Treatments Of Cancer

Source(google.com.pk)
Treatments Of Cancer Biography 
Cancer can be treated in different ways depending on what type of cancer it is, where it is in the body, and whether it has spread (its stage). You may have more than one type of treatment. Your doctors will discuss with you the best treatment for your situation. When planning your treatment, they will take into account your general health as well as the type and stage of the cancer.
Treatment types
Treatments for cancer include chemotherapy, radiotherapy, surgery, hormonal therapies and biological therapies.

Complementary therapies
Find out about the most common therapies and why people use them

Clinical trials
Find out about websites where you can search for cancer research trials in the UK and Europe. Clinical trials are carried out to try to find new and better treatments for cancer

Getting treatment
If you've been diagnosed with cancer, it can help to know what to expect and what to consider. Here we cover topics such as making decisions about treatment, asking for a second opinion or wanting a treatment that's not readily available

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Treatments Of Cancer

Tests For Kidney Function

Source(google.com.pk)
Tests For Kidney Function Biography

Abstract
Recent trends in weight loss diets have led to a substantial increase in protein intake by individuals. As a result, the safety of habitually consuming dietary protein in excess of recommended intakes has been questioned. In particular, there is concern that high protein intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration. There is, however, a serious question as to whether there is significant evidence to support this relationship in healthy individuals. In fact, some studies suggest that hyperfiltration, the purported mechanism for renal damage, is a normal adaptative mechanism that occurs in response to several physiological conditions. This paper reviews the available evidence that increased dietary protein intake is a health concern in terms of the potential to initiate or promote renal disease. While protein restriction may be appropriate for treatment of existing kidney disease, we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein

Western diet.
Dietary protein intake and renal function
Dietary protein intake can modulate renal function [1] and its role in renal disease has spawned an ongoing debate in the literature. At the center of the controversy is the concern that habitual consumption of dietary protein in excess of recommended amounts promotes chronic renal disease through increased glomerular pressure and hyperfiltration [2,3]. Media releases often conclude that, "too much protein stresses the kidney" [4]. The real question, however, is whether research in healthy individuals supports this notion. In fact, studies suggest that hyperfiltration in response to various physiological stimuli is a normal adaptative mechanism [5-10].

The purpose of this paper is to review the available evidence regarding the effects of protein intake on renal function with particular emphasis on renal disease. This review will consider research regarding the role of dietary protein in chronic kidney disease, normal renal function and kidney stone formation and evaluate the collective body of literature to ascertain whether habitual consumption of dietary protein in excess of what is recommended warrants a health concern in terms of the initiation and promotion of renal disease. In the following review, high protein (HP) diets will be defined as a daily consumption of greater than or equal to 1.5 g/kg/day, which is almost twice the current Recommended Dietary Allowance but within the range of current Dietary Reference Intakes (DRIs) for protein [11]. The Institute of Medicine DRI report concluded that there was insufficient scientific evidence for recommendations of an upper limit of protein intake but suggested an acceptable macronutrient distribution range of 10–35% of total energy for protein intake [11].

While the optimal ratio of macronutrient intake for adults has typically focused on fat and carbohydrate [12], contemporary discussions include the role of dietary protein [13-15]. This is particularly true given the recent popularity of high protein diets in weight management [16]. Although the efficacy of these diets with regard to weight loss is still subject to debate, several studies have demonstrated favorable physiological effects [12,16-24]. This has led to a substantial increase in protein intake by individuals adhering to contemporary weight loss plans. As a result, the safety of habitually consuming dietary protein in excess of the Recommended Daily Allowance (RDA) has been questioned.

An overview of chronic kidney disease
Chronic Kidney Disease (CKD) is defined as either kidney damage or a decline in renal function as determined by decreased glomerular filtration rate (GFR) for three or more months [25]. It is estimated that 1 in 9 adults in the United States meet this criteria, while an additional 1 in 9 adults are at increased risk for CKD [26]. In the general population, a decline in renal function is considered an independent risk factor for both cardiovascular disease and all-cause mortality [27]. However, the extent to which a mild diminution in renal function influences this risk is not known [28].

According to the National Kidney Foundation guidelines, CKD is classified into five stages, each of which directly correlates with the severity of the disease [25]. As one progresses from stage 1 to 5 there is a concomitant decline in GFR and thus renal function. The final stage, known as end stage renal disease, represents the most severe manifestation of CKD [29]. This classification system provides a universal standard for application of clinical treatment guidelines.

Hypertension is the second leading cause of CKD and accounts for approximately 30% of all cases in the U.S. [30,31]. In one study, hypertension was associated with a premature decline in renal function in men with normal kidney function [32]. Although, initial estimates of CKD prevalence in hypertensive individuals were about 2%, recent evidence suggests that prevalence rates may be significantly higher [33]. Blood pressure control is of particular importance in hypertensive individuals with CKD. This point has been demonstrated in several trials in which antihypertensive therapy slowed the progression of CKD [34-36].

Race, gender, age and family history are four risk factors for CKD [37-40]. Recent findings suggest that modifiable lifestyle risk factors (i.e., physical inactivity, smoking, obesity) are also associated with CKD. Limited data exist regarding the role of dietary protein intake as an independent risk factor for either the initiation or progression of renal disease but population studies have consistently demonstrated an inverse relationship between dietary protein intake and systemic blood pressure [41,42]. In a randomized control trial [43], dietary protein and fiber had additive effects in lowering 24-hour and awake systolic blood pressure in a group of 36 hypertensives. While these findings suggest that high protein diets may be beneficial to hypertensive individuals, additional research is warranted since increased protein intakes often result in increased consumption of certain micronutrients known to impact blood pressure (e.g., potassium, magnesium, calcium) [44].

Dietary protein and renal function
The relationship between dietary protein and renal function has been studied for over half a century [1]. In 1923, Addis and Drury [45] were among the first to observe a relationship between level of dietary protein and rates of urea excretion. Soon after, it was established that increased protein intake elevated rates of creatinine and urea excretion in the dog model [46]. The common mechanism underlying increased excretion rates was eventually attributed to changes in GFR [47,48] and Van Slyke et al. [49] demonstrated that renal blood flow was the basis for GFR mediated changes in clearance rates in response to increased protein intake. Clearly dietary protein effects GFR [50], with both acute and chronic increases in protein consumption elevating GFR [50,51].

Dietary protein and the progression of renal disease
Observational data from epidemiological studies provide evidence that dietary protein intake may be related to the progression of renal disease [52]. In the Nurses' Health Study, protein intake, assessed with a semi-quantitative food frequency questionnaire, was compared to the change in estimated GFR over an 11-year span in individuals with pre-existing renal disease [53]. Regression analysis showed an association between increased consumption of animal protein and a decline in renal function suggesting that high total protein intake may accelerate renal disease leading to a progressive loss of renal capacity. However, no association between protein intake and change in GFR was found in a different cohort of 1,135 women with normal renal function (Figure 1.). The latter finding led the authors to conclude that there were no adverse effects of high protein intakes on kidney function in healthy women with normal renal status.

