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Τετάρτη 28 Οκτωβρίου 2020

Effect of continuous positive airway pressure on gastroesophageal reflux in patients with obstructive sleep apnea: a meta-analysis

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Abstract

Purpose

Gastroesophageal reflux disease (GERD) often occurs in patients with obstructive sleep apnea (OSA). Although continuous positive airway pressure (CPAP) is considered to be the preferred treatment for OSA, the effect of CPAP therapy on reflux events remains controversial. In this study, we utilized meta-analysis to investigate whether or not CPAP treatment reduces the incidence of reflux.

Methods

Two independent reviewers obtained the data sources from the database of PubMed, Elsevier, Cochrane library, and CNKI using search terms, and then filtered the target articles based on the inclusion and exclusion criteria. RevMan (version 5.3) and STATA (version 12.0) were used for data synthesis. The effect of CPAP treatment on GERD was studied by calculating the weighted mean difference (WMD) and standard deviation (SD) before and after CPAP treatment.

Results

Ten studies involving a total of 272 participants were included in this study. The results showed that the total of WMD before and after CPAP was − 17.68 (95% CI − 30.67 to − 4.69) for percentage time pH < 4, − 24.66 (95% CI − 36.15 to − 13.18) for the longest reflux duration, − 27.53 (95% CI − 49.53 to − 5.52) for number of reflux events, − 49.76 (95% CI − 60.18 to − 39.35) for DeMeester score, − 1.85 (95% CI − 3.00 to − 0.71) for reflux diseases questionnaire (RDQ) score, and − 8.95 (95% CI − 16.00 to − 1.89) for reflux symptom index (RSI). The subgroup analysis demonstrated that the improvement of reflux symptoms was more obvious with the extension of treatment time.

Conclusions

This meta-analysis showed that CPAP treatment significantly reduces the incidence of reflux events in patients with OSA.

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Degos disease

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Degos disease
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Degos disease
Other names Köhlmeier-Degos disease
Degos-disease.jpg
Skin lesions in a person with Degos disease
Specialty Cardiology, dermatology Edit this on Wikidata
Degos disease, also known as Köhlmeier-Degos disease or malignant atrophic papulosis, is an extremely rare condition caused by blockage of arteries and veins. Individuals with this condition will develop papules. Those diagnosed with this disease may also develop complications due to impairment of internal organs. The exact underlying mechanism is still unknown, and an effective treatment is still being developed.[1] There are fewer than 50 living patients presently known worldwide, and fewer than 200 reported in medical literature. However, many individuals may go undiagnosed due to rarity of the disease.[2][3] Most individuals develop symptoms between the ages of 20–50; however, cases outside of this age range have been reported as well.[1]


Contents
1 Symptoms and signs
2 Causes
3 Mechanism
4 Diagnosis
5 Treatment
6 Recent research
7 History
8 References
8.1 Notes
8.2 Further reading
9 External links
Symptoms and signs
The characteristic symptom of Degos disease is the development of papules. Initially, individuals may have skin lesions or rashes, but they will proceed to develop distinct bumps, or papules.[4] Papules are circular in shape, have a porcelain-white center and red border. As papules age, the white centers will skin in and only the border will remain raised. Typically, papules range from 0.5 to 1 cm in width. Papules appear on the trunk and upper extremities and are not found on the individual's palms, soles, scalp, or face.[1]

Symptoms vary, depending on whether an individual has the benign variant or malignant variant of the disease. Both the benign and malignant forms have development of the characteristic papules. Individuals with the benign form will have the typical papules persisting anywhere from a few years to throughout their whole lives. In the benign form, no inner organs are affected. If an individual develops the malignant form, it means that not only are the papules present, but inner organs are involved. Most malignant cases involve problems of the gastrointestinal tract leading to small intestine lesions, abdominal pain, diarrhea, and bowel perforation. If the central nervous system is involved, symptoms can include headaches, dizziness, seizures, paralysis of cranial nerves, weakness, stroke, damage to small areas of the brain due to artery blockage (cerebral infarcts, and cerebral hemorrhage). Additional organs commonly impacted include the heart, lungs, and kidneys. Symptoms that may dev elop from damage to these organs include double vision (diplopia), clouding of lenses of eyes, swelling of the optic disc (papilledema), partial loss of vision, shortness of breath, chest pain, epilepsy, and thickening of pericardium.[3][4]

Someone with the benign form may suddenly develop symptoms of the malignant form.[1] Symptoms can last anywhere from a few weeks to several years. Onset of symptoms typically begins to manifest between the ages of 20–50.[5] A few cases of this condition in newborns have also been described.[6]

