scholarly journals SAT-689 Amantadine Induced Severe Hypoglycemia in a Patient With Type 1 Diabetes and Multiple Sclerosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Basem M Mishriky ◽  
Doyle M Cummings, PharmD ◽  
James R Powell

Abstract Introduction: Amantadine is one of the few options commonly used to treat fatigue associated with multiple sclerosis. However, in a previous trial investigating the effect of amantadine on oral glucose tolerance test results, amantadine caused a reduction in plasma glucose and glucagon levels while increasing insulin levels in healthy volunteers [1]. If amantadine can reduce glucagon levels, we hypothesized that it might also cause hypoglycemia in patients with type 1 diabetes. Case presentation: The patient is a 34-year-old African American male who has a past medical history of type 1 diabetes and multiple sclerosis. His baseline hemoglobin A1c values ranged from 6.9% to 7.6% and his weight was 88 Kg. His insulin glargine dose was 28 units daily while his insulin lispro was 10 units before meals. For almost one year he was followed in clinic and had no episodes of severe hypoglycemia (defined as hypoglycemia requiring assistance from another person). The patient complained about gait imbalance and fatigue from multiple sclerosis for which he was followed by a neurologist. To treat these symptoms, he was prescribed amantadine 100 mg twice daily. A couple of hours following his first dose of amantadine after eating his usual breakfast (with his sister), the patient was found unconscious by his sister. Emergency Medical Services (EMS) was called and he was found to have a blood glucose of 22 mg/dL. He was admitted to the hospital. During that admission, amantadine was discontinued, and he was discharged on insulin glargine 24 units daily and insulin lispro 10 units with meals. Discussion: We present a case of suspected amantadine induced severe hypoglycemia. In patients with type 1 diabetes, there is a loss of the pancreatic β-cells while the α-cells are preserved [2, 3]. We hypothesize that if amantadine reduces glucagon production from the α-cells, patients would be prone to severe hypoglycemia, presumably because of the unopposed insulin action. Although it is unlikely that the severe hypoglycemia was secondary to insulin since the patient was on stable doses, it cannot be completely excluded. We recommend caution when prescribing amantadine to patients on insulin therapy particularly within the first two hours after rapid acting insulin administration. More research is needed to explore this possibility. References: [1] Diabetes Metab Syndr Obes 2009; 2: 203. [2] Br J Diabetes Vasc Dis 2014; 14: 45. [3] Peptides 2018; 10: 54.

2020 ◽  
Vol 3 (1) ◽  
pp. 1-5
Author(s):  
Fövényi J ◽  
Pánczél P ◽  
Thaisz E

The 26-year-old woman was diagnosed with type 1 diabetes in 2014. The diagnosis was confirmed while there was a slight increase in blood glucose and HbA1c levels using oral glucose tolerance test, determination of insulin levels and GADA testing. This was followed by a 2-year period with complete remissions and partial remissions of 2-8 U daily basal insulin glargine. Thereafter, the patient became pregnant. The minimal basal insulin used to date has been switched to human rapid-acting and NPH insulins five times daily, which had to be increased to 11 times the initial dose in the third trimester of pregnancy. After a successful spontaneous birth of a healthy baby girl, our patient wished to return to one-tenth of the maximum insulin dose that was used during pregnancy, to once daily insulin glargine. After three months, her blood glucose levels began to rise, with oral glucose challenge test showing a marked increase in blood glucose and a drastic reduction in C-peptide levels. This was when we switched to multiple daily insulin administration using glargine basal- and glulisine analogue insulins. Later, glargine was switched to insulin degludec, and with a 30-33 U total daily insulin dose and CGM for the past two years, the patient was in a satisfactory metabolic state.


2021 ◽  
Vol 9 (1) ◽  
pp. e002099
Author(s):  
Yuji Komorita ◽  
Masae Minami ◽  
Yasutaka Maeda ◽  
Rie Yoshioka ◽  
Toshiaki Ohkuma ◽  
...  

IntroductionType 1 diabetes (T1D) is associated with higher fracture risk. However, few studies have investigated the relationship between severe hypoglycemia and fracture risk in patients with T1D, and the results are controversial. Besides, none has investigated the risk factors for fracture in Asian patients with T1D. The aim of the present study was to investigate the prevalence of bone fracture and its relationship between severe hypoglycemia and other risk factors in Japanese patients with T1D.Research design and methodsThe single-center cross-sectional study enrolled 388 Japanese patients with T1D (mean age, 45.2 years; women, 60.4%; mean duration of diabetes, 16.6 years) between October 2019 and April 2020. The occurrence and circumstances of any fracture after the diagnosis of T1D were identified using a self-administered questionnaire. The main outcomes were any anatomic site of fracture and fall-related fracture. Severe hypoglycemia was defined as an episode of hypoglycemia that required the assistance of others to achieve recovery.ResultsA total of 92 fractures occurred in 64 patients, and 59 fractures (64%) were fall-related. Only one participant experienced fracture within the 10 years following their diagnosis of diabetes. In logistic regression analysis, the multivariate-adjusted ORs (95% CIs) of a history of severe hypoglycemia were 2.11 (1.11 to 4.09) for any fracture and 1.91 (0.93 to 4.02) for fall-related fracture. Fourteen of 18 participants with multiple episodes of any type of fracture had a history of severe hypoglycemia (p<0.001 vs no fracture).ConclusionsWe have shown that a history of severe hypoglycemia is significantly associated with a higher risk of bone fracture in Japanese patients with T1D.


2019 ◽  
Vol 20 (4) ◽  
pp. 408-413
Author(s):  
Heba M. Ismail ◽  
Carmella Evans‐Molina ◽  
Linda A. DiMeglio ◽  
Dorothy J. Becker ◽  
Ingrid Libman ◽  
...  

2019 ◽  
Vol 4 (2) ◽  
pp. 56-60
Author(s):  
Malihe Mohammadi ◽  
Seyedeh Solmaz Moosavi

Introduction: The association between the incidence of glutamic acid decarboxylase antibodies(GADAs) and risk of diabetes in pregnant women is controversial. Here, our aim was to investigate the incidence and clinical relevance of GADA and its association with development of post-delivery diabetes in women with gestational diabetes mellitus (GDM).Methods: This cohort study was conducted in Torbat–e Heydarieh (Khorasan Razavi, Iran) from October 2015 to March 2017. A total of 147 pregnant women with GDM were included in case group. The control group consisted of 147 healthy controls. A GAD diagnostic kit (Diametra Co.,Italy) was used for diagnosis of GADA. The history of insulin therapy and the development of diabetes one year after delivery were investigated.Results: Of 147 pregnant women with GDM, 9 (6.1%) had GADA in their sera. 14.3% (21 out of 147) of women with GDM had history of insulin therapy. 33.3% (7 of 21) of women who had received insulin developed diabetes one year after delivery. Type 1 and type 2 diabetes were observed in, respectively, 1 (0.7%) and 7 (4.8%) of women with GDM at one year after delivery.At one year after delivery, no women in GADA negative women was diagnosed with type 1 diabetes. However, type 2 diabetes was observed in 2.9% of GADA negative pregnant women.Type 1 and type 2 diabetes were also noticed in, respectively, 11.1% and 33.3% of GADA positive mothers at one year after delivery.Conclusion: The prevalence of GADA was 6.1% in diabetic pregnant women. The GADA positivity and history of insulin therapy during pregnancy were significant risk factors for diabetes at one year after delivery. In addition, development of type 1 diabetes was higher in GADA positive pregnant women with GDM than GADA negative women.


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