Sex: U
Vaccine: FLUX
Symptoms: Haemoglobin normal, Haemorrhage urinary tract, Hepatitis C RNA decreased, Immune thrombocytopenic purpura, Immunoglobulin therapy
Clinical narrative: This case was reported in a literature article and described the occurrence of epistaxis in a elderly male patient who received Flu Seasonal TIV Dresden (Flu trivalent vaccine) for prophylaxis. Co-suspect products included Flu Seasonal TIV Dresden (Flu trivalent vaccine) for prophylaxis and Flu Seasonal TIV Dresden (Flu trivalent vaccine) for prophylaxis. The patient's past medical history included cholecystectomy and tonsillectomy. Concurrent medical conditions included hepatitis c (diagnosed 4 years prior, treatment with ledispavir/sofosbuvir having been completed 2 months prior from the event at 68 years), pre-diabetes, hypertriglyceridemia, chronic back pain, anxiety, smoker (smoking half a pack of cigarettes daily as well as occasional marijuana use, with no use of alcohol or other drugs) and chest pain (The patient did take aspirin once 2 days prior for an episode of chest pain (no chest pain currently at the event at 68 years)). Concomitant products included ledipasvir + sofosbuvir, tamsulosin hydrochloride (Tamsulosin) and pneumococcal 13 serotypes vaccine. On an unknown date, the patient received the 1st dose of Flu trivalent vaccine, the 2nd dose of Flu trivalent vaccine and the 3rd dose of Flu trivalent vaccine. On an unknown date, less than a week after receiving Flu trivalent vaccine and not applicable after receiving Flu trivalent vaccine and Flu trivalent vaccine, the patient experienced epistaxis, epistaxis, epistaxis (serious criteria hospitalization), thrombocytopenia (serious criteria hospitalization and GSK medically significant), haematuria (serious criteria hospitalization), gingival bleeding (serious criteria hospitalization), mouth hemorrhage (serious criteria hospitalization) and primary immune thrombocytopenic purpura (serious criteria hospitalization and GSK medically significant). The patient was treated with fenofibrate, fluticasone propionate (Fluticasone), acetylsalicylic acid (Aspirin), platelets, human blood (Platelet Transfusion), immunoglobulins nos (Immunoglobulin), dexamethasone and prednisone. Rechallenge with Flu trivalent vaccine was positive. Rechallenge with Flu trivalent vaccine was positive. On an unknown date, the outcome of the epistaxis, epistaxis, epistaxis, thrombocytopenia, haematuria, gingival bleeding, mouth hemorrhage and primary immune thrombocytopenic purpura were recovered/resolved. Additional information was provided. This case was reported in a literature article and described the event of epistaxis; severe thrombocytopaenia in an elder male patient between 66 and 68- year-old who was vaccinated with unspecified trivalent inactivated influenza vaccine (manufacturer unknown) for prophylaxis. The patient's medical history included hepatitis C (diagnosed 4 years prior, treatment with ledispavir/sofosbuvir having been completed 2 months prior from the event at 68 years), pre-diabetes, hypertriglyceridaemia, chronic back pain and anxiety. The patient's surgical history included cholecystectomy and tonsillectomy. The patient social history included smoking half a pack of cigarettes daily as well as occasional marijuana use, with no use of alcohol or other drugs. The patient's home medications included tamsulosin 0.4 mg daily, fenofibrate 145 mg daily and fluticasone 50 mg actuation to each nostril daily. The patient did take aspirin once 2 days prior for an episode of chest pain (no chest pain currently at the event at 68 years). No information on patient's family history or concurrent condition were provided. On an unspecified date, the patient received unspecified trivalent inactivated influenza vaccine (administration route and site unspecified, dosage unknown; batch number not provided). The age of vaccination was not provided. On an unspecified date, within 1 week after the vaccination, the patient developed epistaxis that lasted for a couple of hours and then resolved spontaneously. Next year, on an unspecified date, the patient received unspecified trivalent inactivated influenza vaccine (administration route and site unspecified, dosage unknown; batch number not provided). The age of vaccination was not provided. On an unspecified date, within 1 week after the vaccination, the patient developed epistaxis that lasted for a couple of hours and then resolved spontaneously. It was reported that the patient always had normal platelet counts. Next year, on an unspecified date, the patient received unspecified trivalent inactivated influenza vaccine and unspecified pneumococcal conjugate vaccine 13 (administration route and site unspecified, dosage unknown; batch number not provided for both). The age of vaccinations was not provided. On an unspecified date at the age of 68 years, 1 day after vaccination, the patient experienced epistaxis, gross haematuria, and bleeding gums. 2 days after the vaccination, the patient presented to the urgent care with epistaxis that lasted for 1 day, gross haematuria, and bleeding gums. The patient had presented with bloody urine. The urgent care personnel forwarded him to the emergency department. The patient stated, "he consistently had epistaxis after obtaining the influenza vaccine for the last 3 years. However, this time was unusual in that while the epistaxis would usually last for a couple of hours and then resolve spontaneously, it was more prolonged this time." The patient also developed bleeding oral ulcers. Review of systems was negative for fever, night sweats, recent infections, diarrhoea. The patient also denied having epistaxis throughout other times in the year. The patient's physical examination was significant for non-tender sores over the buccal mucosa, blood in the oropharynx and blood clots in bilateral nares with no active bleeding. The nasal mucosa was otherwise unremarkable. The patient also had a petechial rash scattered over bilateral lower extremities and his trunk. On an unspecified date, the patient underwent laboratory investigation, the patient's complete blood count reported as, thrombocytes 0/µL (reference range 150 000-400 000), compared with 210 000-267 000/µL in the past; leucocytes11.1×10E9/L/; haemoglobin 132 g/L were within normal limits. Peripheral blood smear confirmed severe thrombocytopaenia with no thrombocyte