Browsing by Author "Cassim, Bilkish."

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Capsular endoscopy: a single centre experience.
(2021) Naicker, Nisholini.; Cassim, Bilkish.; Newton, Keith.
Abstract Background: Capsule endoscopy (CE) is a relatively new modality in the assessment of obscure occult and obscure overt gastroenterological (GI) bleeding in South Africa. Objectives: The aim of this study was to describe the indications, findings and outcomes of CE at a referral hospital in the public sector in Kwa-Zulu Natal (KZN). Methods: Ethical approval was obtained from the Biomedical Research Ethics Committee of the University of Kwa-Zulu Natal (UKZN). A retrospective electronic chart review of 27 subjects who underwent CE from its introduction in 2013 to 2018 was undertaken. A structured data sheet was used to extract demographic and clinical details and the endoscopist‘s report. Indications were classified as obscure occult GI bleeding, obscure overt GI bleeding, suspected Crohn‘s disease and unexplained macrocytic anaemia (in a single subject). The findings at endoscopy were categorised as vascular (angiodysplasia, varices), inflammatory (villous oedema, erythematous mucosa erosions, ulcers or stenosis), normal, inconclusive or other (villous atrophy, polyps, tumours). Results: The mean age of the 27 patients was 51.2 years ± 21.3 years, with a majority of women (15, 56%) and 12 (44.4%) men. The most common indications for CE were either obscure occult GI bleeding or obscure overt GI bleeding. One patient each had unexplained anaemia and suspected Crohn‘s disease. All subjects had had previous oesophagogastroduodenoscopy (OGD) and colonoscopy prior to the CE, 15 subjects (55.5%) had had a CT scan of the abdomen and seven (26%) underwent red cell scans. Of the 14 subjects with occult GI bleeding, 12 had severe iron deficiency anaemia, with symptom duration ranging from one year to 40 years. These subjects had undergone a minimum of one up to a maximum of six OGDs, with a total of 38 OGDs prior to CE. Abnormal findings on CE were reported in nine subjects (64.3%), the commonest of which was inflammatory, and a definitive diagnosis was made in six (42.9%) subjects. The 11 subjects with obscure overt GI bleeding had undergone a total of 27 prior OGDs prior to CE. Abnormal findings on CE were reported in three of the 11 subjects (27.3%) with obscure overt GI bleeding and a definitive diagnosis made in two subjects (18%). In addition, the diagnosis was supported in the patient with Crohn‘s disease who had been symptomatic for eight years and had had several previous OGDs and colonoscopies. In the total group who underwent CE, nine (33.3%) subjects attained a definitive diagnosis. A further 18.5% attained a diagnosis following subsequent investigations. In three subjects (11.1%) the initial indication resolved requiring no further therapy or investigation and two patients (7.4%) were lost to follow up. Capsule retention occurred in two patients and the capsule was successfully retrieved via laparoscopic surgery. Conclusion: Capsule endoscopy is a useful modality to further investigate select patients with unexplained GI bleeding, including the identification of lesions outside the small bowel. A guideline for the application of CE in the South African context is required.
The effect of ultradistance running on premenopausal women of different ethnic groups.
(2005) McGregor, Avril.; Mars, Maurice.; Cassim, Bilkish.
No abstract available.
Hip fracture and osteoporosis : a comparison of the demographic profile, risk factors, outcomes and health care costs in geriatric patients with and without osteoporotic hip fractures in the public health sector in the eThekwini area.
(2014) Paruk, Farhanah.; Cassim, Bilkish.
Abstract available in PDF file.
A profile of geriatric admissions admitted to King Edward VIII hospital, Durban, in 2005.
(2011) Maharaj, Rasha.; Cassim, Bilkish.
