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Britto IMPA, Aguiar-Oliveira MH, Oliveira-Neto LA, Salvatori R, Souza AHO, Araujo VP, Corraini P, Pannuti CM, Romito GA, Pustiglioni FE: Periodontal disease in adults with untreated congenital growth hormone deficiency: a case–control study. J Clin Periodontol 2011; doi: 10.1111/j.1600-051X.2011.01721.x. Abstract Aim: The aim of this study was to investigate the possible associations between isolated growth hormone deficiency (IGHD) and periodontal attachment loss (PAL) in adults affected by congenital IGHD. Materials and methods: Forty-five previously identified IGHD subjects were eligible for this study. The final study sample comprised 32 cases (gender:20M/12F; age:44.8 ± 17.5) matched for age, gender, diabetes, smoking status and income to 32 controls (non-IGHD subjects). Participants were submitted to a full-mouth clinical examination of six sites per tooth and were interviewed using a structured, written questionnaire. Periodontitis was defined as proximal PAL5 mm affecting 30% of teeth. Results: No significant differences were observed in the percentage of sites with visible plaque between IGHD and non-IGHD subjects (59.4%versus 46.9%, p=0.32). IGHD subjects had significant less supragingival calculus (31.3%versus 59.4%, p=0.02) and more bleeding on probing (71.9%versus 18.8%, p

OBJECTIVE Although chronotropic incompetence (CI) represents an independent predictor of mortality and incidence of coronary artery disease, its pathophysiological mechanisms remain unknown. The purpose of this investigation was to evaluate wall motion abnormalities of the left ventricle and location of coronary arterial lesions in patients with and without CI. METHODS After exclusion of confounding factors, 610 patients (mean age of 58.4 +/- 11 years; 275 men) with ischaemia who underwent exercise echocardiography were studied. Based on heart rate (HR) reached in treadmill testing, patients were divided into two groups: Chl (97 patients who did not reach 85% of maximum HR recommended for age) and ChC (513 patients who achieved 85% of the maximum age-predicted HR). RESULTS There was a higher frequency of dyspnoea (5.2% vs. 0.6%, P = 0.003), systemic hypertension (69.1% vs. 57.3%, P = 0.031) and obesity (38.1% vs. 22.6%, P = 0.001), and a lower tolerance to effort (dyspnoea as limitation of physical effort: 36.1% vs. 8.0%, P < 0.0001; duration of treadmill test: 4.4 +/- 2.2 vs. 7.2 +/- 2.8, P < 0.0001; METs: 6.0 +/- 2.6 vs. 8.4 +/- 2.9, P = 0.002) in Chl compared to ChC. The wall motion score index (WMSI) was higher in Chl than in ChC, both at rest (1.15 +/- 0.29 vs. 1.07 +/- 0.19, P = 0.011) and after exercise (1.24 +/- 0.29 vs. 1.15 +/- 0.19, P = 0.002). Systolic function, which was evaluated in peak exercise through WMSI, was significantly more altered in the Chl group. The presence of severe injuries in right coronary was independently associated with CI (adjusted OR = 3.57, CI 95%: 1.86-6.87). CONCLUSION Chronotropic incompetence is associated with ventricular dysfunction in peak exercise and critical right coronary artery lesions.

ObjectiveGH replacement therapy (GHRT) in adult-onset GH deficiency (AOGHD) reduces carotid intima-media thickness (IMT) and increases myocardial mass, with improvement of systolic and diastolic function. These observations have reinforced the use of GHRT on AOGHD. Conversely, we have previously reported that in adults with lifetime congenital and severe isolated GH deficiency (IGHD) due to a mutation in GHRH receptor gene (GHRHR), a 6-month treatment with depot GH increased carotid IMT, caused the development of atherosclerotic plaques, and an increase in left ventricular mass index (LVMI), posterior wall, and septal thickness and ejection fraction. Such effects persisted 12 months after treatment (12-month washout – 12mo).MethodsWe have studied the cardiovascular status (by echocardiography and carotid ultrasonography) of these subjects 60 months after completion of therapy (60-month washout – 60mo).ResultsCarotid IMT reduced significantly from 12 to 60mo, returning to baseline (pre-therapy) value. The number of individuals with plaques was similar at 12 and 60mo, remaining higher than pre-therapy. LVMI, relative posterior wall thickness, and septum thickness did not change between 12 and 60mo, but absolute posterior wall increased from 12 to 60mo. Systolic function, evaluated by ejection fraction and shortening fraction, was reduced at 60mo in comparison with 12mo returning to baseline levels. The E/A wave ratio (expression of diastolic function) decreased at 60mo compared with both 12mo and baseline.ConclusionsIn adults with lifetime congenital IGHD, the increase in carotid IMT elicited by GHRT was transitory and returned to baseline 5 years after therapy discontinuation. Despite this, the number of subjects with plaques remained stable at 60mo and higher than at baseline.

