Calcitonin and Parathyroid Hormone – Relation to Early Neonatal Hypocalcemia in Infants of Diabetic Mothers

Bergman, Lars R.; Kjellmer, Ingemar; Selstam, Urban

doi:10.1159/000240646

Cited by 53 publications

(16 citation statements)

References 8 publications

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“…This hypothesis warrants further investigation once the molecular identity of the renal magnesium transporters has been described. The serum PTH concentration of 8-wk-old OD was lower than that of OC rats in the current study, which is in accordance with observations in human neonates (2,19,20). A number of hypotheses have been proposed to account for the apparent paradox of hypocalcemia and low PTH concentration.…”

Section: Discussionsupporting

confidence: 92%

“…A number of hypotheses have been proposed to account for the apparent paradox of hypocalcemia and low PTH concentration. Bergman et al (19) suggested that the fall in glucose and consequent increase in glucagon that arises in the neonate post partum stimulates an increase in calcitonin secretion. This inhibits bone resorption and results in hypocalcemia despite low PTH concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…We assessed renal function in rats at 4 wk of age, before puberty, and at 8 wk of age, after puberty, to determine whether in utero exposure to maternal diabetes exerts a long-term programming effect on offspring kidney function. We also measured serum PTH concentration, as this has been reported to be lower in human offspring of diabetic pregnancy (2,19,20) and may contribute to altered renal calcium and magnesium handling.…”

mentioning

confidence: 99%

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Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

et al. 2005

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Diabetic pregnancy has a marked influence on offspring calcium and magnesium homeostasis. Urinary excretion of calcium and magnesium is reduced, yet offspring of diabetic pregnancy exhibit hypomagnesemia and hypocalcemia. The aim of this study was to measure renal hemodynamic and tubular function in the offspring of diabetic (OD) and control, nondiabetic (OC) rats at 4 and 8 wk of age to determine the glomerular and tubular mechanisms through which renal calcium and magnesium handling are programmed in utero. The fraction of filtered calcium that was excreted was significantly lower in OD at both 4 and 8 wk of age [8 wk: OC (n ϭ 6), 11.8 Ϯ 2.9 versus OD (n ϭ 5), 4.3 Ϯ 0.6%; p Ͻ 0.05] and that of magnesium was lower at 8 wk of age [OC (n ϭ 6), 42.4 Ϯ 7.5 versus OD (n ϭ 5), 13.0 Ϯ 1.7%; p Ͻ 0.01]. This increased reabsorption occurred despite an elevated GFR in OD. These findings clearly indicate that tubular reabsorptive mechanisms for calcium and magnesium are increased markedly in OD. Serum PTH concentration was reduced in 8-wk-old OD [OC (n ϭ 7), 539.4 Ϯ 142.1 versus OD (n ϭ 9), 174.3 Ϯ 69.4 pg/ml; p Ͻ 0.05], consistent with previous reports in human infants. Taken together, these observations suggest that the basis for the altered renal magnesium and calcium handling in OD involves increased tubular transport activity and possibly increased sensitivity of these mechanisms to PTH. Diabetic pregnancy has a marked impact on maternal calcium and magnesium homeostasis in both humans and rats. Hypomagnesemia has been widely reported in human diabetic pregnancy (1-3), and diabetic pregnant rats display a marked increase in urinary magnesium excretion (4,5). A reduction in third-trimester plasma calcium concentration has been observed in human diabetic pregnancy in one study (3), but the majority of studies have found no difference in calcium concentrations between normal and diabetic pregnancies. However, in the diabetic rat, pregnancy is associated with marked increases in urinary calcium (4,5) and hypocalcemia in some (4) but not all studies (6).These changes in maternal divalent ion handling have a profound impact on the developing fetus. Human offspring of diabetic pregnancy exhibit hypomagnesemia and hypocalcemia as neonates (2,7-9). In the rat, renal handling of calcium and magnesium is also altered in the offspring of streptozotocin (STZ)-treated diabetic rats (OD). We recently reported that OD retain both calcium and magnesium as neonates and that this continues into adulthood (10). These changes in divalent ion homeostasis also occur in conjunction with changes in bone structure. Human offspring of diabetic pregnancy are susceptible to congenital malformations, including skeletal abnormalities (11), and have lower bone mineral content (12). Reduced bone mineral content and abnormal skeletal development have also been observed in the offspring of STZ-treated diabetic rat mothers (13,14). We recently extended these observations and showed that offspring of STZ-treated diabetic rats have reduced trabecular and ...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

et al. 2005

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“…Wolfe, et al (12), have demonstrated C cells in the normal neonatal thyroid gland to be relatively greater in number and to have greater CT content than those of the normal adult. Elevated levels of plasma CT have been described in neonates (9,13,14) and in cord blood compared with matched matemal blood (8).…”

Section: Introductionmentioning

confidence: 99%

Calcitonin secretion in congenital nongoitrous cretinism.

