Indian Journal of Dermatology
: 2015  |  Volume : 60  |  Issue : 3  |  Page : 324-

Transfusion associated graft versus host disease

Kikkeri Narayanshetty Naveen1, Sharatchandra B Athanker1, Umesh Rajoor2, Jayaraj Sindhoor2,  
1 Department of Dermatology, Sri Dharmasthala Manjunatheshwara College of Medical Sciences and Hospital, Dharwad, Karnataka, India
2 Department of Medicine, Sri Dharmasthala Manjunatheshwara College of Medical Sciences and Hospital, Dharwad, Karnataka, India

Correspondence Address:
Kikkeri Narayanshetty Naveen
Department of Dermatology, Sri Dharmasthala Manjunatheshwara College of Medical Sciences and Hospital, Dharwad, Karnataka

How to cite this article:
Naveen KN, Athanker SB, Rajoor U, Sindhoor J. Transfusion associated graft versus host disease .Indian J Dermatol 2015;60:324-324

How to cite this URL:
Naveen KN, Athanker SB, Rajoor U, Sindhoor J. Transfusion associated graft versus host disease . Indian J Dermatol [serial online] 2015 [cited 2021 Sep 26 ];60:324-324
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Full Text


Transfusion-associated graft-vs-host disease (TA-GVHD) is a rare but usually fatal complication of transfused cellular blood components. In immunocompetent hosts, TA-GVHD has been observed after the transfusion of cellular components from HLA-homozygous donors to recipients heterozygous for that human leukocyte antigen (HLA) haplotype. Transfused, viable, donor T-lymphocytes homozygous for an HLA haplotype for which the recipient is heterozygous may not be recognized as foreign and may engraft within the host and initiate GVHD. Most of these cases have been observed in Japan and the Middle East. Many reported cases of TA-GVHD have been seen in patients with defects in cellular-mediated immunity, patients receiving transfusions from blood relatives, fetuses receiving intrauterine transfusions, and rarely in immunocompetent patients from homogeneous genetic populations. [1]

A 63-year-old male who was HBsAg positive was brought to the institution with fever and generalized redness. The patient was suffering from benign prostatic hypertrophy from 2 years and he underwent transurethral retrogradel prostectomy. The patient was transfused 2 pints of blood on that day and 1 pint the following day. The blood was given from the blood bank from unrelated donor. Post operatively the patient was started with tab amoxicillin and tab paracetamol. He was discharged 5 days later. Eighth day after transfusion he developed fever with chills and rigors which persisted despite the antibiotic therapy. He developed erythematosus macules and patches over the chest which gradually involved the entire body giving a reddish hue to the whole body. He denied history of itching, loose stools and abdomen pain. The patient was a diabetic and hypertensive and was on treatment for the same.

He came to our institution on 18 th day. On examination the patient was febrile. The skin involving the face, trunk, extremities and back and buttocks was bright pink in color with desquamation [Figure 1]. Hemorrhagic macules were present over the lower limbs. Face was edematous. Hemorrhagic crusts were present over the lips. Oral mucosa was otherwise uninvolved. The investigations done outside revealed platelet count 1.25 l/mm. Two days later the report showed platelets count 86000/mm 3 and WBC -3100.{Figure 1}

On admission the investigations were repeated which revealed HBsAg positive. Total count was 2120 cells/mm 3 , and platelets were 32000/mm 3 . Liver function test and renal function tests were normal. Investigations for dengue, malaria and widal were negative.

The patient was started on parental fluids, dexamethasone, azithromycin, oral ofloxacin and parental insulin. Repeat platelet count showed very low count of 7000/mm 3 . Four pints of random donor platelets were given. The next day complete hemogram was done which showed total count 800/mm 3 with marginal improvement of platelet count to 31000/mm 3 . SGOT was raised to 1500. 21 st day report revealed again falling platelet count and WBC counts. TA-GVHD was suspected; however, biopsy was not performed, as platelet counts were very low. On 22 nd day afternoon the patient developed breathlessness and was transferred to medicine. There he succumbed to aspiration pneumonia.

The pathophysiology of TA-GVHD is similar to GVHD associated with bone marrow transplantation (BMT) but, the clinical course in TA-GVHD is more fulminant with marrow aplasia and consequent complication of infections. [2],[3] Marrow involvement does not occur in GVHD associated with BMT, as antigenically, marrow is similar to the graft. In TA-GVHD, the marrow is antigenically similar to the host tissue, against which the graft T cells react.

The clinical features involving skin, liver, gastrointestinal tract and bone marrow should arouse the suspicion of GVHD. The median interval between the transfusion and the onset of fever is 4-10 days. An erythematosus maculopapular rash is observed on the trunk. It then spreads to involve the extremities, including the palms and soles. It may progress to generalized erythroderma or bullae formation. Involvement of the liver is variable. Pancytopenia due to bone marrow aplasia is a late manifestation; occurring after a median interval of 16 days. Uncontrolled infections are the most common cause of death which frequently occurs within 3 weeks of the onset of GVHD. Overall mortality is reported to be more than 90%. [2],[3] In the present case, drug reaction is a possibility, but the course of events, pancytopenia, temporal relationship with blood transfusion strongly suggest TA-GVHD. The findings of skin biopsy, though suggestive, but not pathognomonic of TA-GVHD and doesn't differentiate it from drug reaction. [2],[3]

TA-GVHD in immunocompetent individuals is very rare, unless when a blood donor is homozygous for one of the recipients major HLA types. [4] The reported frequency of one-way matching or sharing HLA haplotype in a non-first degree relative in Japan ranges from 1 in 312 to 1 in 874, which increases the risk of developing TA-GVHD in immunocompetent individuals even after receiving transfusion from unrelated donors. Use of fresh blood and directed donation also contribute to increased risk of TA-GVHD in Japanese population. [5] In the present case stored blood was used and it was from unrelated donor. The data regarding genetic homogeneity is not available in the Indian population. We reported a case of TA-GVHD in a girl child from Karnataka, where the blood was taken from her father. [6] There are no other reports of TA-GVHD from unrelated donor from Karnataka, so the frequency of sharing haplotypes in our population may not be very high. A similar case has been reported from Gujarat and they proposed that TA-GVHD should be strongly suspected if cytopenias develop within 90 days of blood transfusion. [5] In the present case, there was no history of any immunosuppressive disease or consumption of immunosuppressive medications recently or in the past. Probably transient immunosuppression following surgery and blood transfusion may be responsible for the event. [5]

Tissue damage from the recipient's underlying disease, infection and pretransplant conditioning plays a key role in GVHD through pro-inflammatory cytokine production and antigen presenting cell activation. [7] In our patient, Hepatitis-B virus infection might have contributed to GVHD by antigen-presenting cell activation.

The present case is reported to raise the awareness regarding TA-GVHD following blood transfusions during surgeries, as it may go unnoticed and frequently misdiagnosed as drug reaction.


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