HistoryThis section has been translated automatically.
The Somogyi effect was first described in 1959 by the Hungarian Michael Somogyi, after whom it was named (Somogyi 1959).
DefinitionThis section has been translated automatically.
A Somogyi effect is a reactive hyperglycemia in diabetics as a hormonal counter-regulation after nocturnal hypoglycemia (Kolossa 2014).
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OccurrenceThis section has been translated automatically.
The Somogyi effect occurs only very rarely (Howorka1988). It mainly affects children and adolescents with a pronounced hormonal diurnal rhythm (Hien 2007).
In addition to the Somogyi effect, the Dawn phenomenon can also occur on different days in one and the same diabetic (Kolossa 2014).
EtiologyThis section has been translated automatically.
In the Somogyi effect, an excessive evening insulin dose induces nocturnal hypoglycemia, which then leads to reactive morning hyperglycemia (Herold 2020).
PathophysiologyThis section has been translated automatically.
In the Somogyi effect, hypoglycaemia leads to a rise in blood glucose as part of a hormonal counter-reaction, which also leads to insulin resistance (Mehnert 2003).
Clinical pictureThis section has been translated automatically.
Nocturnal hypoglycaemia can cause nightmares and night sweats.
In children, however, nocturnal hypoglycaemia is completely asymptomatic in up to 20% of cases (Hien 2007).
A Somogyi effect may be suspected if, in addition to morning hyperglycaemia, headaches, fatigue (Reinhardt 2004) and night sweats are also present (Wehling 2006).
DiagnosticsThis section has been translated automatically.
The diagnosis is made by several nocturnal BG checks, a fasting BG check and urine sticks for ketones (Hien 2007).
In the case of morning hyperglycaemia triggered by the Somogyi effect, these checks should be carried out between 3 - 4 h (Herold 2020), as the greatest insulin effectiveness occurs between 0.00 h and 3.00 h (Hien 2007).
In the Somogyi effect, BG can be low at night and high in the morning (Reinhardt 2004), but much more often BG is also low or normal in the morning. In these cases, the BG rises only postprandially, even though she has consumed the prescribed BE and the required insulin dose has been maintained (Hien 2007).
Positive urine stix for ketones is suggestive of nocturnal hypoglycemia (Hien 2007).
CGM
The Somogyi effect can mask a Dawn phenomenon. Continuous tissue glucose monitoring (CGM) should be used to differentiate (Kolossa 2014).
LaboratoryThis section has been translated automatically.
Typical for nocturnal hypoglycemia is a positive detection of ketones in the (glucose-free) morning urine (Hien 2007).
Differential diagnosisThis section has been translated automatically.
- Dawn Phenomenon (Herald 2020)
TherapyThis section has been translated automatically.
Patients who have already experienced nocturnal hypoglycemia should not have a BG < 120 mg / dl before bedtime. If this is the case, the patient is recommended to take 2 - 3 BE. To avoid further occurrences of this type, the evening insulin dose should be reduced (Herold 2020).
Hien (2007) recommends reducing the evening NPH dose or switching to an analog insulin that does not show the typical nocturnal peak effect of NPH.
PrognoseThis section has been translated automatically.
In rare cases, the evening insulin dose may no longer be sufficient for the Dawn phase. In this case, it is recommended to leave the dose of the NPH late injection and to consume long-acting, resorption-delayed carbohydrates such as wholemeal bread with butter, wholemeal cookies with cottage cheese, crackers with cheese shortly before bedtime (Hien 2007).
Note(s)This section has been translated automatically.
Recent studies conducted at Washington University School of Medicine suggest that diabetics with nocturnal hypoglycemias have hypo- rather than hyperglycemia in the morning.
Nocturnal hypoglycemias do not lead to hyperglycemia the following day. No correlation has been found between elevated glucose levels and counter-regulatory hormones such as epinephrine, cortisol, glucagon, and growth hormones.
This would disprove the Somogyi effect (Reyhanoglu 2021).
LiteratureThis section has been translated automatically.
- Herold G et al (2020) Internal medicine. Herold Publishers 738
- Hien et al (2007) Diabetes- Handbuch: a guide for practice and clinic. Springer Verlag Heidelberg 167 - 168
- Howorka K (1988) Functional, near-normoglycemic insulin substitution. Springer Verlag Heidelberg 105 - 106
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 2412
- Kolossa R (2014) Insulin pump therapy. Diabetologist (10) 472 - 476. doi 10.1007/s11428-013-1148-6.
Mehnert H et al (2003) Diabetology in clinic and practice. Georg Thieme Verlag Stuttgart 327
- Reinhardt D (2004) Therapy of diseases in childhood and adolescence. Springer Verlag Berlin / Heidelberg 94, 153
- Reyhanoglu G et al (2021) Somogyi Phenomenon. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. PMID: 31855369, Bookshelf ID: NBK551525.
- Somogyi M (1959) Exacerbation of diabetes by excess insulin action. The American Journal of Medicine 26 (2) 169 - 191.
- Wehling M et al (2006) Clinical pharmacology. Georg Thieme Verlag Stuttgart / New York 273, 275
