Scan Science and Technology
Contact Leading Edge Experts & Companies
Adjuvant Disease
The Experts below are selected from a list of 105 Experts worldwide ranked by ideXlab platform
S L Aaron – One of the best experts on this subject based on the ideXlab platform.
-
HUMAN Adjuvant Disease REVISITED : A REVIEW OF ELEVEN POST-AUGMENTATION MAMMOPLASTY PATIENTS
Clinical and experimental rheumatology, 1994Co-Authors: T K Fenske, Phillip E. Davis, S L AaronAbstract:Objectives We have reviewed 11 women post-augmentation mammoplasty who were referred to our clinic with diffuse rheumatic complaints. All patients had undergone mammoplasty with silicone gel-filled implants prior to the onset of their locomotor symptoms (mean latency time 7.8 years). One physician interviewed and examined each of these patients following a standardized format for clinical retrieval. Results Of the patients reviewed, 6 patients had clinical fibromyalgia based on the ACR criteria, and the remaining 5 patients had symptoms consistent with the “chronic fatigue syndrome.” None of our patients were found to have evidence of a defined connective tissue Disease. Antinuclear antibodies were detected in 4 (36%) patients and low level titres of extractable nuclear antigens in only 2 (18%). Conclusions Previously a causal relationship between the use of silicone gel-filled breast implants and the subsequent development of symptoms referred to as human Adjuvant Disease (HAD) has been proposed. On the basis of currently accepted criteria we have preferred to diagnose our post-mammoplasty patients without specific connective tissue Disease, as having chronic fatigue syndrome (CFS), or when tender points are present, as having fibromyalgia (FMS), rather than implying that such cases represent a separate and unique rheumatological Disease entity. In the light of our current understanding of CFS and FMS, a relationship between them and the previous silicone mammoplasty seems possible.
Barrie Vernon-roberts – One of the best experts on this subject based on the ideXlab platform.
-
A comparison of the Disease-modifying and cytokine-regulating activities of tenidap, piroxicam and cyclosporin-A using the Adjuvant-induced model of arthritis in rats
InflammoPharmacology, 1998Co-Authors: David R. Haynes, Martin J. Hutchens, Michael W Whitehouse, Barrie Vernon-robertsAbstract:This study compared the antiarthritic activity of tenidap, piroxicam and cyclosporin-A (CsA) using the model of Adjuvant-induced arthritis in rats. The aim of the study was to correlate any Disease-modifying effects of tenidap with its in-vivo regulation of cytokines. Both tenidap and piroxicam reduced arthritic Disease when administered orally from the time the first signs of arthritis are expressed. Disease suppression correlated with a significant reduction in interleukin-6 production and a slight reduction in interleukin-1 and tumour necrosis factor production. When coadministered with the Adjuvant, tenidap and CsA prevented Disease in 50% and 100% of animals, respectively, whereas piroxicam had no effect. This Disease prevention induced by tenidap and CsA coincided with reduced interferon-γ and interleukin-2 production by lymph node cells one day following initiation of Adjuvant Disease. This inhibition of T-cell cytokines might be consistent with tenidap acting as a Disease-modifying drug.
T K Fenske – One of the best experts on this subject based on the ideXlab platform.
-
HUMAN Adjuvant Disease REVISITED : A REVIEW OF ELEVEN POST-AUGMENTATION MAMMOPLASTY PATIENTS
Clinical and experimental rheumatology, 1994Co-Authors: T K Fenske, Phillip E. Davis, S L AaronAbstract:Objectives We have reviewed 11 women post-augmentation mammoplasty who were referred to our clinic with diffuse rheumatic complaints. All patients had undergone mammoplasty with silicone gel-filled implants prior to the onset of their locomotor symptoms (mean latency time 7.8 years). One physician interviewed and examined each of these patients following a standardized format for clinical retrieval. Results Of the patients reviewed, 6 patients had clinical fibromyalgia based on the ACR criteria, and the remaining 5 patients had symptoms consistent with the “chronic fatigue syndrome.” None of our patients were found to have evidence of a defined connective tissue Disease. Antinuclear antibodies were detected in 4 (36%) patients and low level titres of extractable nuclear antigens in only 2 (18%). Conclusions Previously a causal relationship between the use of silicone gel-filled breast implants and the subsequent development of symptoms referred to as human Adjuvant Disease (HAD) has been proposed. On the basis of currently accepted criteria we have preferred to diagnose our post-mammoplasty patients without specific connective tissue Disease, as having chronic fatigue syndrome (CFS), or when tender points are present, as having fibromyalgia (FMS), rather than implying that such cases represent a separate and unique rheumatological Disease entity. In the light of our current understanding of CFS and FMS, a relationship between them and the previous silicone mammoplasty seems possible.
Jeffrey A. Goldstein – One of the best experts on this subject based on the ideXlab platform.
-
Investigation of silicone oil and fumed silica in an Adjuvant animal model
Plastic and reconstructive surgery, 1997Co-Authors: George J. Picha, Jeffrey A. GoldsteinAbstract:Human Adjuvant Disease is the label given to a syndrome that resembles a connective tissue Disease such as scleroderma and that has been hypothesized to follow augmentation mammoplasty with silicone gel implants or silicone with adulerants. To date, there is no proof that pure silicone is the cause of these symptoms. The cases presented in the literature suggest a comparison to the events seen in the rat Adjuvant arthritis model. Male Lew/SsN rats (n = 65) were used. To evaluate both the Adjuvant and antigenic properties of the gel implant, variations of the standard Freund’s complete Adjuvant inoculum were prepared. Tested were the abilities of low molemolecular weight silicone to act as an Adjuvant and for fumed silisilica to act as an antigen by modifying a rat Adjuvant arthritis model to include silicone and fumed silisilica. On day 0, 0.25 ml of each inoculum was injected intradermally into the plantar aspect of the hindfoot of each rat. The foot diameter was recorded at each time period, compared with the contralateral hindfoot, and normalized to controls at regular time periods over the course of 120 days. Silicone oil did not act as an Adjuvant. Furthermore, fumed silisilica alone did not act as an antigen; however, it is capable of eliciting a reaction that is both delayed and uncharacteristic of the rat Adjuvant arthritis model. These results indicate that “human Adjuvant Disease” may be inappropriate and misleading. (Plast. Reconstr. Surg. 100: 643, 1997.)
David R. Haynes – One of the best experts on this subject based on the ideXlab platform.
-
A comparison of the Disease-modifying and cytokine-regulating activities of tenidap, piroxicam and cyclosporin-A using the Adjuvant-induced model of arthritis in rats
InflammoPharmacology, 1998Co-Authors: David R. Haynes, Martin J. Hutchens, Michael W Whitehouse, Barrie Vernon-robertsAbstract:This study compared the antiarthritic activity of tenidap, piroxicam and cyclosporin-A (CsA) using the model of Adjuvant-induced arthritis in rats. The aim of the study was to correlate any Disease-modifying effects of tenidap with its in-vivo regulation of cytokines. Both tenidap and piroxicam reduced arthritic Disease when administered orally from the time the first signs of arthritis are expressed. Disease suppression correlated with a significant reduction in interleukin-6 production and a slight reduction in interleukin-1 and tumour necrosis factor production. When coadministered with the Adjuvant, tenidap and CsA prevented Disease in 50% and 100% of animals, respectively, whereas piroxicam had no effect. This Disease prevention induced by tenidap and CsA coincided with reduced interferon-γ and interleukin-2 production by lymph node cells one day following initiation of Adjuvant Disease. This inhibition of T-cell cytokines might be consistent with tenidap acting as a Disease-modifying drug.