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Prednisone and reactive hypoglycemia. Case Reports in Endocrinology |
Drug-induced low blood sugar: MedlinePlus Medical Encyclopedia - Alternative Names
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❿Low Blood Sugar (Hypoglycemia) | UVA Health.
Prednisone and reactive hypoglycemia.
The condition may also occur when someone without diabetes takes a medicine used to treat diabetes. In rare cases, non-diabetes-related medicines can cause low blood sugar. Management of patients with diabetes in the intensive care unit. Critical Care Nephrology. Philadelphia, PA: Elsevier; chap Anti-insulin antibodies and the measurement of sulfonylureas in urine were both negative. These results supported the diagnosis of adrenal insufficiency.
A careful medical history found that for over 10 years the patient had been using a cream containing 0. On subsequent outpatient follow-up and while the patient continued to receive replacement therapy with hydrocortisone 20 mg daily, normalization occurred in ACTH The patient had not received hormone blockade therapy. Steroid treatment suppresses the production of corticotropic hormone and ACTH, decreasing adrenal cortisol synthesis and causing adrenal gland atrophy.
Adrenal insufficiency is an uncommon cause of clinically relevant hypoglycemic in adults, and very few cases have been reported. Cortisol deficiency therefore promotes mild fasting hypoglycemia which, however, only tends to occur in metabolic stress situations, especially during infectious processes.
Several causative factors are frequently associated, and the exact mechanism of hypoglycemia is difficult to establish. In the reported case, the final diagnosis was iatrogenic, secondary adrenal insufficiency caused by the suppression of the hypothalamic—pituitary—adrenal axis by chronic treatment with topical glucocorticoids. Sudden glucocorticoid withdrawal at a time of high metabolic stress triggered the occurrence of an adrenal crisis of which hypoglycemia was the initial manifestation.
Potential factors considered to be involved in the development of hypoglycemia included infection, quinolone treatment, malnutrition, and exacerbated chronic renal failure, which completed the complex underlying pathogenesis. The authors state no conflicts of interest. Endocrinol Nutr. ISSN: Previous article Next article. Issue 9. Pages ee22 November More article options. DOI: Diabetes Care 1 September ; 36 9 : — The metabolic effects of low-dose prednisolone and optimal management of glucocorticoid-induced diabetes are poorly characterized.
The aims were to investigate the acute effects of low-dose prednisolone on carbohydrate metabolism and whether long-term low-dose prednisolone administration increases visceral adiposity, amplifying metabolic perturbations. Subjects with inflammatory rheumatologic disease without diabetes mellitus were recruited. Basal endogenous glucose production EGP was estimated by 6,6- 2 H 2 glucose infusion, insulin sensitivity was estimated by two-step hyperinsulinemic-euglycemic clamp, insulin secretion was estimated by intravenous glucose tolerance test, and adipose tissue areas were estimated by computed tomography.
Prednisolone acutely increased basal EGP 2. Low-dose prednisolone acutely perturbs all aspects of carbohydrate metabolism. Long-term low-dose prednisolone induces hepatic insulin resistance and reduces peripheral nonoxidative glucose disposal. We conclude that hepatic and peripheral insulin sensitivity should be targeted by glucose-lowering therapy for glucocorticoid-induced diabetes. Glucocorticoids GCs are potent anti-inflammatory agents that are commonly used to treat a broad range of inflammatory and autoimmune conditions.
Despite the advent of disease-modifying antirheumatologic drugs and biologic therapies, long-term GC prescription rates are still increasing 1. The acute effects of high-dose GCs on carbohydrate metabolism have been extensively investigated. High-dose GCs cause peripheral tissue insulin resistance 3 , because they reduce both oxidative and nonoxidative glucose disposal 4. The effects of high-dose GCs on endogenous glucose production EGP and hepatic insulin sensitivity are less clear, but a number of studies report a deleterious effect 3 , 5 , 6.
