Zusammenfassung
Während der Stillzeit kommt es über die Muttermilch zur Übertragung einer substanziellen
Menge von Kalzium von Mutter zu Kind. Aufgrund des physiologischen, hyperprolaktinämischen
Östrogenmangels und sekundärer Amenorrhö während der Laktationsphase kann der Körper
diesen Kalziumverlust nur zum Teil durch kompensatorische Mechanismen ausgleichen.
Jede Wöchnerin nimmt mit der Entscheidung, ob und wie lange sie ihr Kind stillt, aktiv
Einfluss auf den eigenen Knochenstoffwechsel. Die Mobilisation von Kalzium aus dem
maternalen Skelett während der Stillzeit ist deutlich variabler als während der Schwangerschaft.
Bei einer Stillzeit von 6 Monaten würde das mütterliche Skelett schätzungsweise 4
- 6 % an Knochenmineraldichte verlieren. Dieser Knochendichteverlust geht typischerweise
mit einem Abfall der biochemischen Laborparameter der Knochenformation (Osteocalcin,
knochenspezifische alkalische Phosphatase) sowie einem Anstieg der Marker der Knochenresorption
(N-Telopeptid, Desoxpyridinoline DPD und Hydroxyprolin-Ausscheidung im Urin) einher.
Eine prolongierte Stillzeit kann in Abhängigkeit von der Ausgangsknochendichte zu
einem deutlich stärker ausgeprägten Knochendichteverlust führen. Die genauen Mechanismen,
die den in einer verlängerten Laktationsperiode deutlich stärker ausgeprägten Knochendichteabfall
wieder ausgleichen, sind zurzeit völlig unbekannt. Eine besondere Rolle im Knochenstoffwechselumsatz
in der Stillzeit könnte das Parathormon verwandte Protein (PTHrP) spielen, das im
laktierenden Mammagewebe nachgewiesen werden konnte. Mit dem Abstillen und dem Wiedereinsetzen
der Menstruation folgt eine Erholungsphase mit erneutem Anstieg der Knochendichte
und einem Anstieg der Marker der Knochenformation sowie einem Abfall der Marker der
Knochenresorption. Das genauere Verständnis der physiologischen Zusammenhänge des
Knochenstoffwechsels während der Stillzeit, insbesondere die Modulation der Regeneration
des Knochens, könnte auch zu einem besseren Verständnis des Krankheitsbildes Osteoporose
und dem Management von Osteoporose-Patientinnen führen.
Abstract
During lactation calcium is directly transferred from the mother to child by breast
milk. Secondary amenorrhea caused by the elevated prolactin level associated with
a suppression of the hypothalamic-pituitary axis during lactation leads to a substantial
loss of calcium. The increased calcium demand is regulated by renal and intestinal
compensatory mechanisms as well as mobilization of the maternal skeletal depot. Each
puerpera influences the bone metabolism by the duration of breastfeeding or primary
weaning . Thus mobilization of calcium from the maternal skeleton during lactation
is more highly variable than in pregnancy. 6 months of lactation would approximately
lead to a loss of 4 - 6 % of the maternal mineral skeleton. The loss of bone mass
density is accompanied by a decrease of biochemical markers of bone formation (osteocalcin,
bone specific alkaline phosphatase) and by an increase of biochemical markers of bone
resorption (N-telopeptide, deoxypyridinoline [DPD], hydroxyproline excretion). Prolonged
lactation could induce a severe loss of bone mass density dependent on the peak bone
mass. Compensatory mechanisms explaining the increase of calcium availability are
still unknown. Parathyroid hormone-related protein (PTHrP) might have an important
role in calcium metabolism during lactation. PTHrP has been shown to be synthesized
in lactating mammary tissue. Weaning and the time until the return of menses was consistently
associated with the time of bone recovery. This is also demonstrated by a change in
markers of bone formation and resorption. Today the mechanisms associated with both
the rapid bone loss during lactation as well as the rapid recovery of bone that follows
weaning are still unknown. Particularly an understanding of bone mineral recovery
might influence the future treatment of postmenopausal osteoporosis.
Schlüsselwörter
Osteoporose - Stillzeit - Schwangerschaft - Knochendichte - Knochenstoffwechsel
Key words
Osteoporosis - lactation - pregnancy - bone mass density - bone metabolism
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Dr. med. Lars Hellmeyer
Philipps-Universität Marburg
Klinik für Geburtshilfe und Perinatalmedizin
Pilgrimstein 3
35037 Marburg
eMail: Lars.Hellmeyer@t-online.de
