Salvage Focal Cryotherapy Offers Similar Short-term Oncologic Control and Improved Urinary Function Compared With Salvage Whole Gland Cryotherapy for Radiation-resistant or Recurrent Prostate Cancer

BackgroundWe compared the short-term oncologic and functional outcomes of salvage focal cryotherapy (SFC) with those of salvage total cryotherapy (STC) for radiotherapy (RT)-persistent/recurrent prostate cancer.Materials and MethodsWe queried the Cryo On-Line Database registry for men who had undergone SFC and STC of the prostate for RT-persistent or recurrent disease. Propensity score weighting was used to match age at treatment, presalvage therapy prostate-specific antigen level, Gleason sum, and presalvage cryotherapy androgen deprivation therapy status. The primary outcome was progression-free survival.ResultsA total of 385 men with biopsy-proven persistent or recurrent prostate cancer after primary RT were included in the present study. The median follow-up, age, prostate-specific antigen, and Gleason sum before salvage cryotherapy was 24.4 months (first and third quartile, 9.8 and 60.3), 70 years (first and third quartile, 66 and 74 years), 4 ng/dL (first and third quartile, 2.7 and 5.6 ng/dL), and 7 (first and third quartile, 6 and 8), respectively. After propensity score weighting, the difference in progression-free survival was not statistically significant between the patients who had undergone STC and those who had undergone SFC (79.8% vs. 76.98%; P = .11 on weighted log-rank test). SFC was associated with a lower probability of post-treatment transient urinary retention (5.6% vs. 22.4%; P < .001). No significant differences were found in the incidence of rectal fistula (1.4% vs. 3.8; P = .30), new-onset urinary incontinence within 12 months (9.3% vs. 15.1%; P = .19), or new-onset erectile dysfunction within 12 months (52.6% vs. 59.6%; P = .47) between the SFC and STC groups, respectively.ConclusionsSTC resulted in similar 2-year oncologic outcomes compared with SFC in the RT-persistent/recurrent disease population. However, the patients who had undergone SFC had a lower urinary retention rate compared with those who had undergone STC.     

Development of a Device for Removing a Partial Denture in a Patient with Scleroderma

Scleroderma is a chronic disease that has been associated with immune dysfunction. One of the oral manifestations is microsomia, a result of collagen deposition in the perioral tissues. The complexity of treating these patients includes limited mouth opening ability, and difficulty inserting and removing dentures due to finger deformity. This article will describe an appliance specially designed especially for scleroderma patients, which facilitates treatment of the patient with removable partial dentures (RPD).     

Resolution of skin fibrosis and joint contractures in aggressive diffuse systemic sclerosis using autologous stem cell transplantation

The use of haematopoietic stem cell transplantation (HSCT) has now expanded beyond the domain of haematological diseases. Increasingly, the benefits of intense immunosuppression in the management of severe autoimmune diseases are being recognized. In diffuse systemic sclerosis (SSc), there has been increasing evidence of the efficacy of HSCT in improving morbidity and mortality. We present the first Australian patient to undergo autologous HSCT for SSc and review the current literature in the use of HSCT in SSc. Remarkably, the patient had complete resolution of skin disease (modified Rodnan skin score 27/51–0/51), tenosynovitis, synovitis and myositis.     

Ultrastructural observations on the histogenesis of localized fibrous tumours of the pleura (benign mesothehoma)

Summary Five localized fibrous tumours of the pleura (benign mesothelioma) were studied ultrastructurally in order to elucidate their histogenesis. The histological subtypes of this benign fibrous lesion of the visceral pleura, i.e. the cellular, the collagenous, and the hyaline, were separately analysed.The tumours are composed of undifferentiated mesenchymal cells, intermediate and differentiated fibroblasts as well as collagenous interstitial tissue. The varying distribution of these cell elements account for the various histological subtypes. Morphological similarities between the mesenchymal tumour cells and the superficial mesothelial cells, which are always separated from the true tumour tissue by an intact basement membrane, were not observed.The different cellular elements can be regarded as parts of a continuous spectrum of cytodifferentiation, in which the mature fibroblasts are derived via intermediate forms from the undifferentiated cells. It is concluded that the localized fibrous tumours of the pleura arise from immature mesenchymal stem cells, which seems to be normally found in the submesothelial layer of the visceral pleura.     

