scholarly journals Increased plasma β-hydroxybutyrate levels during the fasting test in patients with endogenous hyperinsulinaemic hypoglycaemia

2013 ◽  
Vol 169 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Alexandre Buffet ◽  
Delphine Vezzosi ◽  
Jean Christophe Maiza ◽  
Solange Grunenwald ◽  
Antoine Bennet ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Partial Pancreatectomy ◽  
C Peptide ◽  
Fasting Test ◽  
Group 2 ◽  
Design And Methods ◽  
Rule Out ◽  
Group 1

ObjectiveThe objective of the present study was to determine whether a plasma β-hydroxybutyrate (BOHB) level >2700 μmol/l during the 72-h fasting test is sufficient to rule out the diagnosis of endogenous hyperinsulinaemic hypoglycaemia (EHH).Research design and methodsWe retrospectively studied BOHB levels in 39 patients with EHH who had undergone a 72-h fasting test to make the diagnosis of EHH, and we compared EHH patients with BOHB levels >2700 μmol/l (group 1), EHH patients with BOHB levels <2700 μmol/l (group 2) and 59 controls (median glycaemia: 3.2 mmol/l and median BOHB: 6095 μmol/l).ResultsDuring a 72-h fasting test, nine patients (group 1) had BOHB levels >2700 μmol/l (median 6140 and range 2957–7824) and 30 patients (group 2) had BOHB levels <2700 μmol/l (median 542 and range 0–2607). In group 1, four patients had undergone partial pancreatectomy previously and were evaluated for the recurrence of hypoglycaemia, whereas none of the group 2 patients had been operated. The duration of the fasting test was longer in group 1 than in group 2 (P<0.0001), and at the end of the fasting test, plasma glucose concentrations were not significantly different (P=0.0617), but insulin (P=0.004), C-peptide (P=0.0015) and proinsulin (P=0.0038) levels were significantly lower in group 1 patients than in group 2 patients, suggesting lower insulin secretion and/or impaired glycaemic counter-regulation.ConclusionDuring a fasting test, a BOHB level >2700 μmol/l is observed in some EHH patients, suggesting that BOHB levels cannot rule out the recurrence of EHH, in particular, after partial pancreatectomy.

scholarly journals Fever as a predictor of adverse outcomes in COVID-19

QJM ◽  
2021 ◽  
Author(s):  
N W Chew ◽  
J N Ngiam ◽  
S M Tham ◽  
Z Y Lim ◽  
T Y W Li ◽  
...  
Keyword(s):  
Tertiary Hospital ◽  
Adverse Outcomes ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
End Point ◽  
Group 4 ◽  
Group 3 ◽  
Group 2 ◽  
Design And Methods ◽  
Group 1

Summary Background/Introduction There are little data on outcomes of COVID-19 patients with the presence of fever compared to the presence of symptoms. Aim We examined the associations between symptomology, presence of fever and outcomes of a COVID-19 cohort. Design and Methods Between 23 January and 30 April 2020, 554 COVID-19 patients were admitted to a tertiary hospital in Singapore. They were allocated into four groups based on symptomology and fever—Group 1: asymptomatic and afebrile, Group 2: symptomatic but afebrile, Group 3: febrile but asymptomatic and Group 4: symptomatic and febrile. The primary outcomes were intensive care unit (ICU) admissions and mortality. The composite end-point included ICU admissions, mortality or any COVID-19 related end-organ involvement. Results There were differences in ferritin (P=0.003), C-reactive protein (CRP) levels (P&lt;0.001) and lymphopenia (P=0.033) across all groups, with the most favourable biochemical profile in Group 1, and the least in Group 4. Symptomatic groups (Groups 2 and 4) had higher ICU admissions (1.9% and 6.0%, respectively, P=0.003) than asymptomatic groups (Groups 1 and 3). Composite end-point was highest in Group 4 (24.0%), followed by Group 3 (8.6%), Group 2 (4.8%) and Group 1 (2.4%) (P&lt;0.001). The presence of fever (OR 4.096, 95% CI 1.737–9.656, P=0.001) was associated with the composite end-point after adjusting for age, pulse rate, comorbidities, lymphocyte, ferritin and CRP. Presence of symptoms was not associated with the composite end-point. Discussion/Conclusion In this COVID-19 cohort, presence of fever was a predictor of adverse outcomes. This has implications on the management of febrile but asymptomatic COVID-19 patients.

