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.     

Locking compression plate fixation of Vancouver type-B1 periprosthetic femoral fractures

BACKGROUND: Fractures occurring at or near the distal tip of a hip prosthesis with a stable femoral stem (Vancouver type-B fractures) are associated with many complications because of the inherently unstable fracture pattern. Locking compression plates use screws that lock into the plate allowing multiple points of unicortical fixation. Such unicortical fixation may lower the risk of damage to the cement mantle or a stable femoral stem during the treatment of a periprosthetic femoral fracture. The purpose of this study was to analyze clinically and radiographically a group of patients with a Vancouver type-B1 periprosthetic femoral fracture treated with open reduction and internal fixation with use of a locking compression plate. METHODS: Fourteen consecutive patients (fourteen hips) with a Vancouver type-B1 periprosthetic femoral fracture were treated with a locking compression plate. There were five men and nine women with an average age of sixty-eight years at the time of fracture. All of the fractures occurred after a total hip arthroplasty performed with cement, and eleven of the arthroplasties were revisions. In addition to the plate, cortical strut allografts were used to stabilize five fractures. The patients were assessed clinically and radiographically. RESULTS: The average duration of follow-up was twenty months. Eight fractures healed uneventfully at an average of 5.4 months. Three treatment constructs failed with fracture of the plate within twelve months after surgery. An additional three constructs also failed because of plate pullout. All failures except one occurred in constructs in which a cortical strut allograft had not been utilized. CONCLUSIONS: On the basis of the high failure rate in this series of patients, locking compression plates do not appear to offer advantages over other types of plates in the treatment of type-B1 periprosthetic femoral fractures. Despite the potential to preserve the cement mantle, the locked screws did not appear to offer good pullout resistance in this fracture type. We believe that supplementation with strut allografts should be used routinely if this type of locking compression plate is selected to treat these fractures.     

Viability of impacted bone allografts under metal mesh at the calcar in revision surgery of the hip

Metal meshes are used in revision surgery of the hip to contain impacted bone grafts in cases with cortical or calcar defects in order to provide rotational stability to the stem. However, the viability of bone allografts under these metal meshes has been uncertain. We describe the histological appearances of biopsies obtained from impacted bone allografts to the calcar contained by a metal mesh in two femoral reconstructions which needed further surgery at 24 and 33 months after the revision procedure. A line of osteoid and viable new bone was observed on the surface of necrotic trabeculae. Active bone marrow between these trabeculae showed necrotic areas in some medullary spaces with reparative fibrous tissue and isolated reactive lymphocytes. This is interpreted as reparative changes after revascularisation of the cancellous allografts. These pathological findings are similar to those reported in allografts contained by cortical host bone and support the hypothesis that incorporation of morcellised bone under metal meshes is not affected by these devices.