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Diabetes treatment in two pregnant women with permanent neonatal diabetes mellitus due to a KCNJ11 mutation.
Stanik, J, Barak, L, Dankovcikova, A, Valkovicova, T, Skopkova, M, Gasperikova, D
Diabetic medicine : a journal of the British Diabetic Association. 2020;(11):1956-1958
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2.
Treatment-Induced Neuropathy of Diabetes (TIND) in Pediatrics: A Case Report and Review of the Literature.
Chandler, E, Brown, M, Wintergerst, K, Doll, E
The Journal of clinical endocrinology and metabolism. 2020;(2)
Abstract
CONTEXT Treatment-induced neuropathy of diabetes (TIND) is a rarely reported but important consideration in patients presenting with an acute onset of neuropathic symptoms following rapid correction of hyperglycemia in diabetes. Although it has been reported in children, the preponderance of literature focuses on adults with TIND. CASE DESCRIPTION We report an 18-year-old male with this condition and his clinical course. We then discuss the proposed pathophysiology of TIND and review the literature. We also provide a standard workup for the diagnosis of TIND. CONCLUSION In both pediatric and adult populations, TIND should be considered in diabetic patients who develop neuropathy acutely following rapid correction of hyperglycemia. Because the pathophysiology of TIND remains poorly understood, there is insufficient information regarding how to target susceptible individuals and prevent the development of TIND.
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3.
Exogenous Insulin Injection-Induced Stiff-Person Syndrome in a Patient With Latent Autoimmune Diabetes: A Case Report and Literature Review.
Lee, YY, Lin, CW, Chen, IW
Frontiers in endocrinology. 2020;:594
Abstract
Stiff-person syndrome (SPS) is highly associated with anti-glutamic acid decarboxylase (GAD) antibody. However, GAD antibodies alone appear to be insufficient to cause SPS, and they possibly are involved in only part of its pathophysiology. It is suspected that the symptoms of SPS get precipitated by external stimuli. Here, we briefly introduce the case of a patient with latent autoimmune diabetes who developed SPS through the action of subcutaneously injected insulin. A 43-year-old man was diagnosed with diabetes and initially well-controlled with oral hypoglycemic agents but progressed to requiring insulin within 1 year of diagnosis. Two months after the initiation of basal insulin therapy, he presented with abdominal stiffness and painful muscle spasms, involving the lower limbs, which resulted in walking difficulty, and thus, he refused insulin injections thereafter. He had been treated with oral anti-diabetic agents instead of insulin for 10 years until premixed insulin twice daily was started again due to poor diabetes control. Immediately after insulin injection, abdominal muscle rigidity and spasms were noted. When insulin was not administered, frequent episodes of diabetic ketoacidosis occurred. Serum GAD antibody test was positive and there was no positivity for islet antigen-2 antibody. A glucagon stimulation test demonstrated relative insulin deficiency, indicative of latent autoimmune diabetes in adults (LADA). Tolerable muscle rigidity was achieved when the dosage of basal insulin was split into two separate daily injections with lower amounts of units per injection. This case highlights a different form of autoimmune diabetes in SPS. To our knowledge, this is the first report of SPS described shortly after the initiation of insulin therapy that required basal insulin to achieve tolerable muscle symptoms and better glucose control, without the development of diabetic ketoacidosis.
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4.
[Severe sensory-motor axonal neuropathy following diabetic ketoacidosis].
Hamada, Y, Takahashi, K, Hokkoku, K, Kanbayashi, T, Hatanaka, Y, Kobayashi, S, Sonoo, M
Rinsho shinkeigaku = Clinical neurology. 2020;(9):614-619
Abstract
We report a case of severe sensory-motor axonal neuropathy on the lower extremities associated with diabetic ketoacidosis (DKA). A sixteen-year-old boy developed coma and admitted to our hospital. We diagnosed him with DKA based on remarkable hyperglycemia, severe acidosis with hyperketonemia. Intensive glycemic control with insulin was immediately started. He had complications of heart failure, rhabdomyolysis, and renal failure, which required intensive care including mechanical ventilation and hemodialysis. When recovered from the critical condition, he noticed severe weakness, numbness, and pain on the lower limbs, and urinary retention. On nerve conduction studies, both motor and sensory action potentials were absent. Serum anti-ganglioside antibodies were negative. Albuminocytologic dissociation was evident in the cerebrospinal fluid. MRI study revealed marked gadolinium enhancement of the cauda equina. After high-dose intravenous immunoglobulin treatment, he was relieved from leg pain, but the leg weakness and bladder bowel dysfunction did not show immediate improvement. It took approximately six months until he became able to stand and walk using ankle orthosis. Acute neuropathy is a rare complication of diabetes mellitus. Painful neuropathy is known to emerge in association with diabetic treatment, but it seldom causes severe motor disturbance. On the other hand, motor-dominant polyneuropathy has been reported to occur acutely along the treatment of DKA and hyperosmolar hyperglycemia syndrome (HHS). Present case and previous cases with DKA and HHS suggest that rapid correction of glucose level is one of the underlying factors of acute neuropathy related with diabetic treatment.
