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Der Wachstumshormonmangel (GHD) ist eine seltene, aber wichtige Erkrankung, die das körperliche und psychosoziale Wohlbefinden von Kindern beeinträchtigen kann. In der Pädiatrie gilt es, frühzeitig zu erkennen, zu diagnostizieren und zu behandeln, um langfristige Folgen zu verhindern.

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Was ist Wachstumshormonmangel?

Wachstumshormon (GH) wird im Hypothalamus produziert und vom Hypophysenhinterlappen freigesetzt. Es regt die Leber an, Insulin-ähnliche Wachstumsfaktoren (IGF-1) zu produzieren, die das Knochenwachstum fördern. Bei GHD ist diese hormonelle Kette gestört, was zu einer verzögerten Körpergröße führt.

Risikofaktoren und Ursachen

Kategorie Typische Auslöser

Genetisch Mutationen in GH-Produktionsgenen (z.B. GHRH)

Strahlenexposition Frühgeburtlichkeit, Strahlentherapie für Tumore

Chromosomale Anomalien Turner-Syndrom, Prader-Willi

Hypophysenerkrankungen Tumoren, Knochenbrüche, Traumata

Systemische Erkrankungen Chronische Nierenerkrankung, Leberzirrhose

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Klinische Anzeichen

Körpergröße: Unterhalb der 5-ten Perzentile

Verzögerte Pubertät (bei Mädchen)

Gewichtszunahme: Adipositas bei Kindern mit GHD

Kognitive Symptome: Konzentrationsschwierigkeiten, Lernprobleme

Psychosoziale Belastung: Selbstwertprobleme, soziale Isolation

Diagnostik

Anamnese & körperliche Untersuchung

- Messung von Körpergröße, Gewicht und BMI
- Langitudinale Wachstumskurve (mindestens 2 Jahre)

Laboruntersuchungen

- Serum-IGF-1: niedrige Werte trotz normaler GH-Spiegel deuten auf GHD hin

Stimulationstest

- Einsatz von Medikamenten (Arginin, Clonidin) zur Induktion der GH-Freisetzung

Bildgebung

- MRT der Hypophyse, um Tumoren oder strukturelle Anomalien auszuschließen

Therapie

GH-Therapie

- Subkutane Injektionen, tägliche Dosis (typisch 0,05–0,1 µg/kg)
- Regelmäßige Überwachung von IGF-1 und Wachstum

Nebenwirkungen überwachen

- Ödeme, Gelenkschmerzen, Hyperglykämie

Zusätzliche Maßnahmen

- Ernährungsberatung, psychosoziale Unterstützung

Prognose

Mit adäquater GH-Therapie erreichen die meisten Kinder eine Körpergröße nahe dem Durchschnitt. Frühzeitige Intervention ist entscheidend für ein normales Wachstum und zur Vermeidung von psychischen Belastungen.

Fazit für Pädiatrie-Teams

Früherkennung: Regelmäßiges Monitoring bei Risikopatienten

Interdisziplinäre Zusammenarbeit: Endokrinologen, Radiologen, Psychologen

Patienten- und Familienaufklärung: Langzeitbehandlung verstehen und akzeptieren

Durch einen strukturierten Ansatz können Pädiater das Wachstumshormonmangel-Risiko minimieren und Kindern eine gesunde Entwicklung ermöglichen.
Wachstumshormone spielen eine entscheidende Rolle bei der körperlichen Entwicklung von Kindern und Jugendlichen. Wenn diese Hormone nicht ausreichend produziert werden, kann dies zu einer Reihe von Problemen führen, die sowohl das Wachstum als auch die allgemeine Gesundheit betreffen. In diesem Text werden wir uns zunächst mit dem Mangel an Wachstumshormon bei Kindern beschäftigen, anschließend die Ursachen (Ätiologie) dieses Mangels beleuchten und schließlich praktische Tipps sowie mögliche Risiken erörtern.

