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Most cases of nontuberculous mycobacterial pulmonary disease (NTM-PD) have a progressive clinical course, and initiation of treatment is recommended rather than watchful waiting. The NTM-PD medications are frequently associated with adverse reactions, occasionally serious. Optimization of the methods for monitoring and managing adverse events in NTM-PD treatment is thus an important medical issue. Here we report a first case of postprandial hypoglycemia caused by the combination of clarithromycin (CAM) and rifampicin (RFP) in a patient with NTM-PD. A 73-year-old Japanese woman with NTM-PD was hospitalized for treatment with a combination of oral CAM, RFP, and ethambutol. She took the first doses of antibiotics before breakfast, and 3 h later went into a hypoglycemic state. Postprandial hypoglycemia occurred with high reproducibility and was accompanied by relative insulin excess. Continuous glucose monitoring with or without food and in combination with various patterns of medication revealed that the combination of CAM and RFP specifically induced postprandial hypoglycemia. Shifting the timing of administration of the CAM and RFP combination from morning to before sleep corrected the hypoglycemia and enabled continuation of the antimicrobial treatment. In conclusion, our report suggests the importance of introducing NTM-PD medication under inpatient management in order to closely monitor and early detect postprandial hypoglycemia and other serious adverse events.
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Postprandial hypoglycemia is a complication of Roux-en-Y gastric bypass (RYGB), but the effects of postprandial exercise and meal glycemic index (GI) on postprandial glucose and glucoregulatory hormone responses are unknown. Ten RYGB-operated and 10 age and weight-matched unoperated women completed four test days in random order ingesting mixed meals with high GI (HGI, GI = 93) or low GI (LGI, GI = 54), but matched on energy and macronutrient content. Ten minutes after meal completion, participants rested or cycled for 30 min at 70% of maximum oxygen uptake (VÌo2max). Blood was collected for 4 h. Postprandial exercise did not lower plasma nadir glucose in RYGB after HGI (HGI/rest 3.7 ± 0.5 vs. HGI/Ex 4.1 ± 0.4 mmol/L, P = 0.070). Replacing HGI with LGI meals raised glucose nadir in RYGB (LGI/rest 4.1 ± 0.5 mmol/L, P = 0.034) and reduced glucose excursions (Δpeak-nadir) but less so in RYGB (-14% [95% CI: -27; -1]) compared with controls (-33% [-51; -14]). Insulin responses mirrored glucose concentrations. Glucagon-like peptide 1 (GLP-1) responses were greater in RYGB versus controls, and higher with HGI versus LGI. Glucose-dependent insulinotropic polypeptide (GIP) responses were greater after HGI versus LGI in both groups. Postexercise glucagon responses were lower in RYGB than controls, and noradrenaline responses tended to be lower in RYGB, whereas adrenaline responses were similar between groups. In conclusion, moderate intensity cycling shortly after meal intake did not increase the risk of postprandial hypoglycemia after RYGB. The low GI meal increased nadir glucose and reduced glucose excursions compared with the high GI meal. RYGB participants had lower postexercise glucagon responses compared with controls.NEW & NOTEWORTHY We investigate the effect of moderate exercise after a high or a low glycemic index meal on nadir glucose and glucoregulatory hormones in gastric bypass-operated individuals and in matched unoperated controls. Cycling shortly after meal intake did not increase the risk of hypoglycemia in operated individuals. The low glycemic index meal increased glucose nadir and reduced excursions compared with the high glycemic index meal. Operated individuals had lower postexercise glucagon responses compared with controls.
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Derivação Gástrica , Hipoglicemia , Humanos , Feminino , Índice Glicêmico , Glicemia , Glucagon/metabolismo , Consumo de Oxigênio , Oxigênio , Insulina , Refeições , Glucose , Período Pós-PrandialRESUMO
BACKGROUND: Noninsulinoma pancreatogenous hypoglycemia syndrome (NIPHS) is a rare syndrome characterized by postprandial hypoglycemia with neuroglycopenic symptoms occurring 1 to 3 h after a meal. Diagnosis can be elusive, as the vast majority of patients have normal fasting blood glucose levels, and onset of hypoglycemic episodes can be a late complication of gastric surgery. CASE REPORT: We report the case of a 45-year-old woman presenting to the Emergency Department (ED) with new-onset seizures and hypoglycemia worsened by glucose administration. Surgical history is pertinent for a Roux-en-Y gastric bypass approximately 10 years prior to presentation. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Although rare, it is important for emergency physicians to be vigilant of this disease process as a traditional treatment approach for hypoglycemia may be detrimental. Although cases of NIPHS have been documented in literature, its presence in emergency medicine-specific literature is seemingly nonexistent. Noninvasive imaging techniques will be normal, and diagnosis is dependent on awareness of this disease entity coupled with a detailed history.
