Hepatitis E virus (HEV) is the causative agent for enteric non-A, non-B hepatitis. Transmission is mainly via the fecal-oral route but the possibility of an additional parenteric transmission has been raised. Patients undergoing chronic hemodialysis (HD) have an increased risk of exposure to blood transmitted agents. Previous studies concerning prevalence of antibodies to HEV (anti-HEV) among HD patients gave conflicting results. The aim of the study presented here was to determine the prevalence of anti-HEV among HD patients of a well-defined semi-rural region in central Greece (Thessalia region). All patients (n=351, 234 males, mean age 60 ± 14 years) who were being treated in the HD units of central Greece (n=5) during 2001 were tested for anti-HEV antibody. Two commercially available specific solid-phase enzyme-linked immunoassays were applied for anti-HEV detection. Hepatitis B virus markers, antibodies to HCV, HIV and HTLV were also screened in all patients by commercially available assays. Serum aminotransferase (AST, ALT) levels were measured by spectrophotometry. 17 anti-HEV-positive patients were found and prevalence was 4.8%, varying from 1.8 - 9.8% in the various HD units. Prevalence of HBsAg and anti-HCV was 5.7% (2.9 - 15%) and 23.6% (11.5 −36.2%) respectively. The anti-HEV prevalence was increased compared to healthy blood donors in Greece (0.26%, p & 0.01). The highest prevalence of anti-HEV was seen at the HD unit of the General Hospital of Karditsa (9.8%). Risk factors for anti-HEV antibody were not identified: no association was found between anti-HEV positivity and age or sex, duration of HD, hepatitis B or C virus infection markers, previously elevated aminotransferase levels or history of transfusion. Our investigation of HEV infection in the cohort of HD patients in central Greece showed that the prevalence of anti-HEV was greater than in healthy blood donors. There was no association to blood borne infections (HBV, HCV). The high prevalence of anti-HEV we found in one HD unit was probably related to a local infection in the past. However, long-term prospective studies are needed in an attempt to identify whether intra-unit factors are also responsible for the increased prevalence of serologic markers of HEV infection among HD patients.
Endocrine organs are metastatic targets for several primary cancers, either through direct extension from nearby tumour cells or dissemination via the venous, arterial and lymphatic routes. Although any endocrine tissue can be affected, most clinically relevant metastases involve the pituitary and adrenal glands with the commonest manifestations being diabetes insipidus and adrenal insufficiency respectively. The most common primary tumours metastasing to the adrenals include melanomas, breast and lung carcinomas, which may lead to adrenal insufficiency in the presence of bilateral adrenal involvement. Breast and lung cancers are the most common primaries metastasing to the pituitary, leading to pituitary dysfunction in approximately 30% of cases. The thyroid gland can be affected by renal, colorectal, lung and breast carcinomas, and melanomas, but has rarely been associated with thyroid dysfunction. Pancreatic metastasis can lead to exo-/endocrine insufficiency with renal carcinoma being the most common primary. Most parathyroid metastases originate from breast and lung carcinomas and melanoma. Breast and colorectal cancers are the most frequent ovarian metastases; prostate cancer commonly affects the testes. In the presence of endocrine deficiencies, glucocorticoid replacement for adrenal and pituitary involvement can be life saving. As most metastases to endocrine organs develop in the context of disseminated disease, surgical resection or other local therapies should only be considered to ameliorate symptoms and reduce tumour volume. Although few consensus statements can be made regarding the management of metastases to endocrine tissues because of the heterogeneity of the variable therapies, it is important that clinicians are aware of their presence in diagnosis.
Three patients (2 male and 1 female) undergoing maintenance hemodialysis for more than 4 years with tumoral calcifications were treated by sodium thiosulfate. All patients had periarticular and soft tissue calcification. A considerable regression of calcified masses with concurrent clinical improvement was noted in 2 of the 3 patients.