High-dose GCs also acutely reduce insulin secretion 7 , 8 , which will contribute to their hyperglycemic effect. There are fewer data regarding the metabolic consequences of typical long-term lower GC doses, which are generally considered to be modest 9 — Furthermore, which components of carbohydrate metabolism are perturbed by low-dose GCs is not clear.
We recently reported that older patients with inflammatory rheumatologic disease using long-term low-dose prednisolone had a higher postglucose load plasma glucose concentration but a slightly lower fasting plasma glucose concentration than matched controls not using prednisolone Our finding of a lower fasting plasma glucose concentration suggests that basal EGP was not increased in subjects using low-dose prednisolone.
This is consistent with a previous study by van Raalte et al. However, van Raalte et al. The effects of GCs on carbohydrate metabolism predominantly have been studied after short courses in healthy young adults.
Findings in younger patients may not be translatable to older patients in whom increased visceral adiposity is likely to increase susceptibility to the diabetogenic effects of GCs In addition, long-term GC therapy may further increase visceral adiposity and enhance the effects of GCs on carbohydrate metabolism 15 , The aim of this study was to investigate the acute effects of low-dose prednisolone on carbohydrate metabolism in an older population typical of patients for whom prednisolone is most frequently prescribed.
An additional aim was to assess whether there is an increase in visceral adiposity that further amplifies metabolic perturbations during long-term low-dose prednisolone administration. This information will provide a foundation for future studies targeting therapy for GC-induced hyperglycemia at the major metabolic abnormalities induced by low-dose prednisolone.
Subjects aged 40 years or older with inflammatory rheumatologic disease were recruited from the outpatient clinic of our institution. The two groups were matched for sex, age, BMI, inflammatory disease activity assessed by C-reactive protein and physical activity assessed by modified Baecke physical activity score Undiagnosed diabetes mellitus was excluded at a screening visit with an oral glucose tolerance test.
One subject in the GC users group was omitted from the EGP and rate of glucose disposal Rd analysis because of a technical problem with the basal 6,6- 2 H 2 glucose infusion.
To determine the acute effects of prednisolone, non-GC users were studied before and after a 7- to day course of oral prednisolone 6 mg daily. To assess the long-term effects of prednisolone, baseline data from non-GC users were compared with baseline data from the matched GC users. Carbohydrate metabolism and body composition were assessed using a standardized 2-day protocol.
At each visit, subjects presented to the Endocrine Research Unit of the Repatriation General Hospital at h after an overnight fast. The day 1 study protocol involved assessment of basal EGP, followed by a two-step hyperinsulinemic-euglycemic clamp study. On day 2, subjects underwent a frequently sampled intravenous glucose tolerance test, dual-energy X-ray absorptiometry scan, and abdominal computed tomography CT scan. Subjects were asked to refrain from alcohol and exercise for 2 days before the study visits, and no subject smoked during study visits.
Subjects consumed all regular medications with water in the morning before the study visits, including their prescribed prednisolone dose. An intravenous cannula was inserted into the antecubital fossa of one arm for administration of infusions. A distally sited cannula was inserted into the contralateral arm for blood sampling and was heated for the duration of the study to achieve arterialization of venous blood.
Steady state was defined as 90 to min after completion of the priming bolus. A two-step hyperinsulinemic-euglycemic clamp study followed immediately. Blood samples were drawn every 5 to 10 min to titrate the variable glucose infusion and steady state was defined as the last 30 min of each step of the clamp study. EGP was calculated using the Steele equation 18 as modified by Finegood et al.
The calculations accounted for the background natural abundance of 13 C and other isomers with the same gas chromatography—mass spectrometry retention time and mass as 6,6- 2 H 2 glucose. Early initiation of hydrocortisone should be considered in cases of refractory hypoglycemia secondary to overdose of long-acting insulin products to prevent unnecessary interventions, decrease IV fluid requirements, and reduce the risks associated with prolonged hypoglycemia.