Wachstumshormonmangel bei Kindern

Ein Mangel an Wachstumshormon (GH), auch bekannt als Hypopituitarismus, bedeutet, dass der Körper nicht genügend des Hormons produziert, das für die Zellteilung und Knochenentwicklung notwendig ist. Kinder mit GH-Mangel wachsen langsamer als ihre Altersgenossen und erreichen oft ein kleineres endgültiges Körpergewicht. Neben dem offensichtlichen Wachstumsausfall kann es auch zu einer verminderten Muskelmasse, erhöhtem Fettanteil sowie einer verlangsamten Knochendichte kommen.

Die Diagnose erfolgt in der Regel durch Bluttests, bei denen die Konzentration von Insulin-like Growth Factor 1 (IGF-1) gemessen wird. Da IGF-1 direkt vom Wachstumshormon beeinflusst wird, spiegelt ein niedriger Wert häufig einen Mangel wider. Ergänzend kann ein Stimulationstest mit Substanzen wie Clonidin oder Arginin durchgeführt werden, um die Fähigkeit der Hypophyse zu prüfen, GH freizusetzen.

Ätiologie des Wachstumshormonmangels

Die Ursachen für einen Wachstumshormonmangel lassen sich in primäre und sekundäre Formen unterteilen. Bei einer primären Störung liegt das Problem direkt an den Hirnanhangsdrüsen (Hypophysen). Häufige Gründe sind:

Genetische Mutationen – Mutationen im GH-Gen oder in Genen, die die Entwicklung der Hypophyse beeinflussen.

Tumore der Hypophyse – Sowohl gutartige als auch bösartige Tumoren können die Hormonproduktion beeinträchtigen.

Traumatische Verletzungen – Kopfverletzungen oder Operationen im Schädelbereich können die Hirnanhangsdrüse schädigen.

Sekundäre Ursachen, bei denen das Wachstumshormon zwar vorhanden ist, aber nicht wirksam ausgeschüttet wird, umfassen:

Systemische Erkrankungen – Chronische Nierenerkrankungen, Leberzirrhose oder andere schwere Krankheiten können die Hormonproduktion beeinflussen.

Medikamentöse Einflüsse – Einige Medikamente wie Steroide oder bestimmte Chemotherapeutika können die Hypophyse beeinträchtigen.

Ernährungsdefizite – Mangelernährung, insbesondere Proteinmangel, kann die Synthese von Wachstumshormonen verringern.

In vielen Fällen ist die genaue Ursache jedoch nicht eindeutig erkennbar, was die Behandlung erschwert.

Tipps und Risiken

Therapieoptionen

Wachstumshormontherapie – Die häufigste Behandlungsform besteht darin, synthetisches GH zu verabreichen. Dies kann die Wachstumsrate deutlich erhöhen und die Knochendichte verbessern.

Kombination mit anderen Hormonen – In manchen Fällen ist zusätzlich eine Thyroxin- oder Kortikosteroidtherapie notwendig, wenn mehrere Hormonspiegel betroffen sind.

Regelmäßige Kontrolle – Blutwerte, Wachstumskurven und Bildgebung sollten regelmäßig überprüft werden, um die Wirksamkeit der Therapie zu beurteilen.

Praktische Tipps für Eltern

Frühzeitige Diagnose – Bei anhaltend langsamerem Wachstum sollte ein Kinderarzt konsultiert werden.

Ernährung optimieren – Ausgewogene Ernährung mit ausreichendem Protein und Mikronährstoffen unterstützt die Hormonproduktion.

Regelmäßige Bewegung – Körperliche Aktivität fördert nicht nur das allgemeine Wohlbefinden, sondern kann auch die natürliche GH-Freisetzung stimulieren.

Risiken der Therapie

Überdosierung – Zu hohe Dosen können zu Schwellungen, Gelenkschmerzen und in seltenen Fällen zu Herzproblemen führen.

Zuckerstoffwechselstörungen – Wachstumshormon beeinflusst den Glukosestoffwechsel; daher kann es das Risiko für Insulinresistenz erhöhen.