GH reduces insulin sensitivity (IS), whereas IGF-I increases it. IGF-I seems to be critical for the development of the -cells, and impaired IS has been reported in GH deficiency (GHD). Objective: The aim of the study was to assess IS and -cell function in adult patients with untreated isolated GHD (IGHD) due to a homozygous mutation in the GHRH receptor gene. Design, Setting, and Patients: We conducted a cross-sectional study in 24 GH-naive adult IGHD subjects and 25 controls. Intervention:We performed an oral glucose tolerance test with glucose and insulin measurements at 0, 30, 60, 90, 120, and 180 min. Main Outcome Measures: IS was assessed by homeostasis model assessment index of insulin resistance (IR), quantitative IS check index, oral glucose IS in 2 h (OGIS2) and 3 h (OGIS3). -Cell function was assayed by homeostasis model assessment index-, insulinogenic index, and area under the curve of insulin-glucose ratio. Results:During the oral glucose tolerance test, glucoselevelswere higherinIGHD subjects (P0.0001), whereas insulin response presented a trend toward reduction (P 0.08). The number of individuals with impaired glucose tolerance was higher in the IGHD group (P 0.001), whereas the frequency of diabetes was similar in the two groups. Homeostasismodel assessment index of IR was lower (P0.04), and quantitative IS check index and OGIS2 showed a nonsignificant trend toward elevation (P 0.066 and P 0.09, respectively) in IGHD. OGIS3 showed no difference between the groups. Homeostasis model assessment index-, insulinogenic index, and ratio of the areas of the insulin and glucose curves were reduced in the IGDH group (P 0.015, P 0.0001, and P 0.02, respectively). Conclusions: Adult subjects with lifetime congenital untreated IGHD present reduced -cell function, no evidence of IR, and higher frequency of impaired glucose tolerance. (

Background: GH deficiency (GHD) is often associated with cardiovascular risk factors, including abdominal fat accumulation, hypercholesterolemia, and increased C-reactive protein. Despite the presence of these risk factors, adults with congenital lifetime isolated GHD (IGHD) due to an inactivating mutation in the GHRH receptor gene do not have premature atherosclerosis.Objective: The aim was to study the serum levels of adiponectin and leptin (antiatherogenic and atherogenic adipokine, respectively), and the urinary albumin excretion (UAE) in these IGHD individuals.Design and Patients: We conducted a cross-sectional study of 20 IGHD individuals (seven males; age, 50.8 ± 14.6 yr) and 22 control subjects (eight males; age, 49.9 ± 11.5 yr).Main Outcome Measures: Anthropometric factors, body composition, blood pressure, serum adiponectin, leptin, and UAE were measured.Results: Adiponectin was higher [12.8 (7.1) vs. 9.7 (5) ng/ml; P = 0.041] in IGHD subjects, whereas no difference was observed in leptin [7.3 (6.3) vs. 9.3 (18.7 ng/ml] and UAE [8.6 (13.8) vs. 8.5 (11.1) μg/min].Conclusions: Subjects with lifetime untreated IGHD have an adipokine profile with high adiponectin and normal leptin levels that may delay vascular damage and lesions of the renal endothelium.

Context: Reduced longevity observed in hypopituitarism has been attributed to GH deficiency (GHD). It is, however, unclear whether GHD or other confounding factors cause this early mortality. Objective: The aim was to study longevity in subjects from a large kindred with untreated, lifetime isolated GHD (IGHD) due to a homozygous mutation in the GHRH receptor gene and in heterozygous carriers of the mutation. Design, Setting, and Participants: We carried out a retrospective cohort study on three groups. We first compared mortality risk of 65 IGHD individuals and their 128 unaffected siblings from 34 families. We then compared mean age of death of the IGHD to the general population. A transversal study was carried out to compare the rate of heterozygosity for the mutation in two groups of young (20–40 yr old) and old (60–80 yr old) normal-appearing subjects from the same county. Main Outcome Measure: We measured longevity. Results: The risk of death of IGHD subjects was not different from their siblings. Life span in IGHD individuals was shorter than the general population. When stratified by sex, this difference persisted only in females, due to a high frequency of IGHD deaths in females aged 4–20. There was no significant difference in life span between IGHD subjects and siblings or the general population when analyzing subjects who reached age 20. The prevalence of heterozygosity did not differ in young and old groups, suggesting no survival advantage or disadvantage. Conclusions: In a selected genetic background, lifelong untreated IGHD does not affect longevity.