Update on Open Abdomen Management: Achievements and Challenges

The open abdomen technique is one of the greatest advances in recent times and has enormous application in the daily management of the critically ill or injured patient. It results in tremendous benefits to the initial resuscitation of these patients but also brings on many challenges beyond those that might be expected from the primary illness or injury. Recent advances in the management of the open abdomen have provided the means to overcome the challenges and reap the benefits.     

An Update on the Treatment of Chorea

Purpose of review

There are many causes for chorea, including genetic, autoimmune, pharmacological, and structural lesions. Where appropriate, treatment is based on reversing the underlying cause of chorea; many cases are self-limited, resolving when the primary disorder is treated. This review focuses on the management of chorea due to untreatable causes.

Recent findings

There are a limited number of double-blind randomized control trials assessing the efficacy of specific chorea treatments. Most therapeutic recommendations are based on small open-label studies, case reports, and expert opinion. This is in part due to the heterogeneity of chorea and chorea-associated syndromes and the variety of neurodegenerative phenotypes with variable progression rates.

Summary

Chorea can be treated with a variety of medications ranging from antiepileptics to antipsychotics. The recent development of selective vesicular monoamine transporter blocking agents has allowed for targeted chorea management with minimal side effects. Neurosurgical interventions such as deep brain surgery (DBS) and pallidotomy are reserved for medication-refractory chorea. As a symptom of neurodegenerative disease, chorea is only one aspect of the basal ganglia syndromes, and often, a multidisciplinary approach tailored to individual patient needs provides the best management.

     

Distal Radioulnar Joint Osteoarthritis: An Update on Treatment Options

The distal radioulnar joint (DRUJ), the articulation between the sigmoid notch of the radius and the distal ulna, plays a pivotal role in stability and load bearing and allows for pronation and supination of the forearm. Osteoarthritis (OA) of the DRUJ commonly occurs due to distal radius trauma but may also be the result of conditions such as joint instability, septic arthritis, or primary OA. It is initially managed with conservative therapy, but surgery is often considered when nonoperative methods fail. The surgical approaches available to treat this pathology have grown over the years. The procedures have generally favorable outcomes, each with their own unique complications and considerations. This paper comprises a review of the outcomes and complications for the different procedures commonly used to surgically treat DRUJ OA.     

Interventional Radiological Treatment of Hepatocellular Carcinoma: An Update

Hepatocellular carcinoma is the commonest primary liver tumor and its incidence is on an increase.Transplantation and surgical resection are the gold standard curative treatment options but less than 20%patients are surgical candidates because of advanced liver disease and/or co-morbidities.Various interventional radiological procedures have been developed and intensively investigated for treatment of inoperable HCC.This review summarizes the various interventional radiological treatments in HCC including patient selection, procedural considerations and response evaluation. Transarterial chemoembolization, radioembolization and radiofrequency ablation are mainly discussed.     

Pulsed Dye Laser Treatment of Warts: An Update

BACKGROUND: Warts are a therapeutic challenge. New studies indicate that pulsed dye laser therapy may be effective, with clearance rates of 72 to 93%. OBJECTIVE: To determine clearance rate in pulsed dye laser treatment of warts and compare our rate to those of other published studies. METHODS: Thirty-three patients with 96 warts received pulsed dye laser treatment for recalcitrant plantar, digital, peri- and subungual, and body warts. RESULTS: Forty-eight percent of patients had complete wart clearance; 45% partially cleared. Sixty-nine percent of those who cleared remained wart-free for an average of 11 months. Mean fluence was 9.4 J/cm2, with an average of 3.4 treatments. Body and palmar warts responded best, digital and peri- and subungual next, and plantar lesions worst. No significant side effects were observed. CONCLUSION: Pulsed dye laser is an effective treatment option for recalcitrant warts with an excellent side effect profile. However, our response rates were not as high as those previously reported, and we feel that further studies would be useful.     

