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The average age of FQ-induced tendinopathy is 64 years, with a male-to-female ratio of 2:1, and a 27-percent incidence of bilateral involvement

Although more than 95 percent of cases of tendinitis/rupture secondary to FQ involve the Achilles tendon, other reported sites of tendon involvement include the quadriceps, peroneus brevis, and rotator cuff

FQs demonstrate a 3.8-fold greater risk for development of Achilles tendinitis/rupture

a large population-based case control analysis, patients treated with FQs exhibited a substantially increased risk of developing tendon disorders overall (1.7-fold), tendon rupture (1.3-fold), and ATR (4.1-fold)

patients taking FQs with concurrent exposure to corticosteroids were found to experience a compounding effect on the risk of tendon rupture, specifically a 46-fold greater predisposition

Some authors have recommended that patients with a history of Achilles tendinitis and advanced age should not be prescribed FQ antibiotics

Approximately 50 percent of patients will recover within 30 days, with 25 percent of patients having symptoms persistent for longer than two months

The mean latency period between the start of FQ treatment and occurrence of tendinopathy has been reported to be a few hours to months, with a median onset of 6 days

The exact pathophysiology of FQ-induced tendinopathy remains elusive

it is possible that FQs have a direct cytotoxic effect on enzymes found in mammalian musculoskeletal tissue

It has been theorized that FQs disproportionately affect human tendons that have a limited capacity for repair, such as in older patients or structural compromise (i.e., pre-existing tendinopathy or trauma)

histopathological findings are similar to those observed in overuse conditions in athletes

Treatment with a FQ should be discontinued and physical therapy initiated

treatment should include rest and decreasing the physical load on the tendon.

Approximately 85 percent of patients present in less than one month

Because rupture can occur even late in the course of treatment or after discontinuation of FQ use, patients receiving a FQ should be counseled to seek medical attention immediately if symptoms, such as redness, pain, swelling, and stiffness, develop

FQs should be used cautiously in patients with risk factors associated with tendinitis, such as advanced age, history of tendon rupture, corticosteroid use, and/or acute or chronic renal dysfunction

malnutrition progressing to cachexia is another common manifestation of cirrhosis

Malnutrition can be mitigated with BCAA supplementation

Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease

Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis

BCAAs metabolites inhibit proteolysis

Patients with cirrhosis have both insulin deficiency and insulin resistance

BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization

Coadministration of BCAAs and glucose has been found to be particularly useful

BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis

Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity

another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity

BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves

BCAA administration has also been shown to have a positive effect on liver regeneration

A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells

BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue

Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels

long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding

The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation

Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests

patients taking BCAA supplementation report improved quality of life

BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis

BCAAs make up 20-25% of the protein content of most foods

Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran

In addition to BCAAs from diet, oral supplements of BCAAs can be used

Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy

Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms

Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state

the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting

A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs

Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis

hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia

BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver

patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation

Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life

the serum BCAA concentration is strongly correlated with the serum albumin level