The epidemiology of corticosteroid induced osteoporosis

Epidemiology is the method used to find the causes of health outcomes and diseases in populations. In epidemiology, the patient is the community and individuals are viewed collectively. By definition, epidemiology is the study (scientific, systematic, and data-driven) of the distribution (frequency, pattern) and determinants (causes, risk factors) of health-related states and events (not just diseases) in specified populations (neighborhood, school, city, state, country, global). It is also the application of this study to the control of health problems (Source: Principles of Epidemiology, 3rd Edition ).

While most molecular epidemiology studies are still using conventional disease diagnosis and classification systems, it is increasingly recognized that disease evolution represents inherently heterogeneous processes differing from person to person. Conceptually, each individual has a unique disease process different from any other individual (“the unique disease principle”), [20] [21] considering uniqueness of the exposome (a totality of endogenous and exogenous / environmental exposures) and its unique influence on molecular pathologic process in each individual. Studies to examine the relationship between an exposure and molecular pathologic signature of disease (particularly cancer ) became increasingly common throughout the 2000s. However, the use of molecular pathology in epidemiology posed unique challenges including lack of research guidelines and standardized statistical methodologies, and paucity of interdisciplinary experts and training programs. [22] Furthermore, the concept of disease heterogeneity appears to conflict with the long-standing premise in epidemiology that individuals with the same disease name have similar etiologies and disease processes. To resolve these issues and advance population health science in the era of molecular precision medicine , “ molecular pathology ” and “epidemiology” was integrated to create a new interdisciplinary field of “ molecular pathological epidemiology ” (MPE), [23] [24] defined as “epidemiology of molecular pathology and heterogeneity of disease”. In MPE, investigators analyze the relationships between; (A) environmental, dietary, lifestyle and genetic factors; (B) alterations in cellular or extracellular molecules; and (C) evolution and progression of disease. A better understanding of heterogeneity of disease pathogenesis will further contribute to elucidate etiologies of disease. The MPE approach can be applied to not only neoplastic diseases but also non-neoplastic diseases. [25] The concept and paradigm of MPE have become widespread in the 2010s. [26] [27] [28] [29] [30] [31] [32]

There was more neurology taught under Harold G. Wolff at Cornell University Medical College in New York than perhaps anywhere else in the country when I attended from 1948 to 1952. I took my residency at the Veterans Administration Hospital in the Bronx, New York, a teaching hospital of Cornell, with Wolff as my Director of Training. While a resident, we thought we had found a treatment for multiple sclerosis. To test our conclusion, the first Class 1 treatment trial ever conducted for multiple sclerosis was performed. This showed no effect, but the participants began investigating multiple sclerosis among the 16 million persons at prime age for symptom onset who had served in the military in World War II. This led me to study its epidemiology worldwide, beginning with a detailed review of all published population-based estimates of frequency. Among these were nationwide surveys from Sweden, Denmark, Switzerland and later Norway and Finland, which showed in each country a concentration of the significantly high regions into contiguous areas forming a single 'focus' in each land, maximal in Denmark under the age of 15 years. The primary locus of high frequency multiple sclerosis seemed to be in the south-central inland lake region of Sweden, with spread to its contiguous neighbours. These concentrations in time and space indicated that multiple sclerosis was a disease probably acquired in early adolescence. Migration studies supported this: moves from high to low showed retention of birthplace risk only for those aged >15 years, whereas opposite moves indicated susceptibility limited to some 11-45 year olds. Epidemics of multiple sclerosis would suggest the disease is not only acquired but also infectious. If an infectious origin were true, transmission would have to occur before clinical onset, and would have to involve a much greater number of subjects than clinically involved. I believe there have been epidemics in Iceland, Shetland-Orkney and the Faroe Islands. On the Faroes there were no cases of multiple sclerosis among native-born resident Faroese from 1900 until 1943, when the first of 21 cases had clinical onset, heralding a type 1 epidemic with peak incidence rates >10 per 100,000 for 1945-46. British troops who occupied the islands from April 1940 to September 1945 we believe brought a widespread (because of the scatter of Faroese cases), asymptomatic (because they were healthy troops), persistent infection we called the primary multiple sclerosis affection that involved a large proportion of Faroese, with clinical multiple sclerosis ensuing in a very small proportion. Primary multiple sclerosis affection itself may have been manifest there as a newly introduced cause of acute infectious gastroenteritis and is possibly the underlying cause of multiple sclerosis in general.

Stroke occurred in 134 (%) patients. Incidence varied according to procedure (coronary bypass %, isolated valve %, valve/coronary bypass %, and ascending aorta %). Patients who had a stroke had a higher perioperative mortality rate than that of patients who did not (% vs %; P < .0001) and a longer period of hospitalization (median 30 days vs 7 days; P < .0001). Multivariate logistic analysis identified 10 preoperative predictors of stroke: gender, age, aortic surgery, previous stroke, critical preoperative state, poor ventricular function, diabetes, peripheral vascular disease, unstable angina, and pulmonary hypertension. A logistic model was developed on the basis of these risk factors to predict the likelihood of stroke.

whereas if the integral is greater than one the disease will not die out and there may be such resonances. For example, considering the periodically varying contact rate as the 'input' of the system one has that the output is a periodic function whose period is a multiple of the period of the input. This allowed to give a contribution to explain the poly-annual (typically biennial) epidemic outbreaks of some infectious diseases as interplay between the period of the contact rate oscillations and the pseudo-period of the damped oscillations near the endemic equilibrium. Remarkably, in some cases the behavior may also be quasi-periodic or even chaotic.

The epidemiology of corticosteroid induced osteoporosis

the epidemiology of corticosteroid induced osteoporosis

Stroke occurred in 134 (%) patients. Incidence varied according to procedure (coronary bypass %, isolated valve %, valve/coronary bypass %, and ascending aorta %). Patients who had a stroke had a higher perioperative mortality rate than that of patients who did not (% vs %; P < .0001) and a longer period of hospitalization (median 30 days vs 7 days; P < .0001). Multivariate logistic analysis identified 10 preoperative predictors of stroke: gender, age, aortic surgery, previous stroke, critical preoperative state, poor ventricular function, diabetes, peripheral vascular disease, unstable angina, and pulmonary hypertension. A logistic model was developed on the basis of these risk factors to predict the likelihood of stroke.

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