Kronična opstruktivna plućna bolest karakterizirana je trajnom, progresivnom opstrukcijom dišnih putova uzrokovanom upalnom reakcijom u tim putovima i plućnom parenhimu na inhalacijske toksične ...čestice ili dim. Osnovni su ciljevi farmakološkog liječenja KOPB-a smanjenje simptoma, učestalosti i težine egzacerbacija te poboljšanje podnošenja fizičkog napora i zdravstvenog statusa. Osnova farmakološkog liječenja stabilnoga simptomatskog KOPB-a jesu bronhodilatatori (beta-agonisti i antikolinergici) sami ili u kombinaciji s inhalacijskim kortikosteroidima (ICS). Za pacijente koji imaju trajne simptome preporučuje se redovita primjena dugodjelujućih bronhodilatatora. Oni znatno poboljšavaju plućnu funkciju, kvalitetu života vezanu uza zdravlje i smanjuju učestalost egzacerbacija u usporedbi s placebom. Ukupno gledajući, dugodjelujući muskarinski antagonisti (LAMA) dovode do većeg poboljšanja parametara plućne funkcije, smanjenja učestalosti akutnih egzacerbacija uz manje neželjenih događaja u odnosu prema dugodjelujućim beta2-agonistima (LABA). U pacijenata čija bolest nije dobro kontrolirana primjenom monoterapije preporučuje se kombinacijska terapija koja se sastoji od dva dugodjelujuća bronhodilatatora različita mehanizma djelovanja. Kombinacijska terapija LABA-LAMA znatno poboljšava plućnu funkciju, simptome i zdravstveni status s obzirom na monoterapiju. Sigurnosni profil kombinacije LAMA-LABA usporediv je s LABA-om i LAMA-om kada se daje kao monoterapija. U pacijenata koji su skloni egzacerbacijama kombinacija ICS-a s LABA-om učinkovitija je nego bilo koja od ovih komponenata samostalno u poboljšanju plućne funkcije, zdravstvenog statusa i smanjenja učestalosti egzacerbacija. U bolesnika s teškim i jako teškim stupnjem KOPB-a i povišenim rizikom od egzacerbacija trojna terapija koja se sastoji od ICS-a, LABA-e i LAMA-e dodatno poboljšava plućnu funkciju, reducira učestalost egzacerbacija i smanjuje zaduhu u odnosu prema kombinaciji ICS-LABA.
As the SARS-CoV-2 virus started its fulminate spread, due to strict epidemiological measures, athletes were transferred to unsupervised online training. This resulted in injury increase occurrence in ...elite sport. Some of many reasons for this are detraining process linked with reversible decrease in muscle mass and increase in body fat content.
We present the unique case of the 13-year-old healthy, junior female figure skater who suffered from multiple injuries associated with unsupervised training and detraining during COVID-19 lockdown. This case reports injuries described in elite athletes’ population, but never reported cumulatively in three months’ time period. Healthy elite athlete with magnetic resonance imaging was diagnosed
with a stress fracture of the second and stress reaction of the fourth metatarsal bone, which occurred during online unsupervised training. The same patient also suffered from lumbar discus protrusion on L4-L5 segment and discus bulging sign on L3-L4 and L5-S1 segments, which occurred after lockdown period, in immediate return to sport. Individual rehabilitation program, which included different modalities of physical therapy during which special attention was given to strengthening, stretching, proprioceptive and dynamic neuromuscular stabilization exercises, resulted in safe and pain free return to sport.
A multi-faced controlled exercise program should be considered as part of successful rehabilitation program in elite sport. As part of injury prevention program, we suggest that sporting federations in collaboration with medical and sport experts develop and implement different and convenient sport- specific guidelines to prevent a rapid increase of injuries in different sport disciplines.
Ozljeda prednjeg križnog ligamenta najčešća je ozljeda ligamenta koljena, naročito kod sportaša, zbog velikih tjelesnih napora i zahtjeva tijekom redovnih sportskih aktivnosti. LCA (lat. ligamentum ...cruciatum anterius) je ključna struktura koljena za održavanje njegove funkcionalne stabilnosti i pravilne biomehanike. Ne samo da ozljeda LCA nije rijetkost, već predstavlja jednu od težih akutnih
ozljeda u sportu pa je shodno tome postala predmetom brojnih istraživanja. Veći rizik od ove ozljede imaju žene zbog brojnih anatomskih i hormonalnih čimbenika, a kao najčešće beskontakne mehanizme ozljeđivanja u literaturi se navode nagla zaustavljanja, promjene smjera kretanja ili doskoci. Liječenje LCA ozljede je konzervativno i operativno. Sportaši, izloženi velikim opterećenjima tijekom treninga i natjecanja, uglavnom biraju operativno liječenje, nakon kojeg slijedi dugotrajan i zahtjevan proces rehabilitacije u koji su uključeni liječnici, fizioteraputi i tim stručnjaka koji se brine o zdravlju sportaša. Motiviranost sportaša utječe na krajnje ishode liječenja. Ciljevi akutne faze rehabilitacije su fokusirani na smanjenje edema i hematoma, postepeno vraćanje opsega pokreta te pravilnu aktivaciju mišića kvadricepsa. Nakon početne faze slijedi progresivno jačanje svih mišića koji sudjeluju u funkcionalnoj stabilnosti koljena, vježbe propriocepcije, ravnoteže, stabilnosti, brzine aktivacije muskulature
i sportu specifično prilagođene vježbe kako bi se sportaš na što bolji i kvalitetniji način pripremio za puni povratak sportskim aktivnostima. Iako postoje propisane smjernice i protokoli za rehabilitaciju te prevenciju LCA ozljede, liječenje sportaša je usredotočeno na potpuno individualni pristup liječenju. Povratak redovnim treninzima i sportskom natjecanju predviđa se otprilike 6 – 9 mjeseci nakon ozljede, no novija saznanja ukazuju da je ponekad preporučljiva i značajno dulja rehabilitacija koja ovisi o samom sportašu, sportu i sportaševu reagiranju na cjelokupni tijek liječenja. Kako bi se rizik od ponovne ozljede smanjio na minimum, prije sigurnog povratka sportu potrebno je napraviti objektivna testiranja funkcionalne stabilnosti koljena.