Causes
The papules characteristic for this disease develop due to infarctions, or blockages in small-medium arteries and veins. The underlying cause is unknown for this disease.[1] Though not confirmed, some cases have shown signs of inheritance between first-degree relatives. It has been suggested that the disease has a familial inheritance pattern; it is thought to be an autosomal dominant disorder. In most cases of familial inheritance, the benign variant of the disease has been present.[4][7][8]

Due to the lack of knowledge of the pathomechanism for this condition prevention strategies are not known. However, in order to prevent worsening of symptoms, consistent evaluations should be conducted by a physician.[1]

Mechanism
Although this disease has been known for around 70 years, the pathomechanism underlying it is still unknown.[1] Several hypotheses have been developed regarding the underlying mechanism for Degos disease. One theory suggests that inflammation of blood vessels may trigger the condition. Another theory has to do with Degos disease as a coagulopathy. Development of a thrombus and resulting reduction of blood flow is common in this condition. A reduction in blood flow throughout the body can lead to damaged endothelial cells and may perhaps lead to the formation of the characteristic papules. Another hypothesis suggests that abnormal swelling and proliferation of the vascular endothelium can lead to intestinal and central nervous system thrombosis, and ultimately lead to development of symptoms associated with Degos disease. Overall, individuals with Degos disease have abnormal blockages in their arteries and veins; however, the cause of these blockages is unknown.[1]

Diagnosis
Clinical evaluation and identification of characteristics papules may allow a dermatologist to diagnose Degos disease.[4] The papules have a white center and are bordered with a red ring. After lesions begin to appear, the diagnosis for Degos disease can be supported by histological findings. Most cases will show a wedge-shaped connective tissue necrosis in the deep corium. This shape is due to the blockage/occlusion of small arteries.[1]

Individuals may be diagnosed with the benign form if only the papules are present. However, an individual may be diagnosed with the malignant form if involvement of other organs like the lungs, intestine and/or central nervous system occurs. The malignant, or systematic form of this condition may suddenly develop even after having papules present for several years. In order to quickly diagnose this shift to the malignant variant of the disease, it is important for individuals to have consistent follow-up evaluations. In these evaluations, depending on which organs are suspected to be involved, the following procedures and tests may be conducted: skin inspection, brain magnetic resonance tomography, colonoscopy, chest X-ray, and/or abdominal ultrasound.[1]

Treatment
Due to the lack of knowledge around the underlying mechanism of malignant atrophic papulosis, an effective treatment method has not been developed.[1][1] Treatment for this condition is symptomatic.[4] However, several treatment methods have been tested and are still being developed as more information regarding the condition is found. Fibrinolytic and immunosuppressive therapeutic regimens were tested and found to be mostly unsuccessful as treatment methods.[1][8]

After treating conditions comorbid with Degos disease, physicians have recently found improvement in symptoms with the use of eculizumab and treprostinil.[9][10] Discovered by dermatopathologist, Cynthia Magro, response to eculizumab is often immediate and dramatic, but has been of limited duration and is expensive, needing to be infused every 14 days.[9] Treprostinil use has been reported to result in clearing of gastrointestinal and central nervous system findings as well as clearing of cutaneous lesions, but reports are limited. Treprostinil may be more effective than other vasodilators because it may also increase the population of circulating endothelial cells, allowing angiogenesis.[1]

Recent research
A 46-year-old male patient was diagnosed with the malignant, systemic form of the disease and was severely ill. The diagnosing dermatopathologist, Cynthia Magro MD, identified the presence of C5b-9 complexes in the involved vessels of the skin biopsy. For treatment of the thrombotic microangiopathy in this patient, she suggested the use of eculizumab, a humanized monoclonal antibody drug developed by Alexion Pharmaceuticals and approved by the Food and Drug Administration for treatment of Paroxysmal nocturnal hemoglobinuria. The patient experienced a dramatic improvement in his condition.[9] Lee Shapiro MD and Aixa Toledo-Garcia MD at Albany Medical College learned of the success with the adult patient, and became the first physicians to successfully treat a pediatric Degos patient with eculizumab.[10]

Dr. Shapiro later observed the resolution of Degos skin lesions in an adult patient with an overlap syndrome involving systemic lupus, systemic sclerosis, and Degos disease who was treated with treprostinil for her pulmonary hypertension. His pediatric Degos patient was developing significant complications despite treatment with eculizumab, so Dr. Shapiro's group became the first to treat a Degos patient with treprostinil.[10] To this point, all known long-term survivors of systemic Degos disease are being treated with a combination of eculizumab and treprostinil.[9][10]