Abstract 1924: Carriers of Loss-of-Function Mutations in ABCA1 Display Pancreatic Beta Cell Dysfunction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Menno Vergeer ◽  
Liam R Brunham ◽  
Joris Koetsveld ◽  
Janine K Kruit ◽  
C B Verchere ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Sensitivity Index ◽  
Loss Of Function ◽  
Β Cell ◽  
C Peptide ◽  
Cell Dysfunction ◽  
Time Interaction

Background The ATP Binding Cassette transporter A1 (ABCA1) transports free cholesterol to nascent high-density lipoproteins (HDL) and maintains plasma HDL levels. In mice, ABCA1 is essential in regulating intracellular cholesterol homeostasis and insulin secretion in the β cell. The role of ABCA1 in human glucose metabolism is unclear. Objective and methods To assess the effects of ABCA1 dysfunction on glucose homeostasis in humans , we matched heterozygous carriers of disruptive mutations in ABCA1 and non-carriers for age, gender and BMI and performed oral glucose tolerance tests (OGTT; 9 vs. 8 respectively) and hyperglycemic clamping experiments (6 vs. 6). Results Carriers had lower HDL-C levels than non-carriers (0.58 ± 0.3 vs. 1.46 ± 0.4 mmol/L, p=0.001) but LDL-C did not differ (3.4 ± 1.0 vs. 2.8 ± 0.8 mmol/L, p=0.21). Fasting plasma glucose was not different (5.2 ± 1.5 vs. 5.0 ± 0.4 mmol/L). Glucose curves after OGTT were significantly higher in carriers than in non-carriers (genotype * time interaction, p=0.005; plasma glucose at t=60 min 9.0 ± 3.0 mmol/L vs. 6.0 ± 1.4 mmol/L respectively, p=0.02). During hyperglycemic clamps, carriers showed a lower first phase insulin and C-peptide response than non-carriers (genotype * time interaction, p<0.05 and p<0.01 respectively; insulin at t=5 min 164±118 vs. 352 ±141 pmol/L, p<0.05; C-peptide at t=5 min 1033 ± 628 vs. 1942 ± 723 pmol/L, p<0.05) but no difference in insulin sensitivity index (0.0216 ± 0.012 mg kg −1 . min −1 . pM −1 for carriers and 0.0197 ± 0.005 mg kg −1 . min −1 . pM −1 for non-carriers; p=0.73). Disposition index - a measure of β cell function, adjusted for insulin sensitivity - was lower in carriers than in non-carriers (1037 ± 610 vs. 2718 ± 1524; p<0.05). Non-carriers responded to an arginine stimulus with an increase in C-peptide levels (from 3558 ± 1240 pM to 6817 ± 1665 pM; p<0.005), whereas in carriers this increase did not reach statistical significance (from 3727 ± 1843 pM to 5480 ± 1757 pM; p=0.12). Conclusion Carriers of loss-of-function mutations in ABCA1 show impaired insulin secretion without insulin resistance, resulting in glucose intolerance. Our data confirm previous studies in mice and provide evidence for a role of ABCA1 in β cell dysfunction and the pathophysiology of diabetes mellitus in man.

Effects of training and detraining on dose-response relationship between glucose and insulin secretion

1989 ◽  
Vol 256 (5) ◽  
pp. E588-E596 ◽  
Author(s):  
K. J. Mikines ◽  
B. Sonne ◽  
B. Tronier ◽  
H. Galbo
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Plasma Glucose ◽  
Response Relationship ◽  
Cell Secretion ◽  
Dose Response Relationship ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Beta Cell Secretion ◽  
Training And Detraining