Introduction: Ageing is a phenomenon that has preoccupied the minds of humankind for generations but it was only in the twentieth century that medical care dedicated to the elderly was created. The field of Geriatric Medicine has grown in South Africa and globally, to be recognized as a subspecialty of Internal Medicine in its own right. Physiological changes in the elderly impact on the increased prevalence of non–communicable diseases and the raised burden of disease in this age group. The altered spectrum of diseases in this age group and atypical manifestations of these conditions make geriatric health care truly unique. In spite of the recognition that the elderly have specific medical conditions, a dedicated health care policy to improve geriatric health care is yet to be developed In South Africa. For such a policy to be created, more needs to be known about the causes of mortality and morbidity that contributes to the burden of disease in this age group. Method: A retrospective chart review was conducted on 218 admissions of persons aged 60 years and over to the medical wards of King Edward VIII Hospital. This is a regional facility in Durban, South Africa, that provides mainly secondary and tertiary levels of care. An ethical waiver was obtained from the Biomedical Research Ethics Committee of the University of KwaZulu- Natal and all data sheets were de-identified. A structured data extraction sheet was used to record demographic and clinical data, including the admission diagnoses, presence of concomitant diseases, management and complications of some of these diseases, length of hospitalization and outcome of admission. Results: The study population comprised 191 patients aged 60 years and over, with a mean age of 70.5 ± 7.4 years (range 60 – 90 years). The patients were predominantly female (61.3%) and Black African (83.8%). While the majority of patients had only 1 admission, most were admitted with multiple diagnoses. Four or more diagnoses were recorded for 58.1% of the patients, with 50 patients (26.2%) having four diagnoses and 38 patients (19.9%) having five diagnoses. A history of current smoking was recorded in 38% of males and 7.2% females. Respiratory disease was the most common admission diagnosis (42.7%), followed by cardiac (42.2%) and renal disease (40.4%). An infection was present in 116 cases (53.2%) on admission, the commonest being pneumonia in 71 (61.2%), followed by urinary tract infection in 34 (28%) and septicaemia in 11 (9.5%). Cardiovascular disease was the most common underlying chronic disease, with hypertension being present in 150 patients (68.8%) and cardiomyopathy in 60 patients (25.5%). Of the patients with hypertension, evidence of end organ damage was present in 128 patients (85.3%), with hypertensive heart disease in 97 patients (75.8%), renal disease in 61 patients (47.7%), cerebrovascular disease in 37 patients (28.91%), hypertensive retinopathy in 11 patients (8.6%) and peripheral vascular disease in 5 patients (3.91%). The most common risk factors for congestive cardiomyopathy were hypertension in 55 cases (67%) and diabetes mellitus in 24 cases (40%). In addition, infection was the most common identifiable precipitating factor for cardiac failure in 40 % of cardiac failure cases Eleven patients were on anticoagulant therapy, of which three (27.3%) presented with overwarfarinization. More importantly, eight of the 17 patients (47%) with atrial fibrillation were not on anticoagulants. Neurological disease was present in 27.5% of the admissions with cerebrovascular disease being the most common (75% of all neurological cases) A diagnosis of malignancy was recorded in 13.1% of admissions with the most common primary site being the lung. In eight patients (32 % of those with malignancy) there was evidence of metastatic disease. Men were more likely than women to be admitted with respiratory disease (22.8% vs. 2.2%, p < 0.0001) such as chronic obstructive airways disease (57% vs. 34.5%, p = 0.001). Although pneumonia was more common in men than in women, this did not reach clinical significance (40.5% vs. 28.8%, p = 0.053). In contrast, more women were admitted with arrhythmias (16.5% vs. 6.3%, p = 0.03), congestive cardiac failure (30.2% vs. 15.2%, p = 0.013) and endocrine diseases (23.7% vs. 12.7%, p = 0.048). Renal disease was more common in women than in men, but did not reach statistical significance (44.6% vs. 32.9%, p = 0.060) In the 191 patients, 64 deaths (33.7%) were recorded during hospitalization. The mortality rate was found to be significantly higher in patients with 15 cerebrovascular accidents, acute renal failure, diabetes mellitus, and infection (including pneumonias). Conclusion: This study confirms the high prevalence and disease burden of non-communicable diseases in older patients, with the majority of patients having multiple diagnoses on admission. Hypertension and other cardiovascular diseases were identified as being most common with a high prevalence of target organ damage. Furthermore, in the patients with malignancy metastatic disease was common. These findings suggest that older patients may present late due to a lack of awareness, limited access to appropriate health care, or lack of adequate treatment and screening programmes. In addition to the burden of non-communicable diseases (NCD), infection (particularly pneumonia) emerged as a common cause for admission and mortality. These findings confirm the high burden of non-communicable diseases and their complications in the older population and highlight the need screening programs to improve detection and better management of these conditions. Furthermore the association of a high mortality with infections, finding underscores the need for implementation and adherence to treatment guidelines, and to develop and adhere to vaccination guidelines. Furthermore, training of health care personnel at all levels should be intensified in an attempt to decrease the burden of disease in older persons and to improve their quality of life.
