The outside layer of these glands makes hormones that help your body respond to stress and regulate your blood pressure and water and salt balance. Addison disease happens if the adrenal glands don't make enough of these hormones. The immune system mistakenly attacks your own tissues, damaging your adrenal glands.

Weight loss muscle weakness fatigue that gets worse over time low blood pressure patchy or dark skin lab tests can confirm that you have addison disease. It should say that you have the disease, list your medicines and say how much you need in an emergency. There are limited data describing the clinical presentation of addison’s disease in south africa. It is hypothesised that patients may present in advanced state of ill health, compared to western countries. A national database of patients was compiled from primary care, referral centres and private practices. Biochemical data were obtained from folder reviews and laboratory archived results. The median and inter quartile age range iqr of patients at enrolment was 46.0 32.0–61.0 years, with a wide range from 2.8–88.0 years.

The median and iqr age at initial diagnosis was 34.0 20.0–45.0 years range 0.02–77.0 years, indicating that at the time of enrolment, the patients, on average, were diagnosed with addison’s disease 12 years previously. Hyperpigmentation was observed in 76%, nausea and vomiting occurred in more than 40%, and weight loss was noted in 25%. Loss of consciousness as a presenting feature was recorded in 20%. with a 95% confidence interval ci of 14–28% and shock occurred in 5% ci 1.5–8.5%. The usual constellation of hyperpigmentation, nausea, vomiting and weight loss suggests addison’s disease, but a significant proportion present with an advanced state of ill health and addisonian crises. citation: ross il, levitt ns 2013 addison’s disease symptoms – a cross sectional study in urban south africa.

Doi:10.1371/journal.pone.0053526 editor: saeed dastgiri, tabriz university of medical sciences, islamic republic of iran received: august 17, 2012 accepted: december 3, 2012 published: january 7, 2013 copyright: © 2013 ross, levitt. This is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. funding: ilr is the recipient of the swedish research links grant no: 65390/2007. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This does not alter the authors’ adherence to all the plos one policies on sharing data and materials.

In the absence of national insurance there is an unequal access to health care, which consists of a vast public health sector and a small, but expanding private health sector 1. Addison’s disease primary adrenal insufficiency results from the destruction of the adrenal cortex, leading to decreased cortisol and aldosterone production. These hormones are vital for survival during stressful situations including infection 2. The study by ross et al describes the underlying aetiology of addison’s disease in a cohort of south africans, which is predominated by autoimmunity 6 . Addison’s disease, like syphilis has been referred to as one of the great mimickers of medicine. It is therefore not surprising that a cross sectional study from germany found a significant delay in making the diagnosis, as 20% of the subjects had symptoms for longer than five years prior to being diagnosed 7.

The vast majority of cohort studies of addison’s disease emanate from western countries and only isolated reports from africa describe the clinical presentation 8. We wished to describe the clinical presentation of addison’s disease in south africa, with the hypothesis that the presentation may be similar to western countries, albeit that the signs and symptoms may be more severe due to the lack of access to health care. It is expected that a description of the clinical presentation of this disorder will serve to remind clinicians of this disorder so that this diagnosis is not missed. A national database of patients with addison’s disease was compiled from primary care, referral centres and private practices. Since databases in south africa were not available for addison’s disease, a systematic approach was adopted of initially inviting patients attending quaternary hospitals, followed by patients attending tertiary hospitals and private care facilities.

This was followed by inviting prospective participants attending both secondary and primary health care facilities between the years 2005–2010. A private commercial database medpages of medical specialists and general practitioners sent in addition, 9 600 personalised e mails to all specialist physicians, paediatricians and general practitioners registered with this organisation. As addison’s disease is designated as a medical condition that enjoys the prescribed minimum benefit, it is a statutory requirement that patients belonging to a medical aid have the total cost of their treatment reimbursed. 10 the medical insurance companies were only able to communicate the names of the treating physicians of addison’s patients to our research group of those patients registered, in order to prevent a breach of confidentiality.

These treating physicians were then requested by letter or e mail to invite his or her patients to participate in the study. Approval to conduct the study was obtained from the research and ethics committee of the university of cape town, which endorses the latest declaration of helsinki. Ethics approval was also obtained from the respective research and ethics committees overseeing the various faculties of health sciences including nelson mandela school of medicine, university of kwazulu natal, university of the free state, university of stellenbosch, university of pretoria and the university of witwatersrand. The diagnosis of addison’s disease was made on the basis of a suggestive clinical presentation, low basal cortisol concentration and simultaneously elevated adrenocorticotrophic hormone acth concentration, or where indicated, a peak cortisol, following 250 µg acth stimulation of less than 550 nmol/l, associated with a basal raised plasma acth, exceeding 10.1 pmol/l. Addison’s disease was confirmed in each case by specialist internist, paediatrician or endocrinologist. The clinical symptoms of the patients at diagnosis of addison’s disease were elicited by interviewing them at the time of enrolment and where possible, the clinical details from the notes at the time of presentation were included in the database. Patient characteristics with non normal distribution were described using median and interquartile range.

Continuous data were compared between groups using the mann whitney and chi squared tests were used for comparisons of binary and categorical variables. Binomial confidence intervals ci were used as a measure of the precision of the estimate. All analyses were conducted were conducted using stata tm version 10.0 stata corp. There were 161 patients who were referred for enrolment in the south african addison’s study. Seven patients with an original label of addison’s disease were excluded: two had a normal acth stimulation test, two had secondary hypoadrenalism, one had a bilateral adrenalectomy for cushing’s disease, and two had suppression of the hypothalamic pituitary adrenal hpa axis, related to previous steroid use for another indication. Three patients declined to participate, citing personal reasons and a further three patients were too late to be enrolled in this observational study. Thus, a total of 148 patients were enrolled in the study and we had obtained 92 62.1% transcripts describing the original clinical presentation.

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The referral pattern for the patients enrolled in the study is illustrated in figure 1. Expand