutritional education from the parents. After about 4 weeks, their insulin requirements probably decreased due to the diabetes honeymoon. Conclusion. COVID-19 can induce acute onset diabetes and diabetic ketoacidosis in children. More research data are needed to improve our knowledge of this constellation and to guide the most appropriate therapies.


2005 ◽  
Vol 35 (3) ◽  
pp. 307-311 ◽  
Author(s):  
C. R. M. Dibben ◽  
S. S. Kalavalapalli ◽  
H. E. J. Linnington ◽  
F. A. Hynes ◽  
S. F. Dinneen ◽  
...  

Objective: To draw attention to severe presentations of atypical neuroleptic related diabetes and to document that a marked degree of remission can take place after drug withdrawal. Method: We describe two patients who presented with diabetic ketoacidosis after treatment with quetiapine and risperidone, respectively. Results: Both patients were negative for islet cell antibodies. They both required treatment with insulin, one in very high dosage, but their insulin requirements fell progressively after the atypical antipsychotic was withdrawn. After several months, neither patient required antidiabetic treatment. Conclusions: Atypical antipsychotic-induced diabetes does not always take a “type 2” presentation in which weight gain and insulin resistance are implicated. Sometimes the presentation is with diabetic ketoacidosis, requiring insulin treatment, which can nevertheless be reversible.


2019 ◽  
Vol 26 (1) ◽  
Author(s):  
C. Sakaguchi ◽  
K. Ashida ◽  
S. Yano ◽  
K. Ohe ◽  
N. Wada ◽  
...  

Nivolumab, an anti–PD-1 antibody, is now considered an important therapeutic agent in several advanced malignancies. However, immune-related adverse events such as endocrinopathies have been reported with its use. Thyroid disorder and isolated adrenocorticotropic hormone deficiency have frequently been reported as nivolumab-induced immune-related adverse events. Another endocrinopathy is nivolumab-induced type 1 diabetes mellitus (t1dm), described as diabetes mellitus with rapid onset and complete insulin insufficiency, at times leading to fulminant t1dm.   We report the case of a 68-year-old woman who developed pancreatic islet–related autoantibody-negative t1dm, possibly induced by nivolumab, under continuous glucocorticoid administration. She was treated with nivolumab for advanced malignant melanoma, concomitant with 10 mg prednisolone daily for thrombophlebitis tapered to 5 mg after 13 courses of nivolumab therapy.   At approximately the 27th course of nivolumab therapy, she showed elevated plasma glucose levels despite preserved insulin secretion. A month later, she developed diabetic ketoacidosis. Her insulin secretion decreased and finally was exhausted. She was diagnosed with acute-onset rather than fulminant t1dm because of a rapidly progressive course to diabetic ketoacidosis during just more than 1 week. She is currently receiving insulin replacement. There has been no recurrence of the melanoma.   Thus, nivolumab might induce autoimmune diabetes mellitus, with patients having t1dm-sensitive human leucocyte antigen being more susceptible even when receiving glucocorticoids. Physicians should be aware that nivolumab could potentially induce t1dm as a critical immune-related adverse event..


Author(s):  
Ploutarchos Tzoulis ◽  
Richard W Corbett ◽  
Swarupini Ponnampalam ◽  
Elly Baker ◽  
Daniel Heaton ◽  
...  

Summary Five days following the 3rd cycle of nivolumab, a monoclonal antibody, which acts as immune checkpoint inhibitor against the programmed cell death protein-1, for metastatic lung adenocarcinoma, a 56-year-old woman presented at the hospital critically ill. On admission, she had severe diabetic ketoacidosis (DKA), as evidenced by venous glucose of 47 mmol/L, blood ketones of 7.5 mmol/L, pH of 6.95 and bicarbonate of 6.6 mmol/L. She has had no personal or family history of diabetes mellitus (DM), while random venous glucose, measured 1 week prior to hospitalisation, was 6.1 mmol/L. On admission, her HbA1c was 8.2% and anti-GAD antibodies were 12 kIU/L (0–5 kU/L), while islet cell antibodies and serum C-peptide were undetectable. Nivolumab was recommenced without the development of other immune-mediated phenomena until 6 months later, when she developed hypothyroidism with TSH 18 U/L and low free T4. She remains insulin dependent and has required levothyroxine replacement, while she has maintained good radiological and clinical response to immunotherapy. This case is notable for the rapidity of onset and profound nature of DKA at presentation, which occurred two months following commencement of immunotherapy. Despite the association of nivolumab with immune-mediated endocrinopathies, only a very small number of patients developing type 1 DM has been reported to date. Patients should be closely monitored for hyperglycaemia and thyroid dysfunction prior to and periodically during immunotherapy. Learning points: Nivolumab can induce fulminant type 1 diabetes, resulting in DKA. Nivolumab is frequently associated with thyroid dysfunction, mostly hypothyroidism. Nivolumab-treated patients should be monitored regularly for hyperglycaemia and thyroid dysfunction. Clinicians should be aware and warn patients of potential signs and symptoms of severe hyperglycaemia.


