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Creation Denso QR Bar Code in Microsoft Office THE METABOLIC AND TOXIC MYOPATHIES

THE METABOLIC AND TOXIC MYOPATHIES
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muscle bers (rhabdomyolysis), myoglobin and other muscle proteins may enter the bloodstream and appear in the urine The latter is cola -colored (burgundy red or brown), much like the urine in hemoglobinuria In hemoglobinuria, however, the serum is initially pink, because hemoglobin (but not myoglobin) is bound to haptoglobin, and this complex is not excreted in the urine as readily as myoglobin; also, the hemoglobin molecule is three times as large as the myoglobin molecule (The hemoglobin-haptoglobin complex is removed from the blood plasma over a period of hours and haptoglobin may be depleted, so that hemoglobinuria is present without grossly evident hemoglobinemia) Differentiation of the two pigments in urine is dif cult; both are guaiac-positive and may be detected by a dipstick, a test that can be used to advantage at the bedside in appropriate circumstances Only small differences are seen on spectroscopic examination The most sensitive means of detecting myoglobin is by radioimmunoassay It should be mentioned that porphyrins are another cause of discoloration of the urine The clinical picture in porphyria is one of a polyneuropathy and not a myopathy Many of the causes of myonecrosis and myoglobinuria have already been mentioned above and in previous chapters Myoglobinuria may be detected in cases of acute in ammatory myopathy, in several types of glycogenosis (see Table 51-1), in carnitine palmityltransferase de ciency, and as a result of poisoning or therapeutic use of a vast array of drugs (including the combination of steroids and pancuronium, discussed earlier), toxins, and venoms (see Table 51-2) Myoglobinuria is an important feature of many other medical conditions: crush injury; extensive infarction of muscle; excessive use or repeated injury of muscles as occurs in status epilepticus, generalized tetanus, malignant neuroleptic syndrome, agitated delirium, prolonged marching, conga drumming, or simply excessive exercise although the latter always suggests an underlying metabolic disease of muscle; electrical and lightning injuries; etc Two noteworthy conditions that are characterized by myonecrosis and myoglobinuria are acute alcoholic intoxication and malignant hyperthermia The former is described further on and the latter in Chap 54, with the membrane channel disorders Regardless of the cause of the rhabdomyolysis, the affected muscles become painful and tender within a few hours Power of contraction is diminished Sometimes the skin and subcutaneous tissues overlying the affected muscles (nearly always of the limbs and sometimes of the trunk) are swollen and congested There may be a low-grade fever and leukocytosis If myoglobinuria is mild, recovery occurs within a few days and there is only a residual albuminuria When myoglobinuria is severe, renal damage may ensue and lead to anuric renal failure requiring dialysis The mechanism of the renal damage is not entirely clear; probably it is not simply a mechanical obstruction of tubules by precipitated myoglobin (although this does occur) It is more likely to result from massive rhabdomyolysis and, correspondingly, there is a very high CK level in the serum Treatment Alkalinization of the urine by ingestion or infusion of sodium bicarbonate is said to protect the kidneys by preventing myoglobin casts, but in severe cases it is of doubtful value, and the sodium may actually be harmful if anuria has already developed Diuresis induced by mannitol or by loop diuretics such as furosemide and by the administration of intravenous uids also reduces the chances of anuric renal failure if given in time Therapy is much the same as for the anuria that follows shock (see Harrison s Principles of Internal Medicine)
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Statin-Induced Myopathy With the widespread use of these lipid-lowering medications, myotoxicity has become a welldescribed but probably overrated problem Symptoms range in severity from mild muscular aches with slightly elevated CK concentrations in the serum to a rare but potentially fatal rhabdomyolitic syndrome The rst generation of these drugs were fungal metabolites (lovastatin, paravastatin, simvastatin) and were infrequently implicated in muscle damage, but the new synthetic ones (atorvastatin, uvastatin, cerivastatin) are more frequently toxic, especially when given with gem brizil (The last of these has reportedly led to over 50 deaths from myoglobinuric renal failure and has been removed from the market) Few cases are this dramatic This subject has been reviewed by Thompson The mechanism of muscle damage is not well understood but it is likely that inherent enzymatic defects are present in a proportion of the severe cases (see the brief review by Farmer) In addition, the chronic use of statin drugs reduces levels of both ubiquinone and small guanosine triphosphate (GTP)-binding proteins, also plausible factors in statin-induced muscle toxicity As mentioned, the combination of one of these medications with gem brizil is particularly likely to result in muscle damage Drugs in the statin class with higher lipid solubility appear to have a greater potential for toxicity as a result of their increased muscle penetration A clinical problem arises when the CK level is elevated but the patient taking one of these medications has no muscular symptoms It has been our general practice to continue the medication if the elevation of CK is in the low range and does not rise over time and if the medication is considered necessary If alternative and safe means of lowering the lipid level are available, then they should be tried in lieu of a statin but each patient s circumstances differ In a small series, Phillips and colleagues have called attention to a similarly vexing and not uncommon problem: myopathic symptoms such as muscle stiffness, tenderness, and weakness with normal CK concentrations A trial of discontinuing the medication may be appropriate Finally, we have encountered a number of patients whose CK levels have remained high for months or longer after the medications have been stopped In a few of these patients, most otherwise asymptomatic, CK levels have remained high over years but we have had no way to ensure that the test was not abnormal before taking the statin Noted on page 1134 is a polyneuropathy in which statin drugs have been tentatively implicated Colchicine Myoneuropathy This condition is included here as much for its clinical interest as for its curious histopathologic features The drug, used widely in the treatment of gout, often gives rise to a mild subacute proximal muscular weakness, but has also produced an acute necrotizing myopathy Most instances of the latter have occurred in patients with a degree of renal failure, which allows accumulation of the drug (even though the drug is metabolized predominantly by the liver) In a few instances it has affected the cranial musculature and the diaphragm Many cases also show clinical or electrophysiologic evidence of a polyneuropathy as pointed out by Kuncl and colleagues, leading to the term colchicine myoneuropathy The re exes are diminished and there is mild distal sensory loss Rare cases of colchicine-induced hypokalemic periodic paralysis and also of myotonia have been reported The serum CK concentration may be elevated or normal The muscle biopsy shows elements of both myopathic and neuropathic disease, with the special feature in muscle of rimmed vacuoles on
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