Totally endoscopic lateral parathyroidectomy: prospective evaluation of 200 patients. ESES 2010 Vienna presentation.

PURPOSE: Several new minimally invasive techniques (mini-open, video-assisted, and endoscopic procedures) for parathyroidectomy have been described. However, totally endoscopic lateral approach parathyroidectomy (Henry technique) is not routinely performed. METHODS: This is a prospective study of 200 consecutive patients that underwent totally endoscopic lateral parathyroidectomy. RESULTS: Two hundred of 387 patients (52%) with primary hyperparathyroidism were included. Fifty-six patients (28%) were converted to open parathyroidectomy. Causes for conversion were lack of intraoperative localization (11%), difficult dissection (10%), bleeding (4%), failure of normalization of IOPTH results (2%), and other causes (1%). Gland localization (areas 1 to 2 versus area 3) and CaPTHus score (<3 versus ≥3) were not associated with the risk of conversion. Mean postoperative follow-up was 13 months, and 196 patients (98%) were cured. CONCLUSIONS: Totally endoscopic lateral approach can be proposed in more than half of the patients with good immediate results. Conversion rate remains important and may explain low acceptance rate of this technique.

Endocrine response after severe subarachnoid hemorrhage related to sodium and blood volume regulation.

BACKGROUND: Hyponatremia is often associated with, and worsens, the prognosis of severe aneurysmal subarachnoid hemorrhage (SAH). Several possible endocrine perturbations of variable severity and variable sodium and water intake have been described in SAH. However, a comprehensive study of the different hormonal systems involved in sodium and water homeostasis and circulating blood volume modifications is still needed. Our aim was to assess water and sodium regulation after severe SAH by investigating blood volume and several hormonal regulatory systems in the context of hyponatremia prevention by controlled sodium intake. METHODS: Nineteen mechanically ventilated patients with severe SAH, were prospectively studied. Replacement of sodium was at least 4.5 mmol x kg(-1) x d(-1) and adjusted on natriuresis. Hormones involved in electrolyte and water homeostasis: vasopressin, renin, angiotensin, aldosterone, and natriuretic peptides were assessed every 3 days for 12 days. Red blood cell volume was measured by the isotopic method (technetium-labeled red blood cells), in the first 48 h after admission and at day 7. Cardiac function was assessed using electrocardiogram, transthoracic echocardiography, and troponin Ic (cTnI). Outcome was assessed at 3 mo. RESULTS: After SAH onset, hyponatremia, but not decreased circulating blood volume, was prevented by high sodium and water infusion adapted to renal excretion. The hormonal profiles were characterized by an increase in renin, angiotensin II, natriuretic peptide concentrations associated with increased troponin Ic, stable low levels of vasopressin, and the absence of increased aldosterone concentrations. There were no correlations between hormone concentrations and natriuresis. CONCLUSION: After severe SAH, in the context of multiple clinical interventions, increased natriuresis and low blood volume are consistent with cerebral salt wasting syndrome, probably related to the sequence of severe SAH, highly increased sympathetic tone, hyperreninemic hypoaldosteronism syndrome, and increased natriuretic peptides release.

Comparison of arginine vasopressin, terlipressin, or epinephrine to correct hypotension in a model of anaphylactic shock in anesthetized brown Norway rats.

BACKGROUND: Arginine vasopressin (AVP) and terlipressin were proposed as alternatives to catecholamines in shock states characterized by decreased plasma AVP concentrations. The endogenous plasma AVP profile in anaphylactic shock is unknown. In an ovalbumin-sensitized anesthetized anaphylactic shock rat model, the authors investigated (1) plasma AVP concentrations and (2) the dose versus mean arterial pressure response for exogenous AVP and terlipressin and compared them with those of epinephrine. METHODS: In a first series of rats (n = 12), endogenous plasma AVP concentrations were compared with a model of pharmacologically induced hypotension (nicardipine, n = 12). A second series was randomly assigned to three groups (AVP, n = 7; terlipressin, n = 7; epinephrine, n = 7) and dose (AVP: 8 doses, 0.03-100 U/kg; terlipressin: 7 doses, 0.03-30 microg/kg; epinephrine: 7 doses, 0.3-300 microg/kg)-response mean arterial pressure curves were plotted. Data are expressed as mean +/- SD. RESULTS: Endogenous plasma AVP concentrations were significantly lower in anaphylactic shock (57 +/- 26 pg/ml) than in the nicardipine group (91 +/- 43 pg/ml; P < 0.05). The ED50 was 10.6 microg/kg (95% confidence interval, 7.1-15.9) for epinephrine and 4.1 U/kg (95% confidence interval, 3.0-5.6) for AVP. Terlipressin did not change mean arterial pressure, regardless of the dose used. CONCLUSIONS: In a rat model, anaphylactic shock is associated with inadequately low plasma AVP concentrations. For clinically relevant doses, AVP and epinephrine had comparable effects on mean arterial pressure and heart rate values, whereas, unexpectedly, terlipressin was ineffective. These results are consistent with reports in humans experiencing anaphylaxis where AVP injection restored arterial pressure.