History
In 1941, this disease was first described by Kohlmeier. However, it was not until 1942 that the disease was recognized as a new clinical entity by Robert Degos. Initially the condition was referred to as Degos Disease or Kohlmeier-Degos disease. However, Degos himself subsequently suggested the name "papulose atrophiante maligne," translated as malignant atrophic papulosis.[11]

References
Notes
Theodoridis, Athanasios; Makrantonaki, Evgenia; Zouboulis, Christos C. (2013-01-14). "Malignant atrophic papulosis (Köhlmeier-Degos disease) - A review". Orphanet Journal of Rare Diseases. 8: 10. doi:10.1186/1750-1172-8-10. ISSN 1750-1172. PMC 3566938. PMID 23316694.
"Degos Disease: Background, Pathophysiology, Epidemiology". 2017-02-07.
De Breucker S, Vandergheynst F, Decaux G (2008). "Inefficacy of intravenous immunoglobulins and infliximab in Degos' disease". Acta Clin Belg. 63 (2): 99–102. doi:10.1179/acb.2008.63.2.007. PMID 18575050. S2CID 34148667.
"Degos Disease - NORD (National Organization for Rare Disorders)". NORD (National Organization for Rare Disorders). Retrieved 2017-12-13.
Snow, J. L.; Muller, S. A. (June 1995). "Degos syndrome: malignant atrophic papulosis". Seminars in Dermatology. 14 (2): 99–105. doi:10.1016/S1085-5629(05)80004-5. ISSN 0278-145X. PMID 7640203.
Torrelo, A.; Sevilla, J.; Mediero, I.g.; Candelas, D.; Zambrano, A. (2002-05-01). "Malignant atrophic papulosis in an infant". British Journal of Dermatology. 146 (5): 916–918. doi:10.1046/j.1365-2133.2002.04677.x. ISSN 1365-2133. PMID 12000397.
Katz, Sara K.; Mudd, Leslie J.; Roenigk, Henry H. (1997). "Malignant atrophic papulosis (Degos' disease) involving three generations of a family". Journal of the American Academy of Dermatology. 37 (3): 480–484. doi:10.1016/s0190-9622(97)70151-8. PMID 9308565.
Powell; Bordea; Wojnarowska; Farrell; Morris (1999-09-01). "Benign familial Degos disease worsening during immunosuppression". British Journal of Dermatology. 141 (3): 524–527. doi:10.1046/j.1365-2133.1999.03050.x. ISSN 1365-2133. PMID 10583060.
Magro, CM; Poe, JC; Kim, C; Shapiro, L; Nuovo, G; Crow, MK; Crow, YJ (2011). "Degos disease: A C5b-9/interferon-α-mediated endotheliopathy syndrome". Am J Clin Pathol. 135 (4): 599–610. doi:10.1309/ajcp66qimfarlzki. PMID 21411783.
Shapiro, LS; Toledo-Garcia, AE; Farrell, JS (April 4, 2013). "Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil--early experience". Orphanet J Rare Dis. 8: 52. doi:10.1186/1750-1172-8-52. PMC 3636001. PMID 23557362.
Degos R.; Delort J.; Tricot R. (1942). "Dermatite papulosquameuse atrophiante". Bulletin de la Société Française de Dermatologie et de Syphiligraphie et de Ses Filiales. 49: 148–150.
Further reading
Scheinfeld N (September 2007). "Malignant atrophic papulosis". Clin. Exp. Dermatol. 32 (5): 483–7. doi:10.1111/j.1365-2230.2007.02497.x. PMID 17692056.
Fazio S (June 13, 2014). "Rash, Myalgia, and Weakness". Now@NEJM.
External links
Classification D
ICD-9-CM: 447.8OMIM: 602248MeSH: D054853DiseasesDB: 29425
External resources
eMedicine: derm/931
vte
Cardiovascular disease (vessels)
Categories: Rare diseasesDisorders causing seizures
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Degos disease is a very rare syndrome with multisystem vasculopathy of unknown cause. It can affect the skin, gastrointestinal tract, and central nervous system. However, other organs such as the kidney, lungs...
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The feasibility and safety of photoselective vaporization for prostate using a 180-W XPS Greenlight laser in day-surgery pattern in China

