Postnatal involution of the human adrenal fetal zone: Stereologic description and apoptosis

Bocian-Sobkowska, J; Woźniak, W; Malendowicz, Ludwik K.

doi:10.3109/07435809809032718

Cited by 28 publications

(19 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The sudden postnatal involution of the fetal zone is connected with notable hemorrhagic lesions and the entire process may be divided into 2 distinct phases, the rapid one, lasting from the birth till the end of the second week of life, followed by a slower one [14,123]. As revealed by stereology, this decrease is highly correlated with the decrease of both the volume of fetal zone and quantity of its cells.…”

Section: Involution Of the Fetal Zonementioning

confidence: 84%

“…Only scattered apoptotic nuclei were seen in central part of the fetal zone and their number increases with the length of gestation [121,122]. In postnatal period, apoptotic index of fetal zone cells was highest during the second week of life, and subsequently declined (from ca 30% to 20%) [14,16,123].…”

Section: Proliferative Activity Of Fetal Adrenocortical Cells and Apomentioning

confidence: 99%

“…As mentioned, during two weeks after birth, the fetal zone of human adrenal cortex practically disappears, however fragments of the zone may persist in the adrenals till the end of the 2 year of life [13,14,124]. It is worth to emphasize marked individual variations in the rate of involution of that zone.…”

Section: Involution Of the Fetal Zonementioning

confidence: 99%

“…At the end of gestation, a developing adrenal gland is organized into distinct zones: glomerulosa, transitory (appears between weeks 22-24, the future zona fasciculata) and dominant fetal zone. Immediately after birth, the fetal zone undergoes rapid involution, but its elements may persist up to the end of the second year of life [13,14]. In human adrenal gland zona reticularis starts to develop at the age of 4-6 or even 8 years, while structure typical to adults stabilizes at the age of 10-20 years [4,11,15,16].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

Malendowicz

2011

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

Section: Involution Of the Fetal Zonementioning

confidence: 84%

Section: Proliferative Activity Of Fetal Adrenocortical Cells and Apomentioning

confidence: 99%

Section: Involution Of the Fetal Zonementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

Malendowicz

2011

Folia Histochem Cytobiol.

View full text Add to dashboard Cite

“…Sabe-se que a adrenal fetal produz grande quantidade de DHEA e DHEA-S, devido à não expressão da enzima 3β hidroxiesteróide-desidrogenase (3bHSD) neste tecido. Existe grande quantidade de receptores AT2, expressos principalmente no segundo trimestre da gestação; quando estes receptores são ativados, inicia-se o processo de redução do tamanho da glândula, secundário ao desaparecimento da zona fetal por apoptose (20)(21)(22)(23).…”

unclassified

Triagem de mutações nos receptores de Angiotensina II, AGTR1 e AGTR2 e avaliação dos polimorfismos C573T e A1166C do gene AGTR1 em pacientes com adrenarca precoce idiopática

