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Anemia has also been identified as an adverse prognostic factor

mild (10 g/dl—normal), moderate (8–10 g/dl), severe (6.5–8 g/dl) and life threatening (<6.5 g/dl or unstable patient) anemia

anemia in cancer patients is often multifactorial.

Cancer itself can directly cause or exacerbate anemia either by suppressing hematopoiesis through bone marrow infiltration or production of cytokines that lead to iron sequestration, or by reduced red blood cell production

in inflammatory anemia, iron deficiency should be defined by a low transferrin saturation of <20%, ferritin levels of <100 ng/ml and a low reticulocyte hemoglobin concentration of <32 pg

anemia to thrombocytosis, as commonly seen in cancer patients

TNF-α inhibits hemoglobin production

treatment itself may be a major cause of anemia

Other cytokines, such as interleukin-6 (IL-6), IL-1 and interferon-γ, have also been shown to inhibit erythroid precursors in vitro [9], albeit to a lesser extent

In inflammation, from whatever cause, IL-6 induces the liver to produce hepcidin. Hepcidin decreases iron absorption from the bowel and blocks iron utilization in the bone marrow

Numerous in vitro studies have illustrated the central role of TNF-α in the pathogenesis of anemia

nephrotoxic effects of particular cytotoxic agents such as platinum salts can also lead to the persistence of anemia through reduced Epo production by the kidney

Currently two options are at the disposal of the clinician for the treatment of anemia in cancer patients: transfusion of packed red blood cells and the use of erythropoiesis-stimulating agents (ESAs)

The goal of the treatment is to relieve the symptoms of anemia such as fatigue and dyspnea.

Transfusion of 1 unit of packed red blood cells has been estimated to result in an increase in the hemoglobin level of 1 g/dl in a normal-sized adult

a higher mortality rate in patients receiving ESA treatment

Recent concerns regarding the risk of thromboembolism in patients treated with ESA have been corroborated by the meta-analyses conducted by Tonnelli and Bennett

Non-recombinant urate oxidase (Uricozyme®)

recombinant urate oxidase (Rasburicase®)

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

cyclophosphamide and ifosfamide

O3 not only remedied infection, but also had hemodynamic and anti-inflammatory properties

Stimulation of oxygen metabolism

In fungi, O3 inhibits cell growth at certain stages

With viruses, the O3 damages the viral capsid and upsets the reproductive cycle by disrupting the virus-to-cell contact with peroxidation.

Inactivation of bacteria, viruses, fungi, yeast and protozoa: Ozone therapy disrupts the integrity of the bacterial cell envelope through oxidation of the phospholipids and lipoproteins

Activation of the immune system

30 and 55 μg/cc

production of interferon and the greatest output of tumor necrosis factor and interleukin-2

Mechanism of action of O3 on the human lung

cascade of reactions like peroxidation of lipids leading to changes in membrane permeability,[41] lipid ozonation products (LOP) act as signal transducer molecules

Dietary antioxidants or free radical scavengers like vitamin E, C, etc., can prevent aforementioned effects of O3