Risk factors for morphometric vertebral fractures in subjects aged 60 years and over in the eThekwini Municipality, KwaZulu-Natal, South Africa.
(2020) Esaadi, Mohidin Amar.; Cassim, Bilkish.; Paruk, Farhanah.
Abstract available in PDF
The role of kinins and cytokines in rheumatoid arthritis.
(2001) Cassim, Bilkish.; Bhoola, Keshavlal Daya Narotam.
Introduction: Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by inflammatory synovitis. The histopathological features include synovial hyperplasia, an inflammatory cell infiltration, angiogenesis and an inflammatory exudate into the synovial joint with progression to bone and joint destruction. While the exact aetiology of RA is unknown, a number of inflammatory cells and mediators have been implicated in the pathogenesis. Kinins are vasoactive peptides that have the capacity to induce the cardinal features of inflammation and considerable evidence exists for a role for the kallikrein-kinin cascade in inflammatory arthritis. The proinflarnmatory cytokines are also important mediators in rheumatoid arthritis and there is evidence for a functional relationship between the kallikrein-kinin and cytokine cascades in rheumatoid arthritis. Methods: Following approval from the Ethics Committee of the University of Natal, synovial tissue samples were obtained at arthroscopy from patients with RA and at autopsy (for controls). The tissue samples were processed for light microscopy and immunostained by the immunoperoxidase method to detect tissue kallikrein and the kinin B 1 and B2 receptors. The intensity of the immunostaining was quantified by image analysis. Blood and synovial fluid samples were obtained from patients with RA and blood from age and sex matched healthy volunteers. The RA patients were assessed clinically to determine the degree of disease activity and the presence or concomitant diseases. Disease activity was determined by the duration of morning stiffness, the twenty eight tender and swollen joint counts, pain on a visual analogue scale, patient's and physician's global assessment of disease activity (Likert scale), a local activity index, the modified Health Assessment Questionnaire (HAQ), disease activity score (DAS) and the erythrocyte sedimentation rate (ESR) and C reactive protein (CRP). In the synovial fluid (SF) samples, the functional activity of tissue kallikrein (TK) was demonstrated using an amidolytic assay and the total amount of TK was measured in a sandwich enzyme linked immunosorbent assay (ELISA). The Pearson's correlation coefficient was used to correlate the TK levels with measures of disease activity. Further, basal and generated kinins were measured in the SF by competitive ELISA, and the levels correlated with measures of disease activity. In the cytokine study, interleukin lP (IL IP) and tumour necrosis factor p (TNFP) were measured in the synovial fluid samples by ELISA, and the relationship between the cytokine levels and disease activity as well as TK, basal and generated kinins determined. Neutrophils were isolated from the blood and synovial fluid samples from the rheumatoid arthritis patients and from the blood samples from healthy volunteers. The circulating and synovial fluid neutrophils were immunostained to detect tissue kallkrein, the kinin moiety in the kininogen molecule and kinin BI and B2 receptors, and the immunofluorescence visualized by confocal microscopy. The images were digitally analysed using the Analysis 2.1 Pro system. The Kruskal Wallis and one-way ANOVA tests were used to compare the mean intensity of imrnunostaining in the control neutrophils with that present on the circulating and SF neutrophils harvested from RA patients. The intensity of labeling for these antigens was correlated with measures of disease activity. Results: 1. Synovial tissue samples: Labeling for tissue kallikrein was observed in the synovial lining and endothelial cells in control and rheumatoid tissue. There was a significant increase in the intensity of TK labeling in the endothelial cells of the rheumatoid tissue (p < 0.05). The kinin Bl and B2 receptor were visualized in the synovial lining cells, endothelial cells and the subintimal fibroblasts and macrophages in the control and rheumatoid synovial samples, with a significant increase in B 1 receptor labeling in the synovial lining cells in rhewnatoid synovial tissue (p < 0.01). 