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Abstract

To evaluate the feasibility and safety of photoselective vaporization for prostate (PVP) with a 180-W XPS Greenlight laser as day surgery in the Chinese population. We retrospectively collected 114 cases undergoing the day surgery PVP and 198 cases undergoing conventional inpatient surgery PVP from April 2017 to March 2020. All patients' data including baseline characteristics, peri-operative data, post-operative outcomes, and complications were recorded and evaluated. The day-surgery procedures were successful in 110 patients. There were no significant differences in baseline characteristics in both groups. The catheterization time and hospitalization time were much shorter and economic cost was much lower in the day-surgery group than in the conventional inpatient surgery group. As for the post-operative complications, the incidence rate of the urinary retention is higher in the day-surgery group than in conventional inpatient surgery group. During the follow -up periods, the International Prostate Symptom Score (IPSS), quality of life (QoL), maximal urinary flow rate (Qmax), and post-void residual urine (PVR) improved significantly in both groups, and no differences were observed between the two groups. Compared to the conventional inpatient surgery, the day-surgery PVP is feasible and safe, which can reduce the hospitalization time and economic cost.

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Τρίτη 27 Οκτωβρίου 2020

The Effect of Wheel Exercise on Functional Indices of Cachexia

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imageIntroduction Cancer-related fatigue and muscle wasting have received significant attention over the last few decades with the goal of establishing interventions that can improve cancer patient life quality and survival. Increased physical activity has shown to reduce cancer-associated fatigue and has been proposed as a promising therapeutic to attenuate cancer-induced wasting. However, significant gaps remain in our understanding of how physical activity affects the compositional and functional changes that initiate muscle wasting. The purpose of the current study was to determine the effect of wheel exercise on body composition and functional indices of cancer cachexia before the development of significant wasting. Methods Thirteen-week-old male ApcMin/+ (MIN) and C57BL/6 (B6) mice were given free wheel access (W) or a locked wheel (Sed) for 5 wk. Results Wheel activity was reduced in the MIN compared with B6; however, wheel access increased complex II expression in isolated skeletal muscle mitochondria regardless of genotype. Wheel access had no effect on tumor burden or plasma interleukin-6 in the MIN. MIN-W increased body weight and lean mass compared with MIN-Sed, and there was a direct correlation between wheel distance and lean mass change. MIN-W increased grip strength and treadmill time to fatigue compared with MIN-Sed. Within MIN-W mice, skeletal muscle fatigability was only improved in high runners (>60 min·d−1). Conclusions Our results suggest that there were therapeutic benefits of increased activity related to body composition, behavior, and whole-body function that were not dependent on exercise duration; however, there was an exercise threshold needed to improve skeletal muscle fatigability in tumor-bearing mice. Interestingly, wheel access was able to improve compositional and functional outcomes without mitigating tumor number or size.
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Respiratory Muscle Fatigue Alters Cycling Performance and Locomotor Muscle Fatigue

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imagePurpose This study aimed to determine if preexisting respiratory muscle fatigue (RMF) alters motoneuronal output, locomotor muscle fatigue, and cycling performance. Methods Eight trained male cyclists performed 5-km cycling time trials after a resistive breathing task that induced RMF and under control conditions (CON). Motoneuronal output was estimated using vastus lateralis surface electromyography, and locomotor muscle fatigue was quantified as the change in potentiated quadriceps twitch force from preexercise to postexercise. Results Time to complete the time trial was 1.9% ± 0.9% longer in RMF compared with CON (P
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PLCD1: A Potential Therapeutic Target in the Treatment of Esophageal Squamous Cell Carcinoma?

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Apical pelvic organ prolapse repair via vaginal‐assisted natural orifice transluminal endoscopic surgery: Initial experience from a tertiary care hospital

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Abstract

Introduction

Natural orifice transluminal endoscopic surgery has been used for gynecologic operations in recent years. The aim of the study is to describe our initial experience using vaginal‐assisted natural orifice transluminal endoscopic surgery (vNOTES) for apical pelvic organ prolapse repair.

Methods

After patients underwent vaginal hysterectomy, vNOTES sacrocolpopexy (n = 4) or vNOTES high uterosacral ligament suspension (n = 7) were performed to treat symptomatic apical pelvic organ prolapse. Sociodemographic and clinical characteristics, Pelvic Organ Prolapse Quantification results, and recorded surgical data (eg, duration of surgery, intraoperative complications, additional prolapse and incontinence surgeries) were obtained from patient files and the hospital's database. Information from postoperative follow‐up visits, including complications and anatomical results, were also recorded.

Results

The mean age of the patients was 60.7 ± 9.1 years. The mean total operative time was 121.3 ± 22.7 minutes. The mean operative time for vaginal hysterectomy, vNOTES sacrocolpopexy, and vNOTES uterosacral ligament suspension was 46 ± 11.9, 65 ± 38, 25 ± 8.2 minutes, respectively. There were no intraoperative and postoperative complications observed. The mean postoperative 24‐hour visual analog scale score was 3.5 ± 1.9 for vNOTES sacrocolpopexy patients and 3.2 ± 0.9 for vNOTES uterosacral ligament suspension patients. Only one patient in the vNOTES sacrocolpopexy group had a recurrence; she experienced stage 2 anterior compartment prolapse 8 months after surgery.

