Glucose toxicity adverse effects

The modes of action for niclosamide are interference with respiration and blockade of glucose uptake. It uncouples oxidative phosphorylation in both mammalian and taenioid mitochondria (22,23), inhibiting the anaerobic incorporation of inorganic phosphate into adenosine triphosphate (ATP). Tapeworms are very sensitive to niclosamide because they depend on the anaerobic metaboHsm of carbohydrates as their major source of energy. Niclosamide has selective toxicity for the parasites as compared with the host because Httle niclosamide is absorbed from the gastrointestinal tract. Adverse effects are uncommon, except for occasional gastrointestinal upset. 

Albendazole selectively blocks glucose uptake and depletes glycogen stores. ATP formation is thus inhibited. It should be administered on an empty stomach for intraluminal parasites and with a fatty meal for tissue parasites. It is metabolized to an active sulfoxide metabolite resulting in very low Albendazole blood levels. Albendazole sulfoxide is excreted in the urine with an elimination half-life of about 8 h. Used for 1-3 days in doses recommended for intestinal worms the incidence of adverse effects is similar in treatment and control groups. Hepato-toxicity may occur, especially after the higher doses that are needed for hydatid disease. Also alopecia has been reported. 

The aldose reductase inhibitors inhibit or reduce secondary complications induced by diabetes, specifically in tissues in which glucose uptake is not insulin-dependent (probably neural tissue, the lens, and glomeruli). Many of them (including alrestatin, imirestat, ponalrestat, and sorbinil) have been used in clinical trials, but have been withdrawn because of adverse effects or lack of effect (2). Their main adverse effects include fever, nausea, diarrhea, increases in liver enzymes, skin rashes, including toxic epidermal necrolysis and Stevens-Johnson syndrome, marked thrombocytopenia, lymphadenopathy, splenomegaly, and adult respiratory distress syndrome. 

Adverse Effects. Common side effects of tacrolimus include gastrointestinal disturbances (cramps, nausea, diarrhea, constipation), weakness, fever, and skin rashes and itching. More serious problems include renal and central nervous system (CNS) toxicity (headache, anxiety, nervousness, seizures).41 Tacrolimus is also associated with problems with glucose metabolism (hyperglycemia, glucose intolerance), and can cause diabetes mellitus in certain individuals.73... 

Claims that consumption of massive doses of ascorbate (1-2 g/d or even higher quantities) can prevent or cure common cold, cancer, or other ailments have no basis in fact. Although ascorbate has low toxic effects, adverse effects at high dose, such as hyperoxalemia (oxalate is a catabolite of ascorbate) in patients undergoing dialysis, or hemolysis in subjects with glucose-6-phosphate dehydrogenase deficiency, have been reported. 

The adverse ejfects of systemic administration of glucocorticoids are well known (see Chapter 59), but treatment for brief periods (5-10 days) causes relatively little dose-related toxicity. The most common adverse effects during a brief course are mood disturbances, increased appetite, impaired glucose control in diabetics, and candidiasis. 

C. Toxicity Cardiovascular adverse effects, which are extensions of the beta blockade induced by these agents, include bradycardia, atrioventricular blockade, and congestive heart failure. Patients with airway disease may suffer severe asthma attacks. Premonitory symptoms of hypoglycemia from insulin overdosage, eg, tachycardia, tremor, and anxiety, may be masked, and mobilization of glucose from the liver may be impaired. CNS adverse effects include sedation, fatigue, and sleep alterations. Atenolol, nadolol, and several other less lipid-soluble beta-blockers are claimed to have less marked CNS action because they do not enter the CNS as readily as other members of this group. 

Statistical analysis of the data suggests significant changes in cecum, liver, and kidney weights between browned and nutritionally equivalent control diets in the 12-mo rats (Table IX). Serum GOT, alkaline phosphatase, and serum glucose levels are all significantly different for these twoadverse effects become more and more pronounced. This pattern indicates that there is a cumulative effect and that it resembles, in many instances, the effect expected of a toxic compound. 

Heavy metals stimulate or inhibit a wide variety of enzyme systems (16, 71, 72), sometimes for protracted periods (71, 73). These effects may be so sensitive as to precede overt toxicity as in the case of lead-induced inhibition of 8 ALA dehydrase activity with consequential interference of heme and porphyrin synthesis (15, 16). Urinary excretion of 8 ALA is also a sensitive indicator of lead absorption (74). Another erythrocytic enzyme, glucose-6-phosphatase, when present in abnormally low amounts, may increase susceptibility to lead intoxication (75), and for this reason, screens to detect such affected persons in lead-related injuries have been suggested (76). Biochemical bases for trace element toxicity have been described for the heavy metals (16), selenium (77), fluoride (78), and cobalt (79). Heavy metal metabolic injury, in addition to producing primary toxicity, can adversely alter drug detoxification mechanisms (80, 81), with possible secondary consequences for that portion of the population on medication. 

An insulin infusion should be considered for severe cases of calcium channel blocker toxicity." Case reports suggest that an intravenous bolus of regular insulin (0.5-1 units/kg) with 50 mL dextrose 50% (0.25 mg/kg for children) followed with a continuous infusion of regular insulin (0.5-1 units/kg per hour) may improve myocardial contractility. The effect of insulin is presently unclear, but it may improve myocardial metabolism that is adversely affected by calcium channel blocker overdoses, such as decreased cellular uptake of glucose and free fatty acids and a shift from fatty acid oxidation to carbohydrate metabolism. This insulin regimen is titrated to improvement in systolic blood pressure over 100 mm Hg and heart rate... 

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