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Derivação Gástrica , Hipoglicemia , Obesidade Mórbida , Feminino , Derivação Gástrica/efeitos adversos , Glucose , Humanos , Hipoglicemia/diagnóstico , Hipoglicemia/etiologia , Pessoa de Meia-Idade , SíndromeRESUMO
Hypoglycemia is a rather frequent complication of diabetes treatment, however it can occur also in non-diabetic patients. The article presents a brief differential diagnosis of hypoglycemia in non-diabetic patients.
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Diabetes Mellitus Tipo 2 , Hipoglicemia , Insulinoma , Neoplasias Pancreáticas , Diagnóstico Diferencial , Humanos , Hipoglicemia/induzido quimicamente , Hipoglicemia/diagnóstico , Insulinoma/diagnóstico , Neoplasias Pancreáticas/diagnósticoRESUMO
Migraine is a common neurological disorder that significantly impacts patients around the world. In the United States, one in six individuals suffers from a migraine disorder. Despite its high prevalence, the etiology of migraine is not well understood. Multiple factors likely contribute to the development of both acute and chronic migraine, making the consensus as to the cause and treatment difficult. Presented here are three case studies involving adult males suffering from chronic migraine. Each subject provided a medical history and underwent physical, psychological, and neurological examinations. In addition, relevant bloodwork and cervical spine X-rays were obtained. Physical examination, laboratory studies, imaging, and psychological metrics were unremarkable with the notable exception of the three-hour oral glucose tolerance tests. All three patients displayed hypoglycemia at three hours. Furthermore, their symptoms markedly improved with the initiation of a ketogenic diet. These data are suggestive of a potential link between postprandial hypoglycemia and chronic migraine. Despite the small sample size, we feel that this report presents possible evidence for a connection between postprandial hypoglycemia and chronic migraine. Furthermore, properly controlled studies of larger sample sizes are required, but we suggest that clinicians consider screening patients for this easily overlooked metabolic disturbance, especially in the absence of other options.
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Objectives: Reaching optimal postprandial glucose dynamics is a daily challenge for people with type 1 diabetes (T1D). This study aimed to analyze the postprandial hyperglycemic excursion (PHEs) and late postprandial hypoglycemia (LPH) risk according to prandial insulin time and type. Research Design and Methods: Real-world, retrospective study in T1D using multiple daily injections (MDI) analyzing 5 h of paired continuous glucose monitoring and insulin injections data collected from the connected cap Insulclock®. Meal events were identified using the rate of change detection methodology. Postprandial glucometrics and LPH (glucose <70 mg/dL 2-5 h after a meal) were evaluated according to insulin injection time and rapid (RI) or ultrarapid analog, Fiasp® (URI), use. Results: Meal glycemic excursions (n = 2488), RI: 1211, 48.7%; UR: 1277, 51.3%, in 82 people were analyzed according to injection time around the PHE: -45 to -15 min; -15 to 0 min; and 0 to +45 min. In 63% of the meals, insulin was injected after the PHE started. Lower PHE was observed with URI versus RI (glucose peak-baseline; mg/dL; mean ± standard deviation): 106.7 ± 35.2 versus 111.2 ± 40.3 (P = 0.003), particularly in 0/+45 injections: 111.6 ± 40.2 versus 118.1 ± 43.3; (P = 0.002). One third (29.1%) of participants added a second (correction) injection. The use of URI and avoiding a second injection were independently associated with less LPH risk, even in delayed injections (0/+45), (-36%, odds ratio [OR] 0.641; confidence interval [CI]: 0.462-0.909; P = 0.012) and -56% (OR 0.641; CI: 0.462-0.909 P = 0.038), respectively. Conclusions: URI analog use as prandial insulin reduces postprandial hyper- and hypoglycemia, even in delayed injections.