Carey¹,

Jones²,

Parthemore³

et al. 1980

J. Clin. Invest.

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A B S T R A C T Plasma calcitonin (CT) was measured in the basal state and/or during provocative tests of hormone secretion in 11 children with congenital nongoitrous cretinism (CNC), in 1 girl with a lingual thyroid, and in 11 normal children. Basal and stimulated CT concentrations were significantly lower in the patients with CNC than in the normal subjects. Mean basal CT (± SE) was 41±4 pg/ml in the normal children, 24±3 pg/ml in the children with CNC, and 20±2 pg/ml in the patient with the lingual thyroid. The mean incremental CT responses to calcium infusion were 7.0±2 pg/ml in the children with CNC, 6.0 pg/ml in the patient with the lingual thyroid, and 146±47 pg/ml in the normal children. The children with CNC also demonstrated a significant delay in the return of the total serum calcium to basal level after the calcium infusion. The mean incremental CT response after infusion of pentagastrin was 7.6+2 pg/ml in the children with CNC, 10.0 pg/ml in the child with the lingual thyroid, and 34.4±11 pg/ml in the normal children. These data indicate that CT deficiency is present in children with CNC and suggest that the deficiency is a consequence of the defective embryologic development of the thyroid gland.

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“…Bergman et at. (6) speculated that neonatal hypoglycemia in IDM might lead to increased glucagon secretio n, and because glucagon is known to both lower serum Ca (24) and stimulate CT secretion (6), it might, th eoretically, directly and ind irectly cause neonatal hypocalcemia . A recent study from our group demonstrated that, in asphyxiated infants, there is an increased seru m CT concentration (presumably stressinduced) and that postnatal seru m Ca concentrations correlate inversely with serum CT conce ntrations (25).…”

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confidence: 99%

Postnatal Surge in Serum Calcitonin Concentrations: No Contribution to Neonatal Hypocalcemia in Infants of Diabetic Mothers

1990

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MAT ERIALS AND METH OD S (2, 3). However, it was shown in a prospective, matched-control study that NHC in IDM is significant even after contro lling for the aforementioned variables ( I). Leadin g theori es related to th e path oph ysiology of NHC in IDM includ e: 1) maternal-fetal Mgdeficient state, du e to matern al glycosuria (4), leading to fetal hypoparath yroidism and subsequent NH C ( I, 5) and 2) neonatal hyperca lcitoninemia (6, 7). The latter theory is supported by evidence that the neonatal surge in serum CT concentrations found in normal neonates also occurs in IDM , which might seem inappropriate when one considers the concomitant decrease in serum Ca. Stu dies supporting th is theory were limited by sma ll sample size, with only one showing an inverse correlation between serum Ca and CT conce ntrations in II IDM (6). We conducted this prospective study to determine whether CT plays any role in NHC in IDM when simultan eous measurements of serum Mg and PTH concentrations are taken int o account.Patients. Since 1979,47 full-term (37-4 1 wk gestation) infants of insulin-dependent diabetic mothers (White classes B-RT) (8) were prospectively studied as part of an NIH-funded program project grant, "Diabetes in Pregnancy." Preterm infants were excluded from this study because of the confounding influences of gestational age on neonatal calcium metabolism (I). The 47 IDM were compared with a group of 31 term infants of nondiabetic pregnant women [norm al glucose challenge test at 28 wk gestation (9)] born after un com plicated pregnan cies, labors, and deliveries. Th is study was approved by the Review Board on Investigations Involving Human Beings of the Uni versity of Cincinn ati Medical Center Hospital. Written informed consent was obtained from one of the legal guardians of each infant before enrollment int o the study.Th e aims of glycemic cont rol in diabetic pregnan cy were a preprandial blood glucose concentration below 5.55 mm ol/L ( 100 mg/dl. ) and a 90-min postprandial blood glucose concentration below 7.7 1 mrnol/ L ( 140 mg/dl.). Pregnant patients were hospitalized when necessary to maint ain these goals of glycem ic contro l. Matern al blood glycosylated Hb A I contents were measured every 4 wk to determine if adequ ate glycemic control was achieved. Pre-or postprandial capillary glucose concentration was alterna tively measured at each weekly visit. In each patient, pre-or postprandi al blood glucose values were averaged over each trimester as mean pre-or postprand ial blood glucose concentrations per trim ester (10).Data collection. Diabetes was categorized using the Whit e classification (8). Blood samples were collected from infants in both groups at birth from a double-clamped segment of umbilical cord and at 24 h of life for determination of Ca, Mg, PTH, and CT. Gestational age was calculated from the last menstrual period and confirmed within ± 2 wk of Ballard score (10). We defined NHC, using the traditional definition supported by the data 493 Abbreviations IDM, infant of diabetic ...

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Calcitonin and Parathyroid Hormone – Relation to Early Neonatal Hypocalcemia in Infants of Diabetic Mothers

Cited by 53 publications

References 8 publications

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

Increased Renal Tubular Reabsorption of Calcium and Magnesium by the Offspring of Diabetic Rat Pregnancy

Calcitonin secretion in congenital nongoitrous cretinism.

Postnatal Surge in Serum Calcitonin Concentrations: No Contribution to Neonatal Hypocalcemia in Infants of Diabetic Mothers

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