Glucagon and insulin cord blood levels in very preterm, late preterm and full-term infants.

BACKGROUND: The cause of hyperglycemia, a frequent disorder of glucose homeostasis in very preterm infants, is still unknown. OBJECTIVES: Determine the glucagon and insulin plasma levels at birth in healthy, appropriate for gestational age (AGA) infants born by elective cesarean section (ECS), at different gestational age. METHODS: Glucagon, insulin and the homeostasis model of assessment-insulin resistance (HOMA-IR) index were measured in cord blood in 52 AGA infants divided into three groups: ≤30 weeks, very preterm (VP, n=16); 35-37 weeks, late preterm (LP, n=18); ≥38 weeks, full term (FT, n=18). RESULTS: In all enrolled infants, Apgar score at 5 min after birth was 7 to 9. In VP infants, glucagon levels were higher than those in LP (533±116 vs. 211±28 pg/mL) (p<0.001) and FT infants (533±116 vs. 226±20 pg/mL) (p<0.001). Insulin levels were higher in VP than in LP (8.61±2.48 vs. 3.98±0.94 mU/L) (p<0.001) and FT infants (8.61±2.48 vs. 4.56±1.2 mU/L) (p<0.001). HOMA-IR index was higher in VP than in LP and FT infants (30.6±10.2 vs. 11.9±3.04 and 13.5±1.6, respectively) (p<0.001). CONCLUSION: We concluded that very low gestational age is associated with high glucagon plasma levels and insulin-resistance, which could explain hyperglycemia in the very preterm infants.

Effects of Acute Recombinant Human TSH on Serum Ghrelin Levels.

UNLABELLED: Recent findings showed the presence of a reciprocal relationship between thyroid hormones and ghrelin, although the exact mechanism is not known. DESIGN: Our study is addressed to evaluate the effect of acute exogenous rhTSH administration on serum ghrelin levels in athyreotic patients on replacement l-thyroxine therapy. The study group included 50 patients (16 males and 34 females) submitted to total thyroidectomy and 131-iodine remnant ablation for differentiated thyroid cancer on l-thyroxine therapy. Mean age was 47.5 ± 16.5 years and mean BMI was 25.6 ± 5.01 kg/m(2). rhTSH was administrated at the dosage of 0.9 mg i.m. once daily for two consecutive days. Blood samples were taken between 08.00 and 09.00 after a overnight fasting for measurement of TSH, FT3, FT4, and ghrelin before the first administration of rhTSH and for measurement of TSH and ghrelin 24, 48, 72, and 96 h after the first administration of rhTSH. RESULTS: Mean ± SD values of basal TSH were 0.54 ± 0.77 µU/ml without significant difference between females and males. As expected, after rhTSH administration TSH concentrations increased at 24 and 48 h with peak TSH values ranging from 20.20 to 313 µU/ml (mean ± SD 98.4 ± 66.7 µU/ml). Mean ± SD values of basal ghrelin were 1085 ± 373 pg/ml without significant difference between males and females. After rhTSH administration ghrelin concentrations decreased significantly (p < 0.01) at 24 h (mean ± SD 934 ± 314 pg/ml p < 0.01) and returned to pre-treatment levels at 96 h. CONCLUSION: Our study demonstrates that acute exogenous TSH administration has a suppressive effect on ghrelin secretion independent from changes in thyroid status.

Prevalence of parietal cell antibodies in a large cohort of patients with autoimmune thyroiditis.

BACKGROUND: Autoimmune thyroiditis (AIT) may be associated with other organ-specific autoimmune disorders, including autoimmune gastritis, but the prevalence of this association is not entirely quantified. The aim of this study was to investigate the prevalence of parietal cell antibodies (PCA) in a large cohort of consecutive patients with AIT. METHODS: We retrospectively studied 2016 consecutive women and 258 men with AIT seen at our referral center in the period from 2004 to 2008. All patients were screened for the presence of PCA in the serum. RESULTS: The prevalence of serum PCA in female patients was 29.7% and progressively increased from 13% in the first-second decade of life to peak at 42% in the ninth decade. During follow up, 21.1% of the PCA-positive patients converted to PCA-negative status. Mean (±standard deviation) basal PCA levels in this group were significantly lower (32 ± 28 U/mL) compared with those remaining PCA positive (129 ± 200 U/mL). A similar prevalence (29.8%) with a similar age-dependency was found in male patients. CONCLUSIONS: In conclusion, our study demonstrates a high, age-dependent prevalence of PCA in an unselected large population of patients with AIT.

