DefinitionThis section has been translated automatically.
Hypoglycaemia factitia is hypoglycaemia artificially induced by injection of insulin or ingestion of sulphonylureas (Herold 2020).
Occurrence/EpidemiologyThis section has been translated automatically.
More women than men are affected, predominantly in the age range of 20 - 40 years, who work almost exclusively in the medical sector (Thomas 2005).
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EtiopathogenesisThis section has been translated automatically.
The causes of hypoglycaemia factitia may be:
- accidental
- psychotic
- suicidal
- criminal (Herold 2020)
Clinical featuresThis section has been translated automatically.
The typical symptoms of hypoglycaemia occur irregularly and independently of food intake (Herold 2020), such as trembling, sweating, restlessness, ravenous hunger (Berlit 2005), diaphoresis, pallor (Kasper 2015). For more details see. Hypoglycemia.
LaboratoryThis section has been translated automatically.
After objectification of hypoglycemia by BG measurement and subsequent stabilization of the patient, the following data should be collected for the diagnosis of hypoglycaemia factitia or the corresponding differential diagnostic diseases:
C-peptide determination in serum
Analysis:
A clear increase is found in:
- insulinoma
- multiple endocrine neoplasia
- diabetes mellitus
- hypoglycaemia factitia due to sulfonylureas (Tiller 2005)
Suppressed in:
- Hypoglycaemia factitia due to insulin (Tiller 2005)
Insulin / Proinsulin
When sulfonylureasare abused, insulin and proinsulin are elevated. It is not uncommon to see an insulin value of > 100 mU / l = 600 pmol / l (Thomas 2005).
Sulfonylurea detection
Negative in: insulinoma, hypoglycaemia factitia due to insulin
Positive in: Hypoglycaemia factitia due to sulfonylureas(Niederau 2021)
Insulin antibody determination
In cases of frequent misuse of insulin, insulin antibodies can sometimes be detected (Thomas 2005).
72 h starvation test
The starvation test is used, among other things, to detect hypoglycemia caused by inadequately high (pro-) insulin release, as can occur, for example, in endogenous hyperinsulinism or insulinoma(Krebs 2018).
Here, serum insulin, blood glucose, insulin / glucose quotient and C- peptide are determined.
Results:
- Insulin and C- peptide show parallel increase in endogenous secretion.
- C-peptide is decreased with exogenous insulin supply (e.g. hypoglycaemia factitia).
- Insulin and C-peptide are elevated when sulfonylureas are taken (e.g., hypoglycaemia factitia).
- Detection of proinsulin i. S. or glibenclamide i. S. in the normal range when taking therapeutic doses of sulfonylureas, elevated in insulinoma (Herold 2020)
Differentiation between insulinoma and hypoglycaemia factitia is possible by determining the sulfonylurea preparation in serum.
Hypoglycaemia factitia caused by insulin can be detected by the suppressed C-peptide value (Thomas 2005).
Differential diagnosisThis section has been translated automatically.
- In non-diabetics:
- Insulinoma
- Epilepsy
- Apoplexy (Herold 2020)
In diabetics:
- Hypoglycemia (etiology see d.)
Complication(s)This section has been translated automatically.
Dementia: Dementia is presumed to occur more frequently in recurrent hypoglycaemia (Herold 2020).
Acute coronary syndrome: Occurs especially in elderly patients > 70 years in the first 10 days after a hypoglycemic coma (Cruz 2020).
Apoplexy: The risk of apoplexy is increased by hypoglycaemia (Cruz 2020).
TherapyThis section has been translated automatically.
Symptomatic therapy of hypoglycaemia factitia depends on the severity of hypoglycaemia:
- 1. a Mild hypoglycemia: The patient should take glucose (= dextrose) orally with an initial dose of 20 - 40 mg orally. Sucrose (= cane or beet sugar) or oligosaccharide drinks (= fruit juices, cola) can also be administered (Kasper 2015) such as:
- Dextrose: 4 platelets of 5 g or 4 teaspoons of 5 g.
- Lump sugar: 6 lumps
- Cola: 200 ml
- Apple juice: 200 ml (Danne 2016).
If the patient is not capable of oral intake because of any concomitant diseases, parenteral treatment with glucose infusion is recommended (Kasper 2015).
- 1. b Severe hypoglycemia: In severe hypoglycemia, 40 ml of 40% glucose should be rapidly injected i. v., followed by an infusion of 5% glucose until a BG of about 200 mg / dl can be achieved.
If i.v. administration is not possible, e.g. because the patient is receiving initial care from a layperson or is reacting aggressively due to hypoglycaemia, 1 mg glucagon can be injected i.m. or s.c. (Herold 2020). This should be done as soon as the patient is able to eat, as glucose can only increase the plasma glucose concentration in the short term (Kasper 2015).
The patient should receive immediate psychiatric follow-up after achieving a stable metabolic state.
Progression/forecastThis section has been translated automatically.
Hypoglycemia-no matter the cause-can lead to coma, seizures, and death if left untreated (Haak 2018).
Note(s)This section has been translated automatically.
Hypoglycemia indicated by sulfonylurea can last for hours and even days. This should be considered in therapeutic measures (Kasper 2015).
LiteratureThis section has been translated automatically.
- Berlit P (2005) Therapielexikon Neurologie. Springer Verlag Heidelberg / Berlin 660
- Cruz P (2020) Inpatient hypoglycemia: the challenge remains. J Diabetes Sci Technol. 14 (3) 560 - 566
- Danne T et al (2016) Compendium of pediatric diabetology. Springer Verlag Berlin / Heidelberg 298
- Haak T et al. (2018) S3 guideline therapy of type 1 diabetes. AWMF Register Number: 057-013
- Herold G et al (2020) Internal medicine. Herold Publishers 511, 748
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 2430 - 2435
- Krebs M (2018) Workup for suspected endogenous hyperinsulinemia: SOP starvation test. J Clin Endocrinol. Stoffw. 11, 61 - 63. https://doi.org/10.1007/s41969-018-0027-6.
- Niederau C et al. (2021) Clinical guide to laboratory diagnostics. Elsevier Ltd. tab 7.9
- Thomas L (2005) Laboratory and diagnosis: indication and evaluation of laboratory findings for medical diagnosis. TH- Books Verlagsgesellschaft mbH Frankfurt / Main 218
- Tiller F W et al. (2005) The clinical laboratory. Ecomed Medizinverlag 149
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