Moura

Melo

Longui

et al. 2006

Arq Bras Endocrinol Metab

View full text Add to dashboard Cite

RESUMOPubarca precoce é o aparecimento de pêlos pubianos antes dos 8 anos em meninas e 9 anos em meninos, sendo sua etiologia mais freqüente a adrenarca precoce idiopática, a longo prazo, associada à síndrome metabólica. Dentre os fatores envolvidos na gênese da adrenarca precoce podemos citar a Angiotensina II (Ang II), a qual promove proliferação celular e esteroidogênese, podendo agir através de dois receptores, o tipo 1 (AT1) e o tipo 2 (AT2). Com o intuito de estudar mutações dos genes dos receptores da AngII, foram avaliadas 50 crianças com diagnóstico de adrenarca precoce idiopática e comparadas ao grupo controle de indivíduos normais. Não foram detectadas mutações dos genes AGTR1 e AGTR2, contudo dois polimorfismos foram identificados no gene AGTR1: o polimorfismo C573T (localizado no exon 5) e o A1166C (na região 3' não codificadora). A freqüência do alelo polimórfico T573 foi de 35% nos pacientes e 38% nos controles. O alelo polimórfico C1166 esteve presente em 24% dos pacientes e em 26% dos controles. Não houve diferença significante entre os grupos, assim como não houve correlação entre a freqüência dos polimorfismos C573T e A1166C e as variáveis clínicas e laboratoriais dos pacientes, ou com sua história familial de síndrome metabóli-ca. Precocious pubarche is the appearance of pubic hair before the age of 8 years in girls and 9 years in boys. The most frequent etiology is idiopathic precocious adrenarche, suggested, after long-term follow-up, to be associated with metabolic syndrome. One of the factors involved in the genesis of precocious adrenarche is Angiotensin II (Ang II), which promotes cell proliferation and steroidogenesis through type 1 (AT1) and type 2 (AT2) receptors. In order to study Ang II receptors mutations, 50 children with idiopathic precocious adrenarche were evaluated and compared to a control group of normal individuals. Mutations were not detected in the AGTR1 and AGTR2 genes; however, two polymorphisms were identified in the AGTR1 gene: the C573T (exon 5) and the A1166C (3' untranslated region). The polymorphic allele T573 was found in 35% of the patients and 38% of controls. The polymorphic allele C1166 was present in 24% of the patients and 26% of controls. There was no statistical difference between groups. There was also no correlation between the polymorphisms and clinical and laboratory findings, as well as their family history of metabolic syndrome.

show abstract

Neonatal McCune‐Albright Syndrome: A Unique Syndromic Profile With an Unfavorable Outcome

et al. 2019

View full text Add to dashboard Cite

Somatic gain‐of‐function mutations of GNAS cause a spectrum of clinical phenotypes, ranging from McCune‐Albright syndrome (MAS) to isolated disease of bone, endocrine glands, and more rarely, other organs. In MAS, a syndrome classically characterized by polyostotic fibrous dysplasia (FD), café‐au‐lait (CAL) skin spots, and precocious puberty, the heterogenity of organ involvement, age of onset, and clinical severity of the disease are thought to reflect the variable size and the random distribution of the mutated cell clone arising from the postzygotic mutation. We report a case of neonatal MAS with hypercortisolism and cholestatic hepatobiliary dysfunction in which bone changes indirectly emanating from the disease genotype, and distinct from FD, led to a fatal outcome. Pulmonary embolism of marrow and bone fragments secondary to rib fractures was the immediate cause of death. Ribs, and all other skeletal segments, were free of changes of typical FD and fractures appeared to be the result of a mild‐to‐moderate degree of osteopenia. The mutated allele was abundant in the adrenal glands and liver, but not in skin, muscle, and fractured ribs, where it could only be demonstrated using a much more sensitive PNA hybridization probe‐based FRET (Förster resonance energy transfer) technique. Histologically, bilateral adrenal hyperplasia and cholestatic disease matched the abundant disease genotype in the adrenals and liver. Based on this case and other sporadic reports, it appears that gain‐of‐function mutations of GNAS underlie a unique syndromic profile in neonates characterized by CAL skin spots, hypercortisolism, hyperthyroidism, hepatic and cardiac dysfunction, and an absence (or latency) of FD, often with a lethal outcome. Taken together, our and previous cases highlight the phenotypic severity and the diagnostic and therapeutic challenges of MAS in neonates. Furthermore, our case specifically points out how secondary bone changes, unrelated to the direct impact of the mutation, may contribute to the unfavorable outcome of very early‐onset MAS. © 2018 The Authors JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

show abstract

Postnatal involution of the human adrenal fetal zone: Stereologic description and apoptosis

Cited by 28 publications

References 1 publication

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

Triagem de mutações nos receptores de Angiotensina II, AGTR1 e AGTR2 e avaliação dos polimorfismos C573T e A1166C do gene AGTR1 em pacientes com adrenarca precoce idiopática

Neonatal McCune‐Albright Syndrome: A Unique Syndromic Profile With an Unfavorable Outcome

Contact Info

Product

Resources

About