Tumorentwicklung – Obwohl selten, besteht ein erhöhtes Risiko für die Entstehung von Tumoren im Gehirn oder anderen Organen bei langfristiger GH-Behandlung.

Langzeitfolgen

Nach Abschluss der Therapie ist eine kontinuierliche Überwachung wichtig, da das Wachstum in der Regel bis zum Alter von etwa 18 Jahren anhalten kann. Einige Kinder können trotz Therapie noch nicht ihr volles Potenzial erreichen, insbesondere wenn die Behandlung verspätet begonnen wurde oder andere hormonelle Störungen vorliegen.

Fazit

Wachstumshormonmangel bei Kindern ist ein komplexes Problem, das sowohl medizinische als auch psychosoziale Auswirkungen hat. Eine frühzeitige Diagnose und gezielte Therapie können den größten Unterschied machen. Eltern sollten sich bewusst sein, dass die Behandlung nicht ohne Risiken ist und eine sorgfältige Überwachung erfordert. Durch Kombination aus medizinischer Intervention, gesunder Ernährung und regelmäßiger körperlicher Aktivität lassen sich jedoch oft positive Ergebnisse erzielen und das volle Wachstumspotenzial des Kindes erreichen.

Micki Carnarvon, 20 years

Endurance athletes in particular benefit, as testosterone affects stamina just as much as strength. Athletes with optimized testosterone levels are often able to train harder, more frequently, and with fewer injuries. Studies have shown that elevated testosterone levels are directly correlated with improved recovery rates. Besides, the idea that a naturally occurring variation in some women’s bodies is somehow unfair doesn’t mesh with how much we exalt male athletes with unusual abilities.
All volunteers gave written informed consent to participate in the original study including subsequent analysis and publication of the data. Volunteers gave written consent to participation and this included a statement confirming that they had not misused any banned drug or anabolic agent and this was confirmed by finding no abnormal testosterone/LH ratios. One way ANOVA was used to assess the differences in body composition and endocrine profiles between the sports and binary logistical regression to ascertain the characteristic of a given sport compared to the others.). This will require longitudinal transgender athlete case-comparison studies that control for variations in hormonal exposure and involve numerous indices of performance (Table 1). These observations also question the required testosterone suppression time of 12 months for transwomen to be eligible to compete in women’s sport, as most advantages over ciswomen were not negated after 12 months of HRT.|Ideally, these would need to replicate adult male circulating testosterone concentrations for sufficient time in women to investigate the effects on muscle, hemoglobin, bone, and other androgen-sensitive measures that display consistent sex dichotomy in the population. These show that during the first 12 months muscle mass (area) was decreased by 9.4% and hemoglobin levels by 14% in 20 transwomen (M2F transgender) treated with an estrogen-based regimen that reduced circulating testosterone concentrations from the male range to the female range. Conversely, testosterone suppression (using an estrogen-based treatment regimen) in 20 transwomen (M2F transgender) that reduced circulating testosterone levels from adult male range to adult female range led to a 9.4% reduction in muscle mass (measured as cross-sectional area). Nevertheless, there is also evidence that hyperandrogenic women, mostly with PCOS, have increased muscle mass and strength that correlates with mildly increased circulating testosterone in the high-normal female range (36, 47). Whereas numerous genes and environmental factors (including genetics, physical activity, and diet) may contribute to muscle mass, the major cause of the sex difference in muscle mass and strength is the sex difference in circulating testosterone.Age-grade competitive sports records show minimal or no female disadvantage prior to puberty, whereas from the age of male puberty onwards there is a strong and ongoing male advantage. Furthermore, endogenous circulating testosterone has minimal effects on skeletal muscle mass and strength in female mice because of its low levels. "This wide bimodal sex difference in circulating testosterone concentrations and the clear dose-response relationships between circulating testosterone and muscle mass and strength, as well as the hemoglobin level, largely account for the sex differences in athletic performance."