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Diabetes Mellitus Tipo 1 , Hiperglicemia , Hipoglicemia , Humanos , Insulina/uso terapêutico , Diabetes Mellitus Tipo 1/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Automonitorização da Glicemia/métodos , Estudos Retrospectivos , Glicemia , Hipoglicemia/induzido quimicamente , Hipoglicemia/prevenção & controle , Hiperglicemia/prevenção & controle , Insulina Regular Humana , Período Pós-Prandial , Estudos Cross-OverRESUMO
BACKGROUND: Abdominal pain and postbariatric hypoglycemia (PBH) are common after bariatric surgery. OBJECTIVES: This study aimed to explore the potential relationship between abdominal pain, gastrointestinal symptoms, and PBH more than a decade after Roux-en-Y gastric bypass (RYGB) and whether continuous glucose monitoring (CGM) with dietary intervention has an educational role in reducing symptoms. SUBJECTS: At two public hospitals in Norway (one University Hospital) 22 of 46 invited patients who reported abdominal pain more than weekly took part. Recruited from a prospective follow-up study of 546 patients 14.5 years after RYGB. METHODS: They used a CGM for two 14-day periods, with a dietary intervention between periods. The Gastrointestinal Symptom Rating Scale (GSRS) and the Dumping Severity Score (DSS) questionnaires were completed at the start and end of the study. RESULTS: The 22 women had preoperative age 39.6 ± 7.7 years and body mass index (BMI) 42.0 ± 4.0 kg/m2, present age 54.6 ± 7.7 years and BMI 29.8 ± 4.8 kg/m2. The total GSRS score and DSS of early dumping decreased after the diet intervention. The number of events with Level 1 (<3.9 mmol/L) or Level 2 (<3.0 mmol/L) hypoglycemia did not change in the second period. Half of the patients had fewer, three had unchanged, and eight had more frequent events with Level 1 hypoglycemia after the intervention. Ten patients had Level 2 hypoglycemia. CONCLUSION: Though inconclusive findings, a personalized dietary intervention reduces GSRS. This intervention was accompanied by lower mean absolute glucose in patients with recurrent abdominal pain after bariatric surgery. However, further studies are needed to explore the benefits of CGM in this setting.
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Derivação Gástrica , Hipoglicemia , Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Derivação Gástrica/efeitos adversos , Monitoramento Contínuo da Glicose , Automonitorização da Glicemia , Seguimentos , Estudos Prospectivos , Glicemia , Dor Abdominal/etiologia , Hipoglicemia/etiologiaRESUMO
Cataract surgery is one of the most frequently performed surgical procedures and is often performed under topical anesthesia in conscious patients. Sweating, palpitations, and anxiety may be seen in patients about to undergo surgery. However, these are typical adrenergic symptoms of hypoglycemia and should be further investigated if occurring before surgery. Here, we report five cases of postprandial or reactive hypoglycemia observed in hospital settings just before conducting cataract surgeries in non-diabetic 52-78-year-old patients from 2019 to 2023.
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Insulin autoimmune syndrome (IAS) or Hirata disease is a rare condition presenting as recurrent hypoglycemia, and associated with elevated insulin levels in the presence of insulin autoantibodies (IAAs) in patients who were never exposed to exogenous insulin and with no evidence of pancreatic abnormalities. IAS is much more frequent in East Asians, especially the Japanese population, compared to the lower incidence in Caucasians. However, it can be associated with other autoimmune diseases or drug use like methimazole and alpha-lipoic acid (ALA). We report a case of a 47-year-old Caucasian male presenting with a 12-month history of worsening episodes of fasting and post-prandial hypoglycemia associated with symptoms of dizziness, tremors, palpitations, and unconsciousness associated with hypoglycemia. Symptoms resolved with the administration of carbohydrate-containing foods, establishing Whipple's triad. At an outside facility, he had initial labs that showed elevated insulin levels (141 µU/ml) with normal glucose, C-peptide, and proinsulin levels, but there was no availability of an IAA lab assay. Given his symptoms, severity, and frequency of hypoglycemia, he was admitted to the hospital for a 72-hour fast, which showed the lowest glucose level of 64 mg/dl with inappropriately high insulin of 22.2 µU/ml, low C-peptide of 0.57 ng/ml, and undetectable proinsulin of <1.6 pmol/L, but with IAA being >50 U/ml (0.0-0.4 U/ml). He was treated with intensive dietary counseling with a low-carbohydrate diet and prednisone 20 mg twice daily initially. Additionally, he could not tolerate octreotide, diazoxide, and acarbose due to side effects. He is currently on prednisone 10 mg daily and nifedipine with no further hypoglycemic episodes, but still has a high IAA of >50 U/ml and serum insulin levels of 70-112 µU/ml. Our case highlights the importance of recognizing hypoglycemia and checking for IAA levels as first-line diagnostic tests, in the absence of which there could be a delay in diagnosis and leading to unnecessary lab and imaging testing. Our case is unique since it happened in a Caucasian without any prior exposure to a triggering factor and has not undergone self-remission yet, which happens in most of IAS cases.
