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Short-chain 3-hydroxyacylCoA dehydrogenase (SCHAD) deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Another presentation is with hyperinsulinemic hypoglycemia [11, 12]. In one Pakistani family in which parents were doubly heterozygous, hyperinsulinism required treatment with diazoxide [8]. Of four affected children, two died. One had impaired mental development and one had developed normally. An infant in another family had hyperinsulinism that was readily controlled with diazoxide and hydrochlorthiazide [11].
Surgery for Severe Obesity
Published in James M. Rippe, Lifestyle Medicine, 2019
Robert F. Kushner, Lisa A. Neff
Patients with symptoms of dumping syndrome can usually be managed by dietary modification, including avoidance of concentrated sweets and simple sugars, consumption of small frequent meals, and inclusion of protein at every meal. Patients with symptoms suggestive of postprandial hypoglycemia that are not ameliorated by dietary modification should undergo evaluation for the presence of endogenous (or “post-bypass”) hyperinsulinemic hypoglycemia.10,48 Patients with more severe neuroglycopenic symptoms (such as confusion or loss of consciousness) should also undergo evaluation for this condition, which can occur after gastric bypass. For most patients with post-bypass hypoglycemia, dietary modification, including carbohydrate restriction to less than 30 grams per meal, can significantly reduce the frequency and severity of symptoms.49 However, when symptoms persist, pharmacologic therapies, such as acarbose, diazoxide, somatostatin analogs, and calcium channel blockers, may be required.
Noninsulinoma pancreatogenous hypoglycemia syndrome and postbariatric hypoglycemia
Published in Demetrius Pertsemlidis, William B. Inabnet III, Michel Gagner, Endocrine Surgery, 2017
Spyridoula Maraka, Adrian Vella
NIPHS was first described in 1999 [13]. It is a rare syndrome characterized by endogenous hyperinsulinemic hypoglycemia in the absence of a discrete insulinoma. The predominant clinical feature of NIPHS is neuroglycopenia 2–4 hours postprandially but not in the fasting state. In contrast, most patients with insulinomas have fasting hypoglycemia [14]. Although a significant minority report postprandial symptoms, the occurrence of symptoms solely postprandially is seen in approximately 6% of patients with insulinoma [7]. During episodes of hypoglycemia, patients with NIPHS have elevated plasma insulin, C-peptide, and proinsulin levels; a low plasma β-hydroxybutyrate concentration; and a negative sulfonylurea/meglitinide screen.
A unique allosteric insulin receptor monoclonal antibody that prevents hypoglycemia in the SUR-1−/− mouse model of KATP hyperinsulinism
Published in mAbs, 2018
Puja Patel, Lawrenshey Charles, John Corbin, Ira D. Goldfine, Kirk Johnson, Paul Rubin, Diva D. De León
It has been previously shown that XMetD, a NAM of the INSR, ameliorates hypoglycemia in mice receiving exogenous insulin.7 In healthy volunteers, a single dose of XMetD resulted in a significant elevation of postprandial plasma glucose concentration and a significant attenuation of the decrease in plasma glucose induced by insulin in the setting of an insulin tolerance test.8 Our study extends these findings in a mouse model relevant to the human condition of endogenous hyperinsulinemic hypoglycemia. Although SUR-1−/− mice are relatively normoglycemic in the fed state,9,10 they develop hypoglycemia with fasting, which allowed us to test the potential for an insulin receptor allosteric inhibitor to normalize fasting plasma glucose in the absence of functional KATP channels. Our studies confirmed previous reports highlighting the phenotype of the SUR-1−/− mice.9,10 Compared to wild-type littermates, SUR-1−/− mice are more hypoglycemic when fasted and more hyperglycemic when glucose loaded, and the glucose intolerance is the result of impaired glucose-stimulated insulin secretion.
A case report of methadone-associated hypoglycemia in an 11-month-old male
Published in Clinical Toxicology, 2018
Michael S. Toce, Margaret A. Stefater, David T. Breault, Michele M. Burns
We report a case of severe hypoketotic, hyperinsulinemic hypoglycemia after methadone exposure. Alternative explanations for hypoketotic hypoglycemia, namely sulfonylurea exposure, fatty oxidation disorders, and persistent hyperinsulinism, were negative. Other causes of hypoglycemia, like starvation or sepsis, would be expected to cause a hyperketotic hypoglycemia due to increased fatty acid oxidation. Administration of epinephrine would be protective against hypoglycemia through increased gluconeogenesis, glycogenolysis, and decreased glucose utilization. It is interesting to note that upon arrival to the presenting hospital, the patient was hyperglycemic, and only became hypoglycemic 3 h later. One possible explanation for the delay in hypoglycemia is that methadone has a delayed time to peak concentration and clinical findings, like respiratory depression, can occur after peak analgesic effect [3]. It is conceivable that methadone-associated hypoglycemia is similarly delayed. With this in mind, a proposed mechanism of opioid-induced insulin secretion is suspected.
Hydroxychloroquine Sulfate Related Hypoglycemia In A Non-Diabetic COVİD-19 Patient: A Case Report and Literature Review
Published in Postgraduate Medicine, 2021
Narimana Imanova Yaghji, Elif Kilic Kan, Songul Akcan, Ramis Colak, Aysegul Atmaca
ACTH, cortisol, growth hormones, liver, and kidney functions were normal. HbA1c level was 4.7% (28 mmol/mol) (Normal Range %4,5–5,7) (Table 1). To confirm or rule out hyperinsulinemic hypoglycemia including insulinoma, 72-h fasting test was performed. He complained about headache and weakness at 72nd hours of the test. The PG level was determined as 49 mg/dl during these symptoms. Concurrent insulin and C-peptide levels were <2 mU/mL and 0.553 ng/mL, respectively. Therefore, insulinoma was excluded (Figure 1). After the exclusion of adrenocortical and pituitary insufficiency, hyperinsulinemia, liver or kidney insufficiency and alcohol consumption, hypoglycemia is attributed to HCQ treatment.