Figure 1. This figure is a plot of multivariate linear regression for change in estimated GFR according to quintile of total protein intake* in participants with normal renal function (n = 1135). Data are taken from Knight et al., Ann Intern Med 2003 Mar 18;138(6):460-7 [53].
Research by Johnson et al. [54], showed protein intake as a possible risk factor for progressive loss of remaining renal function in dialysis patients. Indeed, dietary protein restriction is a common treatment modality for patients with renal disease [55,56] and practice guidelines exist regarding reduced dietary protein intakes for individuals with chronic renal disease in which proteinuria is present [57]. The National Kidney Foundation (NKF) has extensive recommendations with regard to protein intake, which are a byproduct of the Dialysis Outcome Quality Initiative [58]. Again, it is important to note that these recommendations are not indicated for individuals with normal renal function nor are they intended to serve as a prevention strategy to avoid developing CKD. Despite the clarity of these guidelines, their mere existence has resulted in concern regarding the role of dietary protein in the onset or progression of renal disease in the general population [59].

Dietary protein and renal disease
Allen and Cope's observation that increased dietary protein induced renal hypertrophy in dogs [60] led to speculation that dietary protein intake may have deleterious effects on the kidney. Later research in the rat model produced evidence supporting earlier observations from canine research [61-63]. Recently, Hammond and Janes [64] demonstrated an independent effect of increased protein intake on renal hypertrophy in mice. In this study, changes in renal function (i.e., increased glomerular filtration rate and renal hypertrophy) were observed.

Currently, a combination of hormonal interactions and renal processes are thought to explain protein-induced hyperfiltration [65]. Increased glucagon secretion in response to protein administration induced hyperfiltration [66] subsequent to a cascade of events referred to as the"pancreato-hepatorenal cascade" [67]. It has been hypothesized that cAMP works in concert with glucagon to mediate GFR [68]. To date, however, this hypothesis has not been tested and other competing hypotheses suggest other novel mechanisms of protein-induced hyperfiltration [69].

While the effect of hyperfiltration on renal function in those individuals with pre-existing renal disease is well documented [52], the application of these observations to healthy persons with normal renal function is not appropriate. To date, scientific data linking protein-induced renal hypertrophy or hyperfiltration to the initiation or progression of renal disease in healthy individuals is lacking. The possibility that protein-induced changes in renal function are a normal physiological adaptation to nitrogen load and increased demands for renal clearance is supported by changes noted in renal structure and function during pregnancy [70]. GFR increases by as much as 65% in healthy women [8] during pregnancy, typically returning to nonpregnant levels by three months postpartum [7]. Despite these changes in renal function, pregnancy is not a risk factor for developing CKD [6].

The renal hypertrophy and accompanying improvements in renal function in the contralateral kidney that occur subsequent to unilateral nephrectomy also suggest these processes are an adaptive, and possibly beneficial, response [5]. Studies show, despite prolonged hyperfiltration, remnant kidney function remained normal and did not deteriorate during long-term (> 20 yrs) follow-up in nephrectomized patients [9,10]. Thus, compensatory hyperfiltration appears to be a biological adaptation to a variety of renal challenges that is not associated with increased risk of chronic kidney disease in healthy individuals.

The Brenner Hypothesis
Perhaps the most consistently cited reference with regard to the potentially harmful effects of dietary protein intake on renal function is that of Brenner et al. [3]. In brief, the Brenner Hypothesis states that situations associated with increased glomerular filtration and glomerular pressure cause renal injury, ultimately compromise renal function, and potentially increase the risk for or progression of renal disease. Brenner proposed that habitual consumption of excessive dietary protein negatively impacted kidney function by a sustained increased in glomerular pressure and renal hyperfiltration [3]. Since the majority of scientific evidence cited by the authors was generated from animal models and patients with co-existing renal disease, extension of this relationship to healthy individuals with normal renal function is inappropriate. Indeed, a relationship between increased glomerular pressure or hyperfiltration and the onset or progression of renal disease in healthy individuals has not been clearly documented in the scientific literature. Rather, findings from individuals with compensatory hyperfiltration during pregnancy and following unilateral nephrectomy suggest otherwise [9].

The Modification of Diet in Renal Disease (MDRD) study was the largest randomized multicenter, controlled trial undertaken to evaluate the effect of dietary protein restriction on the progression of renal disease [71]. Several variables, including GFR, were measured in patients with chronic renal disease at baseline and throughout the approximately 2 year follow-up period. Patients with renal disease randomized to the very low-protein diet group had slightly slower decline in GFR decline compared with patients randomized to the low-protein diet group. Further data analyses showed patients with lower total protein intake would have a longer time to renal failure and suggested that a lower protein intake postponed the progression of advanced renal disease. Using meta-analysis to assess the efficacy of dietary protein restriction in previously published studies of diabetic and nondiabetic renal diseases, including the MDRD Study, Pedrini et al. concluded that the progression of both nondiabetic and diabetic renal disease could be effectively delayed with restriction of dietary protein [56]. Indeed, current clinical guidelines for the management of patients with renal disease continue to be based on the premise that protein intake greater than that recommended or which results in a renal solute load in excess of the kidney's excretory capabilities will contribute to progressive renal failure in persons with compromised renal function. However, of significance to this review, is the fact that imposing these guidelines on healthy individuals with normal renal function is overzealous given the current status of the scientific literature in this area.

Dietary protein and renal strain
Concerns about level of dietary protein and renal function are often presented in public health guidelines [59]. In addition to the claims that high protein intake causes renal disease, some studies have suggested that renal function may be negatively affected by routine consumption of high protein diets [72-75]. Although high protein diets cause changes in renal function (i.e., increased GFR) and several related endocrine factors [1,76,77] that may be harmful to individuals with renal disease [52,53], there is not sufficient research to extend these findings to healthy individuals with normal renal function at this time.

The lay public is often told that high protein diets "overwork" the kidney and may negatively impact renal function over time [78]. In addition, a number of highly regarded organizations appear to support this line of reasoning [79] given the physiological processes required for excretion of protein-related metabolic waste products to maintain homeostasis following consumption of protein at levels in excess of recommended amounts. Increased consumption of dietary protein is linearly related to the production of urea [80] and urea excretion is controlled by the kidney. These processes are of significant energetic cost to the kidney and represent the physiological "strain" associated with increased protein intake [81].

The word "strain" is misleading given its negative connotation. In a press release [82], one group asserted that increased dietary protein "strains" the kidney via increased urea production, and causes dehydration and accumulation of blood urea nitrogen. This press release also suggested that these events synergistically overwork the kidney and predispose humans to CKD. Scientific research is often misrepresented in this context. Research from our laboratory [83] which is cited in the press release, does not support these contentions. Rather, we found that habitual consumption of a high protein diet minimally affected hydration indices. Changes in total body water and renal function were not measured.