We studied the effect of training and detraining on the dose-response relationship between plasma glucose and beta-cell secretion in seven trained young men using sequential hyperglycemic clamp technique (7, 11, and 20 mM). Experiments were performed in the habitual state 15 h after last training session (T) as well as after 5 days of detraining (DT). Results were compared to data from seven untrained subjects (UT). Glucose-stimulated insulin, proinsulin, and C-peptide levels were lower in T than in UT. They increased during detraining but not to levels seen in UT. Furthermore, in T and DT, but not in UT, increases in C-peptide and proinsulin leveled off with increasing glucose concentrations. Estimated by C-peptide-to-insulin ratios, clearance of endogenous insulin was not influenced by T. Glucose uptake in tissue was the same in T, DT, and UT during clamps, despite lower insulin levels in T and DT. Differences between groups in counterregulatory hormones, fat metabolites, alanine, or electrolytes did not account for these findings. Oxygen consumption was higher in the basal state in T and DT compared with UT but increased similarly in all groups in response to glucose. Conclusions: regular physical activity causes an adaptive decrease in glucose-mediated beta-cell secretion in humans. The training-induced decrease in glucose-stimulated insulin secretion is accurately matched to increased insulin action, keeping glucose disposal constant at any given plasma glucose concentration. Finally, training increases basal metabolic rate but does not influence glucose-induced thermogenesis or clearance of endogenous insulin.

scholarly journals The relationship between fasting hyperglycemia and insulin secretion in subjects with normal or impaired glucose tolerance

2008 ◽  
Vol 295 (2) ◽  
pp. E401-E406 ◽  
Author(s):  
Muhammad A. Abdul-Ghani ◽  
Masafumi Matsuda ◽  
Rucha Jani ◽  
Christopher P. Jenkinson ◽  
Dawn K. Coletta ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Plasma Glucose ◽  
Early Phase ◽  
Mexican Americans ◽  
Late Phase ◽  
Oral Glucose ◽  
C Peptide ◽  
The Relationship

To assess the relationship between the fasting plasma glucose (FPG) concentration and insulin secretion in normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) subjects, 531 nondiabetic subjects with NGT ( n = 293) and IGT ( n = 238; 310 Japanese and 232 Mexican Americans) received an oral glucose tolerance test (OGTT) with measurement of plasma glucose, insulin, and C-peptide every 30 min. The insulin secretion rate was determined by plasma C-peptide deconvolution. Insulin sensitivity (Matsuda index) was measured from plasma insulin and glucose concentrations. The insulin secretion/insulin resistance (IS/IR) or disposition index was calculated as ΔISR/ΔG ÷ IR. As FPG increased in NGT subjects, the IS/IR index declined exponentially over the range of FPG from 70 to 125 mg/dl. The relationship between the IS/IR index and FPG was best fit with the equation: 28.8 exp(−0.036 FPG). For every 28 mg/dl increase in FPG, the IS/IR index declined by 63%. A similar relationship between IS/IR index and FPG was observed in IGT. However, the decay constant was lower than in NGT. The IS/IR index for early-phase insulin secretion (0–30 min) was correlated with the increase in FPG in both NGT and IGT ( r = −0.43, P < 0.0001 and r = −0.20, P = 0.001, respectively). However, the correlation between late-phase insulin secretion (60–120 min) and FPG was not significant. In conclusion, small increments in FPG, within the “normal” range, are associated with a marked decline in glucose-stimulated insulin secretion and the decrease in insulin secretion with increasing FPG is greater in subjects with NGT than IGT and primarily is due to a decline in early-phase insulin secretion.

Mechanism, temporal patterns, and magnitudes of the metabolic responses to the KATP channel agonist diazoxide

2005 ◽  
Vol 288 (1) ◽  
pp. E80-E85 ◽  
Author(s):  
Bharathi Raju ◽  
Philip E. Cryer
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Temporal Patterns ◽  
Metabolic Responses ◽  
Nonesterified Fatty Acid ◽  
Nonesterified Fatty Acids ◽  
C Peptide