Anaphylactic shock: a form of distributive shock without inhibition of oxygen consumption.

BACKGROUND: The pathophysiology of anaphylactic shock during anesthesia is incompletely characterized. It is described as distributive by analogy with septic shock (anaerobic metabolism, high tissue oxygen pressure [Ptio2] values). The Ptio2 profile and its metabolic consequences during anaphylaxis are not known. METHODS: Ovalbumin-sensitized anaphylactic shock rats (n = 11) were compared to nicardipine-induced hypotension rats (n = 12) for systemic hemodynamics, Ptio2, sympathetic nervous system activation, skeletal muscle blood flow, and interstitial lactate and pyruvate concentrations using combined microdialysis and polarographic Clark-type oxygen probes. RESULTS: In both groups, the time course and the magnitude of arterial hypotension were similar. The ovalbumin group but not the nicardipine group displayed decreased skeletal muscle blood flow (from 45 +/- 6.2 ml x 100 g(-1) x min(-1) to 24.3 +/- 5 ml x 100 g(-1) x min(-1); P < 0.0001) and Ptio2 values (from 42 +/- 5 to 5 +/- 2; P < 0.0001). The ovalbumin group had more intense sympathetic nervous system activation with higher plasma epinephrine and interstitial norepinephrine concentrations. For the ovalbumin group, there was skeletal muscle anaerobic metabolism (lactate concentration increased from 0.446 +/- 0.105 to 1.741 +/- 0.459 mm; P < 0.05) and substrate depletion (pyruvate concentration decreased from 0.034 +/- 0.01 mm to 0.006 +/- 0.002 mm; P < 0.05) leading to increased interstitial lactate/pyruvate ratios (from 17 +/- 6 to 311 +/- 115; P < 0.05). CONCLUSIONS: This profile suggests decreased skeletal muscle blood flow and oxygen delivery. Persistent energy consumption results in decreased Ptio2 and substrate depletion through anaerobic glycolysis leading to complete failure of cellular energy production. This could explain rapid organ dysfunction and resuscitation difficulties.

Age-related femoral bone loss in men: evidence for hyperparathyroidism and insulin-like growth factor-1 deficiency.

BACKGROUND: We sought to determine the extent to which the age-related decline of femoral neck (FN) bone mineral density (BMD) might be explained by the age-related change of body composition and biological parameters and the mechanisms by which these factors might influence FN BMD in men. METHODS: The relationships between FN BMD and anthropometric, hormonal, and biochemical parameters and bone turnover markers were studied in 82 men aged 25-86 years. RESULTS: Age was associated with a decline of FN BMD and osteocalcin (OC), bone alkaline phosphatase (bALP), and urinary C-telopeptide (p <.05). The significant relationship between FN BMD and OC (p <.01) did not remain after adjustment for age. With use of multiple linear regression and adjusting for all significant variables associated with FN BMD in univariate analysis (p <.01) (age, weight, lean and fat mass, height, and levels of dehydroepiandrosterone sulfate, insulin-like growth factor [IGF-1], testosterone, and parathyroid hormone [PTH]), age accounted for 29.5% of FN BMD variance. When age was excluded from the model, PTH accounted for 19.5% and IGF-1 for 10% of the FN BMD variance. Bone turnover markers were significantly intercorrelated, and levels of IGF-1 were positively associated with those of bALP and OC (p <.05). CONCLUSIONS: These results show that age is a strong predictor of FN BMD in men, resulting in a decline of bone remodeling, especially of bone formation. The results also show that, after taking into account anthropometric and other biological factors possibly involved in bone aging, the major part of the effect of age on bone is explained by the age-related increase of PTH and decrease of IGF-1 in men, suggesting that all measures taken to limit these age-related changes may be effective in the prevention of the age-related decline of FN BMD in men.

Serum leptin level is a predictor of bone mineral density in postmenopausal women.

To assess whether leptin is an independent predictor of bone mineral density (BMD) in postmenopausal women, we studied the relationships of BMD to serum leptin, 25(OH)D, 1,25(OH)(2)D, PTH, E2, dehydroepiandrosterone sulfate, GH, IGF-I, creatinine clearance, calcium intake, fat mass, and lean mass in 107 women aged 50-90 yr. We also related serum leptin to markers of bone formation [serum bone alkaline phosphatase and osteocalcin (OC)] and resorption (urine C-telopeptide of type I collagen). In stepwise multiple linear regression, lean mass explained 28.5%, age 10.3%, and leptin 7.2% of the whole body BMD variance. Age explained 21.1%, lean mass 12.8%, and leptin 3.7% of the femoral neck BMD variance. After adjustment for fat mass and creatinine clearance, correlations between leptin and bone alkaline phosphatase (positive) and OC (negative) disappeared but, remained significant with urine C-telopeptide of type I collagen (r = -0.27, P < 0.01). Markers of bone formation and resorption were strongly intercorrelated. These data demonstrate that leptin is an independent predictor of whole body and femoral neck BMD in postmenopausal women. Although the relationships between leptin and markers of bone formation appear complex, leptin may exert a protective effect on bone by limiting the excessive bone resorption coupled to bone formation associated with bone loss after menopause.