The concept that increased dietary protein leads to dehydration may have originated from an unsubstantiated extension of a 1954 review of the nitrogen balance literature [84]. This review focused on the design of survival rations for military operations in the desert or at sea, when water supply and energy intake are limited. Since the excretion of 1 gram of urea nitrogen requires 40 – 60 mL of additional water, increased protein intakes in the study translated into an increased water requirement (i.e., +250 mL water per 6 grams of dietary nitrogen in a 500 Kcal diet) for excretion of urea nitrogen. This increased fluid requirement is situation specific and is not necessarily applicable to individuals whose calorie and water intakes are adequate. Presently, we know of no studies executed in healthy individuals with normal renal function which demonstrate a clear relation between increased dietary protein intake and dehydration or a detrimental "strain" on the kidney. Therefore, claims that a high protein diet promotes dehydration or adversely "strains" the kidney remain speculative.

Evidence in healthy individuals
Although the efficacy of high protein diets for weight loss has been evaluated, there have been no reports of protein-induced diminutions in renal function despite subject populations that are generally at risk for kidney disease (e.g., dyslipidemia, obesity, hypertension) [14,15,22,85-87]. A randomized comparison of the effects of high and low protein diets on renal function in obese individuals suggested that high protein diets did not present a health concern with regard to renal function their study population [65]. In this study, 65 overweight, but otherwise healthy, subjects adhered to a low or high protein diet for six months. In the high protein group, both kidney size and GFR were significantly increased from that measured at baseline. No changes in albumin excretion were noted for either group and the authors concluded that, despite acute changes in renal function and size, high protein intake did not have detrimental effects on renal function in healthy individuals. Similar findings were recently reported by Boden et al. [88] in a study of 10 subjects who consumed their typical diet for 7 days followed by strict adherence to a high protein diet for 14 days. No significant changes were noted in serum or urinary creatinine and albumin excretion, suggesting no ill-effects of a high protein diet on renal function.

Athletes, particularly in sports requiring strength and power, consume high levels of dietary protein [89,90]. In fact, many athletes habitually consume protein in excess of 2.0 g/kg/day [91]. Supplementation with amino acids will further increase dietary protein levels in these individuals [92]. Yet there is no evidence that this population is at greater risk for kidney disease or losses in renal function [90]. Poortsmans and Dellalieux [93] found that protein intakes in the range of ~1.4–1.9 g/kg/day or 170–243% of the recommended dietary allowance did not impair renal function in a group of 37 athletes. We found no data in the scientific literature to link high protein intakes to increased risk for impaired kidney function in healthy, physically active men and women.

Dietary protein and renal function in animal models
Although there is limited research regarding the long-term effects of high protein intakes on renal function in humans, animal models have provided insight into this quandary. Mammals fed acute and chronic high protein diets exhibit increases in GFR and renal blood flow [94]. These changes, which are comparable to those observed in humans, led to the hypothesis that high protein intakes are associated with progressive glomerulosclerosis in the rat. Recently, Lacroix et al. [95] studied the effects of a diet containing 50% protein on renal function in Wistar rats and noted no abnormalities in renal function or pathology. Collins et al. [96] also reported no adverse effects of long-term consumption of high protein diets on renal function when two years of a diet containing 60% protein failed to evoke changes in the percentage of sclerotic glomeruli in rats. Robertson et al., [97] studied the effect of increased protein intake on hyperperfusion and the progression of glomerulosclerosis in dogs that were 75% nephrectomized. After four years of feeding diets that were either 56, 27 or 19% protein, no association between diet and structural changes in the kidney were observed.

To the best of our knowledge, there has been only one report of a potentially toxic effect of excessive protein intake on renal function in the rat. Stonard et al. [98] found a diet containing 33% protein produced tubular damage in a specific strain of female rats. However, findings from this study are limited by the fact that damage was induced by a bacterial single-cell protein (Pruteen).

In summary, studies documenting high protein intake as a cause of renal disease in any animal model have not been done. Rather, studies have typically focused on the interaction between protein intake and renal function in the diseased state. As a result, findings from these investigations should not be used as a basis for dietary recommendations for humans. Studies designed to characterize the effects of dietary protein intake on renal function in healthy subjects are warranted.

Dietary protein and kidney stones
The role of high protein diets in kidney stone formation has received considerable attention. Excessive protein intake increases excretion of potentially lithogenic substances such as calcium and uric acid [99,100]. Reddy et al. [101] noted that consumption of a high protein diet for six weeks was associated aciduria and urinary calcium and claimed that this constituted increased risk of stone formation in ten healthy subjects although none of the ten subjects developed renal stones. The severe carbohydrate restriction imposed in this study may have increased keto-acid production thereby contributing acid formation. Since consumption of fruits and vegetables usually produces a marked base load [102], restriction of these foods subsequent to the diet intervention may have also contributed to the net acid load.

Studies that claim an increased propensity for stone formation as a result of increased protein intake should be taken at face value because propensity is a surrogate marker and does not represent actual stone formation. Further, randomized control trials have not been done to test whether an increased tendency for stone formation is enhanced with consumption of a high protein diet.

Epidemiological studies provide conflicting evidence with regard to the association between protein intake and the predisposition for kidney stone formation. In a prospective study of over 45,000 men, researchers found a direct correlation between animal protein intake and risk of stone formation [103]. However, findings in women are difficult to interpret due to conflicting reports in the literature. While some studies have shown a direct relationship between animal protein intake and risk of stone formation in women [104,105], other work suggests an inverse relationship exists [106].

Conflicting findings regarding the role of dietary protein in kidney stone formation limit the development of universal guidelines with regard to a recommended protein intake for individuals at increased risk for stone formation [107]. It is not likely that diet alone causes kidney stone formation [108]. Rather, metabolic abnormalities are typically the underlying cause [109]. For example, Nguyen et al. [110] found that high intakes of animal protein adversely affected markers of stone formation in those afflicted with a stone causing disorder, while no changes were observed in healthy individuals. It has been suggested that one must have a preexisting metabolic dysfunction before dietary protein can exert an effect relative to stone formation [108]. This notion has been coined the "powderkeg and tinderbox" theory of renal stone disease by Jaeger [111]. This theory asserts that dietary excesses, such as high protein intake, serve as a tinderbox which, only in tandem with a metabolic abnormality (the powderkeg), can bring about stone formation. At the present time, however, evidence showing that a high protein intake is an inherent cause of this renal abnormality or is consistently associated with increased kidney stone formation does not exist.

Conclusion
Although excessive protein intake remains a health concern in individuals with pre-existing renal disease, the literature lacks significant research demonstrating a link between protein intake and the initiation or progression of renal disease in healthy individuals. More importantly, evidence suggests that protein-induced changes in renal function are likely a normal adaptative mechanism well within the functional limits of a healthy kidney. Without question, long-term studies are needed to clarify the scant evidence currently available regarding this relationship. At present, there is not sufficient proof to warrant public health directives aimed at restricting dietary protein intake in healthy adults for the purpose of preserving renal function.

Function Of Kidney

Source(google.com.pk)
Function Of Kidney Biography

Along with the liver, the kidneys are another part of the waste processing system of the body -- thus urine goes from the kidneys into the bladder.  The liver filters metabolic waste products, excess sodium and water from the blood, thereby helping to eliminate them from the body.  The kidneys also help regulate blood pressure and the production of red blood cells.