Sclerostin Protects Against Vascular Calcification Development in Mice

Sclerostin is a negative regulator of the Wnt/β-catenin signaling and is, therefore, an important inhibitor of bone formation and turnover. Because ectopic vascular calcification develops in a similar way to bone formation, one might reasonably attribute a role to sclerostin in this pathological process. Ectopic calcification, especially vascular calcification, importantly contributes to mortality in elderly and patients with diabetes, osteoporosis, chronic kidney disease (CKD), and hypertension. The central players in this ectopic calcification process are the vascular smooth muscle cells that undergo dedifferentiation and thereby acquire characteristics of bonelike cells. Therefore, we hypothesize that depletion/deactivation of the Wnt/β-catenin signaling inhibitor sclerostin may promote the development of ectopic calcifications through stimulation of bone-anabolic effects at the level of the arteries. We investigated the role of sclerostin (encoded by the Sost gene) during vascular calcification by using either Sost^−/− mice or anti-sclerostin antibody. Sost^−/− and wild-type (WT) mice (C57BL/6J background) were administered an adenine-containing diet to promote the development of CKD-induced vascular calcification. Calcifications developed more extensively in the cardiac vessels of adenine-exposed Sost^−/− mice, compared to adenine-exposed WT mice. This could be concluded from the cardiac calcium content as well as from cardiac tissue sections on which calcifications were visualized histochemically. In a second experiment, DBA/2J mice were administered a warfarin-containing diet to induce vascular calcifications in the absence of CKD. Here, warfarin exposure led to significantly increased aortic and renal tissue calcium content. Calcifications, which were present in the aortic medial layer and renal vessels, were significantly more pronounced when warfarin treatment was combined with anti-sclerostin antibody treatment. This study demonstrates a protective effect of sclerostin during vascular calcification. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Current Update on HIV-associated Vascular Disease and Endothelial Dysfunction

Highly active antiretroviral therapy (HAART) has greatly reduced the risk of early death from opportunistic infections and extended the lifespan of people infected with the human immunodeficiency virus (HIV). Thus, many complications and organic damage in the HIV-infected population emerge. Cardiovascular disease as coronary artery disease has become a matter of particular concern. Its incidence is greatly increased in the HIV-infected population over that of people of the same age in the absence of general cardiovascular risk factors. Despite several clinical and laboratory studies in the association between HIV infection and cardiovascular disease, the pathogenic mechanisms of this significant clinical problem are largely unknown and are now under active investigation. Endothelial dysfunction is possibly the most plausible link between HIV infection and atherosclerosis. Increased expression of adhesion molecules such as intercellular adhesion molecule (ICAM)-1 and endothelial adhesion molecule (E-selectin) and inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL-6 has been reported in HIV-positive patients. The effect of HAART on endothelial function in HIV-positive patients is also demonstrated. In this review, we focus on the recent research update of HIV-associated vascular disease and vascular injury. We analyze and discuss the recent clinical and laboratory investigations on the effect of HIV, viral protein, and HAART therapy on endothelial injury and vascular disease; identify the areas of controversy and clinical relevance; and suggest some directions for future research. This work was presented at the Molecular Surgeon Symposium on Vascular Injury, Repair and Remodeling at the Baylor College of Medicine, Houston, Texas, May 15 and 16, 2006. The symposium was supported by a grant from the National Institutes of Health National Institute of Health (to C. Chen: R13 HL0836500)     

Nedd4 Deficiency in Vascular Smooth Muscle Promotes Vascular Calcification by Stabilizing pSmad1

The nonosseous calcification process such as atherosclerosis is one of the major complications in several types of metabolic diseases. In a previous study, we uncovered that aberrant activity of transforming growth factor β (TGF‐β) signaling pathway could contribute to the vascular smooth muscle cells’ (VSMCs) calcification process. Also, we identified NEDD4 E3 ligase as a key suppressor of bone morphogenetic protein (BMP)/Smad pathway via a polyubiquitination‐dependent selective degradation of C‐terminal phosphorylated Smad1 (pSmad1) activated by TGF‐β. Here, we further validated and confirmed the role of Nedd4 in in vivo vascular calcification progression. First, Nedd4 deletion in SM22α‐positive mouse tissues (Nedd4^fl/fl;SM22α‐Cre) showed deformed aortic structures with disarranged elastin fibers at 24 weeks after birth. Second, vitamin D–induced aorta vascular calcification rate in Nedd4^fl/fl;SM22α‐Cre mice was significantly higher than their wild‐type littermates. Nedd4^fl/fl;SM22α‐Cre mice showed a development of vascular calcification even at very low‐level injection of vitamin D, but this was not exhibited in wild‐type littermates. Third, we confirmed that TGF‐β1–induced pSmad1 levels were elevated in Nedd4‐deficient primary VSMCs isolated from Nedd4^fl/fl;SM22α‐Cre mice. Fourth, we further found that Nedd4^fl/fl;SM22α‐Cre mVSMCs gained mesenchymal cell properties toward osteoblast‐like differentiation by a stable isotope labeling in cell culture (SILAC)‐based proteomics analysis. Finally, epigenetic analysis revealed that methylation levels of human NEDD4 gene promoter were significantly increased in atherosclerosis patients. Collectively, abnormal expression or dysfunction of Nedd4 E3 ligase could be involved in vascular calcification of VSMCs by activating bone‐forming signals during atherosclerosis progression. © 2016 American Society for Bone and Mineral Research.