Dextrose Infusion Research Articles

Assessment of fetal cord blood acid-base status following intrapartum maternal glucose infusion

Background and Aim: Supplementation of intravenous fluids is associated with with increased incidence of neonatal hypoglycemia. However, WHO guideline recommends no restriction of liquid or solid food to a parturient mother. Therefore, the aim of the study is to compare fetal acid-base status and neonatal blood glucose levels following intrapartum infusion of ringer lactate (RL) solution or dextrose normal saline (DNS) solution in active labor. Methods: It is a prospective, analytical study conducted on hundred women in active labor and they were randomly allocated into two groups. First group (Group A) received intravenous infusion of DNS, and the other group (Group B) was given RL infusion for at least 1 h before delivery. Results: There was no significant difference in fetal acid-base status between the two groups although neonatal blood glucose levels were higher in the DNS group (Group A). Conclusion: Intrapartum infusion of DNS can raise neonatal blood glucose level but does not cause fetal acidosis or any alteration in fetal acid-base status.

A case of severe hyponatremic anuric acute kidney injury safely treated with continuous renal replacement therapy with continuous infusion of dextrose 5％ in water

A case of severe hyponatremic anuric acute kidney injury safely treated with continuous renal replacement therapy with continuous infusion of dextrose 5％ in water

Insulin Glargine and Insulin Aspart Overdose With Pharmacokinetic Analysis

ABSTRACT Objective: Insulin glargine is a long-acting insulin analogue with biotransformation, at the injection site, to a primary active metabolite (glargine-M1). Combined therapy with rapid-acting insulin aspart is common, but pharmacokinetics with supra-therapeutic doses have not been reported. We present clinical and pharmacokinetic findings for 2 episodes of overdose with glargine and aspart in a 43-year-old male with type 1 diabetes. Methods: Liquid chromatography–tandem mass spectrometry was used to detect and quantitate the M1 and insulin aspart levels in the serum of an individual who administered large supra-therapeutic doses of these medications. Results: Prolonged insulin analogue action was associated with measurable aspart levels in the circulation for the first day and with glargine-M1 for up to 5 days. Dextrose infusion rate correlated closely with the circulating levels of aspart and glargine-M1. Throughout the clinical treatment, glargine concentrations were near or below the threshold o...

Wernicke's Encephalopathy Complicating Hyperemesis during Pregnancy.

Wernicke's encephalopathy is caused by severe thiamine deficiency; it is mostly observed in alcoholic patients. We report the case of a 28-year-old woman, at 17 weeks of gestational age, with severe hyperemesis gravidarum. She presented with disturbance of consciousness, nystagmus, ophthalmoplegia, and ataxia. The resonance magnetic imagery showed bilaterally symmetrical hyperintensities of thalamus and periaqueductal area. The case was managed with very large doses of thiamine. The diagnosis of Wernicke's encephalopathy was confirmed later by a low thiamine serum level. The patient was discharged home on day 46 with mild ataxia and persistent nystagmus. Wernicke's encephalopathy is a rare complication of hyperemesis gravidarum. It should be diagnosed as early as possible to prevent long-term neurological sequela or death. Thiamine supplementation in pregnant women with prolonged vomiting should be initiated, especially before parenteral dextrose infusion. Early thiamine replacement will reduce maternal morbidity and fetal loss rate.

