Guyan Arscott

Chemical burns as assault injuries in Jamaica

A three-fold greater incidence of chemical burn injuries in Jamaican hospitals, compared to burn centres in other industrial countries, underscores the problem of the use of common chemicals for assault weapons in this country. With the increased availability of guns for personal use, many Jamaicans learned the value of carrying household chemicals such as sulphuric acid from batteries or sodium hydroxide obtained from cleaning supplies. Chemicals carried in a container, such as one might carry mace, afforded a means of defence among the lower socioeconomic groups who could not afford handguns. This use of dangerous chemicals for defensive weapons has extended to the use of chemicals for assault. The pattern of chemical injury differs significantly from most reports in the literature in both prevalence and aetiology. This review was prepared to examine these injuries with a view to planning strategies for prevention.

Genetic susceptibility to Keloid scarring : SMAD gene SNP frequencies in Afro-Caribbeans

Abstract:  Keloid disease (KD) is a fibroproliferative dermal tumour of unknown aetiology. The increased familial clustering in KD, its increased prevalence in certain races and increased concordance in identical twins suggest a strong genetic predisposition to keloid formation. The highest incidence of keloids is found in the black population, where it has been estimated around 4–6% and up to 16% in random samples of black Africans. SMAD genes 3, 6 and 7 were investigated as candidate genes in Jamaican patients with keloid scars (n = 183) and a matched control population (n = 121) because of their previously reported involvement in fibrotic disorders and to determine if they were associated with keloid disease susceptibility. Thirty Five SNPs across these genes were genotyped using Time‐of‐Flight Mass Spectrometry (MALDI‐TOF MS) and iPLEX assay. Linkage disequilibrium (LD) was established between several of the SNPs investigated. In the Jamaican population, the SMAD SNPs investigated for this study were not strongly associated with increased risk of developing KD. Identification of genetic markers in candidate genes such as the SMAD family may be of significant importance in diagnosis, prognosis and development of new therapies in the management of keloid scarring.

Association of HLA‐DRB1* and keloid disease in an Afro‐Caribbean population

Background.  Keloid disease (KD) is a fibroproliferative dermal tumour of unknown aetiology. The high incidence of familial clustering in KD, its prevalence in certain races and its concordance in identical twins suggest a strong genetic predisposition to keloid formation. The highest incidence of keloids is found in black populations, where the incidence has been estimated to be up to 16%. The most polymorphic genetic system in vertebrates is the major histocompatibility complex (MHC) also known as the human leucocyte antigen (HLA) system. The MHC has been shown to be strongly associated with numerous conditions. Of particular relevance is the association of DR2 with dermal fibrotic diseases including sarcoidosis and systemic sclerosis.

The Aldo-Keto Reductase AKR1B10 Is Up-Regulated in Keloid Epidermis, Implicating Retinoic Acid Pathway Dysregulation in the Pathogenesis of Keloid Disease

Keloid disease is a recurrent fibroproliferative cutaneous tumor of unknown pathogenesis for which clinical management remains unsatisfactory. To obtain new insights into hitherto underappreciated aspects of keloid pathobiology, we took a laser capture microdissection-based, whole-genome microarray analysis approach to identify distinct keloid disease-associated gene expression patterns within defined keloid regions. Identification of the aldo-keto reductase enzyme AKR1B10 as highly up-regulated in keloid epidermis suggested that an imbalance of retinoic acid metabolism is likely associated with keloid disease. Here, we show that AKR1B10 transfection into normal human keratinocytes reproduced the abnormal retinoic acid pathway expression pattern we had identified in keloid epidermis. Cotransfection of AKR1B10 with a luciferase reporter plasmid showed reduced retinoic acid response element activity, supporting the hypothesis of retinoic acid synthesis deficiency in keloid epidermis. Paracrine signals released by AKR1B10-overexpressing keratinocytes into conditioned medium resulted in up-regulation of transforming growth factor-β1, transforming growth factor-β2, and collagens I and III in both keloid and normal skin fibroblasts, mimicking the typical profibrotic keloid profile. Our study results suggest that insufficient retinoic acid synthesis by keloid epidermal keratinocytes may contribute to the pathogenesis of keloid disease. We refocus attention on the role of injured epithelium in keloid disease and identify AKR1B10 as a potential new target in future management of keloid disease.

Continuous intravenous versus bolus parenteral midazolam: a safe technique for conscious sedation in plastic surgery

Conscious intravenous sedation is a safe alternative method to general anaesthesia. We have used a technique of continuously titrated, as opposed to incremental boluses of, intravenous or intramuscular midazolam for conscious sedation, with tumescent adrenaline-lignocaine solution for local anaesthesia, routinely in 421 plastic surgical procedures between 1997 and 2000. All patients were American Society of Anesthesiologists (ASA) class I or II. Conscious sedation was administered through our protocol of continuously titrated doses of midazolam in dextrose saline. The operative field was injected subcutaneously with varying volumes of diluted lignocaine and adrenaline, depending on the anatomical region. Preoperative sedation was administered 1 h before the procedure in the form of an intramuscular injection of pethidine and promethazine (Phenergan). Intraoperatively, a subset of patients received up to four divided diluted doses of pethidine. A preoperative 4 h starvation period pronounced the effect of the sedative. No intraoperative conversions to general anaesthesia were needed, and no sedation complications occurred. No unplanned re-admissions secondary to nausea, prolonged drowsiness or pain were required. All patients who were treated using this technique had an uneventful postoperative course. Hospital stay was substantially shorter than following general anaesthesia, which provided a significant reduction in medical-care expenses and a faster return to work. In conclusion, conscious sedation administered by titrated intravenous midazolam is a well-tolerated, safe, consistent, predictable and effective anaesthetic choice for a variety of plastic surgical procedures, many of which would commonly be performed under general anaesthesia.

Assessment of the influence of HLA class I and class II loci on the prevalence of keloid disease in Jamaican Afro-Caribbeans

Keloid disease (KD) is a common abnormal cutaneous fibrotic disorder of unknown aetiopathogenesis. KD is reported to have a strong genetic component as it is often familial and has a high incidence in certain ethnicities, in particular those of Afro-Caribbean origin. Genetic risk factors combined with aberrant lesional inflammatory responses point to the human leukocyte antigen (HLA) system as a viable target for investigating disease aetiology. Sequence specific primer polymerase chain reaction with allele sequencing was used to determine HLA-DQA1 and DQB1 allele frequencies (AF) for 165 KD patients and 119 healthy controls of black Jamaican Afro-Caribbean origin. HLA class I alleles A*01, A*03, A*25, B*07 and Cw*08:02, previously identified as KD associated in a different ethnicity, were also analysed. Allele sequencing confirmed typing accuracy but no statistically significant differences in AF were identified between KD patients and controls. Furthermore, KD subgroups including patient gender, family history and multiple- or single-site scarring did not show significant allele-disease associations.