Cases reported "Anaphylaxis"

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1/10. An unusual case of anaphylaxis. Mold in pancake mix.

    Anaphylactic reactions involve contact with an antigen that evokes an immune reaction that is harmful. This type of reaction is a rapidly developing immunologic reaction termed a type I hypersensitivity reaction. The antigen complexes with an IgE antibody that is bound to mast cells and basophils in a previously sensitized individual. Upon re-exposure, vasoactive and spasmogenic substances are released that act on vessels and smooth muscle. The reaction can be local or systemic and may be fatal. The authors report the death of a 19-year-old white male who had a history of "multiple allergies," including pets, molds, and penicillin. One morning, he and his friends made pancakes with a packaged mix that had been opened and in the cabinet for approximately 2 years. The friends stopped eating the pancakes because they said that they tasted like "rubbing alcohol." The decedent continued to eat the pancakes and suddenly became short of breath. He was taken to a nearby clinic, where he became unresponsive and died. At autopsy, laryngeal edema and hyperinflated lungs with mucous plugging were identified. Microscopically, edema and numerous degranulating mast cells were identified in the larynx. The smaller airways contained mucus, and findings of chronic asthma were noted. Serum tryptase was elevated at 14.0 ng/ml. The pancake mix was analyzed and found to contain a total mold count of 700/g of mix as follows: penicillium, fusarium, mucor, and aspergillus. Witness statements indicate that the decedent ate two pancakes; thus he consumed an approximate mold count of 21,000. The decedent had a history of allergies to molds and penicillin, and thus was allergic to the molds in the pancake mix. The authors present this unusual case of anaphylaxis and a review of the literature.
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2/10. Serum tryptase analysis in a woman with amniotic fluid embolism. A case report.

    BACKGROUND: Recent studies have noted a striking similarity between amniotic fluid embolism (AFE) and anaphylaxis. Serum tryptase levels may therefore serve as a marker of mast cell degranulation in AFE cases. CASE: A 40-year-old woman, gravida 6, para 4, experienced the acute onset of facial erythema, eclampsia-type seizures, severe hypoxia, cardiac arrest and disseminated intravascular coagulation while in early active labor. The patient was declared dead 37 minutes after the onset of resuscitative efforts. At autopsy, fetal squames were found within the pulmonary tree, uterine blood vessels and brain. A peripheral venous blood specimen, obtained approximately one and a half hours postmortem, revealed a tryptase level of 4.7 ng/mL (normal, < 1). CONCLUSION: An elevated serum tryptase level, in conjunction with our patient's clinical history, adds further supporting evidence to the concept of AFE as an anaphylactoid syndrome of pregnancy.
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3/10. anaphylaxis to isosulfan blue.

    BACKGROUND: Isosulfan blue 1% is a dye used in medical procedures such as lymphangiography and sentinel lymph node biopsy. Anaphylactic reactions to this dye have been rarely reported. OBJECTIVE: We are reporting two patients who experienced anaphylaxis after subcutaneous administration of isosulfan blue. methods: Two female patients with breast cancer were evaluated by our allergy service after suspected intraoperative anaphylactic episodes during sentinel lymph node biopsies in which they had received isosulfan blue 1% for the purpose of visualization of the lymph vessels. In the first case, the patient suffered hypotension and hypoxia requiring intubation. In the second case, the patient suffered prolonged hypotension. Both patients recovered without sequelae. The patients were seen in our clinic, and skin tests were performed to isosulfan blue in addition to other agents the patients had received during anesthesia. RESULTS: In both cases, the patients demonstrated positive skin tests to isosulfan blue. Neither patient had positive skin tests to any other agent used for skin testing. Isosulfan blue skin tests were performed in nine control subjects and all skin tests in the control subjects were negative. CONCLUSIONS: Isosulfan blue may be a cause of anaphylactic reactions and this seems to be an immunoglobulin e-mediated event as confirmed by positive skin tests.
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4/10. Successful treatment with erwinia L-asparaginase for recurrent natural killer/T cell lymphoma.

    We describe a patient with natural killer (NK)/T cell lymphoma who relapsed after autologous peripheral blood stem cell transplantation (auto-PBSCT) and was successfully treated with escherichia coli (E. coli) and erwinia L-asparaginase. A 38-year-old male patient with ulcerated tumor at the left thigh was diagnosed as having nasal type NK/T cell lymphoma on the basis of histopathological and flowcytometric findings of tumor, revealing diffuse infiltration of atypical lymphoid cells into blood vessels and expression of CD7 and CD56 antigens, but not CD3. He had tumor infiltration in the bone marrow and at the right lower lung field. After five cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) therapy, the patient achieved complete remission and received high-dose chemotherapy with auto-PBSCT, although the tumor recurred in the right leg 10 months later. Despite salvage chemotherapy, followed by local irradiation and surgical amputation, a tumor recurred at the left upper gingiva 10 days after. Using E. coli L-asparaginase (6000 U/m2/day), the tumor regressed, fever was alleviated and the serum lactate dehydrogenase decreased to normal range after several days. The asparagine synthetase expression in tumor cells was immunohistochemically negative on paraffin-embedded tissues. Because of the anaphylactoid reaction developing after E. coli L-asparaginase, alternative erwinia L-asparaginase (6000 U/m2/day) was administered, resulting in regression of tumor and fever lysis. L-asparaginase is a promising agent for the treatment of NK/T cell lymphoma.
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5/10. Anaphylactic shock due to rupture of a hepatic hydatid cyst into a pericystic blood vessel following blunt abdominal trauma.