Medscape (you may need to register to access this article), has a paper on Chronic Kidney Disease: Chronic Kidney Disease: It's Time to Recognize Its Presence in Our Patients With Hypertension. Posted 10/22/2004, by Jan Basile, MD.  This is an informative article about kidney function.

Definitions
Renal - pertaining to the kidneys.

Drug-induced

As an example of drug-induced kidney problems consider Zometa. The prescribing directions require measuring the creatinine level prior to administering Zometa. Clinical trial data showed increased renal(kidney) function deterioration when Zometa was given times shorter than 15 minutes and at higher than 4 mg doses (e.g., 8mg/5 minutes). Thus the criteria for dosing at 4mg/>15 minutes.

There are other drugs that can impact the kidney  as well.

What tests are run to assess kidney function?2
You cannot live without adequately functioning kidneys and liver.  Therefore, it may be necessary with certain drugs to run some of the following tests periodically to determine whether those drugs are harming these vital organs.  Liver and kidney insufficiency are also dangerous associated diseases that can aggravate the problem of cancer. The following tests are often given monthly as part of the complete metabolic panel with blood drawn before chemotherapy or during regular monitoring of your disease.

Please refer to the references for a more complete description of the various tests listed below.

BUN (Blood Urea Nitrogen or Urea Nitrogen).   This is the concentration of nitrogen(within urea) in the serum(but not in red blood cells).  A waste product, derived from protein breakdown, produced in the liver and excreted by way of the kidneys. High values may mean that the kidneys are not working as well as they should. BUN is also elevated by blood loss, dehydration, high protein diets and/or strenuous exercise which may temporarily and artificially raise levels. A low BUN level may be the result of liver disease, a low protein diet, pregnancy, or drinking an extreme amount of water.

Creatinine.  A waste product largely from muscle metabolism (breakdown). Concentration of creatinine in the blood depends upon the amount of muscle that you have and the ability of your kidneys to excrete creatinine. High values, especially with high BUN levels, may indicate problems with the kidneys. Low values are generally not considered significant.

Calcium.  Calcium is one of the most important elements in the boby. The parathyroid glands and the kidneys control the amount of calcium in the blood. The parathyroid gland is the main regulator of calcium in the body.  Nearly all of the calcium in the body is found in bone (99%). The remaining 1% is very important for proper clotting, nerve, and cell and enzyme activity. An elevated calcium level can be due to medication (such as too much calcitriol-synthetic vitamin D), inherited disorders of calcium handling in the kidneys, bone disease, or excess parathyroid gland activity or vitamin D. Low calcium can be due to malnutrition, drugs and certain metabolic disorders.

Sodium.  An electrolyte regulated by the kidneys and adrenal glands. This element plays an important role in the water/salt balance in your body.

Potassium.  Potassium is an electrolyte found  primarily inside cells and must be controlled very carefully by the kidneys.  Its role is to maintain water balance inside the cells and to help in the transmission of nerve impulses. A low potassium level can cause muscle weakness and heart problems. A high potassium level can be found in kidney disease or in over ingestion of potassium supplements.

Chloride.   Chloride is an electrolyte regulated by the kidneys and adrenal glands.  Chloride is important to the function of nerves, muscles, and cells.  It is usually associated with a high or low level of sodium or potassium.

Some drugs taken by prostate cancer patients such as estrogens and corticosteriods can cause increased chloride(there are a number of other durgs also that can do this). See (2). Both drugs and other causes can lead to a decrease in serum chloride.

CO2.  Co2 levels reflects the acid status of your blood. See the references listed under (2) for details on the cause of high or low levels.   Corticosteriods as well as kidney disease can be involved.

BUN/Creatinine Ratio - This ratio is sometimes used or diagnostic purposes.

Example Complete Metabolic Panel
Note: the yellow area highlights kidney function tests. Reference ranges may vary from laboratory to laboratory. HI and LO are relative to the Reference Range.

Kidney Functions

Source(google.com.pk)
Kidney Functions Biography
Chronic kidney disease has recently been recognized as a public health problem; it is estimated that by 2030, more than 2 million people in the United States will need dialysis or transplantation for kidney failure.12 Currently, approximately 19 million adults in the United States are in the early stages of the disease,13 defined by either a GFR of less than 60 ml per minute per 1.73 m2 of body-surface area or the presence of kidney damage, regardless of the cause, for three or more months2,14,15 (Table 1TABLE 1
Stages of Chronic Kidney Disease (CKD), Prevalence in the United States in 2000, and Stage-Specific Recommendations for Detection, Evaluation, and Management.
 and Figure 1FIGURE 1
Normal Values for GFR in Men and Women.
). Risk factors for chronic kidney disease include an age of more than 60 years, hypertension, diabetes, cardiovascular disease, and a family history of the disease. Recommendations for evaluating people at increased risk are to measure urine albumin to assess kidney damage and to estimate the GFR with an equation based on the level of serum creatinine.2,5,10,11,16
Once chronic kidney disease is detected, identification of the cause, coexisting conditions, and stage (Table 1) is essential for further evaluation and management. An estimated GFR of less than 60 ml per minute per 1.73 m2 is associated with a graded increase in the risk of each of the major adverse outcomes of chronic kidney disease, which are impaired kidney function, progression to kidney failure, and premature death caused by cardiovascular disease (Figure 2FIGURE 2
Estimated Prevalence of Complications Related to Chronic Kidney Disease, According to the Estimated GFR in the General Population.
).2,11,17-19 The large number of patients who have chronic kidney disease, together with the number of people at increased risk for it, requires primary care providers, as well as specialists in areas other than nephrology, to increase their familiarity with the use of GFR estimates.

MEASUREMENT OF GFR WITH EXOGENOUS FILTRATION MARKERS
GFR is accepted as the best overall measure of kidney function.15,20 Normal values, which are related to age, sex, and body size, are approximately 130 ml per minute per 1.73 m2 in young men and 120 ml per minute per 1.73 m2 in young women. Mean values decline as persons age (Figure 1).15
GFR is measured as the urinary or plasma clearance of an ideal filtration marker such as inulin or of alternative exogenous markers such as iothalamate, EDTA, diethylene triamine pentaacetic acid, and iohexol. Measuring clearance with the use of exogenous markers is complex, expensive, and difficult to do in routine clinical practice.21 Furthermore, research studies have reported a measurement error of 5 to 20 percent (variation within a single clearance procedure or between clearance procedures on different days).22-25 The variation is greater in the higher ranges of GFR on the absolute scale.22

ESTIMATION OF GFR WITH ENDOGENOUS FILTRATION MARKERS
Urinary clearance of an endogenous filtration marker such as creatinine can be computed from a timed urine collection (for example, a 24-hour urine collection) and blood sampling during the collection period without the need for the administration of an exogenous marker. Nonetheless, timed urinary collections are cumbersome and susceptible to error, and 24-hour urine collections for the measurement of creatinine clearance are no longer recommended routinely to estimate the level of kidney function.
In the steady state, the serum level of an endogenous marker is related to the reciprocal of the level of GFR and can be used to estimate the GFR without a urine collection. The serum level of endogenous filtration markers can also be affected by factors other than the GFR, including tubular secretion or reabsorption, generation, and extrarenal elimination of the endogenous filtration marker.

