Abdominal pain, unconsciousness, and skin rash after lung transplantation.

Long-term success of lung transplantation is limited by allograft dysfunction and frequent infections. Varicella zoster virus infection (VZV) is one of the most common opportunistic infections among solid organ transplantation recipients. However the occurrence of visceral involvement or disseminated disease, as seen after bone marrow transplantation, is rare. We report a case of a 59-year-old woman who underwent double-lung transplantation with a fatal visceral and disseminated varicella zoster virus infection.

What does pain signify? A hypothesis concerning pain, the immune system and unconscious pain experience under general anesthesia.

In this paper, I present a case-study that initiates a discussion about the meaning of pain. The case-study concerns a person who was under deep sedation during colonoscopy. The person did not experience pain from a first-person perspective, although pain was evident to the medical team from a second-person perspective. The divergence of pain perspectives raises an interesting quandary. If the body communicates pain while pain consciousness is blocked by the sedation procedure, our conclusion should be that the intersubjective aspect of pain precedes the "subjective," first-person experience of pain. This conclusion is not consistent with the common representational conception of pain that places the intrasubjective point of view prior to the intersubjective point of view. The solution I offer to this quandary is the quasi-paradoxical idea that pain can be experienced unconsciously through the immune system. Following this suggestion, I hypothesize that post-traumatic stress disorders following general anesthesia may result from this unconscious pain experience. If this idea is scientifically grounded, then physicians should: (1) consider ways of blocking the unconscious pain experience produced by the immune system without interfering with the immune response, and (2) study pain as a complex cognitive and unconscious system by drawing an analogy with the immune system, which follows similar logic.

Late postprandial hypoglycemia due to bioactive insulin dissociation from autoantibody leading to unconsciousness in a patient with insulin autoimmune syndrome.

We report here the case of an 83-year-old man who was treated for unconsciousness and hypoglycemia (39 mg/dL) accompanied by marked elevation of serum immunoreactive insulin (IRI) (4,760 µIU/mL). We diagnosed his condition as insulin autoimmune syndrome (IAS, Hirata disease) because of a high insulin autoantibody (IAA) titer (>90%: bound/total) and no history of exogenous insulin administration. Reactive hypoglycemia occurred due to immediate association followed by dissociation between insulin and insulin autoantibodies after glucose or food intake. An α-glucosidase inhibitor in combination with frequent small meals reduced the postprandial hyperglycemia (glucose spike) and ameliorated the reactive hypoglycemia.

Influence of total IgE levels on the severity of sting reactions in Hymenoptera venom allergy.

BACKGROUND: Detection of specific IgE for Hymenoptera venoms and skin tests are well established diagnostic tools for the diagnosis of insect venom hypersensitivity. The aim of our study was to analyze the effect of total IgE levels on the outcome of generalized anaphylactic reactions after a Hymenoptera sting. METHODS: Two hundred and twenty patients allergic to bee, wasp, or European hornet venom were included in the study. Their specific and total IgE levels, serum tryptase levels, skin tests, and sting history were analyzed. RESULTS: In patients with mild reactions (grade I, generalized skin symptoms) we observed higher total IgE levels (248.0 kU/l) compared to patients with moderate reactions (grade II, moderate pulmonary, cardiovascular, or gastrointestinal symptoms; 75.2 kU/l) and severe reactions (grade III, bronchoconstriction, emesis, anaphylactic shock, or loss of consciousness; 56.5 kU/l; P < 0.001). Accordingly, 25% of the patients with low levels of total IgE (<50 kU/l), but no individual with total IgE levels >250 kU/l, developed loss of consciousness (P = 0.001). Additionally, specific IgE levels were related to total IgE levels: Specific IgE levels increased from 1.6 to 7.1 kU/l in patients with low (<50 kU/l) and high (>250 kU/l) total IgE levels, respectively (P < 0.001). Specific IgE levels correlated inversely to the clinical reaction grades, however, this trend was not statistically significant (P = 0.083). CONCLUSION: Patients with Hymenoptera venom allergy and high levels (>250 kU/l) of total IgE, predominantly develop grade I and grade II reactions and appear to be protected from grade III reactions. However, this hypothesis should be confirmed by extended studies with sting challenges.

Impaired cell-mediated immunity in Plasmodium falciparum-infected patients with high-parasitemia and cerebral malaria.

Several cell-mediated functions were studied in vivo and in vitro in 63 Thai patients with acute falciparum malaria, including 21 cases with cerebral manifestations and 10 cases with initial parasitemia over 10%. Initial delayed cutaneous reactions to phytohemagglutinin and soluble protein antigens were negative in most cerebral malaria cases. In other patients, skin reactions were impaired or abolished as a direct function of parasitemia. No major alteration in the numbers of blood T and B lymphocytes was found. In lymphocyte cultures, proliferative responses to lectins were generally found within normal ranges; in contrast, proliferative responses to candidin were suppressed in parallel with delayed cutaneous responses to the same antigen. From these data, it can be concluded that the alteration of specific cell-mediated responses are predominantly detectable in acute cases with major parasite invasion, i.e., high parasitemia and/or cerebral manifestations. A direct role of Plasmodium falciparum was further suggested by the rapid restoration of cell-mediated functions observed in several cases under successful antimalarial therapy. These results do not support any evidence in favor of a preexisting cellular immune deficiency in relation with the occurrence of cerebral or high-parasitemia acute malaria in these patients.