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Disease probability

Table 2 lists the distribution of HIV/AIDS in various regions of the world. The heavy infection level in sub-Saharan Africa is the result of several factors. First, the disease probably originated there. The oldest HIV sample came from the Republic of the Congo in 1959, but most researchers believe AIDS had been killing people many decades before then. Second, most of the countries in sub-Saharan Africa are underdeveloped and have lacked the resources to fight the disease or implement effective prevention plans. This region of the world now has 70% of the global total of HIV-infected people but only 10% of the world s... [Pg.14]

Etiology. Most cases of PD are sporadic and appear to arise from a combination of genetic predisposition and environmental or toxic factors. Purely genetic forms of the disease probably account for less than 10% of cases, but the risk of family members of an affected patient to develop PD is significantly increased even in sporadic PD. [Pg.766]

Pulmonary disease probably occurs by inhalation conidia, which convert to the yeast forms in the lungs. It may be acute or chronic and can mimic infection with tuberculosis, pyogenic bacteria, other fungi, or malignancy. [Pg.429]

Among the many factors that affect cotton production are insects and diseases. Probably no other cultivated crop is so attractive to such a wide variety of insects, and in tropical conditions they multiply rapidly and spread. Therefore, the economical production of cotton in these areas, as elsewhere, often depends on whether or not the insects are controlled. [Pg.19]

The importance of nutrition in the dental caries problem is reviewed in 90 pages by Shaw.22 Although we have indicated that metabolic peculiarities in the area of mineral metabolism seem "most likely to be pertinent" to the dental caries problem (p. 218), it does not follow that interest should be restricted to this field. Because teeth are organic structures produced as the result of metabolic processes, there is not a single vitamin, amino acid, or other nutrient factor which may not be implicated in the disease. Probably many different deficiencies are involved in the production of the sum total of all caries existing in all individuals. Much evidence, of course, has been found to indicate the importance of calcium, phosphorus, and vitamin D, but other items may also be very important. [Pg.246]

Coeliac disease probably arose around 10000 bc when humans switched from the hunter-gatherer way of life to cultivation of cereals (barley, wheat and oats). An illness... [Pg.82]

Both case-control and convenience-cohort studies will be biased if the recall of diagnosed patients systematically differs from the recall of others. For instance, case group members, who are struggling to determine why they have a disease, probably recall differently than controls, who may be in the hospital for more routine matters. [Pg.11]

Landes and Posner (1987, Chapter 9) and Robinson (1985) argue that courts should not waste resources determining whether substance X caused malignancy y in individual z. Instead, courts should compensate those who have been exposed to a carcinogen an amount equal to the expected value of damages based on the population s disease probabilities. Such compensation would send the correct signals to both firms and consumers and conserve resources that are currently used in fruitless attempts to determine cause and effect at the individual level (National Research Council 1991,43). Individuals could use the compensation to buy insurance and share the risk of later disease among themselves. [Pg.33]

High doses of reserpine characteristically produce sedation, lassitude, nightmares, and severe mental depression occasionally, these occur even in patients receiving low doses (0.25 mg/d). Much less frequently, ordinary low doses of reserpine produce extrapyramidal effects resembling Parkinson s disease, probably as a result of dopamine depletion in the corpus striatum. Although these central effects are uncommon, it should be stressed that they may occur at any time, even after months of uneventful treatment. Patients with a history of mental depression should not receive reserpine, and the drug should be stopped if depression appears. [Pg.231]

Methotrexate s principal mechanism of action at the low doses used in the rheumatic diseases probably relates to inhibition of aminoimidazolecarboxamide ribonucleotide (AICAR) transformylase and thymidylate synthetase, with secondary effects on polymorphonuclear chemotaxis. There is some effect on dihydrofolate reductase and this affects lymphocyte and macrophage function, but this is not its principal mechanism of action. Methotrexate has direct inhibitory effects on proliferation and stimulates apoptosis in immune-inflammatory cells. Additionally, inhibition of proinflammatory cytokines linked to rheumatoid synovitis has been shown, leading to decreased inflammation seen with rheumatoid arthritis. [Pg.808]

Substantial evidence indicates that high plasma levels of lipoprotein remnants and LDL are atherogenic, while high levels of HDL are atheroprotective. Therefore, the class of lipoproteins that is increased or decreased will determine the clinical feature of a patient. Besides the influence on atherosclerosis, high levels of chylomicrons lead to acute pancreatitis, while markedly decreased levels of VLDL and LDL lead to retinal and neurologic disease, probably due to vitamin E deficiency. [Pg.499]