Creatinine
Creatinine is an amino acid derivative with a molecular mass of 113 D that is freely filtered by the glomerulus. Many studies support the similarity of creatinine clearance to GFR and its reciprocal relationship with the serum creatinine level.26,27 Creatinine is secreted by proximal tubular cells as well as filtered by the glomerulus; thus, the creatinine clearance exceeds the GFR. Tubular secretion of creatinine varies among and within individual persons, especially in those with a mild-to-moderate reduction in the GFR.28 Some drugs, including trimethoprim and cimetidine, inhibit creatinine secretion, thereby reducing creatinine clearance and elevating the serum creatinine level without affecting the GFR.28,29 The generation of creatinine is determined primarily by muscle mass and dietary intake (Table 2TABLE 2
Factors Affecting Creatinine Generation.
), which probably accounts for the variations in the level of serum creatinine observed among different age, geographic, ethnic, and racial groups.28,30,31 Extrarenal elimination of creatinine may be increased at low levels of GFR; this increase is mainly related to the degradation of creatinine by intestinal bacteria and can be affected by the use of antibiotics.26,27 For these reasons, the relationship between the levels of serum creatinine and GFR varies substantially among persons and over time. The use of a single reference range for serum creatinine to distinguish between a normal GFR and an abnormal one can be misleading (Figure 3FIGURE 3
Relationship of Serum Creatinine Level to Measured GFR in the Modification of Diet in Renal Disease Study.
).26-28,32,34

Cystatin C
Cystatin C, a nonglycosylated basic protein with a low molecular mass (13 kD) that is freely filtered by the glomerulus, is currently under investigation as a replacement for serum creatinine in estimating the GFR.35-40 After filtration, cystatin C is reabsorbed and catabolized by the tubular epithelial cells; only small amounts are excreted in the urine. Consequently, although cystatin C is cleared by the kidneys, its urinary clearance cannot be measured, which makes the study of the factors affecting its clearance and generation difficult.
The generation of cystatin C appears to be less variable from person to person than that of creatinine. However, there is preliminary evidence that serum levels of cystatin C are influenced by corticosteroid use41 and are related to age, sex, weight, height, smoking status, and the level of C-reactive protein, even after adjustment for creatinine clearance.42 Other studies show extrarenal elimination of the protein in the presence of high levels of cystatin C.36,37 Recent investigations suggest that cystatin C may be a better filtration marker than creatinine, especially at higher levels of GFR. However, it is less certain whether the measurement of cystatin C is an improvement over creatinine-based equations for estimating the GFR.35,36,43-45

EQUATIONS USED TO ESTIMATE GFR
Estimating equations include variables such as age, sex, race, and body size, in addition to serum creatinine, as surrogates for muscle mass, and therefore, they can overcome some of the limitations of the use of serum creatinine alone. An estimating equation is derived with the use of regression techniques to model the observed relation between the serum level of the marker and the measured GFR in a study population. Estimating equations for GFR have been developed chiefly in study populations consisting predominantly of patients with chronic kidney disease and reduced GFR. Although an equation developed in one population is appropriate for use in that population, evaluation in other populations is necessary to demonstrate the generalizability of the observed relationships. We will focus on two creatinine-based equations that have been extensively studied and widely applied, the Cockcroft–Gault and the Modification of Diet in Renal Disease (MDRD) study equations.32,33,46,47
The Cockcroft–Gault formula was developed in 1973 with the data from 249 men with creatinine clearances (Ccr) from 30 to 130 ml per minute.46,48 The estimating equation is Ccr=[(140− age)×weight/](72×Scr)×0.85 (if the subject is female), where Ccr is expressed in milliliters per minute, age in years, weight in kilograms, and serum creatinine (Scr) in milligrams per deciliter. It systematically overestimates GFR because of the tubular secretion of creatinine. The values are not adjusted for body-surface area; a comparison with normal values for creatinine clearance requires measurement of height, computation of body-surface area, and adjustment to 1.73 m2.49
The MDRD study equation was developed in 1999 with the use of data from 1628 patients with chronic kidney disease. It estimates GFR adjusted for body-surface area.32,33 The estimating equation is GFR=186×(Scr)−1.154×(age)−0.203×0.742 (if the subject is female) or ×1.212 (if the subject is black). This equation was reexpressed in 2005 for use with a standardized serum creatinine assay, which yields serum creatinine values that are 5 percent lower34,47: GFR=175×(standardized Scr)−1.154×(age)−0.203×0.742 (if the subject is female) or ×1.212 (if the subject is black). GFR is expressed in milliliters per minute per 1.73 m2, and race is either black or not. The term for race reflects a higher average serum creatinine level in blacks, partly owing to increased muscle mass. In the MDRD study population, 91 percent of the GFR estimates were within 30 percent of the measured values, and this approach was more accurate than either the use of the Cockcroft–Gault equation or the measurement of creatinine clearance, even after adjustment for body-surface area and correction for systematic bias owing to the overestimation of GFR by creatinine clearance (Figure 4FIGURE 4
Relation of Estimated GFR to Measured GFR in the Participants in the Modification of Diet in Renal Disease (MDRD) Study.
).
To convert the values to SI units (Scr in micromoles per liter), replace 72 in the denominator with 0.84 in the Cockcroft–Gault equation, replace 186 with 32,788 in the original (1999) MDRD study equation,33 and replace 175 with 30,849 in the reexpressed (2005) MDRD study equation.47
Evaluation of Current Estimating Equations
The MDRD study and the Cockcroft–Gault equations have been evaluated in numerous populations, including blacks, whites, and Asians with nondiabetic kidney disease, patients with diabetes and kidney disease, patients with diabetes without kidney disease, kidney-transplant recipients, and potential kidney donors.50-70 The MDRD study equation is reasonably accurate in nonhospitalized patients known to have chronic kidney disease. In four large studies of persons with chronic kidney disease, the mean difference between estimated and measured GFR ranged from –5.5 to 0.9 ml per minute per 1.73 m2.50-52,54 In some studies, the MDRD study equation has been reported to be more accurate than the Cockcroft–Gault equation,50-52,54,71 whereas other studies have found that the two yield similar results.53,63,69,72 The Cockcroft–Gault equation appears to be less accurate than the MDRD study equation in older and obese people.54,69,71
Both the MDRD study and the Cockcroft–Gault equations have been reported to be less accurate in populations without chronic kidney disease, such as in young patients with type 1 diabetes without microalbuminuria and in potential kidney donors.50,52,54,56,57,63 On average, GFR estimates of less than 90 ml per minute per 1.73 m2 in this population are lower than the directly measured values; mean differences between GFR estimates from the MDRD study equation and the direct GFR measurement range from –29 to 3.3 ml per minute per 1.73 m2.50,52,54,63,69 This difference may lead to a false positive diagnosis of chronic kidney disease (a GFR of less than 60 ml per minute per 1.73 m2) in persons who do not have the disease but have a mild reduction in GFR. However, despite the potential misclassification, studies in the general population show that an estimated GFR of less than 60 ml per minute per 1.73 m2 is associated with an increased risk of adverse outcomes of chronic kidney disease.11,17,18,73
There are several possible explanations for reports that higher GFR estimates may be inaccurate (see the Appendix). First, variation among laboratories in calibration of the serum creatinine assay has a larger effect at higher GFR levels and is probably an important reason for the wide variation in the results of published studies.74-77 Furthermore, the biologic and measurement variability of GFR is greater at higher levels. Finally, the use of an equation developed in a population with chronic kidney disease may be limited in a population without the disease.