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Postprandial hypoglycemia (PPH) is a complex and multifactorial complication of bariatric surgery (BS). PPH may cause severe symptoms or be asymptomatic. The treatment of this condition requires dietary changes, but severe cases require drug therapy. The number of therapeutic options is limited and are often associated with adverse side effects. Different classes of drugs have been used and tested, but the resolution of PPH remains a challenge for physicians and patients. In this review, we gathered articles on PPH after BS from PubMed searches (2001 to 2022) and focused on the main drugs tested for the treatment of this condition, such as acarbose, somatostatin analogues, type 2 sodium-glucose cotransporter inhibitors, calcium channel blockers, and liraglutide. Avexitide and glucagon pump are two new therapeutic options that have been recently tested. For the search, the terms "postbariatric hypoglycemia," "bariatric surgery," and "late dumping syndrome" were used. PPH after BS is a frequent condition that should always be evaluated after BS. Treatment should be individualized and the available therapeutic options may be useful based on the condition's pathophysiology.
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Cirurgia Bariátrica , Derivação Gástrica , Hipoglicemia , Obesidade Mórbida , Humanos , Derivação Gástrica/efeitos adversos , Hipoglicemia/tratamento farmacológico , Hipoglicemia/etiologia , Hipoglicemia/diagnóstico , Cirurgia Bariátrica/efeitos adversos , Glucagon , Acarbose/uso terapêutico , Obesidade Mórbida/cirurgia , GlicemiaRESUMO
With a rise in obesity and more patients opting for bariatric surgery, it becomes crucial to understand associated complications like postprandial hypoglycemia (PPH). After bariatric surgery, significant changes are seen in insulin sensitivity, beta cell function, glucagon-like peptide 1 (GLP-1) levels, the gut microbiome, and bile acid metabolism. And in a small subset of patients, exaggerated imbalances in these functional and metabolic processes lead to insulin-glucose mismatch and hypoglycemia. The main treatment for PPH involves dietary modifications. For those that do not respond, medications or surgical interventions are considered to reverse some of the imbalances. We present a few case reports of patients that safely tolerated GLP-1 agonists. However, larger randomized control trials are needed to further characterize PPH and understand its treatment.
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Cirurgia Bariátrica , Derivação Gástrica , Hipoglicemia , Obesidade Mórbida , Humanos , Glicemia/metabolismo , Obesidade Mórbida/cirurgia , Derivação Gástrica/efeitos adversos , Hipoglicemia/etiologia , Cirurgia Bariátrica/efeitos adversos , Peptídeo 1 Semelhante ao Glucagon/metabolismo , Insulina/metabolismoRESUMO
The best-known etiologies of hyperinsulinemic hypoglycemia are insulinoma, non-insulinoma pancreatogenous hypoglycemic syndrome, autoimmune processes, and factitious hypoglycemia. In 2009, a disease not associated with classic genetic syndromes and characterized by the presence of multiple pancreatic lesions was described and named insulinomatosis. We present the clinical and pathologic features of four patients with the diagnosis of insulinomatosis, aggregated new clinical data, reviewed extensively the literature, and illustrated the nature and evolution of this recently recognized disease. One of our patients had isolated (without fasting hypoglycemia) postprandial hypoglycemia, an occurrence not previously reported in the literature. Furthermore, we reported the second case presenting malignant disease. All of them had persistent/recurrent hypoglycemia after the first surgery even with pathology confirming the presence of a positive insulin neuroendocrine tumor. In the literature review, 27 sporadic insulinomatosis cases were compiled. All of them had episodes of fasting hypoglycemia except one of our patients. Only two patients had malignant disease, and one of them was from our series. The suspicion of insulinomatosis can be raised before surgery in patients without genetic syndromes, with multiple tumors in the topographic investigation and in those who had persistent or recurrent hypoglycemia after surgical removal of one or more tumors. The definitive diagnosis is established by histology and immunohistochemistry and requires examination of the "macroscopically normal pancreas." Our case series reinforces the marked predominance in women, the high frequency of recurrent hypoglycemia, and consequently, a definitive poor response to the usual surgical treatment.
