Acquired Inhibitor of Factor VIII Presenting as Delayed Wound Healing

Abstract

A 55-year-old male was admitted following a road traffic accident with scalp suture infection, right preseptal cellulitis and right parotitis. He was treated at a local hospital where primary suturing was done and was referred to our tertiary care hospital following non-healing of wound for further management. There was an eschar on the right side of the face. He had a past history of delusions and hallucinations 22 years back for which he was on chlorpromazine and diazepam. There was no family history of bleeding disorder. On examination, patient was febrile, pale with a pulse-rate of 100 beats/minute, blood pressure of 110/70 mmHg. There were no abnormal heart sounds and the lungs were clear. The abdomen was soft and there was no organomegaly clinically. On admission his haemoglobin was 9.5 gm/dL, total count-7,400 cells/mm 3 with a normal differential count, platelet count 90,000/mm 3 of blood.The peripheral smear showed normocytic normochromic RBCs, erythropenia with few macrocytes, there were no schistocytes, the white blood cells were within normal limits and there was mild thrombocytopenia. The reticulocyte count was 0.1%. Blood urea was 10 mg/dL, creatinine 0.92 mg/dL, serum sodium 139 meq/L, serum potassium 3.9 meq/L and chloride 105 meq/L. The random blood sugar was 96 mg/dL, serum bilirubin 0.4 mg/dL, SGOT-33 units/L, SGPT 53 units/L, serum alkaline phosphatase-98 units/L, gamma glutamyl transferase of 59 units/L, total protein 3.4g/dL. The urine routine was normal. The prothrombin time was normal (15.6 sec with a control of 14.1 sec). The activated partial thromboplastin time was prolonged, 60.6 sec with a control of 29.2 sec. The D-dimer test was negative, ruling out disseminated intravascular coagulation. The bleeding time was normal. The chest X-ray was normal.The X-ray skull showed no evidence of bony injury to the facial bones and there was no evidence of osteomyelitis. The CT scan facial bones showed no evidence of bony injury and CT of the brain was normal. The ultrasound of the right parotid region showed parotitis and multiple enlarged deep cervical lymph nodes on both sides. The ultrasound abdomen showed splenomegaly. There was no evidence of papilloedema. The wound swab culture and sensitivity showed a moderate growth of Staphylococcus aureus which was sensitive to a large number of antibiotics. In view of the prolonged AbSTRACTAcquired coagulation factor VIII inhibitor leads to a rare disease i.e., acquired haemophilia which is idiopathic in majority of cases and is seen with autoimmune diseases, haematologic and solid tumours, infections, in the post-partum period and also with certain long-term use of drugs like penicillin and its derivatives, phenytoin, sulfa antibiotics, chloramphenicol, methyldopa, chlorpromazine, levodopa, interferon-α, fludarabine, clopidogrel. We report a case here, with acquired Factor VIII (FVIII) inhibitor acquisition which presented with delayed wound healing as a result of protracted bleeding into the wound. The inhibitor was acquired due to prolonged chlorp...

Case Report: Effective management of adalimumab-induced acquired hemophilia A with the CyDRI protocol

“…This catalog encompasses medications, such as the antiplatelet drug clopidogrel [ 11 , 12 ], along with alemtuzumab [ 13 – 18 ] and omalizumab [ 19 ], monoclonal antibodies used in treating specific leukemia types and allergic asthma, respectively [ 10 ]. Other drugs that have been associated with AHA include penicillins [ 20 – 22 ], interferons [ 23 – 25 ], chlorpromazine [ 26 ], acetaminophen and chlorpheniramine [ 27 ] and anti-cancer drugs including fludarabine and imatinib [ 10 ].…”

Acquired Factor VIII Inhibitor Presenting as Occult GI Bleeding

“…While there have been other studies highlighting the various presentations of acquired factor inhibitors, no other documented case has been presented with anemia in the setting of occult gastrointestinal and intramuscular bleeding. In other acquired factor VIII inhibitor cases in the literature, patients first presented with gross hematuria or acute evident gastrointestinal bleeding [ 5 ]. Other cases highlight acquired factor VIII inhibitor in patients with underlying malignancy, interstitial lung disease, SLE, and bullous pemphigoid, and yet others presented with delayed wound healing.…”