Non-islet cell tumour hypoglycaemia: A case report

Sir, Hypoglycaemia is usually a manifestation of pancreatic islet cell tumours producing insulin, primary or secondary adrenal insufficiency, advanced liver disease, phaeochromocytoma, insulin growth factor (IGF)-1 secreting tumours, hypothyroidism, substances interfering with insulin, and insulin receptor-mediated metabolism or antibodies interfering with insulin. Non-islet cell tumour hypoglycaemia (NICTH) has been related to the production of IGF-II or its high-molecular-weight precursor (big IGF-II) by tumours, which are mesenchymal malignancies such as fibrous tumours, sarcomas and mesothelioma. It results from inhibited hepatic glycogenolysis, gluconeogenesis and diminished lipolysis, indicating increased insulin-like activity in the body. In addition, there is enhanced glucose utilisation due to the high metabolic needs of a large tumour. Big IGF- II is a form of pro-IGF-II, which is biologically active and has a greater bioavailability.[1] There have been a very few case reports of fasting hypoglycaemia in patients with phyllodes tumour (PT). PTs are rare fibroepithelial lesions that make up 0.3–0.5% of breast tumours. We describe such a case, its management and a brief review of the literature. A 37-year unmarried female presented with a large chest wall tumour (25 cm × 20 cm × 20 cm), which was diagnosed to be PT on core biopsy. On the day of surgery, she complained of dizziness and the blood sugar testing showed a value of 16 mg/dL. On eliciting history, she said that she had experienced such episodes previously. She had difficulty in getting up in the morning, sometimes did not recognise relatives, experienced sweating, and palpitations; mostly during the early morning. The supervised overnight fast test was done. The patient went into hypoglycaemia after 6 h, the critical samples for glucose and insulin C-peptide were tested, levels were very low. This ruled out the possibility of an insulinoma. This suggested that hypoglycaemia might be tumour induced. The growth hormone (GH) and IGF-I levels were low. Oral prednisolone was administered at night and morning 4 am and 6 am and glucose levels were done, which were found to be normal. Pre-operative blood sugar values were low (60 mg%) and supplementary dextrose infusion was continued intraoperatively, titrated with repeated blood samples. Mastectomy was performed and breast reconstructed with deep inferior epigastric perforator flap. Intraoperatively, dextrose requirements decreased after excision of the tumour. Postoperatively, blood sugar was measured 2nd hourly for first 6 h and later 4th hourly and the levels remained normal. The first case of NICTH was reported in 1983 in a 43-year-old woman with a large left breast PT, 28 cm in diameter and weighing 4.2 kg, successfully treated with mastectomy. This patient's hospital course was marked by recurrent profound hypoglycaemia followed by loss of consciousness but recovered without any neurological deficit each time after dextrose administration. The plasma levels of non-suppressible insulin-like protein were increased, whereas levels of insulin were normal.[2] Another similar case presentation was found in a 66-year-old woman who also recovered after removing a 6 kg weight PT, describing elevated values of big IGF-II in the blood and in the tumour extract.[3] Furthermore, a case of hypoglycaemia has been reported in a 54-year-old woman who was treated with surgery (malignant PT of 9 kg and 35 cm), and post-operative medroxyprogesterone acetate because of lung metastasis. In this case, the plasma level of IGF-II was moderately diminished postoperatively, whereas the tumour extract IGF-II level was high.[4] Moreover, an unfortunate case of irreversible hypoglycaemic coma during fine-needle aspiration of a PT breast has been described, but the patient subsequently died on the 8th day of admission due to aspiration pneumonia and renal failure. Low levels of Insulin, IGF-I, C-peptide, and GH suggested an insulinomimetic compound to be the cause of hypoglycaemia. Postmortem of the patient revealed hypoglycaemic brain damage with hippocampal necrosis.[5] To conclude, big sized PTs may manifest with NICTH, and simple management can prevent poor outcomes. The complete resection of the tumour produces a prompt normalisation of the serum glucose level. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

İleri yaşta görülen nadir bir hipoglisemi nedeni: İnsülinoma

Insulinoma is rare pancreatic neuroendocrine tumor that is usually described as benign and sporadic. It is seen mostly in women at the ages between 40 and 60 years. Insulinoma can cause hypoglycemic attacks which may lead to serious consequences. Here we report a case of an 82 years old woman with the diagnosis of insulinoma presented by cerebrovascular disease due to severe hypoglycemia. Early diagnosis of the disease is essential to prevent lethal hypoglycemia. The first choice of treatment is surgery. However in the elderly, medical treatments may be preferred as primary treatment due to the existing comorbidities. For this case, it was possible to control the hypoglycemic attacks by using diazoxide and octreotide treatment. So that continous dextrose infusion is not necessary.