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Hiperinsulinismo , Hipoglicemia , Tumores Neuroendócrinos , Humanos , Feminino , Afeto , HipoglicemiantesRESUMO
Postprandial reactive hypoglycemia, or late dumping syndrome, is a common but underrecognized complication from bypass surgery. We report an unusual case of postprandial reactive hypoglycemia in a patient with a severe esophageal stricture from corrosive agent ingestion who underwent ileocolic interposition and an antecolic Billroth-II gastrojejunostomy. A 22-year-old male patient with a one-year history of corrosive ingestion was referred to the hospital for a surgical correction of severe esophageal stricture. After the patient underwent ileocolic interposition and an antecolic Billroth-II gastrojejunostomy, he experienced multiple episodes of gastroesophageal refluxsymptoms during nasogastric feeding and had onset of hypoglycemic symptoms. His plasma glucose level was 59 mg/dL. After we had intraoperatively re-inserted a jejunostomy tube bypassing the ileocolic interposition, and reintroduced enteral nutrition, his hypoglycemic symptoms resolved. We performed a mixed meal tolerance test by nasogastric tube, but the results did not show postprandial hypoglycemia. Although the specific mechanism is unclear, this case suggests gastroesophageal reflux to the ileal interposition may have caused a state of exaggerated hyperinsulinemic response and rebound hypoglycemia. To the best of our knowledge, we are the first to report case of postprandial hypoglycemia after ileocolic interposition, which may have been caused by exaggerated hyperinsulinemic response due to gastroesophageal reflux to the ileal interposition. This syndrome should be considered in the patient who has had ileocolic interposition surgery and has developed postprandial hypoglycemia.
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Polycystic ovary syndrome (PCOS) is an insulin-resistant state compensated for by the body via hyperinsulinemia. More than 50% of women with PCOS are obese and/or have metabolic syndrome. Weight loss improves both metabolic and reproductive outcomes. Energy/caloric content as well as the nutrient composition of one's diet may also be important. This article will present a series of studies from our research comparing the effects of dietary protein vs. simple carbohydrates (CHOs). The results of the acute challenge studies demonstrate that simple CHO intake causes reactive hypoglycemia in one third of women with PCOS, especially among obese and insulin-resistant individuals. Symptoms of hypoglycemia are associated with secretion of cortisol and adrenal androgens. Simple CHOs suppress the hunger signal ghrelin for a shorter period. During weight loss, women who receive protein supplementation achieve more significant weight and fat mass losses. The amino acid compositions of the protein supplements do not affect the improvements in weight and insulin resistance. It is plausible that simple CHO intake leads to weight gain, or interferes with weight loss, by causing reactive hypoglycemia, triggering adrenal steroid secretion and thus leading to snacking. Since obese women with PCOS are more susceptible to reactive hypoglycemia, a vicious cycle is established. Restriction of simple CHOs may break this cycle.
