Elevated enzymes symptoms and conditions

I was given 2 doses of 750mg IV Levaquin in my local emergency room for a UTI, then sent homw with a RX for 750mg oral. I went back to the emergency room 2 days later with a temp of 101 and complaints of leg pain and numb feet. The emergency again gave me 750mg Levaquin IV admited me into a observation ward when they continued to give me three additional does 750mg Levaquin IV, and sent me home. I went back to the emergency for the third time, severe pain in feet, numbness in feet and swollen and red, burning, elevated temp and this time elevated liver and pancreases enzymes. Admitted into the hospital, they proceed to do a spinal tap to see if I had Guillian Bria Symdrome. I was concluded that I had acute sensoury neuropathy induces by Levaquin toxicity. It is four weeks past, I still have numbness and buring in my feet. I must have had my allergic reaction after the second does because as we look back, I experienced a rash around my abdomen, a sever headache and elevated temp as I received the third does. Because the temp kept stayed elevated and the leg pain got worse, they kept giving me the Levaquin, which resulted in the overdoes toxicity, that was escentially casuing the elevated liver and pancreas enzymes, which was causing the high temp and leg pain. The temp, and elevated enzymes started to decrease when the Levaquin was stopped. As for the nueopathy in the feet and lower legs, only time will tell. If you have never taken this drup before, DON"T. They are other drugs out there that can be used.

Perhaps you could print the following and take with you to your next appointment:

Underappreciated Statin-Induced Myopathic Weakness Causes Disability
Bruce H. Dobkin
University of California Los Angeles, Reed Neurologic Research Center,
bdob...@mednet.ucla.edu

Introduction. Myopathic syndromes induced by 3-hydroxy-3-methylglutaryl

coenzyme A (HMG-CoA) reductase inhibitors (statins) include muscle
complaints, myalgia, myositis, and rhabdomyolysis. No prospective study

of statins, however, included tests of strength, so the incidence of
weakness, with or without muscle symptoms and elevated enzymes, is
unknown, and perhaps overlooked. Methods. From a convenience sample of
patients referred to an outpatient neurorehabilitation clinic over the
course of 1 year, 8 patients with hemiparetic stroke and 10 patients
with other presumed neurologic diseases presented with new difficulty
walking by 3 to 12 months after starting one of 3 statins. They
reported no myalgias, exercise-induced aches, or weakness. Examination
revealed proximal paresis graded 4/5 on the unaffected side in the
hemiparetic patients and symmetrical bilateral proximal limb and neck
flexor weakness graded 4/5 in the others. They stood up with difficulty

and walked with bilateral hip drop and imbalance on turns. Results.
Laboratory tests did not reveal myositis or other causes for paresis.
No improvement in strength or mobility was found 6 weeks after
initiating resistance exercises. The statin agent was stopped. By 3
months off statin, all recovered 5/5 proximal strength. Walking
improved, and they arose from a chair without pushing off with their
arms. Discussion. Serial manual muscle testing after initiating a
statin may detect a reversible cause of disability. A genetic
predisposition to statin-induced myopathic proximal weakness with
normal creatine kinase is consistent with a continuum of previously
reported symptoms and signs but may be underappreciated.

(in the discussion, the author notes that while single-subject,
double-blinded statins vs placebo studies would make the causal
relationship between disabling myopathy more apparent, he notes
recurrences in his patients' symptoms when the investigator was unaware that several of the subjects had been placed back on the statin by their primary physicians. p. 261)