Early initiation of low-level parenteral dextrose induces an accelerated diabetic phenotype in septic C57BL/6J mice

Development of hyperglycemia during sepsis is associated with increased morbidity and mortality. Nutritional support is common practice in the intensive care unit, but the metabolic effects are not well understood. The purpose of this study is to determine the effect of early low-level calorie provision on the development of hyperglycemia in a clinically relevant murine model of sepsis. C57BL/6J mice underwent femoral arterial and venous catheterization followed by cecal ligation and puncture (CLP) or sham surgery and low-dose intravenous dextrose or saline infusion. Blood glucose, plasma insulin, and cytokines were measured after 24 h. Additional septic mice underwent hyperinsulinemic-euglycemic clamps or received intravenous insulin concurrent with dextrose to determine whole-body insulin sensitivity and test the efficacy of insulin to reverse hyperglycemia. Neither dextrose infusion nor CLP alone induced hyperglycemia. Early initiation of low-level dextrose in septic mice produced a variable glycemic response: 49% maintained euglycemia (blood glucose < 200) and 27% developed severe hyperglycemia (blood glucose ≥ 600). Hyperglycemia was associated with increased inflammation and reduced insulin secretion and sensitivity compared with control mice or CLP mice maintaining euglycemia. Insulin prevented the progression to severe hyperglycemia but was ineffective in reestablishing glycemic control once hyperglycemia had developed. In conclusion, early initiation of clinically relevant low-level dextrose (∼ 20% daily caloric requirements) precipitated hyperglycemia akin to an acute diabetic phenotype in septic mice characterized by decreased insulin sensitivity, decreased insulin secretion, and an increased inflammatory response.

Resistance exercise training and circulatory responses to feeding and skeletal muscle protein anabolism in older men.

Sarcopenia, the age-related loss of muscle mass, contributes to frailty and the loss of independence in older adults. It is well known that ageing results in a decreased sensitivity of skeletal muscle to the anabolic effects of dietary protein, and one explanation for this may be the age-related reduction in muscle leg blood flow and microvascular blood volume (MBV). Low MBV could compromise the postprandial transport of key amino acids and insulin to skeletal muscle where they are known to stimulate muscle protein synthesis (MPS) and arrest rates of muscle protein breakdown (MPB), respectively. As a result, strategies that enhance MBV in older adults may augment the delivery of amino acids and insulin to skeletal muscle following a meal and thus serve as a viable means to combat sarcopenia.

Glucocorticoid-Induced Preterm Birth and Neonatal Hyperglycemia Alter Ovine β-Cell Development.

Adults born preterm are at increased risk of impaired glucose tolerance and diabetes. Late gestation fetuses exposed to high blood glucose concentration also are at increased risk of impaired glucose tolerance as adults. Preterm babies commonly become hyperglycemic and are thus exposed to high blood glucose concentration at an equivalent stage of pancreatic maturation. It is not known whether preterm birth itself, or complications of prematurity, such as hyperglycemia, alter later pancreatic function. To distinguish these, we made singleton preterm lambs hyperglycemic (HYPER) for 12 days after birth with a dextrose infusion and compared them with vehicle-treated preterm and term controls and with HYPER lambs made normoglycemic with an insulin infusion. Preterm birth reduced β-cell mass, apparent by 4 weeks after term and persisting to adulthood (12 mo), and was associated with reduced insulin secretion at 4 months (juvenile) and reduced insulin mRNA expression in adulthood. Hyperglycemia in preterm lambs further down-regulated key pancreatic gene expression in adulthood. These findings indicate that reduced β-cell mass after preterm birth may be an important factor in increased risk of diabetes after preterm birth and may be exacerbated by postnatal hyperglycemia.

Stability Studies of Amoxicillin and Gentamicin Injection in Intravenous Infusions

<p style="text-align: justify;"><strong>Context:</strong> Amoxicillinsodium and gentamicin sulfate are commonly antibiotics which used for infection treatment. In Indonesia, injection of antibiotics can be administered concurrently with intravenous infusion. Injection is mixed into the infusion bottle or directly injected into infusion tubing. Before use, mixed of antibiotics and intravenous infusion is usually stored in a refrigerator to maintain stability.<strong>Aims: </strong>The study was designed to examine the stability of amoxicillin sodium and gentamicin sulfate in intravenous infusions. Methods and Material: Each of Amoxicillin sodium and Gentamicin sulfate was mixed into the ringer&rsquo;s dextrose infusion and ringer&#39;s lactate infusion at room temperature (27⁰C) and cold temperature (4⁰C) for 24 hours. The concentration of antibiotics were measured with Reversed-Phase High Performance Liquid Chromatography for 0, 1, 2, 3, 4, 5, 6, and 24 hours after antibiotics mixed to intravenous infusions. <strong>Results:</strong> Quantitative analysis was conducted by RP-HPLC, because this instrument give good separation of antibiotics from other components of intravenous infusion. The values of linearity, accuracy, precision, limit of detection and limit of quantification are fullfilled the criteria for HPLC validation. The stability of Amocixillin sodium influenced by the infusion type, temperature and time, while the stability of Gentamicin sulfate is only influenced by the infusion type. <strong>Conclusion: </strong>Amoxicillin sodium is more stable in ringer&#39;s lactate infusion, whereas Gentamicin sulfate is more stable in ringer&#39;s dextrose infusion. <p style="text-align: justify;"><strong>Key words:</strong> Amoxicillin sodium, Chemical stability, Gentamicin sulfate, Ringer&rsquo;s dextrose, Ringer&rsquo;s lactate.