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Bariatric/metabolic surgery and sodium-glucose cotransporter 2 inhibitors (SGLT2is) are becoming increasingly popular for the management of overweight/obese patients with type 2 diabetes mellitus (T2DM). Consequently, the chance that a patient undergoing bariatric/metabolic surgery is also treated with an SGLT2i would be rather common in clinical practice. Both risks and benefits have been reported. On the one hand, several cases of euglycemic diabetic ketoacidosis have been reported within the few days/weeks after bariatric/metabolic surgery. The causes are diverse but a drastic reduction in caloric (carbohydrate) intake most probably plays a crucial role. Thus, SGLT2is should be stopped a few days (and even more if a pre-operative restricted diet is prescribed to reduce liver volume) before the intervention and reintroduced only when the caloric (carbohydrate) intake is sufficient. On the other hand, SGLT2is may exert a favorable effect to reduce the risk of postprandial hypoglycemia, a complication reported among patients who have been treated with bariatric/metabolic surgery. An increased hepatic glucose production and a reduced production of interleukin-1ß have been proposed as possible underlying mechanisms for this protective effect. Finally, whether SGLT2is could prolong diabetes remission following surgery and improve the prognosis of patients with T2DM who benefit from bariatric/metabolic surgery remains to be investigated.
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Cirurgia Bariátrica , Diabetes Mellitus Tipo 2 , Inibidores do Transportador 2 de Sódio-Glicose , Humanos , Inibidores do Transportador 2 de Sódio-Glicose/uso terapêutico , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/cirurgia , Cirurgia Bariátrica/efeitos adversos , Glucose , Medição de Risco , Carboidratos/uso terapêuticoRESUMO
Background/Objective: Patients with an insulinoma, a type of pancreatic neuroendocrine tumor, typically present with fasting hypoglycemia but can rarely present exclusively with postprandial hypoglycemia. Case Report: A 69-year-old man presented with episodes of postprandial blurry vision, sweating, and confusion for the last 2 years that were becoming more frequent over the last several weeks. Home blood glucose measurements revealed postprandial hypoglycemia (glucose level, 45-70 mg/dL), and symptoms were consistent with the Whipple triad. Continuous glucose monitoring revealed only postprandial hypoglycemia within 2 hours following meals. An outpatient fast was conducted with detectable insulin (6 µIU/mL) and C-peptide (2.0 ng/mL) levels with an elevated proinsulin (20.8 pmol/L) level when the serum blood glucose level dropped to 47 mg/dL (21 hours after the initiation of the fast). A computed tomography scan of the abdomen and pelvis showed a 1.6-cm hyperenhancing lesion in the distal body of the pancreas. He underwent endoscopic ultrasonography with fine-needle aspiration. Pathology revealed a low-grade, well-differentiated, neuroendocrine tumor with lymphovascular invasion and regional lymph node metastases, confirming the diagnosis of a pancreatic neuroendocrine tumor. Discussion: Exclusive postprandial hypoglycemia is estimated to occur in 6% of the insulinomas. Patients with postprandial hypoglycemia may be initially managed as those with reactive hypoglycemia; however, this case highlights the importance of evaluating for an insulinoma in a patient who has failed treatment for reactive hypoglycemia. This case also demonstrates the importance of including proinsulin levels in that evaluation. Conclusion: Pancreatic neuroendocrine tumor should be considered in postprandial hypoglycemia, even in the absence of fasting hypoglycemia. Measuring proinsulin levels is essential in the diagnostic workup of insulinoma causing hypoglycemia.
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Increasing evidence suggests that migraine may be the result of an impaired brain glucose metabolism. Several studies have reported brain mitochondrial dysfunction, impaired brain glucose metabolism and gray matter volume reduction in specific brain areas of migraineurs. Furthermore, peripheral insulin resistance, a condition demonstrated in several studies, may extend to the brain, leading to brain insulin resistance. This condition has been proven to downregulate insulin receptors, both in astrocytes and neurons, triggering a reduction in glucose uptake and glycogen synthesis, mainly during high metabolic demand. This scoping review examines the clinical, epidemiologic and pathophysiologic data supporting the hypothesis that abnormalities in brain glucose metabolism may generate a mismatch between the brain's energy reserve and metabolic expenditure, triggering migraine attacks. Moreover, alteration in glucose homeostasis could generate a chronic brain energy deficit promoting migraine chronification. Lastly, insulin resistance may link migraine with its comorbidities, like obesity, depression, cognitive impairment and cerebrovascular diseases. PERSPECTIVE: Although additional experimental studies are needed to support this novel "neuroenergetic" hypothesis, brain insulin resistance in migraineurs may unravel the pathophysiological mechanisms of the disease, explaining the migraine chronification and connecting migraine with comorbidities. Therefore, this hypothesis could elucidate novel potential approaches for migraine treatment.
