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Endometriosis - A Chameleon: Patients' Perception of Clinical Symptoms, Treatment Strategies and Their Impact on Symptoms.

ABSTRACT: Introduction: Endometriosis is a chronic disease with differing clinical presentations. Treatment strategies depend mainly on clinical presentation and patient lifestyle. In women newly diagnosed with endometriosis, it is often difficult to understand the pathophysiologic origin, the potential individual impairment due to disease and the different treatment options. Compliance with the selected treatment is therefore often not optimal. Material and Methods: In a descriptive study, data of 51 women with endometriosis (mean age 36.2 years ± 11.3) were analyzed according to the predominant clinical presentation: asymptomatic disease, disease with typical symptoms, ovarian cysts or infertility. Results: More than 50 % of patients ascribed a therapeutic benefit to surgical intervention or endocrine treatment, especially women in the subgroup with dysmenorrhea who received combined treatment. It should be noted that in the group of women facing infertility, more than half stated that they could not decide on the value of diagnostic and therapeutic reproductive medicine. Nevertheless, more than half of the women in this group became pregnant within two years after the initial diagnosis. Discussion: When deciding on the best treatment strategy for endometriosis, it is important to take account of potential pain and infertility. Women's perception of endometriosis will vary depending on their symptoms, the time of diagnosis and their lifestyle. Offering continuous information on clinical aspects and manifestations of the disease may improve treatment outcomes. Personalized counseling is an essential part of the clinical management of the disease.

SUBMITTER: Wimberger P

PROVIDER: S-EPMC4210380 | biostudies-other | 2014 Oct

REPOSITORIES: biostudies-other

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Project description:The very first line of defense in humans is innate immunity, serving as a critical strongpoint in the regulation of inflammation. Abnormalities of the innate immunity machinery make up a motley group of rare diseases, named 'autoinflammatory', which are caused by mutations in genes involved in different immune pathways. Self-limited inflammatory bouts involving skin, serosal membranes, joints, gut and other districts of the human body burst and recur with variable periodicity in most autoinflammatory diseases (ADs), often leading to secondary amyloidosis as a long-term complication. Dysregulated inflammasome activity, overproduction of interleukin (IL)-1 or other IL-1-related cytokines and delayed shutdown of inflammation are pivotal keys in the majority of ADs. The recent progress of cellular biology has clarified many molecular mechanisms behind monogenic ADs, such as familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome (or 'autosomal dominant familial periodic fever'), cryopyrin-associated periodic syndrome, mevalonate kinase deficiency, hereditary pyogenic diseases, idiopathic granulomatous diseases and defects of the ubiquitin-proteasome pathway. A long-lasting history of recurrent fevers should require the ruling out of chronic infections and malignancies before considering ADs in children. Little is known about the potential origin of polygenic ADs, in which sterile cytokine-mediated inflammation results from the activation of the innate immunity network, without familial recurrency, such as periodic fever/aphthous stomatitis/pharyngitis/cervical adenopathy (PFAPA) syndrome. The puzzle of febrile attacks recurring over time with chameleonic multi-inflammatory symptoms in children demands the inspection of the mixture of clinical data, inflammation parameters in the different disease phases, assessment of therapeutic efficacy of a handful of drugs such as corticosteroids, colchicine or IL-1 antagonists, and genotype analysis to exclude or confirm a monogenic origin.

Project description:BackgroundTGF-β has potent profibrotic activity in vitro and has long been implicated in systemic sclerosis (SSc), as expression of TGF-β-regulated genes is increased in the skin and lungs of patients with SSc. Therefore, inhibition of TGF-β may benefit these patients.MethodsPatients with early, diffuse cutaneous SSc were enrolled in an open-label trial of fresolimumab, a high-affinity neutralizing antibody that targets all 3 TGF-β isoforms. Seven patients received two 1 mg/kg doses of fresolimumab, and eight patients received one 5 mg/kg dose of fresolimumab. Serial mid-forearm skin biopsies, performed before and after treatment, were analyzed for expression of the TGF-β-regulated biomarker genes thrombospondin-1 (THBS1) and cartilage oligomeric protein (COMP) and stained for myofibroblasts. Clinical skin disease was assessed using the modified Rodnan skin score (MRSS).ResultsIn patient skin, THBS1 expression rapidly declined after fresolimumab treatment in both groups (P = 0.0313 at 7 weeks and P = 0.0156 at 3 weeks), and skin expression of COMP exhibited a strong downward trend in both groups. Clinical skin disease dramatically and rapidly decreased (P < 0.001 at all time points). Expression levels of other TGF-β-regulated genes, including SERPINE1 and CTGF, declined (P = 0.049 and P = 0.012, respectively), and a 2-gene, longitudinal pharmacodynamic biomarker of SSc skin disease decreased after fresolimumab treatment (P = 0.0067). Dermal myofibroblast infiltration also declined in patient skin after fresolimumab (P < 0.05). Baseline levels of THBS1 were predictive of reduced THBS1 expression and improved MRSS after fresolimumab treatment.ConclusionThe rapid inhibition of TGF-β-regulated gene expression in response to fresolimumab strongly implicates TGF-β in the pathogenesis of fibrosis in SSc. Parallel improvement in the MRSS indicates that fresolimumab rapidly reverses markers of skin fibrosis.Trial registrationClinicaltrials.gov NCT01284322.

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Endometriosis - A Chameleon: Patients' Perception of Clinical Symptoms, Treatment Strategies and Their Impact on Symptoms.

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