Jermendy, D. Erdesz, L. Nagy et al. Miller, L. Phillips, D. Ziemer, D. Gallina, C. Cook, and I. Stargardt, L. Gonder-Frederick, K. Krobot, and C. Arem and W. Heinemann, R. Linkeschova, K. Rave, B. Hompesch, M. Sedlak, and T. Rasmussen, E. Mosekilde, and M. Shibutani and C. Tofade and E. Suppl 1, pp. S66—S76, Umpierrez, R. Hellman, M.
Korytkowski et al. Call Schedule Online. Causes of Hypoglycemia Medications for diabetes are the most common cause, particularly when combined with the following factors: Taking too much blood sugar-lowering medication Delaying or missing meals or eating too little at meals Too much or too strenuous exercise Although rare, reactive hypoglycemia may also occur in people without diabetes.
Other causes of hypoglycemia include: Alcohol abuse, especially binge drinking coupled with not eating Starvation Early pregnancy Certain pituitary or adrenal gland conditions Certain liver conditions Kidney disease Certain types of stomach surgery Tumor that makes insulin Hereditary enzyme or hormone deficiencies Severe illness or infection Are You at Risk?
Factors that may increase your chance of hypoglycemia include: Having diabetes Taking medications that lower blood sugar levels Drinking too much alcohol Fasting, particularly in combination with strenuous exercise Symptoms Symptoms may come on slowly or suddenly and may cause: Sweating Nervousness Lightheadedness Heart palpitations Hunger Headache Tingling feeling around the mouth As hypoglycemia worsens, it may cause: Fatigue Weakness Inappropriate behavior or severe confusion Poor control of movements Seizure Loss of consciousness If you have frequent hypoglycemia, you may lose many of the early symptoms and be at particular risk of sudden loss of consciousness, seizure or bizarre behavior.
Diagnosing Hypoglycemia Your doctor will try to document your low blood sugar and measure your blood glucose levels while you're having symptoms. Treatment Talk with your doctor about the best treatment plan for you.
Glucose is a type of sugar your body uses as a main source of energy. Hypoglycemia is a condition where the level of glucose in your blood becomes low enough to cause symptoms. When blood glucose drops too low, your body does not have enough energy to function properly.
Medications for diabetes are the most common cause, particularly when combined with the following factors:. If you have frequent hypoglycemia, you may lose many of the early symptoms and be at particular risk of sudden loss of consciousness, seizure or bizarre behavior.
This could affect your ability to operate machinery or a motor vehicle. Your doctor will try to document your low blood sugar and measure your blood glucose levels while you're having symptoms. If you don't have diabetes, and you don't take medications that lower your blood sugar levels, your doctor may do other tests to see if and why you're having low blood sugar levels.
These tests may include checking your blood levels after periods of not eating. Some people who have prolonged or severe hypoglycemia take glucagon. Glucagon is an injectable hormone that raises blood sugar levels. Edits to original content made by Rector and Visitors of the University of Virginia. This information is not a substitute for professional medical advice. In This Section. Low Blood Sugar Hypoglycemia.
Make an Appointment. Call Schedule Online. Causes of Hypoglycemia Medications for diabetes are the most common cause, particularly when combined with the following factors: Taking too much blood sugar-lowering medication Delaying or missing meals or eating too little at meals Too much or too strenuous exercise Although rare, reactive hypoglycemia may also occur in people without diabetes. Other causes of hypoglycemia include: Alcohol abuse, especially binge drinking coupled with not eating Starvation Early pregnancy Certain pituitary or adrenal gland conditions Certain liver conditions Kidney disease Certain types of stomach surgery Tumor that makes insulin Hereditary enzyme or hormone deficiencies Severe illness or infection Are You at Risk?
Factors that may increase your chance of hypoglycemia include: Having diabetes Taking medications that lower blood sugar levels Drinking too much alcohol Fasting, particularly in combination with strenuous exercise Symptoms Symptoms may come on slowly or suddenly and may cause: Sweating Nervousness Lightheadedness Heart palpitations Hunger Headache Tingling feeling around the mouth As hypoglycemia worsens, it may cause: Fatigue Weakness Inappropriate behavior or severe confusion Poor control of movements Seizure Loss of consciousness If you have frequent hypoglycemia, you may lose many of the early symptoms and be at particular risk of sudden loss of consciousness, seizure or bizarre behavior.