Acute pancreatitis secondary to diabetic ketoacidosis induced hypertriglyceridemia in a young adult with undiagnosed type 2 diabetes.

The triad of acute pancreatitis, hypertriglyceridemia and diabetes is a rare occurrence. A previously well 19-year-old male presented to the emergency department with 24-hour history of epigastric pain, associated with polyuria and nausea. Biochemical markers showed the presence of hyperglycemia (blood sugar level 15 mmol/L) and ketonemia (5.3 mmol/L). Further investigation revealed severe hypertriglyceridemia (4,009 mg/dL) and elevated lipase (1,714 U/L). Abdominal ultrasound confirmed the diagnosis of acute pancreatitis. He was transferred to intensive care, where he received i.v. hydration, insulin and dextrose infusion. His metabolic derangements gradually resolved. His glycosylated hemoglobin was 13%, indicating the presence of chronically elevated blood sugars. The possible pathophysiology and management of this unusual triad: diabetic ketoacidosis, hypertriglyceridemia and acute pancreatitis, are explored in this paper.

Investigating the effect of glucose on aortic pulse wave velocity using pancreatic clamping methodology.

Aortic stiffness, determined by carotid-femoral pulse wave velocity (cfPWV), independently predicts cardiovascular outcomes. Recent studies suggest that glucose levels influence arterial stiffness indices. It is not clear, however, whether glucose affects cfPWV independently of glucoregulatory hormones. The aim of this study was to utilize a pancreatic clamping approach to determine whether plasma glucose independently predicts cfPWV. Healthy participants (N = 10) underwent pancreatic clamping to control glucose at varying concentrations using a 20% dextrose infusion while suppressing endogenous glucagon, insulin, and growth hormone by octreotide and replacing the hormones intravenously to achieve basal concentrations. Tonometric cfPWV, blood pressure, heart rate, plasma glucose, glucagon, insulin, growth hormone, and vasoactive biomarkers were measured. Plasma glucose levels of 150 mg/dl at 1 hr and 200 mg/dl at 2 hr postbaseline were achieved. There were no significant changes in cfPWV (5.8 m/s at 0 hr, 5.9 m/s at 1 hr, and 5.9 m/s at 2 hr) with increased glucose levels. There were small increases in insulin secretion. A definitive role for glucose in cfPWV modulation was not determined; there is a potential role for insulin as a cfPWV modulator. Continued efforts in clarifying the independent roles of glucose and insulin can elucidate novel vessel-related targets for cardiovascular disease prevention and management in patients with impaired glucose tolerance and diabetes.

The effect of intrauterine infusion of dextrose on clinical endometritis cure rate and reproductive performance of dairy cows