To assess the mechanism, temporal patterns, and magnitudes of the metabolic responses to the ATP-dependent potassium channel agonist diazoxide, neuroendocrine and metabolic responses to intravenous diazoxide (saline, 1.0 and 2.0 mg/kg) and oral diazoxide (placebo, 4.0 and 6.0 mg/kg) were assessed in healthy young adults. Intravenous diazoxide produced rapid, but transient, decrements ( P = 0.0023) in plasma insulin (e.g., nadirs of 2.8 ± 0.5 and 1.8 ± 0.3 μU/ml compared with 7.0 ± 1.0 μU/ml after saline at 4.0–7.5 min) and C-peptide ( P = 0.0228) associated with dose-related increments in plasma glucose ( P = 0.0044) and serum nonesterified fatty acids ( P < 0.0001). After oral diazoxide, plasma insulin appeared to decline, as did C-peptide, again associated with dose-related increments in plasma glucose ( P < 0.0001) and serum nonesterified fatty acids ( P = 0.0141). Plasma glucagon, as well as cortisol and growth hormone, was not altered. Plasma epinephrine increased ( P = 0.0215) slightly only after intravenous diazoxide. There were dose-related increments in plasma norepinephrine ( P = 0.0038 and P = 0.0005, respectively), undoubtedly reflecting a compensatory sympathetic neural response to vasodilation produced by diazoxide, but these would not raise plasma glucose or serum nonesterified fatty acid levels. Thus selective suppression of insulin secretion, without stimulation of glucagon secretion, raised plasma glucose and serum nonesterified fatty acid concentrations. These findings define the temporal patterns and magnitudes of the metabolic responses to diazoxide and underscore the primacy of regulated insulin secretion in the physiological regulation of postabsorptive carbohydrate and lipid metabolism.

Sensitivity of insulin secretion to feedback inhibition by hyperinsulinaemia

1981 ◽  
Vol 98 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Ralph A. DeFronzo ◽  
Christian Binder ◽  
John Wahren ◽  
Philip Felig ◽  
Eleuterio Ferrannini ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Feedback Inhibition ◽  
Normal Subjects ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Arterial Plasma

Abstract. The ability of insulin to inhibit its own secretion was examined in 15 normal subjects given an intravenous infusion of insulin in a dose of 0.25, 0.50, 1.0, 5.0 or 10.0 mU/kg/min for two hours. Arterial plasma insulin concentration achieved during the infusion segregated into three levels of hyperinsulinaemia: 35 ± 1 (mean ± sem), 87 ± 15 and 828 ± 210 μU/ml. Plasma glucose concentration was kept constant at the basal level by a variable glucose infusion. Fasting C-peptide (0.29 ± 0.02 pmol/ml) fell significantly in all subjects during hyperinsulinaemia and reached a concentration of 0.19 ± 0.03 pmol/ml at 60 min and 0.14 ± 0.03 at 120 min after the start of the insulin infusion. The C-peptide response was not related to the infusion dose nor to the steady state plasma insulin concentration. It is concluded that (a) basal insulin secretion as evaluated from C-peptide measurements is inhibited by small (24 ± 3 μU/ml) physiological elevations in plasma insulin concentration independent of changes in plasma glucose, and (b) supraphysiological or even pharmacological elevations in plasma insulin do not result in a further decrease in endogenous insulin secretion above that achieved with mild hyperinsulinaemia.

Does high-normal 2-hour post load plasma glucose after myocardial infarction in patients with normal glucose tolerance adversely affect prognosis?

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Chattopadhyay ◽  
A George ◽  
J John ◽  
T Sathyapalan
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Cohort Analysis ◽  
Normal Glucose Tolerance ◽  
Rank Test ◽  
Free Survival ◽  
Net Reclassification Improvement ◽  
Normal Glucose ◽  
Group 2 ◽  
Group 1