Diagnosing Hypoglycemia Your doctor will try to document your low blood sugar and measure your blood glucose levels while you're having symptoms. Treatment Talk with your doctor about the best treatment plan for you. Options include: Sugar Symptoms of low blood sugar can be relieved quickly by: Eating sugar in a rapidly absorbable form, such as: Fruit juice Sugared soft drink Table sugar in water Honey or corn syrup Taking glucose tablets IV glucose in severe cases Medication Some people who have prolonged or severe hypoglycemia take glucagon.
Surgery Some cases are caused by a tumor, which may need to be removed. Prevention To reduce your chance of hypoglycemia, take these steps: For people with diabetes: Monitor your medication. Take it as prescribed. Follow the diet and exercise plans given by your doctor. Avoid drinking alcohol in excess. Non-diabetic people prone to hypoglycemia: Avoid drinking too much alcohol. Eat frequent, small meals.
Eat enough food before exercising. If you are prone to severe hypoglycemia: Wear a medical alert bracelet or other medical alert identification. Learn to recognize symptoms and take quick corrective measures. Low Blood Sugar Hypoglycemia Specialists. No results.
However, due to their narrow therapeutic window, prolonged use increases the risk of hypoglycemia with short-term steroids, especially where single morning. In this patient with inoperable NICTH, the combination of low doses of prednisone and rhGH was a successful long-term therapy for hypoglycemia, with no AEs. He responded well to prednisone therapy with resolution of hypoglycemia and decline in the insulin autoantibody titers. This study concludes that autoimmune. present with postprandial hypoglycemia, marked neuro- glycopenic symptoms of confusion, treatment of IAS, prednisone therapy was started at 12 mg. Ferrets with severe hypoglycemia may be recumbent or having seizures during Published doses for prednisone in ferrets are to 2 mg/kg PO q12h. Axelrod, A. These tests may include checking your blood levels after periods of not eating. If you are prone to severe hypoglycemia: Wear a medical alert bracelet or other medical alert identification.Overdose of long-acting insulin can cause unpredictable hypoglycemia for prolonged periods of time. Refractory hypoglycemia following these interventions presents a clinical challenge in the absence of clear guidelines for management.
Octreotide has sometimes been used, but its use is generally limited to sulfonylurea overdose. In this case report, we present a case of refractory hypoglycemia following an overdose of units of long-acting insulin glargine that failed to respond to usual modes of therapy mentioned above. Stress-dose corticosteroids were then initiated, followed by subsequent improvement in IV dextrose and glucagon requirements and blood glucose levels.
Hence, corticosteroids may serve as an adjunctive therapy in managing hypoglycemia and can be considered earlier in the course of treatment in patients with refractory hypoglycemia to prevent volume overload, especially when large volumes of dextrose infusions are required.
Insulin is a mainstay of treatment in patients with type 1 diabetes mellitus T1DM , and a significant proportion of patients with type 2 diabetes mellitus T2DM are insulin-dependent [ 1 — 3 ]. At the same time, insulin therapy is associated with multiple adverse effects, with hypoglycemia being one of the most common. For example, in the U. Prospective Diabetes Study, the prevalence of hypoglycemia in patients with T2DM who were taking insulin was However, these prevalences represent usual medication use and do not account for the potential for insulin overdose, either intentional or unintentional.
Management of insulin overdose poses a clinical challenge and may require modified treatment strategies, given the lack of consensus and guidelines. The objective of this report is to describe a case of intentional insulin overdose associated with refractory hypoglycemia and to discuss the integrative approach to managing this case. This represented her third intentional insulin overdose in the preceding six months.