The main objective of this study was to evaluate the intrauterine administration use of 200mL of 50% dextrose solution as a treatment against clinical endometritis (CE); CE cure rate and reproductive performance were evaluated. Additionally, the association of several relevant risk factors, such as retained placenta (RP), metritis, CE, anovulation, hyperketonemia, and body condition score with reproductive performance, early embryonic mortality, and CE were evaluated. A total of 1,313 Holstein cows housed on 4 commercial dairy farms were enrolled in the study. At 7±3 DIM cows were examined for metritis and had blood collected to determine serum β-hydroxybutyrate concentration. To determine if cows had ovulated at least once before 44±3 DIM, the presence of a corpus luteum was evaluated by ovarian ultrasonography at 30±3 DIM and at 44±3 DIM. At 30±3 DIM, CE was diagnosed using the Metricheck device (SimcroTech, Hamilton, New Zealand); cows with purulent or mucopurulent vaginal discharge were diagnosed as having CE. Cows diagnosed with CE (n=175) were randomly allocated into 2 treatment groups: treatment (intrauterine infusion of 200mL of 50% dextrose) or control (no infusion). Clinical endometritis cows were re-evaluated as described above at 44±3 DIM, and cows that were free of purulent or mucopurulent vaginal discharge were considered cured. Intrauterine infusion of dextrose tended to have a detrimental effect on CE cure rate, and treatment did not have an effect on first-service conception rate and early embryonic mortality. A multivariable Cox’s proportional hazard model was performed to evaluate the effect of several variables on reproductive performance; the variables RP, CE, parity, anovulation, and the interaction term between parity and anovulation were associated with hazard of pregnancy. Cows that did not have RP or CE were more likely to conceive than cows that were diagnosed with RP or CE. Cows that had RP were at 3.36 times higher odds of losing their pregnancy than cows that did not have RP. In addition, cows diagnosed with CE were at 2.16 higher odds of losing their pregnancy than cows without CE. In conclusion, intrauterine infusion of 200mL of 50% dextrose solution as a treatment for CE had a strong statistical tendency to decrease CE cure rate, did not improve first-service conception rate and early embryonic mortality, and did not decrease calving-to-conception interval.

Risk factors for the development of hypokalemia in neonatal diarrheic calves.

BackgroundNeonatal diarrheic calves have a clear negative potassium balance because of intestinal losses and decreased milk intake but in the presence of acidemia, they usually show normokalemic or hyperkalemic plasma concentrations.ObjectivesTo assess whether marked hypokalemia occurs in response to the correction of acidemia and dehydration and to identify factors that are associated with this condition.AnimalsEighty‐three calves with a clinical diagnosis of neonatal diarrhea.MethodsProspective cohort study. Calves were treated according to a clinical protocol using an oral electrolyte solution and commercially available packages of 8.4% sodium bicarbonate, 0.9% saline and 40% dextrose infusion solutions.ResultsThe proportion of hypokalemic calves after 24 hours of treatment (19.3%) was twice as great as it was on admission to the hospital. Plasma K+ after 24 hours of treatment was not significantly correlated to venous blood pH values at the same time but positively correlated to venous blood pH values on admission (r = 0.51, P < .001). Base excess on admission (Odds ratio [OR] = 0.81, 95% confidence interval [CI] = 0.70–0.94), duration of diarrhea (OR = 1.37, 95% CI = 1.05–1.80), milk intake during hospitalization (OR = 0.54, 95% CI = 0.37–0.79) and plasma sodium concentrations after 24 hours (OR = 1.12, 95% CI = 1.01–1.25) were identified to be independently associated (P < .05) with a hypokalemic state after 24 hours of treatment.Conclusions and Clinical ImportanceFindings of this study suggest that marked depletion of body potassium stores is evident in diarrheic calves that suffered from marked metabolic acidosis, have a low milk intake and a long history of diarrhea.

Life-Threatening Metabolic Coma Caused by Levofloxacin

Patients with diabetes mellitus are often susceptible to hypoglycemic episodes while on therapy. Most of these are attributed to inappropriate dosing of hypoglycemic agents, dietary indiscretion, or acute illness. Medications being used concomitantly should be reviewed closely when the etiology of hypoglycemia is unclear. A fifty-six-year-old woman with a history of diabetes mellitus (on metformin monotherapy) was found unresponsive at home. Her fingerstick glucose was 15 mg/dL for which she received 50% dextrose intravenously. The patient never had any previous documented hypoglycemic episodes. She had recently been diagnosed with pneumonia and was prescribed oral levofloxacin therapy. The patient had taken 4 doses of levofloxacin before the onset of hypoglycemia. These episodes recurred over the next 2 days needing close intensive care unit monitoring, dextrose infusion, and glucagon administration. Basic blood/urine investigations, cortisol and thyroid profile were normal except for low blood glucose and renal insufficiency (serum creatinine 1.4 mg/dL and creatinine clearance 42 mL/min). HbA1c was 6.8% (4.4%-6.4%), insulin 51.3 μU/mL (2.6-24.9 μU/mL), IGF-1 301 ng/mL (27-223 ng/mL), and C peptide 9.3 ng/mL (0.8-3.5 ng/mL). These levels were elevated but were deemed nondiagnostic because of fluctuating glucose values after glucagon administration. A blood screen for sulfonylureas and metaglinides was negative. A seventy-two-hour fast was performed to rule out hyperinsulinemic hypoglycemic syndromes; however, blood glucose values remained consistently above 120 mg/dL during this period. Thus, after exclusion of other causes, we utilized the adverse drug reaction probability scale and concluded that hypoglycemia was probably related to recent use of levofloxacin.