USE OF GFR ESTIMATES
GFR estimates appear to provide a substantial improvement over the measurement of serum creatinine alone in the clinical assessment of kidney function. However, proper interpretation of GFR estimates requires attention to their limitations. The following discussion focuses on the application of current estimating equations for selected aspects of the detection, evaluation, and management of chronic kidney disease (Table 1).
Detection of Chronic Kidney Disease
A persistent reduction in the GFR to less than 60 ml per minute per 1.73 m2 is defined as chronic kidney disease.1,2,5 The differing accuracy of current estimating equations in people with and those without the disease may make it difficult to interpret GFR estimates that are near 60 ml per minute per 1.73 m2. In this range, the interpretation of GFR estimates depends on the clinical context. Patients with markers of kidney damage such as proteinuria or abnormalities on imaging studies or on kidney biopsy have the disease, even if GFR estimates are 60 ml per minute per 1.73 m2 or greater. Patients without markers of kidney damage who have GFR estimates of 60 ml per minute per 1.73 m2 or greater are unlikely to have the disease. There is some uncertainty with respect to patients without markers of kidney damage who have GFR estimates just below 60 ml per minute per 1.73 m2. Some of these patients may have a measured GFR above 60 ml per minute per 1.73 m2 and therefore would not be considered to have chronic kidney disease. Clinical decision making in these cases will depend on other characteristics of the patients, such as the presence or absence of risk factors for the disease or its complications. Clinicians may decide to defer further evaluation in some patients, but it may be prudent to monitor their estimated GFR more frequently, adjust the dose of medications that are excreted by the kidney, and avoid medications toxic to the kidney.

Monitoring Progression of Chronic Kidney Disease
The reciprocal relationship between GFR and serum creatinine levels makes it difficult for clinicians to appreciate the level and rate of change in GFR by simply monitoring serum creatinine levels. For example, in a 50-year-old white man an increase in serum creatinine from 1.0 to 2.0 mg per deciliter (88.4 to 176.8 μmol per liter) reflects a decline in GFR of 46 ml per minute per 1.73 m2, but a further increase in the serum creatinine level from 2.0 to 3.0 mg per deciliter (265.2 μmol per liter) reflects a further decline of only 14 ml per minute per 1.73 m2.

Evaluation and Management of Complications
Decreased kidney function is associated with many complications, such as hypertension, anemia, malnutrition, bone disease, and a decreased quality of life (Figure 2).2 These complications can be treated effectively, especially if detected early.78-81 Accordingly, testing for complications of this disease has been recommended beginning in patients with stage 3 chronic kidney disease (defined by a GFR of 30 to 59 ml per minute per 1.73 m2).2

GFR and Referral to Nephrologists
Complications related to chronic kidney disease and the risk of severe kidney failure are highest among patients with stage 4 or 5 of the disease.11,17-19 Late referral to nephrologists before the initiation of dialysis is associated with increased rates of morbidity and mortality.82-84 Thus, it is important to refer any patient with a GFR estimated to be less than 30 ml per minute per 1.73 m2 to a nephrologist for co-management.

Medications and Chronic Kidney Disease
Many medications are excreted by the kidneys and require adjustment in the dose when the GFR is reduced. The Cockcroft–Gault equation has been widely used in pharmacokinetic studies and in the guidance of drug dosing. In most cases, the GFR estimates from the MDRD study and the Cockcroft–Gault equations fall within the same interval for dose adjustment. Nonetheless, until there are more data based on the MDRD study equation or other new equations, physicians and pharmacists may choose to continue to use the Cockcroft–Gault equation to adjust drug doses in patients with a decreased estimated GFR. The appropriate adjustment in medication dose for patients who are either very large or very small in size requires the expression of GFR estimates in milliliters per minute, rather than in milliliters per minute per 1.73 m2.49
Assessment of Risk for Cardiovascular Disease
An estimated GFR below 60 ml per minute per 1.73 m2 is a risk factor for both new and recurrent cardiovascular disease in the general population and in people at increased risk for cardiovascular disease.11,17-19 In these patients, death from cardiovascular disease is more common than progression to kidney failure.73 Patients with an estimated GFR below 60 ml per minute per 1.73 m2 are therefore considered to be in the high-risk group for cardiovascular disease, and they should undergo intensive evaluation and treatment of risk factors for cardiovascular disease.1,11
Recent studies suggest that the serum level of cystatin C may be a better predictor of outcomes of cardiovascular disease than GFR estimates based on levels of serum creatinine. It is not known whether the prediction is improved because cystatin C is a better marker of GFR than levels of serum creatinine or because factors apart from GFR that affect the level of cystatin C or creatinine also are related to the risk of cardiovascular disease.35-45,85-87 For example, many chronic diseases, including cardiovascular disease, are associated with decreased muscle mass and, consequently, lower serum creatinine levels and higher estimated GFR, which would weaken the association of lower estimated GFR and cardiovascular disease. Factors related to higher levels of cystatin C are less well understood, but a reported positive association with C-reactive protein would strengthen the association of a higher level of cystatin C and cardiovascular disease.
When to Consider Clearance Measurements Instead of Estimated GFR
GFR estimates are less accurate in certain circumstances. One such circumstance occurs in people with unusual body habitus or diet (Table 2); for example, a person with substantial muscle wasting may have a lower GFR than suggested by the GFR estimate, even at GFR levels of less than 60 ml per minute per 1.73 m2, owing to a low level of creatinine generation. Another circumstance is in patients with rapidly changing kidney function; in these patients, changes in GFR estimates lag behind changes in measured GFR. GFR can be estimated from the rate and magnitude of change in the GFR estimate, analogous to the interpretation of changes in the serum creatinine level in the nonsteady state. The third circumstance involves patients with GFR estimates of 60 ml per minute per 1.73 m2 or greater. More accurate estimates may be necessary to evaluate people for kidney donation, administer drugs with marked toxic effects and that are excreted by the kidneys (e.g., high-dose methotrexate), or determine a person's eligibility for research protocols.
Clearance of exogenous filtration markers provides the most accurate measure of GFR and could be used if facilities for administration of the marker and its measurement are available. Creatinine clearance can be measured from a 24-hour urine collection and a single serum sample in the steady state, but the results must be interpreted with caution because of errors in collection of timed urine specimens and because creatinine clearance exceeds GFR. The former source of error might be reduced by repeated measurements and the latter by pretreatment with cimetidine, which partially inhibits creatinine secretion.88 If cystatin C is shown to be a better endogenous marker of GFR, estimation of GFR from cystatin C might be helpful in some of these circumstances.
GFR Reporting by Clinical Laboratories
Reporting the estimated GFR may improve physicians' recognition of chronic kidney disease.89 Current recommendations to clinical laboratories take into account the greater inaccuracy of GFR estimates at higher levels.4 Laboratories should report a specific value of GFR only if the estimated GFR is less than 60 ml per minute per 1.73 m2; higher values should be reported as “GFR is 60 ml per minute per 1.73 m2 or more.”