Antinuclear Antibodies and Anti-DNA Antibodies in Scleroderma

Antinuclear antibodies (ANA), including anti-DNA antibodies, and rheumatoid factors (RAT, Waaler-Rose) were determined prospectively during a 3-year period in 40 patients with localized scleroderma (LS) compared with 77 patients with generalized scleroderma (GS). ANA were increased in 26% of patients with LS, and in 47% with GS, anti-DNA antibodies in 23% of patients with LS, and in 34% with GS. Thus, the anti-DNA antibody level was lower compared with the known level in systemic lupus erythematosus. Rheumatoid factors were present in 6-7% of patients with LS, and in 14-15% of patients with GS. Increased antinuclear antibodies were not associated with any specific type of localized scleroderma, nor with internal disorders, and no case of clinical overlap to discoid or systemic lupus erythematosus was observed. However, six patients with localized scleroderma and complaints of arthralgia all presented increased antibodies, and one patient showed overlap to rheumatoid arthritis. It is suggested that increased ANA and anti-DNA antibodies in localized scleroderma, associated with joint manifestations, represents a systemic component in this type of scleroderma, with activation of the immune system and similarities with generalized collagen diseases.     

Impaired late suppression of Epstein-Barr virus (EBV)-induced immunoglobulin synthesis: A common feature of autoimmune disease

We examined regulation of Epstein-Barr virus-induced plaque-forming cell generation in peripheral blood mononuclear cells from several autoimmune and seronegative diseases and correlated these results with Epstein-Barr virus-induced proliferation. We confirmed the defective regulation of Epstein-Barr virus-induced plaque-forming cells in peripheral blood mononuclear cells of patients with rheumatoid arthritis and scleroderma. Peripheral blood mononuclear cells from patients with seronegative arthropathies and chronic infective inflammation (cystic fibrosis) had normal regulation of Epstein-Barr virus-induced plaque-forming cells. Peripheral blood mononuclear cells from rheumatoid arthritis had excessive plaque-forming cell generation in the face of a normally regulated decrease in Epstein-Barr virus-induced proliferation. In contrast, peripheral blood mononuclear cells from scleroderma had defective suppression of both Epstein-Barr virus-induced proliferation and plaque-forming cell generation. Thus, impaired regulation of Epstein-Barr virus-induced plaque-forming cell generation is a common feature of autoimmune disease and demonstrates some specificity for these disorders.     

Anti-centromere antibodies (ACA) in systemic sclerosis patients and their relatives: a serological and HLA study

Autoantibody reactivity to centromere proteins CENP-A, CENP-B and CENP-C was examined in 58 patients with systemic sclerosis (SSc). 218 first degree relatives and 22 spouses, HLA class II typing for HLA-DRB1 and HLA-DQA1 was performed by restriction fragment length polymorphism (RFLP) analysis in 50 families, and HLA-DRB1, HLA-DQA1 and HLA-DQB1 typing was performed by olignucleolitde typing in 44 families. Eleven probands and two relatives had ACA. The two relatives with ACA also had SSc. One relative was an identical twin sister of a pro band with ACA and the other relative was a sister of a proband with ACA. All ACA-positive probands and relatives were female, and all recognized CENP-A, CENP-B and CENP-C. The presence of at least one HLA-DQB1 allele not coding for leueine at position 26 of the first domain appeared necessary, although not sufficient for the generation of ACA, Therefore within SSc families ACA is strongly associated with female gender and disease phenotype, and is at least in part genetically determined.