The effects of TNF-α on GLP-1-stimulated plasma glucose kinetics.

Glucagon-like peptide-1 (GLP-1) analogs have recently been promoted as antihyperglycemic agents in critically ill patients with systemic inflammation, but the effects of TNF-α on glucose metabolism during GLP-1 administration are unknown. The objective of the study was to determine whether the infusion of TNF-α at high physiological levels impairs GLP-1's effects on glucose metabolism. This was a randomized, controlled, cross-over trial. The study was conducted at a hospital clinical research laboratory. Twelve healthy males (aged 24 ± 3 y; body mass index 22.9 ± 1.3 kg/m(2)). After an overnight fast, either saline (0.9%) or recombinant human TNF-α (1000 ng/m(2) · h) was infused from t = 0-6 hours. At t = 2 hours, GLP-1 infusion (0.5 pmol/kg · min) began. From t = 4-6 hours, the GLP-1 infusion rate was increased to 1.2 pmol/kg · min. Plasma glucose was clamped at 5 mmol/L throughout via a variable rate 20% dextrose infusion. Trials were 7-14 days apart. Endogenous glucose production (EGP) was measured by the [6,6-(2)H2]glucose isotope tracer dilution method. GLP-1 infusion suppressed plasma glucagon (P < .01), elevated plasma insulin, and C-peptide (P < .01) and suppressed EGP (P < .001) during the saline infusion. In contrast, the infusion of TNF-α increased plasma TNF-α and IL-6, elevated body temperature, and blunted the GLP-1-induced suppression of EGP during high-dose GLP-1 infusion (all P < .05, TNF-α vs saline). However, TNF-α infusion lowered plasma GLP-1 during high-dose GLP-1 infusion (P < .001). TNF-α induces systemic inflammation and reduces plasma GLP-1, thereby reducing the suppression of EGP during GLP-1 infusion. This may have clinical relevance if GLP-1 analog drugs are used for the treatment of hyperglycemia in critically ill patients.

Effects of alkalinization and rehydration on plasma potassium concentrations in neonatal calves with diarrhea.

BackgroundIncreased plasma potassium concentrations (K+) in neonatal calves with diarrhea are associated with acidemia and severe clinical dehydration and are therefore usually corrected by intravenous administration of fluids containing sodium bicarbonate.ObjectivesTo identify clinical and laboratory variables that are associated with changes of plasma K+ during the course of treatment and to document the plasma potassium‐lowering effect of hypertonic (8.4%) sodium bicarbonate solutions.AnimalsSeventy‐one neonatal diarrheic calves.MethodsProspective cohort study. Calves were treated according to a clinical protocol using an oral electrolyte solution and commercially available packages of 8.4% sodium bicarbonate (250–750 mmol), 0.9% saline (5–10 L), and 40% dextrose (0.5 L) infusion solutions.ResultsInfusions with 8.4% sodium bicarbonate solutions in an amount of 250–750 mmol had an immediate and sustained plasma potassium‐lowering effect. One hour after the end of such infusions or the start of a sodium bicarbonate containing constant drip infusion, changes of plasma K+ were most closely correlated to changes of venous blood pH, plasma sodium concentrations and plasma volume (r = −0.73, −0.57, −0.53; P < .001). Changes of plasma K+ during the subsequent 23 hours were associated with changes of venous blood pH, clinical hydration status (enophthalmos) and serum creatinine concentrations (r = −0.71, 0.63, 0.62; P < .001).Conclusions and Clinical ImportanceThis study emphasizes the importance of alkalinization and the correction of dehydration in the treatment of hyperkalemia in neonatal calves with diarrhea.