CONCLUSIONS
The main limitation of current GFR estimates is the greater inaccuracy in populations without known chronic kidney disease than in those with the disease. Nonetheless, current GFR estimates facilitate detection, evaluation, and management of the disease, and they should result in improved patient care and better clinical outcomes. The reporting of estimated GFR whenever the measurement of serum creatinine is ordered should be coordinated with a campaign to educate physicians, health care organizations, patients, and the public about chronic kidney disease and the interpretation of GFR estimates.

Lymphoma Disease

Source(google.com.pk)
Lymphoma Disease Biography

Some complementary and alternative medicine (CAM) practitioners blame common symptoms such as fatigue, headache and poor memory on intestinal overgrowth of the fungus-like organism Candida albicans, or yeast syndrome. To cure the syndrome, they recommend a candida cleanse diet, which includes no sugar, white flour, yeast and cheese, on the theory that these foods promote candida overgrowth.

Unfortunately, there isn't much evidence to support the diagnosis of yeast syndrome. Consequently many conventional practitioners doubt its validity. And there are no clinical trials that document the efficacy of a candida cleanse diet for treating any recognized medical condition.

Not surprisingly, many people note improvement in various symptoms when following this diet. If you stop eating sugar and white flour, you'll generally wind up cutting out most processed foods, which tend to be high in calorie content and low in nutritive value. Within a few weeks of replacing processed foods with fresh ones and white flour with whole grains, you may start to feel better in general. That, rather than stopping the growth of yeast in the gastrointestinal tract, is the main benefit of a candida cleanse diet.


Research on the effectiveness of aromatherapy — the therapeutic use of essential oils extracted from plants — is limited. However, some studies have shown that aromatherapy might have health benefits, including:

Relief from anxiety and depression

Improved quality of life, particularly for people who have chronic health conditions
Essential oils used in aromatherapy are typically extracted from various parts of plants and then distilled. The highly concentrated oils may be inhaled directly or indirectly or applied to the skin through massage, lotions or bath salts. Aromatherapy is thought to work by stimulating smell receptors in the nose, which then send messages through the nervous system to the limbic system — the part of the brain that controls emotions.

Many essential oils have been shown to be safe when used as directed. However, essential oils used in aromatherapy aren't regulated by the Food and Drug Administration. When applied to the skin, side effects may include allergic reactions, skin irritation and sun sensitivity. In addition, further research is needed to determine how essential oils might affect children and how the oils might affect women who are pregnant or breast-feeding, as well as how the oils might interact with medications and other treatments.

If you're considering aromatherapy, consult your doctor and a trained aromatherapist about the possible risks and benefits.

What Is Lymphoma

Source(google.com.pk)

What Is Lymphoma Biography

Lymphomas are cancers that develop in the lymphatic system -- the tissues and organs that produce, store, and carry white blood cells. The lymphatic system includes the bone marrow, spleen, thymus, lymph nodes, and a network of thin tubes that carry lymph and white blood cells into all the tissues of the body. Types of lymphoma include non-Hodgkin's, Hodgkin's, and cutaneous T-cell lymphoma.

In non-Hodgkin's lymphoma, the most common form of the disease, cells in the lymphatic system become abnormal. They divide and grow without any order or control, or old cells that should die, don't. Non-Hodgkin's lymphoma can begin or spread to almost any part of the body.

In Hodgkin's disease, cells in the lymphatic system also become abnormal, but the cancer tends to spread in a fairly orderly way from one group of lymph nodes to the next. Eventually, it can spread almost anywhere.

In cutaneous T-cell lymphoma, T-lymphocytes (infection fighting white blood cells) become cancerous, causing skin problems.

Signs and Symptoms:
Lymphoma is accompanied by the following signs and symptoms, by type:

Non-Hodgkin's and Hodgkin's:

Painless swelling in lymph nodes in neck, underarm, or groin
Unexplained fever
Drenching night sweats
Fatigue
Unexplained weight loss
Itchy skin
Cutaneous T-Cell:

Itchiness
Dark patches on skin
Tumors on skin (mycosis fungoides)
Skin infections

Who's Most At Risk?:
People with the following conditions or characteristics are at risk for developing lymphoma, by type:

Non-Hodgkin's:

Congenital immunodeficiency
Infections: Epstein-Barr virus (EBV), Helicobacter pylori, Kaposi's sarcoma herpes virus (HIV related lymphoma), human T-cell leukemia virus type 1
Immunosuppressive therapy following organ transplant
Autoimmune diseases
Prior chemotherapy or radiation exposure or therapy
Exposure to certain chemicals or solvents
Hodgkin's:

Viruses: EBV, mononucleosis, HIV
Tonsillectomy
Genetic predisposition
Caucasians more likely than African Americans
Men more likely than women
Same sex siblings: 10 times greater risk
Cutaneous T-Cell:

Human T-cell leukemia virus type 1
Exposure to certain chemicals or solvents

What to Expect at Your Provider's Office:
If you are experiencing symptoms of lymphoma, you should see your health care provider. Your health care provider will carefully check for swelling or lumps in the neck, underarms, and groin. If the lymph nodes don't feel normal, a biopsy will be performed. The doctor will remove a small piece of the lymph node -- or, in the case of cutaneous T-cell lymphoma, a growth from the skin -- and a pathologist will examine the tissue under a microscope to check for cancer cells.

If you have cancer, your doctor will do more tests to find out if the cancer has spread to other parts of the body (staging). This may involve blood and bone marrow tests, computed tomography (CT) scans, positron emission tomography scans (PET), cobmination PET/CT scans, and, possibly, a laparotomy, in which the doctor cuts into the abdomen and checks the organs for cancer.

Treatment Options:
Treatment Plan

A treatment plan will be based on the diagnosis, the stage of the disease, the size of the tumor, and your general health and age.

Drug Therapies

Your health care provider may prescribe the following drug therapies:

Hodgkin's and Non-Hodgkin's:

Radiation therapy
Chemotherapy, possibly with alpha interferon
Cutaneous T-Cell:

Emollients, moisturizers, topical steroids
Chemotherapy
Electron beam therapy
Retinoids and interferon
Surgical and Other Procedures

Bone marrow transplantation and peripheral blood stem cell transplantation are sometimes performed. Radioimmunotherapy, which is treatment with a radioactive substance that is linked to an antibody that will attach to the tumor when injected into the body, is being tested in clinical trials. Surgical removal of the tumor may also be performed.

Complementary and Alternative Therapies
A comprehensive treatment plan for lymphoma may include a range of complementary and alternative therapies. Be sure to ask your team of health care providers about the best ways to incorporate these therapies into your overall treatment plan. Always tell your health care providers about any supplements you are taking.

