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
