Fructose intake increases MetS and hypertension. The high fructose intake upregulates phosphofructokinase which increases triglyceride production, bypassing central regulation. This results in ATP depletion with reduced capacity to recover. Thus attempts by the cells to increase ATP through AMP deaminase results in uric acid production.
Increasing uric acid concentrations is found to be associated with insulin resistance and metabolic syndrome in both men and women. Equally, it is associated with carotid plaque formation.
Study of Iraqi population at elevated risk of stroke found that both serum and salivary levels of malondialdehyde, glutathione, superoxide dismutase, and uric acid proved useful as potential biomarkers of risk assessment.
Serum lactate elevates early in triathlon. The greatest increase is associated with the swim event. Muscle damage progressed through the 3 events (creatine phosphokinase and LDH). Uric acid levels increased. Recovery was seen out to 6 days post event.
Gout is a result of Insulin resistance? It makes perfect biologic sense. IR causes inflammation and what is Gout? Nothing but an inflammatory condition. So is Gout merely a join representation of metabolic dysfunction? I say yes.
Reduced SOD activity might be responsible for excessive accumulation of superoxide anions leading to increased free radical mediated injury. Increased free radical production has been shown to be responsible for chromosomal damage leading to mutagenecity, cell proliferation and carcinogenesis. SOD activity showed marked improvement after mastectomy indicating the lowering of oxidative stress.
The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions
Superoxide dismutase is an important antioxidant enzyme which decomposes the harmful superoxide anions into hydrogen peroxide thus protects the body from the action of free radicals
Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females
ADA seems to be a promising marker of inflammation in breast cancer thereby suggesting that it can be used as a diagnostic tool to detect the stage of breast cancer along with cytopathological studies
In conclusion, our study confirmed the role of oxidative stress in the pathogenesis of breast cancer.
Another potent antioxidant molecule is reduced glutathione. It acts as reductant which converts hydrogen peroxide into water and reduces lipid peroxidation products into their corresponding alcohols and thus mediates protective action.
In the present study, significantly low SOD activity has been observed in female patients suffering from carcinoma breast both pre as well as post operative in comparison to healthy females.
The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients.
Increased ADA activity in breast cancer patients has also been reported
We observed significantly decreased SOD activity and GSH levels in patients belonging to clinical stage 4 as compared to those having stages 1, 2 or 3 of breast cancer.
increased oxidative stress gives rise to inflammation which could further aggravates the disease
Antioxidant status was highly depressed in advanced stages of breast cancer as compared to initial stage.
In the present study, significantly low GSH levels were observed in female patients of carcinoma breast as compared to normal females
Walia et al. (1995) reported increased ADA activity in breast cancer patients as compared to age matched normal subjects.
These free radicals are able to cause damage to membrane, mitochondria and macromolecules including proteins, lipids and DNA and actively take part in cell proliferation. This cascade in turn generates the inflammatory response and causes the progression of the disease.
Experimental and epidemiological evidences implicate the involvement of oxygen derived free radical in the pathogenesis of breast cancer.
Breast carcinoma involves a cascade of events that are highly inflammatory.
Marked oxidative stress in stage 4 of breast cancer indicated advancement of the disease, hence checking oxidative stress at initial stage could be helpful for controlling the progression of the disease.
They concluded that ADA is a better probable parameter for detection of breast cancer
Adenosine deaminase enzyme (ADA) catalyzes the conversion of adenosine to inosine which finally gets converted to uric acid
serum ADA activity tends to increase with advancing age,
Prevalence of oxidative stress gives rise to inflammation.
Study finds a reduction in SuperOxide Dismutase and Glutathione Perioxidase in advancing breast cancer. Cancer is a high oxidative stress disease that results in inflammation, mitochondrial dysfunction and proliferation. Adenosine Deaminase (ADA) is proposed to be another biomarker to assess tumor stage.
urine alkalisation may induce calcium phosphate deposition
renal replacement therapy should be started on an emergency basis when hydration fails to produce a prompt metabolic improvement or when ARF develops
Up to 50% of patients with newly diagnosed multiple myeloma have renal failure and up to 10% require dialysis
renal ultrasonography remains the method of choice for investigating extra-renal obstruction
The relief of the obstruction, either by percutaneous nephrostomy or through a ureteral stent, is the cornerstone of treatment
TMA may be associated with the cancer itself, with cancer chemotherapy, or with allogeneic BMT
thrombotic microangiopathy (TMA)
it may be as high as 5%
Most of the cases occur in patients with solid tumours, the most common type being adenocarcinoma (stomach, breast and lung)
The pathophysiology of the TMA-malignancy association remains controversial, although many studies suggest an insult to the vascular endothelium
mitomycin C. Subsequently, TMA has been reported with many anti-cancer agents, including gemcita-bine, bleomycin, cisplatin, CCNU, cytosine arabinoside, daunorubicin, deoxycoformycin, 5-FU, azathioprine and interferon α
Plasma exchanges have been shown to improve prognosis in the general population of patients with TMA
Causative factors should be looked for and antihypertensive treatment given. Lastly, in the absence of guidelines, we believe that plasma exchange should be proposed in patients with severe cancer treatment-associated TMA
The most widely used protective measure is saline infusion to induce solute diuresis
During methotrexate infusion and elimination, fluids should be given to maintain a high urinary output and urinary alkalisation should be performed to keep the urinary pH above 7.5. Rescue with folinic acid (50 mg four times a day) should be started 24 hours after each high-dose metho-trexate infusion and serum methotrexate concentrations should be measured every day