Abstract Background Type 2 diabetes mellitus (DM) and pre-DM, newly diagnosed after MI in patients without known DM adversely affects prognosis. 2-hour post-load glucose (2h-PG) predicts post-MI prognosis better than fasting plasma glucose (FPG). Plasma glucose below the conventional threshold for the diagnosis of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), affects post-MI prognosis. Purpose To test whether high-normal post-load plasma glucose in patients with normal glucose tolerance (NGT) would affect post-MI prognosis and whether FPG or 2h-PG increases this risk. Methods Retrospective cohort analysis of 425 MI survivors without known DM and with NGT followed up for (death and non-fatal MI) as MACE. MACE in patients with 2h-PG &gt; median for the whole cohort (Group 2), was compared with those at or below (Group 1). Event free survival in the two groups was estimated from the Kaplan–Meier curves and compared using log-rank test. Cox proportional hazard regression identified predictors of MACE. Continuous net reclassification improvement (NRI&gt;0) and integrated discrimination improvement (IDI) and c-statistics determined the added predictive value of glycaemic matrices. Results Median 2h-PG was 6.3 mmol/l. 219 patients in Group 1 and 206 in Group 2. Group 2 had higher age, prevalence of hypertension, hypercholesterolaemia, ST-segment depression and higher heart rate and GRACE scores. Median follow-up was 40.6 months. MACE was more frequent in Group 2 than Group 1 (OR 2.82, 95% CI 1.55 to 5.16, p&lt;0.001). MACE-free survival was higher in Group 1 (HR 2.43, 95% CI 1.53 to 3.85, p&lt;0.001). Group 2 (HR 2.42, 95% CI 1.44 to 4.04, p&lt;0.001) predicted the MACE-free survival. 2h-PG, but not the FPG independently predicted of MACE (HR 1.73, 95% CI 1.31 to 2.30, p&lt;0.001). Addition of 2h-PG to models containing FPG and other variables improved their predictive performance (NRI&gt;0 0.5062, p&lt;0.001; IDI 0.0376, p=0.003). The c-statistic increased when 2h-PG was added to the GRACE score only model (δAUC 0.037, 95% CI 0.012 to 0.081, p=0.046). Conclusion(s) This study suggests that “high-normal” 2h-PG is an independent predictor of post-MI prognosis. Normoglycaemic patients with 2h-PG ≥6.4 mmol/l, had worse post-MI prognosis compared to those with 2h-PG ≤6.3 mmol/l. The risk of MACE increased with increasing 2h-PG within the normal range. FPG had no effect on prognosis. Funding Acknowledgement Type of funding source: None

scholarly journals Hyperhomocysteinemia is an independent risk factor of atherosclerosis in patients with metabolic syndrome

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Giuseppina Piazzolla ◽  
Mafalda Candigliota ◽  
Margherita Fanelli ◽  
Anna Castrovilli ◽  
Elsa Berardi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Uric Acid ◽  
Folic Acid ◽  
Carotid Stenosis ◽  
Color Doppler ◽  
Elevated Serum ◽  
C Peptide ◽  
Group 2 ◽  
Group 1

Abstract Background Metabolic syndrome (MetS) is a clinical condition potentially promoting the development of atherosclerotic disease. To date, the clinical impact of elevated serum homocysteine (Hcy) levels in MetS is still under discussion. The aim of this cross sectional study was to evaluate the relationship between MetS and hyperhomocysteinemia and the potential role of Hcy in the pathogenesis of atherosclerotic complications of MetS. Methods We recruited 300 outpatients with MetS. All patients underwent a medical history collection, physical examination, blood sampling and carotid ultrasound echo-color Doppler. According to Hcy levels, MetS patients were divided into two groups: “normal” (< 10.7 μmol/l; n = 140, group 1) and “high” Hcy (≥ 10.7 μmol/l; n = 160, group 2). Comparisons between groups were made by Student’s t-test or Chi-square test. The effects of potential covariates on group differences were evaluated by general linear models. The relationships between continuous variables were assessed by simple or multiple correlation and by linear regression. Multiple regression models were built to evaluate the effects of Hcy, together with other potential risk factors, on carotid atherosclerosis. Results Patients with high Hcy were predominantly male and slightly older than group 1 patients. Smokers and non-smokers exhibited similar Hcy levels, nor was a statistical relationship between pack-years and Hcy observed. Group 2 showed lower levels of folic acid, vitamin D, high density lipoprotein (HDL)-cholesterol and glomerular filtration rate (e-GFR) than group 1, but higher levels of C-peptide, uric acid and triglycerides. In all patients, Hcy was positively correlated with C-peptide and uric acid and negatively with folic acid and e-GFR. Intima-media thickness (IMT) and carotid stenosis degree were significantly higher in patients with high Hcy and a positive relationship between Hcy and both IMT and carotid stenosis was detected in all patients. Finally, Hcy atherogenic effects were independent of other well-known atherosclerosis risk factors. Conclusions Our results highlight a link between MetS and hyperhomocysteinemia and a direct effect of Hcy on atherogenic process during MetS. Early correction of folic acid levels may contribute to prevent cardiovascular complications in MetS patients.