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5.
Osmolar-gap in the setting of metformin-associated lactic acidosis: Case report and a literature review highlighting an apparently unusual association.
Elshafei, MN, Alamin, M, Mohamed, MFH
Medicine. 2020;(41):e22492
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Abstract
RATIONALE Metformin-associated lactic acidosis (MALA) is a rare adverse effect that has significant morbidity and mortality. MALA is a high anion gap (AG), nonosmolar acidosis. Associated osmolar-gap (OG) is rarely reported, so finding an OG may make the diagnosis of MALA challenging. PATIENT CONCERNS Forty-five years' old type II diabetic patient on metformin presented to emergency with a two-day history of vomiting, watery diarrhea, and mild abdominal discomfort. On examinations, he looked dehydrated. Investigation revealed acute kidney injury (AKI) with a high lactic acid (LA) level of 24 mmol/L, pH of 6.8, AG of 40, and an OG of 20 mOsm/kg DIAGNOSES The presence of an OG made the diagnosis challenging; the history was negative for alcohol, osmolar substance, or illicit drug ingestion or use. The toxicology screen was negative. After ruling out plausible causes of AG and OG, MALA was deemed the likely reason for his presentation likely precipitated by dehydration and AKI. INTERVENTIONS He underwent two sessions of hemodialysis, afterward managed with fluid hydration. OUTCOMES On day 3, he was in the polyuric phase suggestive of acute tubular necrosis. His serum creatinine improved afterward with improved acidosis; after 8 days, he was discharged in stable condition. LESSONS MALA is a rare side effect of metformin therapy. Acute kidney injury is a known precipitant of MALA. In our review, we highlight the association of MALA and the presence of an OG. We believe that treating physicians should be aware of this relationship to avoid delaying or overlooking such an important diagnosis.
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6.
Heterotaxy syndrome with agenesis of dorsal pancreas and diabetes mellitus: case report and review of the literature.
Riguetto, CM, Pelichek, S, Moura Neto, A
Archives of endocrinology and metabolism. 2019;(4):445-448
Abstract
Heterotaxy syndrome (HS) is a rare congenital condition with multifactorial heritance, characterized by an abnormal arrangement of thoraco-abdominal organs and vessels. Patients present with multiple cardiac, gastrointestinal, hepatosplenic, pancreatic, renal, neurological and skeletal disorders without any pathognomonic alteration. Despite the described increased risk of diabetes mellitus (DM) in patients with altered pancreatic anatomy, just one case was reported in Korea regarding the association of HS and DM in a 13-year-old girl. Our report refers to a 40-year-old female Brazilian patient with a history of DM and HS with polysplenia and agenesis of dorsal pancreas without cardiac abnormalities. She presented a worsening glycemic control associated with weight gain and signs of insulin resistance. After a proper clinical management of insulin and oral medications, our patient developed an improvement in glycemic control. Although it is a rare disease, HS with polysplenia and pancreatic disorders can be associated with an increased risk of DM. This case highlights the importance of investigating DM in patients with HS, especially those with pancreatic anatomical disorders, for proper clinical management of this rare condition.
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7.
Sodium-glucose cotransporter-2 inhibitors induced eu-glycemic diabetic ketoacidosis: The first report in a type 2 diabetic (T2D) Taiwanese and literature review of possible pathophysiology and contributing factors.
Lin, YH
Journal of the Formosan Medical Association = Taiwan yi zhi. 2018;(9):849-854
Abstract
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors are the newest class of oral antidiabetic drugs (OADs), approved to be a second-line OAD for type 2 diabetes in Taiwan since 2016. The U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) had both released statements associating the use of SGLT-2 inhibitors may increase the risk of eu-glycemic diabetic ketoacidosis (euDKA). This review reveals the possible pathophysiology with a chain of metabolic adaptions to decrease plasma glucose and increase plasma ketone bodies through pancreas, kidney, liver and adipose tissue. Moreover, euDKA is a potential and rare complication of treatment with SGLT-2 inhibitors when coexisting with triggering factors. It is an emerging challenge for clinical physicians and patients treated with SGLT-2 inhibitors. Therefore, first report of SGLT-2 inhibitor induced euDKA in a T2D Taiwanese and literature review of possible pathophysiology and contributing factors are presented in order to make more attentions in public.