Improved relaxation and decreased stress, through such activities as guided imagery, tai chi, yoga, and meditation are helpful in promoting a sense of well being. Intimacy and support from others helps promote a positive and empowering attitude.

Nutrition and Supplements
These nutritional tips may help reduce symptoms. Many herbs and supplements can interact negatively with conventional cancer medications and new research about such reactions is ongoing. While supplements may be helpful, it's important to work with knowledgeable provider and inform your doctors about any supplements you're using or considering using.

Try to eliminate potential food allergens, including dairy, wheat (gluten), corn, soy, preservatives, and food additives. Your health care provider may want to test for food sensitivities.
Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes) and vegetables (such as kale, spinach, and peppers).
Avoid refined foods, such as white breads, pastas, and sugar.
Eat cruciferous vegetables (such as broccoli, cabbage, and cauliflower).
Use healthy oils in foods, such as olive oil or vegetable oil.
Reduce or eliminate trans fatty acids, found in such commercially baked goods as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.
Avoid coffee and other stimulants, alcohol, and tobacco.
Drink 6 - 8 glasses of filtered water daily.
Exercise lightly, if possible. Speak to your doctor about what regimen is right for you.
You may address nutritional deficiencies with the following supplements:

Probiotic supplement (containing Lactobacillus acidophilus), 5 - 10 billion CFUs (colony forming units) a day, for maintenance of gastrointestinal and immune health. Some probiotic supplements may need refrigeration - check the label carefully.
Omega-3 fatty acids, such as fish oil, 1 - 2 capsules or 1 tbsp. oil 2 - 3 times daily, to help decrease inflammation. Fish oils may increase bleeding in sensitive individuals, such as those taking blood thinning mediations (including aspirin).
Melatonin, 2 - 5 mg before bed, when needed for sleep. Some alternative health care providers will use higher dosages. Melatonin may interact with a variety of medications, including sedatives, antidepressants, hormonal medications, and others.
Herbs

Herbs can potentially be an important part of an integrated cancer plan but should only be prescribed by a knowledgeable health care provider who is in communication with all of your other doctors.

Homeopathy
Although few studies have examined the effectiveness of specific homeopathic therapies, professional homeopaths may consider the following remedies for the treatment of gastritis symptoms (such as nausea and vomiting) based on their knowledge and experience. Before prescribing a remedy, homeopaths take into account your constitutional type -- your physical, emotional, and psychological makeup. An experienced homeopath assesses all of these factors when determining the most appropriate treatment for you individually.

Homeopathy may help reduce symptoms and strengthen overall constitution and may help decrease the side effects of chemotherapy.

Radium bromatum is specific for radiation poisoning, especially followed by arthritic complaints. Acute dose is 3 - 5 pellets of 12X to 30C every 1 - 4 hours until symptoms are relieved.
Physical Medicine

Contrast hydrotherapy may help enhance immune function and facilitate the transport of nutrients and waste products. End hot showers with 1 - 2 minutes of cold water spray. Since hydrotherapy stimulates lymphatic flow, talk to your physician first before beginning and hydrotherapy regimen.

Acupuncture
Acupuncture may help strengthen immunity and detoxification. It may also reduce the side effects of chemotherapy. For many patients and physicians, acupuncture has become one of the most widely used alternative interventions in cancer treatment. Unlike botanicals and nutrients, acupuncture works without ingesting substances so possible interactions with cancer treatments is unlikely.

Prognosis/Possible Complications:
Prognosis varies depending on the type and stage of lymphoma. Survival rates for Stage I and II non-Hodgkin's lymphoma and Hodgkin's lymphoma are very high.

Potential complications include the following:
Hodgkin's sometimes develops into non-Hodgkin's lymphoma
Radiation and chemotherapy can cause secondary cancers
Infections and pulmonary fibrosis (thickening and scarring of the air sacs of the lungs) may occur

Signs Of Leukemia

Source(google.com.pk)
Signs Of Leukemia Biography

There are two types of leukemia, acute and chronic. In acute leukemia the disease progresses rapidly, there is an accumulation of immature, useless cells in the marrow and blood. In chronic leukemia, the disease develops more slowly and allows more mature, useful cells to be made. Acute leukemia crowds out the good cells more rapidly than chronic leukemia. "Acute" means "sudden onset", while "chronic" means "long-term".

Acute lymphoblastic leukemia, also known as acute lymphocytic leukemia is when the blood and bone marrow have large numbers of white blood cells destined to become lymphocytes.

Acute lymphoblastic leukemia is commonly referred to by the acronym ALL, pronounced as three separate letters - eigh, el, el. ALL is the most common childhood cancer, especially among toddlers aged 2 to 3 years.

In the USA, ALL incidence is significantly higher among Caucasian than African-American children. Incidence is highest among Hispanic children.

In the USA there are about 6,000 new cases of ALL annually, an incidence of 1 in every 50,000 people.

In England and Wales there are approximately 2,400 diagnosed cases of acute leukemia each year, of which about 600 are ALLs. The NHS (National Health Service), UK, informs that 85% of all ALL cases occur among children aged less than 15 years.

Experts say the main causes of ALL are exposure to high levels of radiation or benzene. Smokers are three times as likely to develop ALL compared to non-smokers - benzene is one of the 4,000 substances found in cigarette smoke. Individuals who have spent over 5,000 hours in airplanes have a higher risk of developing ALL (flying exposes you to more of the Sun's radiation). About 1 in every 20 cases are thought to be caused by related genetic disorders, such as Down's syndrome.

Some scientists wonder whether early exposure to germs might protect children from developing ALL. A significantly lower percentage of children who went to playgroups at an early age develop ALL compared to those who didn't. Symptoms of acute lymphoblastic leukemia will usually start slowly, and then escalate in severity as the number of blast cells in the blood rises. Signs and symptoms may include:
Fatigue
Frequent unexplained bleeding, such as nosebleeds or bleeding gums
High fever
Oversweating
Painful joints and/or bones
Panting
Several infections over a short period
Swollen glands (lymph nodes)
Swollen liver
Swollen spleen
The skin bruises easily
The skin is paler than it should be
Unexplained weight loss
If the affected cells spread into the CNS (central nervous system), the patient may have neurological symptoms, such as dizziness, vomiting, blurred vision, fits (seizures) and headaches.

With the right treatment virtually all children will become symptom free (remission) and 85% will be completely cured. Unfortunately, only about 40% of adult patients achieve a complete cure.

Treatment involves a combination of chemotherapy and radiotherapy (radiation therapy). Sometimes a bone marrow transplant may be used.

For those who are not cured, their immune systems, which are very low in white blood cells, become vulnerable to infections, some of them life-threatening. There is also a risk of serious bleeding due to a lack of platelets.

Approximately 230 people die from ALL in England and Wales each year.

Dutch athlete, Maarten van der Weijden, was diagnosed with ALL in 2001. He went on to win the 10 km open water marathon race at the 2008 Summer Olympics in Beijing.

Andrew McMahon, singer of the bands Something Corporate and Jack's Mannequin, was diagnosed with ALL in 2005.