Abstract 16477: Sacubitril/valsartan as a Treatment for Resistant Hypertension in Patients With Heart Failure and Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Pardeep S Jhund ◽  
Alice M 1 ◽  
Marc A Pfeffer ◽  
Faiez ZANNAD ◽  
Martin P Lefkowitz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Resistant Hypertension ◽  
Preserved Ejection Fraction ◽  
Mineralocorticoid Receptor Antagonist ◽  
Drug Classes ◽  
Neprilysin Inhibitor ◽  
Group 2 ◽  
Design And Methods ◽  
Group 1

Objective: Heart failure with preserved ejection fraction (HFpEF) is typically a hypertensive phenotype and many HFpEF patients have difficult to control hypertension. We examined the effect of neprilysin inhibition on resistant hypertension in HFpEF patients in the PARAGON-HF trial. Patients entered a 1 to 4-week valsartan run-in (target dose 80mg bd), followed by sacubitril/valsartan run-in, before randomization to valsartan or sacubitril/valsartan (target doses 160mg bd or 200mg bd respectively). Design and methods: Patients were examined according to different definitions of resistant hypertension using systolic blood pressure (SBP) at the end of valsartan run-in. Group 1: SBP≥140mmHg (≥135mmHg if diabetes) despite treatment with a calcium channel blocker (CCB), diuretic and valsartan, Group 2: SBP≥130mmHg despite treatment with a CCB, diuretic and valsartan, or SBP<130mmHg despite treatment with a CCB, diuretic, mineralocorticoid receptor antagonist (MRA) and valsartan, and Group 3: SBP≥140mmHg (≥135mmHg if diabetes) despite treatment with a CCB, diuretic, MRA and valsartan (≥4 classes of SBP-reducing therapy, including MRA). We examined reduction in SBP from end of valsartan run-in to weeks 4 and 16 after randomization and the proportion of patients with controlled SBP at week 16 on sacubitril/valsartan vs valsartan. Results: Of 4796 patients randomized, criteria for resistant hypertension were fulfilled in 726 (15%) using the Group 1 definition, 1146 (24%) using the Group 2 definition and 132 (3%) in the third group. The combination of neprilysin inhibitor, angiotensin receptor blocker, CCB and diuretic (+/-MRA) reduced SBP and significantly increased the proportion of patients with controlled SBP (Table). Conclusion: Sacubitril/valsartan may be useful in treating resistant hypertension in patients with HFpEF, even in those who continue to have an elevated SBP despite treatment with at least 4 antihypertensive drug classes, including an MRA.

scholarly journals Prevalence, Clinical and Biochemical Spectrum, and Treatment Outcome of Acromegaly With Normal Basal GH at Diagnosis

2018 ◽  
Vol 103 (10) ◽  
pp. 3919-3924 ◽  
Author(s):  
Ana Laura Espinosa de los Monteros ◽  
Ernesto Sosa-Eroza ◽  
Baldomero Gonzalez ◽  
Victoria Mendoza ◽  
Moises Mercado
Keyword(s):  
Care Center ◽  
Tertiary Care ◽  
Real Life ◽  
Success Rates ◽  
Distinctive Features ◽  
Group 4 ◽  
Patient Groups ◽  
Group 2 ◽  
Design And Methods ◽  
Group 1

Abstract Context The term micromegaly has been used to describe a subset of patients who have elevated IGF-1 levels but apparently normal basal GH (bGH) concentrations and often a glucose-suppressed GH of &lt;1 ng/mL. Objective To evaluate the prevalence, clinical spectrum, and therapeutic outcome of acromegaly with normal bGH at diagnosis. Design and Methods Retrospective analysis of a cohort of patients with acromegaly diagnosed and treated at a tertiary care center. Results A cohort of 528 patients with acromegaly was stratified according to bGH at diagnosis: group 1, &lt;2 ng/mL, n = 16; group 2, 2 to 9.9 ng/mL, n = 202; group 3, 10 to 99 ng/mL, n = 294; and group 4, ≥100 ng/mL, n = 16. Patients in group 1 (normal bGH) constituted 3% of the total cohort and were significantly older and more likely to be male than patients in the other groups. The frequency of acromegalic symptoms, signs, and comorbidities was similar between the four patient groups. Patients in group 1 more often harbored microadenomas (75%) and had significantly lower median IGF-1 and postglucose GH levels. Surgical success rates were similar between patients from groups 1 (53.8%), 2 (54.1%), and 3 (36.9%), whereas only 13.3% of patients in group 4 achieved remission. Conclusion Normal bGH acromegaly is uncommon in real life. These patients have some distinctive features that argue against this being simply acromegaly in its early stages.

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