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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to the report by Inam Ahmed and Aasha Amin, arsenic poisoning is contaminating underground water supplies across northern Bangladesh and threatening the lives of millions. In Jessore, a northern district of Bangladesh, almost every home has a child or adult suffering from arsenic poisoning. Villagers have lost count of the casualties, most of them small children. Dr. Mahmudur Rahman of Community Hospital in Dhaka states that children are most severely affected by arsenic poisoning, a situation that is aggravated by poverty and malnutrition. While early diagnosis and treatment may help these affected children, immediate measures must be taken to stop further contamination. An intensive study has found that, in Bangladesh, of the 34 districts from which water samples were collected, 22 had high levels of arsenic. In view of this, experts have suggested a three-pronged action plan to address the problem: 1) arsenic-contaminated tube wells need to be sealed and the public informed to use alum water to neutralize the effect of arsenic; 2) ponds need to be identified and reserved exclusively for drinking water, and the wasting of underground water from deep tube wells has to be stopped; 3) the government needs to initiate watershed management to ensure safe ground water supplies to villages.
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PMID:Arsenic on tap. 1232 Oct 49

Migraine is a pervasive neurologic disorder characterized by recurrent attacks of disabling headache. Despite significant morbidity with impact that may be physical, emotional, social, and economic, treatment of these attacks is often delayed. Patients frequently delay therapy until the more severe or "textbook" symptoms arise, often mistaking the earliest stages as representative of "tension" or "sinus" headaches. Clinicians may recommend deferral of treatment until the more severe levels of pain are seen, perhaps in a misguided attempt to conserve pharmaceutical resources. Patients and clinicians seem more comfortable with perspectives of "being sure it's a migraine" and "not wasting the medication on milder headaches." Therefore, patients and clinicians must learn the latest lessons in migraine: 1) mild migraine usually progresses to more severe levels if left untreated, 2) early treatment is more effective than delayed treatment, 3) early treatment may result in lower rates of adverse events and headache recurrence, and 4) early treatment is cost effective. As clinicians advocate the early treatment of migraine in its mild phase, evidence to support this recommendation has finally become available. I educate my migraineurs to consider each typical headache to be a version of migraine. Most patients with migraine will experience "little" headaches that they often mislabel as tension, sinus, regular, stress, or normal headaches. Instead of these terms, I have them consider their attacks as "small migraines" and "big migraines," with the smaller headaches often evolving into the bigger episodes. Given such a foundation, I advise them to treat at the beginning of the headache, perhaps earlier than they would have previously identified it as a migraine. They must capture the attack while it "whispers migraine" instead of delaying until the attack "shouts migraine." Early treatment of migraine is successful for most patients. However, there are situations in which treatment of the mild phase is not advisable or possible. In patients with frequent or daily migraine, treatment must be reserved for the most disabling attacks. We must advise treatment as soon as the migraine becomes moderate to severe. Certain patients, or certain headaches in some patients, may not progress through a mild phase, perhaps because of rapid escalation or because migraine is already severe upon awakening. Here we encourage migraineurs to treat as soon as possible, often with parenteral formulations of medication. The reaction of the patient (speed of dosing) and the action of the medication (speed of onset of the drug) will ultimately play roles in the successful interception of each attack.
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PMID:Intercepting migraine: results of early therapy with nonspecific and migraine-specific agents. 1634 56

