Transient hyperthyroidism after surgery for secondary hyperparathyroidism: a common problem

Background

Postoperative hyperthyroidism occurs in approximately one third of patients following parathyroidectomy due to primary hyperparathyroidism (PHP), but has only rarely been described in secondary hyperparathyroidism (SHP). The frequency, course, and laboratory markers of postoperative hyperthyroidism in SHP remain unknown. Our purpose was to evaluate the frequency and the clinical course of postoperative hypcrthyroidism following surgery of SHP and to determine the diagnostic value of thyroglobulin in this setting.

Material and Methods

A total of 40 patients undergoing parathyroidectomy because of SHP were included in this study. Thyroid stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fl4), and thyroglobulin (Tg) were determined one day before and on day 1, 3, 5, 10, and 40 after surgery. At each of these visits patients were clinically evaluated for signs or symptoms of hyperthyroidism.

Results

Biochemical evidence of hyperthyroidism was evident in 77% of patients postoperatively despite of preoperatively normal serum levels. TSH dropped from 1.18 ± 0.06mU/L to 0.15 ± 0.07mU/L (p = 0.0015). Free triiodothyronine (fT3) and fT4 levels increased from 2.86 ± 0.02ng/L and 10.32 ± 0.13ng/L, respectively, to their maximum of 4.83 ± 0.17ng/L and 19.35 ± 0.58ng/L, respectively. Thyroglobulin levels rose from 3.8 ± 0.8ng/mL to 111.8 ± 45.3ng/mL (p < 0.001). At day 40 all thyroid related laboratory values were within normal range. Correlation analysis of postoperative values revealed significant correlations for lowest TSH (r = -0.32; p = 0.038), and highest fT3 (r = 0.55; p < 0.001) and fT4 levels (r = 0.67; p < 0.001) with Tg.

Conclusion

Transient hyperthyroidism is frequent after parathyroidectomy for SHP with Tg being a suitable marker. Awareness of this self-limiting disorder is important to avoid inappropriate and potentially harmful treatment.     

Levosimendan induces NO production through p38 MAPK,ERK and Akt in porcine coronary endothelial cells: role for mitochondrial KATP channel

Background and purpose:

Levosimendan acts as a vasodilator through the opening of ATP-sensitive K⁺ channels (K_ATP) channels. Moreover, the coronary vasodilatation caused by levosimendan in anaesthetized pigs has recently been found to be abolished by the nitric oxide synthase (NOS) inhibitor N^ω-nitro-L-arginine methyl ester, indicating that nitric oxide (NO) has a role in the vascular effects of levosimendan. However, the intracellular pathway leading to NO production caused by levosimendan has not yet been investigated. Thus, the purpose of the present study was to examine the effects of levosimendan on NO production and to evaluate the intracellular signalling pathway involved.

Experimental approach:

In porcine coronary endothelial cells (CEC), the release of NO in response to levosimendan was examined in the presence and absence of N^ω-nitro-L-arginine methyl ester, an adenylyl cyclase inhibitor, K_ATP channel agonists and antagonists, and inhibitors of intracellular protein kinases. In addition, the role of Akt, ERK, p38 and eNOS was investigated through Western blot analysis.

Key results:

Levosimendan caused a concentration-dependent and K⁺-related increase of NO production. This effect was amplified by the mitochondrial K_ATP channel agonist, but not by the selective plasma membrane K_ATP channel agonist. The response of CEC to levosimendan was prevented by the K_ATP channel blockers, the adenylyl cyclase inhibitor and the Akt, ERK, p38 inhibitors. Western blot analysis showed that phosphorylation of the above kinases lead to eNOS activation.

Conclusions and implications:

In CEC levosimendan induced eNOS-dependent NO production through Akt, ERK and p38. This intracellular pathway is associated with the opening of mitochondrial K_ATP channels and involves cAMP.     

"Medical high risk" designation is not associated with survival after carotid artery stenting

BACKGROUND: While medical high risk (MHR) has been proposed as an indication for carotid artery stenting (CAS), the impact of MHR on long-term survival and stroke after CAS has not been described. METHODS: A retrospective chart review of CAS procedures at our institution was performed. One hundred seventy-nine consecutive patients who underwent 196 CAS procedures were classified by MHR status based on cardiac, pulmonary, and renal criteria routinely used in high-risk clinical trials. Survival and stroke rates were compared after 90 CAS procedures in MHR patients vs 106 CAS procedures in normal risk patients. Survival results were also compared with 365 contemporaneous carotid endarterectomy (CEA) procedures in 346 patients. RESULTS: The mean age of CAS patients was 72 years, with 87% having a smoking history, 85% hypertension, 38% diabetes, 39% symptomatic, and 74% documented coronary artery disease. Mean follow-up was 23 months. Recurrent stenosis after CEA comprised 21% of all CAS procedures. During the 30-day post-procedure period, there were five minor strokes, one major stroke, and one death, for a combined stroke/death rate of 3.6%. Kaplan-Meier analysis demonstrated mortality of 5% at 1 year and 21% at 3 years for the entire cohort. Cox regression analysis found that MHR designation was not associated with increased mortality or an increase in a composite end point of death or stroke. MHR patients had mortality of 4% at 1 year and 22% at 3 years. Normal risk patients had mortality of 6% at 1 year and 20% at 3 years. Preoperative age over 80 years old, low density lipoprotein (LDL) > or =160 mg/dL, and serum creatinine > or =1.5 mg/dL conferred statistically significant risk for death (Hazard ratios: 2.9, 4.3, and 2.4, respectively). As a point of comparison, a contemporaneous group of CEA patients were analyzed similarly. After adjusting for age over 80 years old and serum creatinine > or =1.5 mg/dL, there was no survival difference between MHR patients undergoing CAS or CEA. CONCLUSIONS: The presence of MHR did not impact long-term survival or stroke rate after CAS, and overall survival of MHR patients in our series was comparable with risk-adjusted controls undergoing CEA. These results suggest the need for more refined predictors of medical risk to optimally guide patients in selecting carotid revascularization strategies.