The patient reported suicidal ideation and worsened depression for three months prior to presentation and decided to inject three full insulin glargine U pens units each , which she had at home from her prior insulin prescription.
At that time, she was closely monitored, but not medically treated, and was sent to the ED. Her physical examination upon arrival was unremarkable and did not reveal any areas of fluctuance at the reported injection sites.
A regular diet was started and carbohydrate intake was encouraged. Fingerstick glucose levels were monitored every 15 minutes for the first seven hours and every 30 minutes thereafter. The patient was then transferred to the medical intensive care unit MICU for close observation. She was transitioned from a standard diet to a bariatric diet due to suspected reactive hypoglycemia associated with her postbariatric surgery status, which consisted of 56 grams of carbohydrate and 18 grams of protein per day.
The IV glucagon infusion was weaned off on hospital day four after three additional doses of hydrocortisone on days 3 and 4. Patients who experience an insulin overdose can present with prolonged, refractory hypoglycemia, especially with the administration of long-acting insulin [ 5 ].
Although the duration of action of insulin glargine is reported to be 24 to 30 hours [ 6 ], these parameters were observed with doses of 0. In cases of overdose, the duration of action may be affected by a number of factors, including the route and site of administration, injection volume, solution concentration e. U , local blood supply, and presence of lipodystrophy or cutaneous amyloidosis at the injection site. For example, insulin injections of larger volumes are more slowly absorbed from the subcutaneous space than smaller volumes, which may result in delayed hypoglycemia following the injection [ 8 ].
Other factors, such as the presence of insulin autoantibodies and renal dysfunction, can prolong the duration of hypoglycemia as well. Therefore, it may be difficult to predict the duration of hypoglycemia in cases of insulin overdose. Based on case reports involving insulin overdose, hypoglycemia has been reported up to several days after injection [ 5 , 9 , 10 ]. The initial treatment for hypoglycemia should primarily involve oral carbohydrate ingestion [ 11 ].
This should be accompanied by frequent monitoring of serum glucose levels and electrolytes, especially serum potassium. Continuous infusions of dextrose e. In cases where hypoglycemia persists despite standard treatment modalities, other treatment options can be explored. The somatostatin analog octreotide has been tried in previous cases of insulin overdose [ 13 , 14 ]. However, its use was associated with inconsistent results and is usually reserved for hypoglycemia secondary to sulfonylurea use [ 15 ].
Another uncommon approach to cases of insulin overdose includes excision of the insulin depot at the injection site when clear fluctuance is present. This theoretically can help in preventing delayed absorption of insulin and associated prolonged hypoglycemia and has been utilized successfully in previous cases [ 16 , 17 ].
However, in cases such as the present one where an area of fluctuance is not visible on physical examination, this option is not possible. Another treatment strategy that may be underutilized involves the use of glucocorticoids. These agents promote hepatic gluconeogenesis and decrease peripheral glucose uptake and are frequently associated with hyperglycemia as a result. Hence, glucocorticoids may serve as an adjunctive therapy option in managing refractory hypoglycemia in cases of insulin overdose.
This approach has been utilized in a prior case of refractory hypoglycemia associated with insulin overdose where hydrocortisone was administered to prevent volume overload associated with the infusion of large volumes of dextrose-containing IV fluids [ 14 ]. The initial management of her hypoglycemic episodes followed guideline recommendations, starting with oral carbohydrate ingestion and parenteral dextrose administration [ 11 , 12 ].
One concern raised with this approach was regarding her history of sleeve gastrectomy and that the carbohydrate ingestion could lead to excess endogenous insulin release and subsequent worsening of hypoglycemia symptoms [ 19 ].
Therefore, the decision was made to place her on a high protein, low carbohydrate bariatric diet to help mitigate this potential issue. Adjunctive measures were required due to her persistent hypoglycemia, and she was therefore given IM glucagon injections in addition to oral and parenteral carbohydrates. An IV glucagon infusion was tried as well, which proved ineffective at completely resolving hypoglycemia.