Mouse models indicate that metastatic dissemination occurs extremely early; however, the timing in human cancers is unknown. We therefore determined the time point of metastatic seeding relative to ...tumour thickness and genomic alterations in melanoma. Here, we find that lymphatic dissemination occurs shortly after dermal invasion of the primary lesion at a median thickness of ~0.5 mm and that typical driver changes, including BRAF mutation and gained or lost regions comprising genes like MET or CDKNA2, are acquired within the lymph node at the time of colony formation. These changes define a colonisation signature that was linked to xenograft formation in immunodeficient mice and death from melanoma. Thus, melanoma cells leave primary tumours early and evolve at different sites in parallel. We propose a model of metastatic melanoma dormancy, evolution and colonisation that will inform direct monitoring of adjuvant therapy targets.
Sentinel lymph node spread is a crucial factor in melanoma outcome. We aimed to define the impact of minimal cancer spread and of increasing numbers of disseminated cancer cells on melanoma-specific ...survival.
We analyzed 1,834 sentinel nodes from 1,027 patients with ultrasound node-negative melanoma who underwent sentinel node biopsy between February 8, 2000, and June 19, 2008, by histopathology including immunohistochemistry and quantitative immunocytology. For immunocytology we recorded the number of disseminated cancer cells (DCCs) per million lymph node cells (DCC density DCCD) after disaggregation and immunostaining for the melanocytic marker gp100. None of the control lymph nodes from non-melanoma patients (n = 52) harbored gp100-positive cells. We analyzed gp100-positive cells from melanoma patients by comparative genomic hybridization and found, in 45 of 46 patients tested, gp100-positive cells displaying genomic alterations. At a median follow-up of 49 mo (range 3-123 mo), 138 patients (13.4%) had died from melanoma. Increased DCCD was associated with increased risk for death due to melanoma (univariable analysis; p<0.001; hazard ratio 1.81, 95% CI 1.61-2.01, for a 10-fold increase in DCCD + 1). Even patients with a positive DCCD ≤3 had an increased risk of dying from melanoma compared to patients with DCCD = 0 (p = 0.04; hazard ratio 1.63, 95% CI 1.02-2.58). Upon multivariable testing DCCD was a stronger predictor of death than histopathology. The final model included thickness, DCCD, and ulceration (all p<0.001) as the most relevant prognostic factors, was internally validated by bootstrapping, and provided superior survival prediction compared to the current American Joint Committee on Cancer staging categories.
Cancer cell dissemination to the sentinel node is a quantitative risk factor for melanoma death. A model based on the combined quantitative effects of DCCD, tumor thickness, and ulceration predicted outcome best, particularly at longer follow-up. If these results are validated in an independent study, establishing quantitative immunocytology in histopathological laboratories may be useful clinically.
Background Sentinel lymph node spread is a crucial factor in melanoma outcome. We aimed to define the impact of minimal cancer spread and of increasing numbers of disseminated cancer cells on ...melanoma-specific survival. Methods and Findings We analyzed 1,834 sentinel nodes from 1,027 patients with ultrasound node-negative melanoma who underwent sentinel node biopsy between February 8, 2000, and June 19, 2008, by histopathology including immunohistochemistry and quantitative immunocytology. For immunocytology we recorded the number of disseminated cancer cells (DCCs) per million lymph node cells (DCC density DCCD) after disaggregation and immunostaining for the melanocytic marker gp100. None of the control lymph nodes from non-melanoma patients (n = 52) harbored gp100-positive cells. We analyzed gp100-positive cells from melanoma patients by comparative genomic hybridization and found, in 45 of 46 patients tested, gp100-positive cells displaying genomic alterations. At a median follow-up of 49 mo (range 3-123 mo), 138 patients (13.4%) had died from melanoma. Increased DCCD was associated with increased risk for death due to melanoma (univariable analysis; p<0.001; hazard ratio 1.81, 95% CI 1.61-2.01, for a 10-fold increase in DCCD + 1). Even patients with a positive DCCD ≤3 had an increased risk of dying from melanoma compared to patients with DCCD = 0 (p = 0.04; hazard ratio 1.63, 95% CI 1.02-2.58). Upon multivariable testing DCCD was a stronger predictor of death than histopathology. The final model included thickness, DCCD, and ulceration (all p<0.001) as the most relevant prognostic factors, was internally validated by bootstrapping, and provided superior survival prediction compared to the current American Joint Committee on Cancer staging categories. Conclusions Cancer cell dissemination to the sentinel node is a quantitative risk factor for melanoma death. A model based on the combined quantitative effects of DCCD, tumor thickness, and ulceration predicted outcome best, particularly at longer follow-up. If these results are validated in an independent study, establishing quantitative immunocytology in histopathological laboratories may be useful clinically. Please see later in the article for the Editors' Summary
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