THROMBOTIC THROMBOCYTOPENIC PURPURA FOLLOWING THE FLU VACCINE. A. Markarian 1 , R.D. Hobbs 1 ; 1 Oakwood Healthcare System, Dearborn, MI LEARNING OBJECTIVE: To recognize thrombotic thrombocytopenic purpura (TTP) as a potential complication of the influenza vaccine. CASE INFORMATION: A 58 year-old man with COPD, diabetes mellitus, and hypertension presented with mental status changes and oliguria. He had felt fatigued for several days and had noted a rash on his shins. His chronic medications were Metformin, Glipizide, Nitrobid, Metoprolol, Omeprazole, and Quinine. He received the flu vaccination two weeks prior to admission. He was afebrile but tachycardic. Physical exam showed flaccid paralysis, diminished deep tendon reflexes and bilateral Babinski signs. The heart, lungs and abdomen were unremarkable. A petechial skin rash was noted on both shins. Laboratory studies revealed mild anemia (Hgb 11.7), schistocytes on the peripheral smear, LDH (1927) and a low haptoglobin. The platelet count was 13,000. PT, PTT, INR, fibrinogen and fibrin degradation products were normal. The BUN was 84 and the creatinine 3.4. ANA was positive with a titer of 1:160; anti ds DNA and Lupus anticoagulant were negative. Total compliment levels were normal. SSA/RO and SSB/LA were negative. Antiglo-merular basement membrane Ab, ANCA, ACLA-IgG and IgM, and C1 Esterase inhibitor were normal. HIV was non reactive. Cultures were negative for enteric pathogens. Von Willebrand' factor activity was normal. Quinine dependant antibodies against platelet glycoprotein were negative but non drug dependant IgM antibody was positive. The patient was treated with plasmapheresis and hemodialysis and recovered. DISCUSSION: The classic pentad of TTP includes microangiopathic hemolytic anemia, thrombocytopenia, neurologic symptoms, renal disease and fever. The etiology is poorly understood although underlying immune complex formation is frequently found. Plateletassociated antibodies and serum reactivity against endothelial cells are positive in some cases. Most cases are idiopathic. Associated conditions include infections (bacterial, viral, and fungal), autoimmune diseases, AIDS, cancer, vaccinations and drugs such as quinidine, quinine and ticlopidine. Cases of TTP following influenza vaccine have been reported (Brown et al, Br Med J 1973; 2(861):303; Symmers, Br Med J 1973; 2(866) :614). In the present case, it is likely that the influenza vaccine triggered the antibody formation and immune complex deposition and led to the development of TTP. CASE INFORMATION: A 55-year old male post myocardial infarction was transferred for cardiac catheterization from a small community hospital. His past medical history per family included closed head trauma as a child, with residual cognitive impairment, hypertension, gout, and some hearing loss over the past 2 months. He has worked as a janitor for a local school for the past 13 years. He was described by his family as``slow'' and had a 6th grade education. On hospital day 6, after stabilization, his disposition became a concern. That morning, he sat in bed watching cartoons, laughing, with the sound off. When examined, he became confused and cried. His answers to questions were intermittently unintelligible. He frequently answered questions not asked. An uncle confirmed that this was his baseline, and that he had exhibited odd behavior since a child; his family had attributed it to falling off a truck and hitting his head. His primary team asked psychiatry if evaluating the level of his cognitive functioning would help, and his supervisor at work was called. She said that he was an excellent and very dependable employee as long as he was shown exactly what to do. When asked if he would follow verbal orders, she again stated that he needed to be shown what to do. Suspecting severe hearing impairment, a stethoscope was placed in his ears. With the communicator shouting into the diaphragm, he could hear clearly and responded appropriately. Audiometry on day #10 revealed complete sensory hearing loss on the right, severe loss on the left, with 10% speech discrimination on the left, which increased to 20% when allowed to lip-read. Further questioning revealed that he remembered being able to hear to some degree as a very young child. He was not aware that his family did not know how profoundly deaf he was. DISCUSSION: Chartlore, the process by which diagnoses are assigned via undocumented notes in the chart, is usually a product of loosely applied terms that, once used, tend to``stick.'' This particular example of chartlore is interesting in that the original misdiagnosis/assumption appears to have been made, not by the medical staff, but by the patient's own family, and tragically for him, perpetuated over decades, preventing its correction. Physicians must recognize the often deceptive nature of chartlore and the need to confirm history gleaned from medical records and family members. This fact is especially true when the``facts'' obtained conflict. 1) Recognize that McArdle disease is the number one glycogen storage disease diagnosed in adults, 2) Recognize the typical history of a patient with McArdle disease, and 3) Increase awareness of the disease for possible earlier detection. CASE INFORMATION: CASE: CC is a 31-year-old male who presented with a one-day history of dark urine. CC had to swim strenuously when a barge he was on sank. He then developed diffuse body aches and dark urine. He had a long history of exercise intolerance, easy fatigability, and on several occasions had dark colored urine after exertion. CC's younger brother had a similar history but his symptoms were not as severe. Meds: none, otherwise negative PMH. Pertinents on PE were BP 131/78, P 101, RR 24, WNWD male in moderate distress from diffuse whole body pain. CV: RRR with mild tachycardia, abd was normal with no HSM. The patient had diffuse muscular tenderness over the thighs, arms, forearms, anterior chest, and back. Labs BUN of 14, Cr of 1.2, AST of 461, ALT of 138, ALK PHOS of 97, LDH of 7,090, and a CK of 87,000. UA showed specific gravity of 1.015, pH 5.0, 4+ prot, 3+ blood, + LE, + NIT, 0 ± 3 RBC's, and +3 myoglobin. The patient had a biceps muscle biopsy which showed the absence of myophosphorylase. DISCUSSION: McArdle Disease or muscle phosphorylase deficiency results in limited ATP production from glycogenolysis and results in glycogen accumulation. It is the most common glycogen storage disease in adults. Inheritance is autosomal recessive, and the abnormal allele is on chromosome 11. Patients usually are diagnosed in the second or third decade but most have had symptoms since childhood. Exercise intolerance with muscle cramps, myoglobinuria, and a second wind phenomenon are common. Most patients have baseline elevated CK's. Diagnosis can be made by after ischemic exercise testing by measuring lactate levels and ammonia. Definitive diagnosis can be made by muscle biopsy and demonstrating myophosphorylase deficiency. DNA based diagnosis and carrier detection are available. Prognosis is generally good since longevity is not affected. Patients should avoid strenuous exercise and know the symptoms for seeking medical care during an exacerbation. High protein diets and oral glucose or fructose may increase exercise endurance.