Background: The literature places the occurrence of paediatric Monteggia lesions between 1.5% and 3% of all childhood elbow injuries. There are circumstances, which may make early correct diagnosis difficult. Failure to make an early correct diagnosis may have catastrophic consequences on joint range of motion in the chronic stage. The goal of this paper is to describe our three-step approach to the treatment of acute Monteggia lesions based on the stability and radiological appearance of the fracture dislocation, to give an overview of possible pitfalls and clinical and radiological signs that aid the diagnostic process. Methods: Retrospective analysis of 23 patients treated for this type of injury at our Department over a period of 6 years was performed. Treatment options were 1. Closed reduction under image intensifier followed by immobilization in over the elbow cast, 2. Open reduction and intramedullary nailing with ESIN, or 3. Open reduction and plate osteosynthesis. Average follow-up was 37 months. In our Department we aim for definitive treatment of fracture-dislocations in children within the acute setting. In the 23 acute cases, the selected procedure-reduction + casting/reduction + ESIN/reduction + plating-was performed within 2 to 16 h of arrival. 10 patients were treated with reduction + casting, 10 with reduction + ESIN and 3 with reduction + plating. Results: 21 patients were available for long-term follow-up. No nerve or tendon injuries or infections were observed in these cases. By managing the patients with the Three Step Method retaining the reduction was successful in all but one of our acute cases in the study period. Excellent range of motion was observed in all three groups. Conclusions: The Three Step Method allows for primary definitive treatment of these lesions with low complication rates and good range of motion result. Implementing the three step method in the acute phase helps avoid catastrophic consequences on joint range of motion in the chronic stage.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine reproductive disorders in women. Vitamin D deficiency is also quite common in this condition. The degree of vitamin D deficiency correlates with the severity of PCOS. Both male and female vitamin D levels play a role in fertility and affect the outcomes of in vitro fertilization (IVF). Moreover, fertility and IVF indicators are improved by vitamin D not only in healthy women but in those diagnosed with PCOS. Both vitamin D deficiency and PCOS increase pregnancy-related complications. Vitamin D supplementation and optimal vitamin D levels decrease both maternal and fetal risk for complications and adverse events. Furthermore, vitamin D supplementation may ameliorate or even prevent pregnancy-related reversible bone loss in mothers. This review emphasizes the roles of vitamin D deficiency and vitamin D supplementation and their correlation with PCOS regarding reproductive health.

Background Andropause and hypertension also increase the risk of coronary artery damage. Aim To investigate the effect of testosterone deficiency and hypertension on intramural coronary vessels. Methods 4 groups of 8-week-old Sprague-Dawley rats were studied: control male (Co, n=10), orchidectomized male (OCT, n=13), angiotensin (AII) hypertensive male (AII, n=10), and AII hypertensive and OCT (AII + OCT, n=8). Surgical orchidectomy was performed, and an osmotic minipump was inserted for chronic angiotensin II infusion (100 ng/min/kg). After 4 weeks, spontaneous tone and biomechanical properties of the intramural coronary resistance artery were investigated in vitro, by pressure microarteriography. Outcomes Morphology and biomechanics of the intramural coronaries were evaluated: the outer diameter, wall thickness–to–lumen diameter ratio, and tangential wall stress in the contracted and relaxed states. Results The outer diameter was reduced in OCT and AII + OCT groups (on 50 mmHg 315 ± 20 Co; 237 ± 21 OCT; 291 ± 16 AII, and 166 ± 12 μm AII + OCT). The increased wall thickness–to–lumen diameter ratio resulted in lower tangential wall stress in AII + OCT rats (on 50 mmHg 19 ± 2 Co; 24 ± OCT; 26 ± 5 AII, and 9 ± 1 kPa AII + OCT). Spontaneous tone was increased in the hypertensive rats (AII and AII + OCT groups) (on 50 mmHg 7.7 ± 1.8 Co; 6.1 ± 1.4 OCT; 14.5 ± 3.0 AII, and 17.4 ± 4.1 % AII + OCT). Clinical Implications Andropause alone can be considered as a cardiovascular risk factor that will further exacerbate vascular damage in hypertension. Strengths & Limitations A limitation of our study is that it was performed on relatively young rats, and the conclusions might not apply to coronary remodelling in older animals with slower adaptation processes. Conclusions Testosterone deficiency and hypertension damage the mechanical adaptation of the vessel wall additively: double noxa caused inward eutrophic remodeling and increased tone.

Objective To better understand factors that may play a role in the development of varicosities. Methods We induced combined flow-pressure disturbance in the saphenous system of the rat by performing chronic partial clipping of the main branch. Biomechanical and quantitative histological testing was undertaken. Results A rich microvenous network developed. Bloodflow decreased to 0.65 ± 0.18 µl/s (control side, 3.5 ± 1.4 µl/s) and pressure elevated to 6.8 ± 0.7 mmHg (control side, 2.3 ± 0.2 mmHg, p < 0.05). Involution of the wall and lumen was observed (16.5%, 28.7% and 35.5% reduction in outer diameter, wall thickness and wall mass respectively, p < 0.05). Elevated macrophage (CD68) and cell division (Ki67) activity was observed. Elastic tissue and smooth muscle actin became less concentrated in the inner medial layers. Conclusions Low-flow induced morphological shrinking of the lumen in veins may override pressure-induced morphological distension. Loosening of the force-bearing elements during flow-induced wall remodeling may be an important pathological component in varicosity.

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