C. J. Boushey et al., A Quantitative Assessment of Plasma Homocysteine as a Risk Factor for Vascular Disease Probable Benefits of Increasing Folic Acid Intakes, J. Am. Med. Assoc. 274 (1995) 1049-57. [Pg.146]

Estrogen replacement therapy may have untoward effects in patients with renal disease, including an increased risk of thrombosis of dialysis access and potentially worsening of coronary artery disease, probably because the excretion of estrogens is impaired (77). [Pg.267]

A4. Allan, J. D., Cusworth, D. C., Dent, C. E., and Wilson, V. K., A disease, probably hereditary, characterised by severe mental deficiency and a constant gross abnormality of amino acid metabolism. Lancet i, 182-187 (1958). [Pg.248]

Although, as shown in Table 10.1, there are plausible mechanisms to suggest that homocysteine is a causative factor in cardiovascular disease, it is possible that hyperhomocysteinemia is a result of the renal damage that is an early event in cardiovascular disease, thus a proxy marker of disease rather than a causative factor (Jacobsen, 1998 hangman and Cole, 1999 Kircher and Sinzinger, 2000). in chronic renal failure, hyperhomocysteinemia is associated with cardiovascular disease, probably because of both impaired excretion of homocysteine and impaired activity of betaine homocysteine methyl-transferase elevated plasma dimethylglycine predicts plasma homocysteine (McGregor et al., 2001). [Pg.294]

Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA 1995 274(13) 1049-57. [Pg.263]

The adverse effects reported with epidural administration are similar to those reported with the intrathecal route. Again, old age and respiratory disease probably dispose to respiratory depression (133). As can be predicted from pharmacokinetic considerations, delayed respiratory depression is more common with epidural morphine than with fentanyl (134). [Pg.2632]

Symptoms in patients with Wilson s disease usually begin in the second or third decade of life, but may be earlier or later. However, mutations that completely destroy gene function may be associated with onset of liver disease as early as 3 years of age. The initial clinical presentation may be hepatic, with presentation similar to acute hepatitis or to chronic active hepatitis neurological (e.g., clumsiness, dysarthria, ataxia, and tremors) renal (renal tubular acidosis with aminoaciduria) or, less commonly, hematological, with hemolysis secondary to acute release of free copper from tissue and subsequent oxidation of erythrocyte membranes. The hepatic, and possibly CNS, damage may also be secondary to copper-induced oxidative damage to mitochondrial membranes. Hepatic levels of Cp messenger ribonucleic acid (mRNA) are reduced in patients with Wilson s disease, probably secondary to inhibition of transcription by increased intracellular levels of apoCp. ... [Pg.558]

Richardson WS, Wilson MC, Guyatt GH, et al. Users guides to the medical literature XV. How to use an article about disease probability for differential diagnosis. Evidence-Based Medicine Working Group. JAMA 1999 281 1214-1219. [Pg.37]

Pilot studies evaluating combination therapy with fluconazole plus flucytosine as initial therapy yielded unsatisfactory results, and this approach is discouraged even in low risk patients. Ketoconazole has been used successfully in the treatment of cutaneous cryptococcosis, but it is not useful in the treatment of CNS disease, probably because of its poor penetration into the CNS. ... [Pg.2174]

At that time, the disease probably caused about one-quarter of all deaths in England. The poets and writers of the so-called Romantic Age often seemed to be almost resigned to their fate. Keats mentions the symptoms in his poem Ode to a nightingale ... [Pg.62]

It has been suggested (KIO) that the role of ERP in a better prognosis with respect to disease-free and overall survival is confined to subjects with positive axillary node involvement at the time of initial presentation. In node negative disease, the differences in prognoses are minimal if any. PRP status also has been associated with increased survival in node negative disease. However, recent data from patients with negative nodes who received adjuvant chemotherapy demonstrated no relationship between ERP status and disease-free survival. Therefore receptor status in node negative disease probably should not be used as either a... [Pg.188]


See other pages where Disease probability is mentioned: [Pg.538]    [Pg.210]    [Pg.57]    [Pg.140]    [Pg.294]    [Pg.215]    [Pg.110]    [Pg.156]    [Pg.74]    [Pg.77]    [Pg.29]    [Pg.40]    [Pg.165]    [Pg.294]    [Pg.294]    [Pg.13]    [Pg.482]    [Pg.828]    [Pg.331]    [Pg.695]    [Pg.50]    [Pg.546]   
See also in sourсe #XX -- [ Pg.140 ]




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