|However, analysis of the existing literature demonstrates a large degree of inter-individual and inter-study variability in hormonal changes during exercise. Exercise has significant health-related benefits and it is proposed to increase plasma testosterone concentrations . Thus, maintaining physiological levels of testosterone has significant health benefits. Age, higher body weight, poor nutritional status, stress, sleep deprivation, and alcohol consumption are known physiological factors leading to lower serum testosterone concentrations. The success of 18-year-old Mboma resulted in further debate about the eligibility of DSD athletes to compete in women's sport, with World Athletics President Sebastian Coe saying that WA would continue to monitor the situation. An athlete would be eligible to compete if her testosterone level was below 10 nmol/L, or if she could prove that 'she has an androgen resistance such that she derives no competitive advantage'. Men and women need the proper amount of testosterone to develop and function normally.|All of this reduces the active (free) form of testosterone in the body. The testes produces less testosterone, there are fewer signals from the pituitary telling the testes to make testosterone. The ovaries of women with PCOS contain multiple cysts. Having too much naturally-occurring testosterone is not a common problem among men. Testosterone levels are too carefully controlled by the brain for that to occur. But having high cholesterol doesn't mean your testosterone will be high. If you thought testosterone was only important in men, you'd be mistaken.|This further supports the key interpretation that the biological effects of exogenous or endogenous testosterone are the same at comparable circulating levels. Male sexual function is maintained by endogenous testosterone at adult male circulating concentrations. Table 1 (25–36) summarizes data from appropriate reported studies using mass spectrometry–based methods to measure serum testosterone in healthy men and women. Using LC-MS measurement, circulating testosterone in adults has a strikingly nonoverlapping bimodal distribution with wide and complete separation between men and women. Prior to puberty, levels of circulating testosterone as determined by LC-MS are the same in boys and girls (16). A reliable threshold for circulating testosterone must be set using measurement by the reference method of liquid chromatography–mass spectrometry (LC-MS) rather than using one of the various available commercial testosterone immunoassays. Separate male and female events in sports is a dominant form of classification that is superimposed on other graduated age group and weight classifications (e.g., in weightlifting, power lifting, wrestling, boxing, rowing), which reflect differences in strength, power, and speed to ensure fairness in terms of opportunity to win and, additionally, safety in contact sports.}
Remember, a holistic approach that includes proper sleep, nutrition, and stress management will contribute to sustained well-being and improved athletic performance. It’s crucial to balance intense exercise with adequate rest to prevent negative impacts on your hormonal balance. Limit alcohol consumption, as excessive intake can impair testosterone production. Avoid overtraining to prevent testosterone depletion, adding rest days in your routine. Maintain a balanced diet rich in healthy fats, proteins, and micronutrients (e.g., vitamin D and zinc) to support hormone synthesis. Prioritize adequate sleep, as quality rest is essential for hormone production, with a target of 7-9 hours per night. Tackle HIIT sessions with short, intense bursts followed by rest periods for effective hormone stimulation.
Over-the-counter analgesics, such as nonsteroidal anti-inflammatory drugs and acetaminophen, may decrease testosterone levels, suggesting cautious use. Sports performance is linked closely to testosterone level, prompting athletes to explore legal and illegal ways to boost testosterone. InterACT, an intersex youth advocacy organization, argued that the policy forces all women to surrender private genetic information and that any framework targeting transgender athletes will also inevitably affect intersex women.
Boys and girls demonstrate differences in a range of physical characteristics, including body composition and skinfold thickness , height, and explosive strength, even before puberty , suggesting that sex chromosome composition plays a role in determining differences in adult athletic performance. The policy, by its admission, is based on a "hypothetical cross-over scenario in which a typical male tackler mass is involved in a tackle against a ball carrier with a typical female mass" . The participation of transgender athletes in the Olympic Games was approved following the 2003 Stockholm Consensus on Sex Reassignment in Sports, which recommended that transwomen athletes undergoing sex reassignment after puberty be eligible for competition 2 years post-gonadectomy, HRT, and legal recognition of assigned sex . How applicable these performance data are from both Harper and Roberts et al. in determining the extent of advantage remaining in transwomen athletes post-gender-affirming treatment remains to be determined. These findings require replication in trained transwomen athletes, although they would suggest a different rate and extent of mitigation of the advantages held by transwomen given that the strength advantages, but not the cardiovascular advantages, of transwomen were mitigated after 2 years of HRT. This finding agrees with previous studies that have shown that baseline muscular strength in transwomen is not significantly diminished after 1 year 51, 53 but is after 2 years of HRT .