Conclusion

As a treatment for apical pelvic organ prolapse, vNOTES is a feasible approach in both sacrocolpopexy and uterosacral ligament suspension.

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Single‐incision laparoscopic full‐thickness anterior abdominal wall repair of a Morgagni hernia using a suture‐assisting needle in a child: A case report

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Abstract

Single‐incision laparoscopic repair of a congenital Morgagni diaphragmatic hernia using a suture‐assisting needle was performed in a 1‐year‐old boy. Three ports were inserted through a single umbilical incision to repair the 2.5 × 2.3‐cm defect. The full‐thickness muscle layer of the anterior abdominal wall and the posterior rim of the defect were penetrated with the suture‐assisting needle holding a thread, which was then released. The needle tip was pulled back over the muscle layer, shifted laterally, and again passed through the muscle layer and the posterior rim. The thread was then captured by the needle and pulled out through the anterior abdominal wall. Five mattress sutures were placed in this way and tied subcutaneously. The postoperative course was uneventful, and the cosmetic outcome was favorable. A suture‐assisting needle is useful for completing full‐thickness anterior abdominal wall repair, which is important for preventing the recurrence of a congenital Morgagni diaphragmatic hernia.

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Does the time from symptom onset to surgery affect the outcomes of patients with acute appendicitis? A prospective cohort study of 255 patients

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Abstract

Introduction

The objective of this study was to evaluate the impact of operative timing on outcomes of acute appendicitis.

Methods

This study examined adult patients who had presented to the hospital with acute appendicitis and had undergone appendectomy from December 2017 to February 2019. Time delay and outcomes of perforated and non‐perforated appendicitis were compared. Patients were classified into five groups based on the period from symptom onset to operation: group 1, <24 hours; group 2, ≥24 and <48 hours; group 3, ≥48 and <72 hours; group 4, ≥72 and <96 hours; and group 5, ≥96 hours. The five groups were compared, with risk of perforation assessed in particular.

Results

A total of 255 patients were included in the analysis. Symptom duration, operative time, and length of postoperative hospital stay (P < .001) were significantly longer in the perforated group (n = 49) than in the non‐perforated group (n = 206). The perforated group also had a higher conversion rate to open procedures (P = .002) and a higher rate of wound infection (P = .034). Group 1 had 53 patients, group 2 had 95 patients, group 3 had 57 patients, group 4 had 32 patients, and group 5 had 18 patients. The incidence of appendiceal perforation and median operative time progressively increased along with symptom duration in the five groups. In multivariate analyses, independent risk factors for appendiceal perforation were male gender (odds ratio = 2.33, 95% confidence interval [CI]: 1.07‐5.08) and symptom duration ≥48 hours (relative to ≥24 and <48 hours) (odds ratio = 4.64, 95%CI: 1.76‐12.27). Patients with symptom duration ≥72 ho urs had a significantly longer operative time than those with symptom duration ≥48 and <72 hours (β = 21.38, 95%CI: 5.66‐37.11, P = .008).

Conclusion

The risk of perforation increased significantly 48 hours after the onset of appendicitis. Symptoms duration ≥72 hours was associated with a longer operative time.

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Laparoscopic surgery in patients with cystic fibrosis: A systematic review

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Abstract

Introduction

Laparoscopic surgery may be advantageous for cystic fibrosis (CF) patients because it leads to fewer complications than open surgery. However, it could still lead to pulmonary and cardiovascular complications in CF patients. We aimed to systematically review the use of laparoscopic surgery in CF patients.

Methods

A systematic review was performed in compliance with PRISMA guidelines. A literature search was performed using PubMed/MEDLINE, ScienceDirect, EMBASE, and Google Scholar, with "cystic fibrosis and laparoscopic surgery" and "cystic fibrosis and minimally invasive surgery" used as the search terms. The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) criteria were applied. The protocol was registered with the PROSPERO register.

Results

Six studies met the predetermined inclusion criteria; accordingly, two studies provided high‐quality evidence and four provided moderate‐quality evidence. The interrater correlation was convincing (r s = .95, P = .02, two‐tailed). Therefore, three quantitative studies and three qualitative studies were assessed and evidence‐graded in accordance with the GRADE protocol.

Conclusion

The benefits of laparoscopic surgical interventions for patients with CF were supported with good evidential value and recognized as a safe and suitable surgical option.

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