Hypomagnesemia is defined as a serum magnesium level less than 1.8 mg/dL (< 0.74 mmol/L). Hypomagnesemia may result from inadequate magnesium intake, increased gastrointestinal or renal losses, or redistribution from extracellular to intracellular space. Increased renal magnesium loss can result from genetic or acquired renal disorders. Most patients with hypomagnesemia are asymptomatic and symptoms usually do not arise until the serum magnesium concentration falls below 1.2 mg/dL. One of the most life-threatening effects of hypomagnesemia is ventricular arrhythmia. The first step to determine the likely cause of the hypomagnesemia is to measure fractional excretion of magnesium and urinary calcium-creatinine ratio. The renal response to magnesium deficiency due to increased gastrointestinal loss is to lower fractional excretion of magnesium to less than 2%. A fractional excretion above 2% in a subject with normal kidney function indicates renal magnesium wasting. Barter syndrome and loop diuretics which inhibit sodium chloride transport in the ascending loop of Henle are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypercalciuria. Gitelman syndrome and thiazide diuretics which inhibit sodium chloride cotransporter in the distal convoluted tubule are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypocalciuria. Familial renal magnesium wasting is associated with hypercalciuria, nephrocalcinosis, and nephrolithiasis. Asymptomatic patients should be treated with oral magnesium supplements. Parenteral magnesium should be reserved for symptomatic patients with severe magnesium deficiency (< 1.2 mg/dL). Establishment of adequate renal function is required before administering any magnesium supplementation.
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PMID:Hypomagnesemia: an evidence-based approach to clinical cases. 2008 Dec 99

Hypophosphatemia is defined as a serum phosphate level of less than 2.5 mg/dL (0.8 mmol/L). Hypophosphatemia is caused by inadequate intake, decreased intestinal absorption, excessive urinary excretion, or a shift of phosphate from the extracellular to the intracellular compartments. Renal phosphate wasting can result from genetic or acquired renal disorders. Acquired renal phosphate wasting syndromes can result from vitamin D deficiency hyperparathyroidism, oncogenic osteomalecia, and Fanconi syndrome. Genetic disorders of renal hypophosphatemic disorders generally manifest in infancy and are usually transmitted as an X-linked hypophosphatemic rickets. Symptoms of hypophosphatemia are nonspecific and most patients are asymptomatic. Severe hypophosphatemia may cause skeletal muscle weakness, myocardial dysfunction, rhabdomyolysis, and altered mental status. The diagnostic approach to hypophosphatemia should begin with the measurement of fractional phosphate excretion; if greater than 15% in the presence of hypophosphatemia, the diagnosis of renal phosphate wasting is confirmed. Renal phosphate wasting can be divided into 3 types based upon serum calcium levels: primary hyperparathyroidism (high serum calcium level), secondary hyperparathyroidism (low serum calcium level), and primary renal phosphate wasting (normal serum calcium level). Phosphate supplementations are indicated in patients who are symptomatic or who have a renal tubular defect leading to chronic phosphate wasting. Oral phosphate supplements in combination with calcitriol are the mainstay of treatment. Parenteral phosphate supplementation is generally reserved for patient with life-threatening hypophosphatemia (serum phosphate < 2.0 mg/dL). Intravenous phosphate (0.16 mmol/kg) is administered at a rate of 1 mmol/h to 3 mmol/h until a level of 2 mg/dL is reached.
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PMID:Hypophosphatemia: an evidence-based problem-solving approach to clinical cases. 2062 6

We present the hypothesis that advanced stage cancer is also a heart failure syndrome. It can develop independently of or in addition to cardiotoxic effects of anti-cancer therapies. This includes an increased risk of ventricular arrhythmias. We suggest the pathophysiologic link for these developments includes generalized muscle wasting (i.e. sarcopenia) due to tissue homeostasis changes leading to cardiac wasting associated cardiomyopathy. Cardiac wasting with thinning of the ventricular wall increases ventricular wall stress, even in the absence of ventricular dilation. In addition, arrhythmias may be facilitated by cellular wasting processes affecting structure and function of electrical cells and conduction pathways. We submit that in some patients with advanced cancer (but not terminal cancer), heart failure therapy or defibrillators may be relevant treatment options. The key points in selecting patients for such therapies may be the predicted life expectancy, quality of life at intervention time, symptomatic burden, and consequences for further anti-cancer therapies. The cause of death in advanced cancer is difficult to ascertain and consensus on event definitions in cancer is not established yet. Clinical investigations on this are called for. Broader ethical considerations must be taken into account when aiming to target cardiovascular problems in cancer patients. We suggest that focused attention to evaluating cardiac wasting and arrhythmias in cancer will herald a further evolution in the rapidly expanding field of cardio-oncology. This article is protected by copyright. All rights reserved.
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PMID:Advanced cancer is also a heart failure syndrome - an hypothesis. 3324 8