2. Tissue kallikrein activity and the total TK concentration was measured in the synovial fluid obtained from 20 patients with RA. There was no direct correlation between the between the enzymic and antigenic tissue kallikrein. There w as a significant negative correlation between the enzymic TK and the twenty eight swollen joint count (r = -0.464; p <0.05). 3. There was a significant negative correlation between the basal kinin and generated kinin levels (r= -0.454; p < 0.05). In addition, there was a negative correlation between the basal kinin levels and the C RP (r = -0.537; p < 0.05) and the disease activity score (r = -0.458; p < 0.05). In contrast, there was a positive correlation between the generated kinin levels and the twenty-eight tender and swollen joint counts (r = 0.536; p < 0.05 and r = 0.509; p < 0.05 respectively), the ESR (r = 0.598; p < 0.01), CRP (r = 0.725; p < 0.01) and the disease activity score (r = 0.676; p < 0.01). There was a significant correlation between the SF levels of IL IP and pain (r = 0.462; p < 0.05), physician's global assessment of disease activity (r = 0.549; p < 0.05), 28 tender joint count (r = 0.4 72; p < 0.05) and CRP (r = 0.530; p < 0.05). Although there appeared to be a correlation between the IL 1 p and disease activity score, this was not significant (r = 0.412; p = 0.07). In addition, the levels of synovial fluid lNF a correlated with the 28 tender joint (r = 0.458; p < 0.05) count and CRP (r = 0.653; p < 0.01). 4. There appeared to be a trend towards a negative correlation between the SF amidase TK levels and IL 1 p, however this was not significant. While there was no direct relationship between the SF levels of IL 1 P and the generated kinins, there was a positive correlation between low to moderate levels of IL 1 p and the generated kinins (r = 0.51, p < 0.05). In contrast, there was a negative correlation with higher levels of IL Ip (r = -0.5, p < 0.05). 5. Immunoreactive TK, kinin moiety and the Bl and B2 receptors were visualized on the circulating neutrophils from the healthy volunteers and the circulating and SF neutrophils from the RA patients. There was no statistically significant difference in the mean intensity of TK labeling in the circulating neutrophils from healthy volunteers (n=8) and the circulating and synovial fluid neutrophils of the RA patients n=8). However, when the intensity of labeling of the SF neutrophils (n=80) from the RA patients was compared to the circulating neutrophils (n=80) of healthy volunteers, there was a significant loss of TK labeling in the SF neutrophils of the RA patients (1-Way ANOVA, p < 0.01). In the RA patients, there was a loss of the kinin moiety from both the SF and circulating neutrophils compared to controls (Kruskal-Wallis: p < 0.05 and < 0.01 respectively). Although there was a clear increase in the intensity of labeling of the kinin BI receptor on the SF neutrophils from RA patients (n=8), when compared to the circulating neutrophils from healthy volunteers (n=8), the mean values did not reach significance (Kruskal Wallis; p > 0.05). However, a significant increase in Bl receptor labeling was observed on both the circulating and SF neutrophils of the RA patients (n=80) when compared to circulating neutrophils of the healthy volunteers (n=80) (1 Way ANOVA, p < 0.01 and < 0.05 respectively). In addition, there was a positive correlation between the immunoreactivity for the BI kinin receptor on the circulating neutrophils from the RA patients and the local activity index (r = 0.783; p < 0.05). Although there was a clear increase of the kinin B2 receptor on the