Author(s):  
Monica N. Naguib ◽  
Jennifer K. Raymond ◽  
Alaina P. Vidmar

AbstractIntroductionMultisystem inflammatory syndrome in children (MIS-C) is a unique clinical complication of SARS-CoV-2 infection observed in pediatric patients. COVID-19 is emerging as a potential trigger for the development of diabetes in children. Here, we report a patient presenting with MIS-C and new onset diabetes, and discuss the implication and clinical management of these concomitant conditions.Case presentationAn eight-year-old female presented with hyperglycemia, ketosis and metabolic acidosis consistent with diabetic ketoacidosis (DKA) in the setting of fever, rash, respiratory distress, hemodynamic instability, reduced systolic function with dilation of the left anterior descending artery, and positive SARS-CoV-2 antibodies suggestive of MIS-C.


2020 ◽  
Vol 7 (2) ◽  
pp. 18-25
Author(s):  
Alexandre Perez ◽  
Benjamin Lazzarotto ◽  
Jean-Pierre Carrel ◽  
Tommaso Lombardi

Background: Lichen planus is a chronic mucocutaneous inflammatory disease. Oral manifestations are common, and may remain exclusive to the oral mucosa without involvement of the skin or other mucosae. A differential diagnosis includes oral lichenoid drug reactions. Allopurinol, which is the first line hypo-uricemic treatment, is often quoted as being a possible offending drug, though oral reactions have rarely been reported. Case presentation: We describe a 59-year-old male gout patient, successfully treated with allopurinol, who developed acute onset of oral lichenoid lesions, involving bilaterally the buccal mucosa, the tongue and the labial mucosa. Histopathology was consistent with a lichen planus or a drug-induced lichenoid reaction. Improvement of the patient’s condition after withdrawal of allopurinol confirmed the lichenoid nature of the lesion. Remission was complete after a few weeks. Discussion: Although unusual, allopurinol may induce a lichenoid drug reaction. These reactions may mimic clinically and histopathologically idiopathic lichen planus. Improvement or complete regression of the lesions may be attempted to confirm the diagnosis. According to the latest WHO recommendations, these lesions have a potential for malignant transformation.


2003 ◽  
Vol 79 (934) ◽  
pp. 454-457 ◽  
Author(s):  
D Kamalakannan

2021 ◽  
Vol 15 (1) ◽  
pp. 48-51
Author(s):  
Gian Luca Vita ◽  
Carmen Terranova ◽  
Maria Sframeli ◽  
Antonio Toscano ◽  
Giuseppe Vita

Introduction: Guillain-Barré Syndrome (GBS) is an acute, immune-mediated, generalized polyradiculoneuropathy often triggered by a bacterial or viral infection, vaccination, or surgery. During the SARS-CoV-2 pandemic, some patients were reported with GBS associated COVID-19 infection. Case Presentation: We report, herein, a patient who had a recurrent GBS after forty years. Intravenous immunoglobulins (IVIg) induced improvement, but her condition worsened suddenly after twenty days, coinciding with a COVID-19 infection. A second IVIg cycle was administered, and she improved again. Conclusion: The take-home message is that in the current pandemic, any re-worsening or lack of improvement after appropriate treatment of GBS or possibly other autoimmune neurological diseases must be checked to determine if it is related to COVID-19 infection.


Author(s):  
Shivani Patel ◽  
Venessa Chin ◽  
Jerry R Greenfield

Summary Durvalumab is a programmed cell death ligand 1 inhibitor, which is now approved in Australia for use in non-small-cell lung and urothelial cancers. Autoimmune diabetes is a rare immune-related adverse effect associated with the use of immune checkpoint inhibitor therapy. It is now being increasingly described reflecting the wider use of immune checkpoint inhibitor therapy. We report the case of a 49-year-old female who presented with polyuria, polydipsia and weight loss, 3 months following the commencement of durvalumab. On admission, she was in severe diabetic ketoacidosis with venous glucose: 20.1 mmol/L, pH: 7.14, bicarbonate 11.2 mmol/L and serum beta hydroxybutyrate: >8.0 mmol/L. She had no personal or family history of diabetes or autoimmune disease. Her HbA1c was 7.8% and her glutamic acid decarboxylase (GAD) antibodies were mildly elevated at 2.2 mU/L (reference range: <2 mU/L) with negative zinc transporter 8 (ZnT8) and islet cell (ICA) antibodies. Her fasting C-peptide was low at 86 pmol/L (reference range: 200–1200) with a corresponding serum glucose of 21.9 mmol/L. She was promptly stabilised with an insulin infusion in intensive care and discharged on basal bolus insulin. Durvalumab was recommenced once her glycaemic control had stabilised. Thyroid function tests at the time of admission were within normal limits with negative thyroid autoantibodies. Four weeks post discharge, repeat thyroid function tests revealed hypothyroidism, with an elevated thyroid-stimulating hormone (TSH) at 6.39 mIU/L (reference range: 0.40–4.80) and low free T4: 5.9 pmol/L (reference range: 8.0–16.0). These findings persisted with repeat testing despite an absence of clinical symptoms. Treatment with levothyroxine was commenced after excluding adrenal insufficiency (early morning cortisol: 339 nmol/L) and hypophysitis (normal pituitary on MRI). Learning points: Durvalumab use is rarely associated with fulminant autoimmune diabetes, presenting with severe DKA. Multiple endocrinopathies can co-exist with the use of a single immune checkpoint inhibitors; thus, patients should be regularly monitored. Regular blood glucose levels should be performed on routine pathology on all patients on immune checkpoint inhibitor. Clinician awareness of immunotherapy-related diabetes needs to increase in an attempt to detect hyperglycaemia early and prevent DKA.


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