In the setting of persistent hypoglycemia three days after the reported overdose and concern for volume overload, other treatment modalities were considered. Octreotide was not given due to the inconsistent results from previous cases along with its high cost and because sulfonylurea coingestion was not suspected [ 13 , 14 ]. Excision of the insulin depot was not possible in our patient because she did not have a clear site of fluctuance at the injection site.
Consistent with use of hydrocortisone in a previous case report [ 14 ], a trial of stress-dose hydrocortisone was started.
Hydrocortisone was chosen due to its shorter duration of action compared to other glucocorticoids, thereby reducing the risk of subsequent hyperglycemia. Following the administration of four doses of hydrocortisone, she was able to be weaned off both the D10 and glucagon infusions and was able to maintain euglycemia.
There are some important limitations to the present case that should be considered as well. We were unable to obtain the insulin product to verify its identity, and there was no recent prescription history to reconcile since the patient was no longer on insulin. However, given the timeline of events and the intensive medical therapy that she required, it seems reasonable to assume that long-acting insulin with adequate potency was used.
We did not rule out other secondary causes of hypoglycemia, such as postprandial hyperinsulinemic hypoglycemia associated with bariatric surgery. However, this is more commonly associated with Roux-en-Y gastric bypass than sleeve gastrectomy and was thought to be more likely associated with the insulin overdose in the present case given the temporal association with insulin administration [ 19 ].
Given the prior cases involving the use of glucocorticoids for insulin-induced hypoglycemia, we felt that the administration of hydrocortisone contributed towards the resolution of hypoglycemia and reduced the continued need for parenteral dextrose and glucagon in the present case. However, given the delay in the administration of hydrocortisone until three days after presentation, it is also possible that the hypoglycemia resolved due to the clearance of the exogenous insulin, as opposed to the effect of glucocorticoid administration.
Finally, while the efficacy of IV glucagon infusion is more established in pediatrics with T1DM and in neonatal hypoglycemia, the efficacy of continuous infusions of IV glucagon for the treatment of insulin-induced hypoglycemia in adults is unclear given the absence of strong supporting evidence in this population [ 14 , 20 , 21 ].
Glucagon acts by promoting glycogenolysis and gluconeogenesis and thus has limited use once glycogen stores have been depleted. On the other hand, insulin itself promotes the conversion of glucose to glycogen for storage in the liver.
These previous overdoses were managed successfully with IV glucagon infusions; therefore, it was reasonable to attempt the use of an IV glucagon infusion for persistent hypoglycemia during the present case. However, her prior suicide attempts involved much smaller doses of insulin, which may explain why the IV glucagon infusion alone failed to resolve hypoglycemia in the present case, thereby requiring hydrocortisone administration.
Insulin overdose often requires intensive care admission and frequent monitoring of blood glucose and electrolytes. Prolonged continuous D10 IV infusions can lead to volume overload, and parenteral administration of higher concentrations of dextrose e. This case adds to the literature supporting the use of glucocorticoids in the management of refractory hypoglycemia associated with overdoses of long-acting insulin.
Additionally, this case involved a patient who was not being treated for diabetes mellitus following sleeve gastrectomy and could be extrapolated to such patients. Early initiation of hydrocortisone should be considered in cases of refractory hypoglycemia secondary to overdose of long-acting insulin products to prevent unnecessary interventions, decrease IV fluid requirements, and reduce the risks associated with prolonged hypoglycemia.
Jermendy, D. Erdesz, L. Nagy et al. Miller, L. Phillips, D. Ziemer, D. Gallina, C. Cook, and I. Stargardt, L. Gonder-Frederick, K. Krobot, and C. Arem and W. Heinemann, R.
Linkeschova, K. Rave, B. Hompesch, M. Sedlak, and T. Rasmussen, E. Mosekilde, and M. Shibutani and C. Tofade and E. Suppl 1, pp. S66—S76, Umpierrez, R. Hellman, M. Korytkowski et al. Groth and E. Tariq, S.
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