Masturbation is prevalent in the general population54; however, the effects of masturbation and abstinence on testosterone levels remain understudied. Results vary, with reports of higher testosterone values in cannabis users,52,173 no difference,12,39,102 and decreased testosterone in users versus nonusers.99 Further research is needed to fully establish the effects of cannabis on testosterone levels. Zinc—a common TB component—has been shown to boost testosterone levels, particularly in people with both with and without zinc deficiency.17,80,88,98,138,148,164,170 Its effects are attributed to antioxidant activity in the testes and activation of steroidogenic enzymes. Fat tissue increases estradiol through aromatization, lowering testosterone levels; however, testosterone deficiency from obesity is rare in athletes.
In the logistic model a low LH featured in male alpine skiers (where an association with a high testosterone was seen) and judo athletes while FSH was low in male handball players. There were no significant differences between sports in women for testosterone, LH or FSH. In order to examine the effects of body composition across the whole group of 15 sports we analysed the available measured data and established a regression model from which we calculated an ‘estimated’ lean body mass (eLBM) and by subtracting this from the measured mass (M), and estimated fat mass (eFM). Growth hormone was lower in handball players, osteocalcin lower in track and field athletes who characteristically had higher levels of PICP. A higher testosterone was seen in basketball and alpine skiing while powerlifters had lower testosterone levels. The testosterone concentrations in the powerlifters are on average remarkably small and 8 of the remaining sports had significantly larger values. There are fewer volunteers and thus less data for women elite athletes but again basketball players are the tallest, weightlifters the shortest and cross-country skiers the lightest.
The governing body of world athletics then justified its decision after a study found that "women with higher testosterone could run longer and had more lean muscle mass." Such decisions should be based on the best available scientific evidence from the best available scientific practice and the decisions made will also require a firm political resolve to fairly integrate transwomen and DSD women athletes into elite female sport. However, the 5 nmol/L level adopted by World Athletics is based on the inference that there is a relationship between performance and testosterone concentrations and is meant to represent the value above which a performance advantage is no longer within the bounds of healthy cisgender females. During the consensus discussions, there was a constructive debate on the testosterone limit in the elite category of female sports. Given the inherent challenges of human studies, investigators need to adopt similar creative approaches if they are to elucidate the role of androgen receptors in elite DSD women and transwomen athletes. This model represents an ideal opportunity to study muscle function in the present context as the different combinations of gonads and sex chromosomes will result in different testosterone concentrations.
In this model, myotrophic or anabolic activity is measured by change in the weight of the rat bulbocavernosus/levator ani muscle, and androgenic activity is measured by change in the weight of the rat ventral prostate (or, alternatively, the rat seminal vesicles), in response to exposure to the AAS. The measurement of the dissociation between anabolic and androgenic effects among AAS is based largely on a simple but outdated and unsophisticated model using rat tissue bioassays. Dissociation between the ratios of these two types of effects relative to the ratio observed with testosterone is observed in rat bioassays with various AAS. Endogenous/natural AAS like testosterone and DHT and synthetic AAS mediate their effects by binding to and activating the AR. Body weight in men may increase by 2 to 5 kg as a result of short-term (muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out. Anabolic-androgenic steroids (AAS) cause these changes by directly impacting the muscle tissue's cellular components.

Amos De Chair, 20 years

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