The highest (3600 IU) reported overdose of insulin glargine ever and management.

Sir, Insulin glargine (LANTUS® SOLOSTAR®; Sanofi Aventis, Deutschland) – relatively a new medication in the treatment of diabetes mellitus – is a long-acting insulin for meeting the basal insulin requirement with an ongoing effect up to 24 h.[1,2] In literature, there are small number of cases regarding with overdose use of insulin glargine. One of these cases with regard to insulin glargine overdose was by Lu and Inboriboon, who had reported a case of suicide attempt with 2700 units of insulin glargine resulting 96 h of hypoglycemia.[3] Herein, we report another case of insulin glargine overdose resulting 120 h of hypoglycemia in a diabetic patient who had attempted suicide with 3600 units of insulin glargine. To our knowledge, this is the highest reported insulin glargine dose ever. In this present case, a 45-year-old-male patient with type-2 diabetes mellitus and major depression was admitted to emergency department with the loss of consciousness after self-administered 3600 units of insulin glargine. Patient's laboratory findings on admission were as follows: Blood glucose level - 20 mg/dl, potassium - 2,8 mmol/L, serum level of sulfonylurea - 0,0 mg/μL, C-peptide - 0.0956 (0.51–2.7 ng/mL normally), and serum insulin value - 216 mU/L (2.6–25 normally). Patient treated with continuous intravenous dextrose infusion and 1 mg of glucagon hydrochloride. On follow-up, the patient needed 120 h of intravenous glucose infusion for the recurrent hypoglycemic episodes. At the end of the 5th day, no hypoglycemia attack was observed. The patient discharged without any permanent complications on the 6th day of hospitalization. Then, he referred to a psychiatry clinic. Hypoglycemia is the most frequent side effect of insulin glargine. The timing of hypoglycemia and its duration differs according to the insulin formulations. Insulin glargine is known to have no peak effect. The plasma concentration versus time profile of insulin glargine is relatively more stable with no peak in 24 h compared to conventional human insulin.[4,5] This allows once-daily administration as basal therapy. However, overdose use of insulin glargine may rarely present with prolonged hypoglycemia attacks.[3] As a result, we aimed to emphasize in this letter that emergency and intensive care physicians should be aware of overdose use of insulin glargine present with prolonged hypoglycemia attacks. In these cases, intensive care physicians should immediately initiate continuous dextrose infusions, and the patients should be monitored closely with frequent blood glucose samples to prevent the risk of prolonged hypoglycemia episodes. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

A case of recurrent hypoglycemia in pregnancy

A 33-year-old female who was 34 weeks into her third pregnancy with no previous medical illness developed giddiness and loss of consciousness and was hospitalized. Her capillary blood glucose was found to be 20 mg%. She fully regained her consciousness after 25% dextrose infusion. Over the next 24 h, she developed three more episodes and was similarly treated. After the fourth episode, she deteriorated and in spite of supportive measures expired th week of pregnancy had showed a hypoglycemic tendency. The combination of raised TLC, suggesting an acute bacterial infection, together with the underlying silent chronic kidney disease probably resulted in severe and recurrent hypoglycemia. This case underlines the need to do serum creatinine as part of a routine antenatal check-up.

Persistent Hypoglycemia in Patient with Hodgkin's Disease.

Hypoglycemia is a rare complication of Hodgkin's disease. Several explanations have been postulated but the exact pathophysiology is not well understood. We are presenting a case of newly diagnosed Stage IV Hodgkin's disease that developed persistent and recurrent hypoglycemia despite giving glucagon, repeated 50% dextrose, and D5 and D10 continuous infusion. Hypoglycemia workup showed the C-peptide level to be low. Patient was suspected of having hypoglycemia related to lymphoma and was given a trial of prednisone which resolved the hypoglycemic episodes and made the patient euglycemic for the rest of his hospital stay. The presence of a substance that mimicked the effects of insulin was highly suspected. Several case reports strengthen the hypothesis of an insulin-like growth factor or antibodies secreted by the cancer cells causing hypoglycemia in Hodgkin's disease but none of them have been confirmed. Further investigation is warranted to more clearly define the pathophysiology of persistent hypoglycemia in patients with Hodgkin's disease.