    Partial drainage of a hepatic hydatid cyst into a pericystic blood vessel caused anaphylactic shock following minimal blunt abdominal trauma in a child. A case report including diagnostic procedures and treatment is presented.
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6/10. Massive fat and necrotic bone marrow embolization in a previously undiagnosed patient with sickle cell disease.

    A case of sickle cell disease diagnosed postmortem is described. A 37-year-old black woman presented with anemia, respiratory distress, and abdominal and back pain. death followed an intramuscular injection of iron, and anaphylaxis was clinically diagnosed. At autopsy, massive fat and necrotic bone marrow embolization of pulmonary and renal vessels was found. In the vertebral column, multifocal areas of ischemic necrosis were present, and proved to be the source of this embolization. Sickled red cells appeared in bone marrow sinusoids, and signs of disseminated intravascular coagulation were present.
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7/10. Protamine sulfate and fatal anaphylactoid shock.

    A 73-year-old male underwent uneventful three-vessel coronary artery bypass grafting after which he received iv protamine sulfate for reversal of systemic heparinization. Shortly thereafter, the patient developed and succumbed to an anaphylactoid reaction attributed to protamine. The patient had none of the previously reported risk factors for hypersensitivity to the drug and was therefore not considered at high risk for such a severe adverse reaction. Although uncommon, the fatal outcome of this low-risk patient seriously addresses the need for alternative measures for heparin reversal.
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8/10. serum sickness triggered by anaphylaxis: a complication of immunotherapy.

    An 8-year-old boy developed anaphylaxis after receiving his maintenance dose of immunotherapy and proceeded to display the signs and symptoms of serum sickness. These consisted of fever, arthralgia, arthritis, urticaria followed by a hemorrhagic palpable rash, edema, lymphadenopathy, splenomegaly, abdominal pain, proteinuria, and neurologic manifestations consistent with vascular compromise of the posterior cerebral circulation. A skin biopsy specimen revealed perivascular infiltrates of lymphocytes and few polymorphonuclear neutrophils. The timing of events in this patient suggests that immunotherapy initiated a chain of events beginning with anaphylaxis and leading to serum sickness. It is hypothesized that the enhanced vascular permeability that accompanied the anaphylaxis allowed immune complexes that may have preexisted in the circulation to deposit in the blood vessels of the patient. These complexes may or may not have been related to the immunotherapy itself. Because antihistamines are known to prevent the induction of serum sickness, early and aggressive treatment of anaphylaxis during immunotherapy may prevent the occurrence of immune complex disease.
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9/10. Fat embolism, intravascular coagulation, and osteonecrosis.

    A triad of intraosseous fat embolism, intravascular coagulation (both thrombosis and hemorrhage), and osteonecrosis was pathologically demonstrated to coexist for the first time in humans. Specimens were evaluated from the earliest nontraumatic (18 hours) and traumatic (29 hours) femoral head lesions yet reported, and the cause and early pathogenesis were confirmed in a third case. An absolute overload of subchondral fat emboli, with hypercoagulability, stasis, and endothelial damage by free fatty acids, appears to cause end-organ death by triggering intravascular coagulation. This intermediary pathway appears to be capable of producing osteonecrosis by progressive fibrin platelet thromboses, which begin in vulnerable subchondral capillaries and sinusoids, especially when associated with arteriolar vasoconstriction and impaired secondary fibrinolysis (reperfusion of necrotic vessels with peripheral marrow hemorrhages). A relative overload of subperiosteal and subchondral fat emboli, which is below the ischemic/anoxic threshold but insufficient for intravascular coagulation, may cause osteopenia.
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10/10. Nucleus pulposus pulmonary embolism. A case report.

    STUDY DESIGN. This postmortem case report describes nucleus pulposus pulmonary embolism occurring in a human. OBJECTIVES. Clinical, pathologic, and pathogenetic features of the case are discussed. Reference is made to warnings in the literature stressing the importance of avoiding, during radiologic procedures, any possibility of intrathecal ingress of iodinated, ionic, hyperosmolar contrast material. SUMMARY OF BACKGROUND DATA. Various tissues have been implicated as pulmonary emboli in humans. Nucleus pulposus has been reported to embolize to spinal cord vessels in animals and humans and to embolize to the lungs in two animal species. This is the first report of nucleus pulposus pulmonary embolism in a human. methods. A patient with refractory low back pain was admitted for lumbar discography using diatrizoate meglumine, 52%, and diatrizoate sodium, 8%. Afterward, an ultimately fatal systemic reaction began, among the symptoms of which were spasmodic extensions of the lower back and legs. Postmortem examination was performed. RESULTS. Nucleus pulposus pulmonary emboli were seen microscopically on random lung sections. The lumbar vertebral column grossly featured acute herniations of disc material into vertebral marrow spaces; nucleus pulposus was identified microscopically in these areas. CONCLUSIONS. We speculate that the spasmodic back extensions imposed compressive forces on vertebrae, causing nucleus pulposus to be extruded into vertebral marrow sinusoids (thus creating emboli) and possibly causing these emboli to flow anteriorly into the anterior external vertebral plexus, which resulted in pulmonary emboli exclusively with no spinal cord emboli.
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