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8.
Sulfonylurea vs insulin therapy in individuals with sulfonylurea-sensitive permanent neonatal diabetes mellitus, attributable to a KCNJ11 mutation, and poor glycaemic control.
Stanik, J, Dankovcikova, A, Barak, L, Skopkova, M, Palko, M, Divinec, J, Klimes, I, Gasperikova, D
Diabetic medicine : a journal of the British Diabetic Association. 2018;(3):386-391
Abstract
BACKGROUND Therapy with sulfonylurea is preferable to insulin in the majority of individuals with KCNJ11 mutations, but not all of these people achieve target levels of HbA1c in long-term follow-up. We aimed to compare sulfonylurea therapy with insulin treatment in two sulfonylurea-sensitive individuals with a KCNJ11 mutation who had poorly controlled permanent neonatal diabetes mellitus. CASE REPORT We report on two individuals with a KCNJ11 mutation (p.R201H) who are currently aged 35 (SVK1) and 21 years (SVK2). These individuals were switched from insulin to sulfonylurea in 2005. Data from the first 4 (SVK2) and 8 years (SVK1) of the follow-up showed improved diabetes control and increased quality of life for both individuals. During the following years, however, both individuals failed to retain good diabetes control (HbA1c ≤ 53 mmol/mol; 7.0%). We therefore changed the therapy to a combination of insulin and sulfonylurea in both individuals, or to insulin monotherapy in SVK1, and compared the effects on HbA1c with those of sulfonylurea monotherapy. HbA1c levels in both individuals worsened after adding insulin to sulfonylurea [67 mmol/mol (8.3%) vs 77 mmol/mol (9.2%) in SVK1 and 106 mmol/mol (11.8%) vs 110±19 mmol/mol (12.2±1.7%) in SVK2], and after switching to only insulin therapy in SVK1 [57 mmol/mol (7.4%) vs 62 mmol/mol (7.8%)] when compared with sulfonylurea monotherapy. DISCUSSION Our data show that sulfonylurea monotherapy might be preferable to insulin in people with permanent neonatal diabetes mellitus sensitive to sulfonylurea even when HbA1c is above target.
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9.
Type 2 diabetes in a 5-year-old and single center experience of type 2 diabetes in youth under 10.
Hutchins, J, Barajas, RA, Hale, D, Escaname, E, Lynch, J
Pediatric diabetes. 2017;(7):674-677
Abstract
The worrisome rise in pediatric type 2 diabetes (T2DM) is most prevalent among minority ethnic/racial populations. Typically, T2DM occurs during puberty in high risk obese adolescents with evidence of insulin resistance. Screening for T2DM in obese youth can be a daunting task for pediatricians and differentiating between pediatric T1DM and T2DM in obese youth can be challenging for pediatric endocrinologists. There is very limited data regarding the prevalence of T2DM among youth < 10 years of age. Here we present the case of a 5-year-old Hispanic male diagnosed with T2DM after referral by his pediatrician for abnormal weight gain, acanthosis nigricans and an elevated HbgA1c. He subsequently became symptomatic for diabetes with confirmed hyperglycemia and HbgA1c of 9.7% (83 mmol/mol) at the time of formal diagnosis. Type 1 diabetes autoantibodies (GAD65, Islet, and ZincT8) and monogenic diabetes genetic tests were negative. Due to elevated liver enzymes and baseline HbgA1c, he received basal insulin as his initial therapy. In this paper, we will discuss this case and present an IRB approved retrospective review of the characteristics of the 20 T2DM patients <10 years of age identified to date in our pediatric diabetes center. This review highlights that while uncommon, the diagnosis of T2DM merits consideration even in prepubertal children. This is especially true when working with a high risk population, such as our Hispanic South Texas youth.
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10.
First case of drug eruption due to ipragliflozin: Case report and review of the literature.
Saito-Sasaki, N, Sawada, Y, Nishio, D, Nakamura, M
The Australasian journal of dermatology. 2017;(3):236-238
Abstract
Ipragliflozin is a new drug for the treatment of diabetes mellitus. Its action of sodium-glucose cotransporter 2 (SGLT2) inhibition induces glucosuria and decreases blood glucose levels. We report the first case of ipragliflozin-related eczematous drug eruption and a review of the past literature on drug eruptions caused by SGLT2 inhibitors.