clumping. Rare small, lightly granulated thrombocytes were present. There were no other significant abnormalities. Serum chemistry had a creatinine of 0.99 mg/ dL, glucose 104 mg/ dL, with other lab values normal. Urine microscopy showed more than 100 erythrocytes with 0-5 leucocytes and no squamous cells or bacteria. Prothrombin time was 10.1 s. Activated partial thromboplastin time was 23.5 s. Fibrinogen: 378 mg/dL. D-dimer was 2.09 mg/L. Nasopharyngeal influenza A, influenza B and respiratory syncytial virus polymerase chain reaction (PCR) was negative. Human immunodeficiency virus (HIV) antigen/antibody was negative. Hepatitis C quantitative viral load was none detected. Flow cytometry was negative. There was no evidence of an infection or lymphoproliferative disorder. The patient was diagnosed with severe thrombocytopaenia due to primary immune thrombocytopaenia purpura (ITP). The epistaxis had resolved with some external pressure prior to arrival to the emergency department and the patient was no longer bleeding. Patient received a platelet transfusion. He was initiated on both intravenous immunoglobulin (IVIG) therapy and dexamethasone 40 mg daily for 3 days. He was then switched to oral prednisone 60 mg daily. All told, the patient received four transfusions of platelets during the admission given his platelet count of 0/µL (abnormal platelet count) and bleeding from both the nose and the urinary tract (platelet transfusion is recommended with platelet counts of less than10 000/µL or when a clinician feels there was severe bleeding). The day after initial treatment, his platelet count improved to 39 000 and on the fourth day, it improved to 101 000. By the 10th day, the platelet count was normal at 342 000/µL. The patient was discharged on 60 mg of prednisone as well as a proton pump inhibitor and advised not to receive any further influenza vaccinations. The patient had achieved platelet recovery and was stable after treatment. The patient continued to follow-up. It had now been one and a half years. He never had another abnormal platelet count or any episodes of bleeding. The case has been considered serious due to hospitalisation. The author considered the events of epistaxis, severe thrombocytopaenia and immuno thrombocytopaenia purpura (ITP) related to unspecified trivalent influenza vaccine. The authors stated that "It is highly likely that the severe thrombocytopaenia in our patient was due to the influenza vaccination due to the temporal association of the vaccination with the thrombocytopaenia and the ruling out of other diagnoses (hepatitis C RNA count was zero and there was no evidence of an infection or lymphoproliferative disorder). He always had normal platelet counts. Only on this occasion of epistaxis when the blood count was checked did he have an abnormal platelet count, which was immensely low at 0/µL. Furthermore, the patient noted that he only had epistaxis after influenza vaccination, and that this was happened consistently after three influenza vaccinations. ITP is linked with different kinds of vaccinations. Prior retrospective studies showed that there is a risk of developing ITP after receiving measles-mumps-rubella, hepatitis A, varicella and diphtheria-tetanus-pertussis vaccines in children and adolescents. A number of case-control studies and case reports regarding post-influenza vaccination ITP have been published. Vaccine-associated ITP may be caused by molecular mimicry, which demands the activation of autoreactive B or T cells by peptides in the vaccine that display structural parallel to antigens found on platelets. In previously reported cases of post-influenza vaccination ITP, patients made a full recovery after treatment. Our patient also achieved platelet recovery and was stable after treatment. Therefore, post-influenza vaccination ITP in elderly patients may respond to steroid and IVIG treatment. The time frame of development of ITP in relation to the epistaxis is notable in this case. At least one case report has had a child develop three occurrences of ITP, each within 1 week of receiving the influenza trivalent vaccine. It is possible that with first exposure, there is a prolonged period of time before symptoms and that repeat exposures produce an anamnestic, symptomatic response which is both more brisk and more severe. This may explain our patient's gross haematuria and oral ulcers with his latest presentation". The article corresponding to this case is not available for submission due to copyright restriction. The reporter considered the epistaxis to be related to Flu trivalent vaccine. The reporter considered the epistaxis to be related to Flu trivalent vaccine. The reporter considered the epistaxis, thrombocytopenia, haematuria, gingival bleeding, mouth hemorrhage and primary immune thrombocytopenic purpura to be related to Flu trivalent vaccine. Lab Comments: Lab tests were performed on unspecified dates. The patient always had normal platelet counts.  Review of systems was negative for fever, night sweats, recent infections, diarrhoea. The patient also denied having epistaxis throughout other times in the year. The patient's physical examination was significant for non-tender sores over the buccal mucosa, blood in the oropharynx and blood clots in bilateral nares with no active bleeding. The nasal mucosa was otherwise unremarkable. The patient also had a petechial rash scattered over bilateral lower extremities and his trunk. Peripheral blood smear confirmed severe thrombocytopaenia with no thrombocyte clumping. Rare small, lightly granulated thrombocytes were present. There were no other significant abnormalities. Urine microscopy showed more than 100 erythrocytes (reference 0-3) with 0-5 leucocytes and no squamous cells or bacteria. Nasopharyngeal influenza A, influenza B and respiratory syncytial virus polymerase chain reaction (PCR) was negative. There was no evidence of an infection or lymphoproliferative disorder. The patient was diagnosed with severe thrombocytopaenia due to primary immune thrombocytopaenia purpura (ITP). The day after initial treatment, his platelet count improved to 39 000 and on the fourth day, it improved to 101 000. By the 10th day, the platelet count was normal at 342 000/µL. The patient continued to follow -up. It had now been one and a half years. He never had another abnormal platelet count or any episodes of bleeding.