Immunologically undetectable human placental lactogen in a normal pregnancy.

Sideri, Mario; Virgiliis, G. De; Guidobono, F.; Borgese, Nica; Sereni, Lucia Piceni; Nicolini, Umberto; Remotti, G

doi:10.1111/j.1471-0528.1983.tb09309.x

Cited by 23 publications

(10 citation statements)

References 8 publications

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“…Deletions of hPL and GH-V are associated with fetal growth failure in a subset of infants (Table 1); of eight patients with hPL gene deletions, four had birth weights of 2600 g or less; of three with combined hPL and GH-V gene deletions, two were normal but one weighed 1270 g [60][61][62][63][64][65][66][67][68][69][70]. This variation might be explained by variable compensation by other (nondeleted) somatogenic (GH-N) or lactogenic hormones (PRL) [4] acting through the GH and/or PRL receptors.…”

Section: Deletion Mutations Of the Human Placental Lactogen And Placementioning

confidence: 99%

Placental hormones and the control of maternal metabolism and fetal growth

Newbern

Freemark

2011

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

412

339

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Section: Deletion Mutations Of the Human Placental Lactogen And Placementioning

confidence: 99%

Placental hormones and the control of maternal metabolism and fetal growth

Newbern

Freemark

2011

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

412

339

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“…The role of this hormone remains obscure. Very rarely, pregnancies progressing normally and resulting in delivery of normal babies are associated with the absence of HPL in maternal plasma throughout pregnancy (Nielsen et al 1979;Borody and Carlton 1981;Alexander et al 1982;Sideri et al 1983; Barbieri et al 1986;Simon et al 1986;Trapp et al1987) or very low concentrations of HPL (Gaede et al1978;Bradford and Hargreaves 1978;Moshirpur et al 1981;Hubert et al 1983;Giampietro et al 1984;Wohlk et al 1984). Some ten pregnancies have been reported in the literature, but only in a few cases have had the genetic background examined in detail using Southern analysis (Nielsen et al 1979;Wurzel et al 1982;Wohlk et al 1984;Parks et al 1985;Simon et al 1986).…”

Section: Introductionmentioning

confidence: 99%

Absence of human placental lactogen and placental growth hormone (HGH-V) during pregnancy: PCR analysis of the deletion

et al. 1998

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Human placental lactogen (HPL) is produced in large amounts in normal pregnancies. We report a pregnancy with complete lack of HPL and the placental variant of the human growth hormone HGH-V. The pregnancy resulted in a severely growth-retarded but otherwise normal male baby. PCR analysis of DNA extracted from the placenta showed that the HPL encoding genes hPL-4 and hPL-3 were deleted along with the human growth hormone variant gene (hGH-V), which is located between these two active hPL genes and also expressed in the normal placenta. Of the five members of this multigene family, hGH-N, which is expressed in the pituitary gland, and hPL-1, a presumed pseudogene, were left intact. The latter (hPL-1) was expressed as RNA transcripts only at very low levels as is usually reported in normal pregnancies. Analysis of the parents' DNA showed that both of them carried a different heterozygous deletion at the 3' end of the hGH/hPL locus.

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“…(J Clin Endocrinol Metab 60: 994,1985) R EPORTS of antenatal deficiency of human chorionic somatomammotropin (hCS) fall into two categories. In the first, there is complete absence of immunoassayable hCS in maternal serum, implying complete deficiency of hCS production by fetal syncytiotrophoblastic cells (1)(2)(3)(4)(5). The second category involves partial hCS deficiency, with peak maternal serum hCS levels on the order of 1 /xg/ml, or approximately one fourth of normal levels (5)(6)(7)(8)(9).…”

mentioning

confidence: 99%

An Effect of Gene Dosage on Production of Human Chorionic Somatomammotropin*

Parks

Nielsen

Sexton

et al. 1985

The Journal of Clinical Endocrinology & Metabolism

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The gene deletions responsible for isolated partial deficiency of fetal human chorionic somatomammotropin (hCS) production were characterized by restriction endonuclease analysis of genomic DNA prepared from the leukocytes of an affected child. The phenotypically normal child was the product of a 38-week pregnancy characterized by peak maternal hCS levels of 1.1 micrograms/microliter (normal, 3-9.2 micrograms/ml) and normal levels of other pregnancy-associated hormones. Two genes, termed hCS-A and hCS-B, specify the same mature hCS peptide and are responsible for fetal hCS production. Digestion of the child's DNA with the enzymes Hind III, Eco RI, Bam HI, Bgl II, Hinc II and Msp I disclosed absence of the restriction fragments that normally contain the hCS-A gene. However, the hCS-B gene was present in the child's DNA. The child's DNA digests contained an abnormally large Eco RI fragment of 10.0 kb containing the hCS-L gene. This abnormal fragment is a marker for a deletion that is responsible for complete deficiency of hCS when present in the homozygous state. The child's DNA restriction patterns were consistent with heterozygosity for two different deletions involving hCS genes. The paternal hGH gene cluster lacked the hCS-A, human GH variant, and hCS-B genes, while the maternal cluster lacked only the hCS-A gene. Thus, the child's DNA contained only one of the normal complement of four functional hCS genes per diploid genome. Material hCS levels approximately one fourth as great as those present at comparable stages of normal pregnancies indicated that there was no compensatory increase in expression of the remaining hCS gene.

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Immunologically undetectable human placental lactogen in a normal pregnancy.

Cited by 23 publications

References 8 publications

Placental hormones and the control of maternal metabolism and fetal growth

Placental hormones and the control of maternal metabolism and fetal growth

Absence of human placental lactogen and placental growth hormone (HGH-V) during pregnancy: PCR analysis of the deletion

An Effect of Gene Dosage on Production of Human Chorionic Somatomammotropin*

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