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Patients receiving reduced intensity regimens, which do not result in marrow ablation, often have a later onset of GVHD. The gastrointestinal manifestations include diarrhea which may become bloody, cramping, nausea, vomiting and failure to thrive [].This is due both to the later engraftment and the damage from the preparative regimen producing cytokines that drive the immune responses resulting in clinical GVHD. While acute GVHD is a clinical diagnosis, there are other conditions that can mimic or coexist with GVHD, such as drug toxicity (especially common in patients post transplant on multiple antimicrobial agents, immunosuppressive drugs, hyperalimentation, receiving methotrexate, .) and infection.Symptoms most frequently start with donor engraftment, but may happen later.Acute GVHD is a clinical diagnosis but, as many the symptoms of acute GVHD are non-specific, histologic confirmation, especially if the symptoms are atypical or involve just the liver or gut, may be extremely useful.].

The earliest and most common manifestation is skin GVHD.

Recent data support the use of the grading system since it is able to subdivide patients into risk categories for complications and mortality.

In this system, patients are divided into one of four grades (I-IV) depending on the degree, or stage, of involvement in three organs.

Clinically, the diagnosis is suspected when a recipient of HSCT develops any or all of the following signs or symptoms: dermatitis (skin rash), cutaneous blisters, crampy abdominal pain with or without diarrhea, persistent nausea and vomiting, hepatitis (with elevation of bilirubin and/or liver enzymes).

Typically, these symptoms occur before day 100 after the HSCT, but may occur later.

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The incidence of grade II-IV acute GVHD is roughly 35%–50%.