Abductor tendon lesions and insertional tendinopathy are the most common causes of lateral thigh pain. Gluteal tendon pathology is more prevalent in women and frequency increases with age. Chronic atraumatic tears result in altered lower limb biomechanics. The chief complaint is lateral thigh pain. Clinical examination should include evaluation of muscle strength, lumbar spine, hip and fascia lata pathology. The hip lag sign and 30-second single leg stance tests are useful in diagnosing abductor insufficiency. Magnetic resonance imaging (MRI) is the gold-standard investigation to identify abductor tendon tears and evaluate the extent of muscle fatty infiltration that has predictive value on the outcome of abductor repair. Abductor tendinosis treatment is mainly conservative, including non-steroidal anti-inflammatory medications, activity modification, local corticosteroid injections, plasma-rich protein, physical and radial shockwave therapy. The limited number of available high-quality studies on treatment outcomes and limited evidence between tendinosis and partial ruptures make it difficult to provide definite conclusions regarding the best management of gluteal tendinopathy. Surgical management is indicated in complete and partial gluteal tendon tears that are unresponsive to conservative treatment. There are various open and arthroscopic surgical procedures for direct repair of abductor tendon tears. There is limited evidence concerning surgical management outcomes. Prerequisites for effective tendon suturing are neurologic integrity and limited muscle fatty infiltration. Chronic irreparable tears with limited muscle atrophy and limited fatty infiltration can be augmented with grafts. Gluteus maximus or/vastus lateralis muscle transfers are salvage reconstruction procedures for the management of chronic end-stage abductor tears with significant tendon insufficiency or gluteal atrophy. Cite this article: EFORT Open Rev 2020;5:464-476. DOI: 10.1302/2058-5241.5.190094
Introduction: The treatment options of chronic abductor insufficiency in the setting of muscle degeneration, are limited and technically demanding. We present the outcomes of a salvage technique for unreconstructable, chronic abductor tears performed by a single surgeon. Methods: We retrospectively evaluated 38 patients who were surgically managed for chronic abductor insufficiency. Patients without hip implants and patients following primary or revision total hip arthroplasty (THA) were involved. All patients had a Trendelenburg gait, impaired muscle strength of abduction (⩽M4) and fatty degeneration of muscles (Goutallier ⩾3). They underwent transfer of a flap of the anterior third of gluteus maximus to the greater trochanter that was sutured under the slightly mobilised vastus lateralis. The level of pain, functional scores, muscle strength and Trendelenburg gait were re-evaluated at 12 postoperative months. Results: The mean age of patients was 70.2 years. 10 patients received the tendon transfer on a native hip, 6 following primary THA and 22 after revision THA. The mean pain level (3.2 vs. 7, p < 0.001) and Harris Hip Score (80.2 vs. 41.6, p < 0.001) and the median abductor strength (4 vs. 3, p < 0.001) was significantly improved compared to the preoperative scores. 26 patients demonstrated negative and 12 positive Trendelenburg sign at 12 postoperative months. No serious complications were reported. Conclusions: This salvage technique improved the strength of abduction and functional results and reduced the level of pain in 80% of patients with chronic abductor tears. The short-term outcomes of the procedure were favourable; however, further evaluation is needed.
Protein synthesis is a central and dynamic process, frequently deregulated in cancer through aberrant activation or expression of translation initiation factors and tRNAs. The discovery of tRNA-derived fragments, a new class of abundant and, in some cases stress-induced, small noncoding RNAs has perplexed the epigenomics landscape and highlights the emerging regulatory role of tRNAs in translation and beyond. Skin is the biggest organ in human body, which maintains homeostasis of its multilayers through regulatory networks that induce translational reprogramming, and modulate tRNA transcription, modification and fragmentation, in response to various stress signals, like UV irradiation. In this review, we summarize recent knowledge on the role of translation regulation and tRNA biology in the alarming prevalence of skin cancer.
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