Age: 48.0
Sex: M
Vaccine: FLUX(H1N1)
Symptoms: Skin haemorrhage, Skin plaque, Splenomegaly, Stool analysis normal, Streptococcus test negative
Clinical narrative: Case number PHHY2013US039400 is an initial literature report received on 22 Apr 2013. The author presented a case of severe serum sickness after H1N1 influenza vaccine administration. This report refers to a 48-years-old male patient. His medical history included a cardiac surgery at the age of 18 for a valvular problem. He was on no medications and denied using over the counter medications, herbal supplements and illicit drugs before the onset of symptoms and he denied any medication allergies. It was reported that five to six weeks earlier he had a febrile respiratory illness with malaise and aches which was possibly a primary H1N1 infection. He denied upper respiratory tract and gastrointestinal symptoms in 3 weeks before events and he did not have lower respiratory tract symptoms. There was no history of previous adverse reactions to stings or recent insect sting. He denied administration of antisera or blood products and recent illness before vaccination. His vaccination history included administration of tetanus vaccine (manufacturer and batch number: not reported) in the past which was well tolerated and he never had influenza vaccination in the past. He was vaccinated with H1N1 (manufacturer and batch number: not reported) on an unknown date. He was in his usual state of good health until 24 to 48 hours after receiving vaccine, after which he developed symptoms. He developed facial swelling and rash, predominantly on the anterior chest wall which was followed by shortness of breath. Subsequently he noted back pain, reduced urine output, brown urine and increasing swelling and was taken to emergency room. Before going to emergency room, he took diphenhydramine as treatment for rash. In emergency room, his blood pressure was 87/38 mm Hg, pulse rate was 155 beats per minute and respiratory rate was 30 breaths per minute. Respiratory distress with accessory muscle use was evident. Lungs were clear to auscultation. Face and neck displayed nonpitting edema, abdomen was distended and legs were edematous. Numerous wheals and raised erythematous plaques, some with central clearing consistent with urticaria were present on the trunk and extremities. Mucosal surfaces were free of lesions. He was presented with renal failure. Laboratory results were performed and the results were reported as follows: White blood cell count was 22.2 x 10^9/L including 20% neutrophils, 58% bands, 5% metamyelocytes/myelocytes, 3% eosinophils and 4% atypical lymphocytes. Blood urea nitrogen was 27 mg/dL and creatinine level was 2.39 mg/dL and the values increased to 86 mg/dL and 5.2 mg/dL respectively. Fibrin degradation product level was >20 mg/mL. Erythrocyte sedimentation rate was 75 mm/hr. C3 was 29 mg/dL and C4 levels was 8.9 mg/dL. Urinalysis revealed proteinuria. Computed tomography scan revealed splenomegaly and extensive lymphadenopathy throughout the chest and abdomen. Infectious causes of the patient's symptoms were suspected and hence he underwent a careful workup to exclude causative agents. Aerobic, anaerobic, fungal and urine cultures were negative. Histoplasma antigen, stool examination for ova and parasites, hepatitis panel, human immunodeficiency virus, Neisseria DNA, assays for acute infection with Coccidioides, Borrelia, Epstein-Barr virus, cytomegalovirus, Bartonella henselae, Brucella and Toxoplasma were negative. Antistreptolysin titers were not suggestive of recent streptococcal infection. Immunoelectrophoresis revealed marked polyclonal increase in IgG and IgA. Bone marrow biopsy revealed polyclonal plasmacytosis only. C1q binding assay was 10.6 mgE/mL indicating presence of circulating immune complexes. Skin biopsy revealed perivascular lymphocytic inflammation and marked dermal hemorrhage consistent with capillaritis and immunofluorescence revealed focal vascular deposits of IgM and C3 in the dermis. Prednisone 1 mg/kg/day was started. There was dramatic improvement in the rash and serum creatinine level was decreased to 1.9 mg/dl. At 6-week follow-up, symptoms had completely resolved and renal function was normalized. It was stated that since the patient and his wife denied administration of antisera or blood products and any history of medication use, insect sting or recent illness in the 4 to 21 day period preceding onset of symptoms of serum sickness and no current infection was identified, the inciting factor was considered to be the influenza vaccination. The author discussed that the patient had history of a respiratory illness which was a possible primary H1N1 infection when reported influenza infections were at the peak in the local region. He did not seek care at that time and was not tested for influenza infection during that illness. It was stated that if he had developed circulating antibodies to influenza haemagglutinin or other proteins due to recent infection, the influenza vaccination might be considered as a second exposure and he would be expected to develop symptoms within 36 hours or less. His explosive onset and severity of symptoms were consistent with a second exposure event. No other potential cause of the event was discovered upon extensive history and laboratory evaluation. The author concluded the article stating that the case emphasizes the importance of early consideration of serum sickness in patients presenting with typical symptoms and recent exposure to a foreign antigen.