L-thyroxine requirement in patients with autoimmune hypothyroidism and parietal cell antibodies.

BACKGROUND: Hypothyroid patients on l-T(4) therapy may require replacement doses exceeding the theoretical needs to normalize serum TSH due to low patient compliance, drugs interference, and malabsorption. OBJECTIVE: We examined whether autoimmune gastritis might cause increased l-T(4) requirement in patients with autoimmune thyroiditis receiving l-T(4) replacement. PATIENTS: We studied 391 patients with clinical or subclinical hypothyroidism from autoimmune thyroiditis who had achieved normal serum TSH concentration (0.3-3.0 microU/ml) under l-T(4) for at least 6 months. Patients were screened for serum parietal cell antibodies (PCA) as a marker of autoimmune gastritis, and the PCA status was correlated with the l-T(4) dose. We also studied a group of 60 patients receiving l-T(4) replacement after total thyroidectomy. RESULTS: PCA-positive (155 of 391) and PCA-negative (236 of 391) patients did not differ for pretherapy serum TSH levels and thyroid volume. The l-T(4) requirement was significantly (P = 0.002) higher in PCA-positive (1.24 +/- 0.40 microg/kg x d) than in PCA-negative patients (1.06 +/- 0.36 microg/kg x d), and a significant positive correlation was found between l-T(4) requirement and serum PCA levels. Among PCA-positive patients, l-T(4) requirement was even higher in those with proven gastritis (1.52 +/- 0.40 microg/kg x d) compared with those without gastric damage (1.15 +/- 0.33 microg/kg x d) (P < 0.0001). The increased l-T(4) requirement was confirmed also in PCA-positive thyroidectomized patients (1.81 +/- 0.27 microg/kg x d) compared with PCA-negative thyroidectomized patients (1.52 +/- 0.24 microg/kg x d). Independent variables affecting l-T(4) requirement were PCA and serum TSH at diagnosis. CONCLUSIONS: Autoimmune gastritis is an additional factor affecting l-T(4) requirement in patients with autoimmune thyroiditis. Serum PCA measurement should be considered in patients with an unexplained high requirement of l-T(4).

Serum ghrelin as a marker of atrophic body gastritis in patients with parietal cell antibodies.

AIM: Autoimmune gastritis is frequently associated with autoimmune thyroiditis and other organ-specific autoimmune diseases, and may lead to atrophic body gastritis (ABG). We studied the diagnostic use of the measurement of serum ghrelin compared with other markers of gastric damage in predicting the presence of ABG in patients with autoimmune gastritis. METHODS: We studied 233 patients with autoimmune gastritis and 211 control subjects. All patients and control subjects were screened for circulating parietal cell antibodies (PCAs) and were tested for serum ghrelin, gastrin, pepsinogen I and II, and anti-Helicobacter pylori antibody levels. A total of 52 patients and 28 control subjects underwent a gastric endoscopy. RESULTS: In PCA/positive patients, mean (+/-sd) serum ghrelin levels were significantly lower (238 +/- 107 pmol/liter), and mean (+/-sd) serum gastrin levels were significantly higher (81.2 +/- 128.3 ng/ml), with respect to PCA/negative patients (282 +/- 104 pmol/liter and 20.7 +/- 13.3 ng/ml, respectively; P < 0.0001). Serum ghrelin and gastrin levels were inversely correlated (P = 0.004). A total of 40 patients had ABG documented by the gastric biopsy (90% in PCA/positive patients and 10% in PCA/negative patients). The receiver operating characteristic curve analysis revealed that a cutoff value for serum ghrelin of 188 pmol/liter was associated with the highest sensitivity and specificity (97.3 and 100%, respectively) in detecting gastric atrophy and was superior to gastrin (P = 0.012), PCA (P = 0.002), and the pepsinogen I/II ratio (P = 0.016) measurements. CONCLUSIONS: Our study demonstrates that ghrelin secretion is negatively affected by autoimmune gastritis, and its serum level represents the most sensitive and specific noninvasive marker for selecting patients at high risk for ABG.