circulating and SF neutrophils from the RA patients compared to circulating neutrophils from healthy volunteers, this was only significant for the circulating neutrophils from the RA patients (Kruskal-Wallis, p = 0.05). There was no correlation between the intensity of labeling of TK, the kinin moiety and the B2 receptor and measures of disease activity. Discussion and conclusions 1. This study provides the first evidence for the localization of TK and the kinin receptors in control and rheumatoid synovial tissue using antibodies specific for each protein and standard immunolabelling techniques. Synovial fibroblasts, macrophages and endothelial cells through the release of enzymes and cytokines have the ability to mediate the inflammatory changes and cartilage and bone destruction in RA. The presence of TK and the kinin receptors in these cells therefore provides evidence for a pathogenetic role for the kallikrein-kinin cascade in RA. 2. In addition, in RA there is an exudation of fluid into the joint space. Tissue kallikrein has been previously reported in the synovial fluid obtained from RA patients, however the correlation of TK levels and disease activity has not been previously studied. The negative correlation between enzymic TK and the twenty-eight swollen joint count, an indicator of disease activity suggests that there is a consumption of TK in inflammation, presumably due to increased kininogenase activity. Similarly, the kinin generating capacity of synovial fluid obtained from RA patients has been previously reported, however, this is the first study demonstrating a link between kinin generating capacity and validated markers of disease activity. The kinin generating capacity is a complex and dynamic cascade involving the bioregulation of all the components of the kallikrein-kinin system and is therefore more likely to accurately define the role of kinins in inflammatory arthritis than are individual components of the kallikrein-kinin cascade. Measurement of tissue kallikrein and basal kinins is affected by the presence of natural inhibitors and their short half-life in biological fluids. In addition to the synovial fluid study a decrease in the urinary TK activity and an increase in urine kinin generated kinins was demonstrated, suggesting that there is a systemic activation of the kallikrein kinin cascade in RA. 3. Although there is evidence for an interaction between the kallikrein-kinin and cytokine cascades in inflammation, in this study a direct correlation between the levels of interleukin 1 J3 and tumour necrosis factor J3 in the synovial fluid and TK and generated kinin levels was not found. This may be due to the wide variations in the levels of cytokines, the presence of inhibitors and anti-inflammatory cytokines, or a complex and dynamic relationship between the two cascades. However, the correlation of both generated kinins and interleukin l J3 and tumour necrosis factor J3 with disease activity provides circumstantial evidence for a synergistic role for these mediators in inflammatory arthritis. 4. In the neutrophil study, loss of immunoreactive tissue kallkrein and kinin moiety from the neutrophils obtained from RA patients was demonstrated. This finding supports the hypothesis that kinins are released from the neutrophils by the enzymatic action of tissue kallkrein and suggests that the kallkrein-kinin system is activated both locally and systemically in patients with RA. Further, there was upregulation of the both the kinin B 1 and B2 receptors on the neutrophils from the RA patients. While the B2 receptor is thought mediate most of the actions of kinins, the correlation of the intensity of B 1 receptors and the local activity index implies that the B 1 receptor may be important in inflammation. 5. These findings provide convincing evidence for the role of the kallikrein-kinin cascade in the pathogenesis of inflammation in RA. Further development of kinin receptor antagonists may provide a novel therapeutic modality.