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Resistência à Insulina , Transtornos de Enxaqueca , Encéfalo , Glucose/metabolismo , Humanos , Insulina/metabolismo , Resistência à Insulina/fisiologiaRESUMO
Purpose: Glucose metabolism disorders are an established risk factor for atherosclerosis. Although reactive hypoglycemia (RH) can be classified as one of these disorders, its role as a potential atherosclerosis risk factor remains unclear. The aim of the study was to assess whether patients with RH have a higher risk of atherosclerosis. Patients and Methods: We recruited 178 patients (N=178) with suspected RH who were hospitalized after 2014 and underwent a prolonged 5-hour oral glucose tolerance test. The study cohort was divided into 2 groups depending on the results of the oral glucose tolerance test: Group 1 - subjects without RH (n=44), Group 2 -subjects with RH (n=134). Results: The analyzed groups differed significantly in terms of the following risk factors for atherosclerosis: high-density lipoprotein (HDL) cholesterol levels (54.3±18.8 mg/dL vs 63±18.5 mg/dL, p=0.003) and atherogenic indices (Castelli I: 3.7±1.2 vs 3.1±1.3, p=0.004; Castelli II: 2.1±0.9 vs 1.7±0.9, p=0.007; the atherogenic index of plasma: 0.34±0.33 vs 0.18±0.3, p=0.006; and the atherogenic coefficient: 2.7±1.2 vs 2.1±1.3, p=0.004). Univariate logistic regression showed that RH should not be considered to be a predictor of an increased atherogenic index of plasma (odds ratio [OR]=0.3 [95% confidence interval [CI] [0.16-0.7], p=0.002). Multivariate logistic regression revealed triglyceride levels (OR 1.14 [1.07-1.2], p=0.001) and body weight (OR 1.07 [1.03-1.12], p=0.002) to be independent risk factors for atherosclerosis. Conclusion: Atherosclerosis risk factors are no more prevalent in patients with RH. RH does not increase the risk of an abnormal atherogenic index of plasma.
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Reactive postprandial hypoglycemia (RPH) is an understudied condition that lacks clinical definition, knowledge of future health implications, and an understanding of precise underlying mechanisms. Therefore, our study aimed to assess the glycemic response after glucose ingestion in individuals several years after the initial evaluation of RPH and to compare glucose regulation in individuals with RPH vs. healthy volunteers. We assessed the inter- and intra-individual differences in glucose, insulin, and C-peptide concentrations during 5-h oral glucose tolerance tests (OGTTs); the surrogate markers of insulin resistance (HOMA-IR and Matsuda index); and beta-cell function (distribution index and insulinogenic index). The study included 29 subjects with RPH (all females, aged 39 (28, 46) years) and 11 sex-, age-, and body mass index (BMI)-matched controls. No biochemical deterioration of beta-cell secretory capacity and no progression to dysglycemia after 6.4 ± 4.2 years of follow-up were detected. RPH subjects were not insulin resistant, and their insulin sensitivity did not deteriorate. RPH subjects exhibited no differences in concentrations or in the shape of the glucose-insulin curves during the 5-h OGTTs compared to age- and BMI-matched controls. No increased incident type 2 diabetes risk indices were evident in individuals with RPH. This dictates the need for further research to investigate the magnitude of future diabetes risk in individuals experiencing RPH.
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Postprandial hypoglycemia is a rare complication after Roux-en-Y gastric bypass (RYGB). The underlying pathophysiology remains to be fully understood. We present a case of a 49-year-old woman with a past medical history of mesenteric thrombosis due to prothrombin-related thrombophilia, which culminated in RYGB 10 years prior to presentation. The patient had been given anticoagulation treatment for several years, which she abandoned one year prior to presentation. She presented to our consultation with episodes of postprandial hypoglycemia and severe anemia due to iron and vitamin B12 deficiencies. Dietary adjustments were set in place to prevent hypoglycemia and neuroglycopenic symptoms. Intravenous iron and intramuscular vitamin B12 supplementation led to full recovery of hemoglobin levels, allowing restart of oral anticoagulation to prevent recurrence of thrombotic events.