4 research outputs found

    Migraine Prevention through Ketogenic Diet: More than Body Mass Composition Changes

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    The ketogenic diet (KD) is gaining attention as a preventive treatment for migraine, which is sustained by many pre-clinical and clinical data. KD is also used for weight loss, and there is a relation between migraine and weight excess, but it is speculated that KD efficacy on migraine may go beyond this effect. We conducted a retrospective observational study on 23 migraine patients who received a KD and were evaluated at the baseline and then after 3 months both from a neurological and a nutritional point of view, including body mass composition analysis. We observed a reduction in monthly headache days (12.5 ± 9.5 vs. 6.7 ± 8.6; p < 0.001) and in days of acute medication intake (11.06 ± 9.37 vs. 4.93 ± 7.99; p = 0.008). We also observed a reduction in patients’ weight (73.8 ± 15.2 vs. 68.4 ± 14.6; p < 0.001) and BMI (26.9 ± 6.2 vs. 23.7 ± 8.1; p < 0.001) with a decrement of the fat mass (28.6 ± 12.5 vs. 20.6 ± 9.8; p < 0.001). Patients who responded to KD and those who did not had no differences with respect to weight or fat mass loss. These data corroborate the utilization of KD as a preventive treatment for migraine and suggest that the efficacy of such an intervention is not only due to weight or fat mass loss but probably relies on other mechanisms specific to KD

    In vitro undetectable PT and Fibrinogen (and in vivo?)

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    A 81 aged woman came to E.R. of Trieste University Hospital with a traumatic head injury. Blood cells count, liver enzymes and other parameters were normal, but with a photometric clot detection method PT and PT-derived Fibrinogen were undetectable, Fibrinogen-Clauss gave different results (157 to 357 mg/dL) and aPTT-Ratio was normal (0.96). When the instrument detection performance was improved, PT was normal and PT-derived Fibrinogen detectable, but Fibrinogen-Clauss was still very unsteady (352/294/558 mg/dL). When a mixing test was performed with normal pool plasma, PT was corrected, PT-derived Fibrinogen was very low (80 mg/dL) and Fibrinogen-Clauss resulted 360 mg/dL. Fibrinogen-Antigen was 368 mg/dL by a nephelometric immunoassay. In another Lab with a different optical analyzer, PT and aPTT yielded the same results, Fibrinogen-Clauss was 557 mg/dL with 35 IU/ml Thrombin reagent (and a very steep clot formation curve), but 113 mg/dL with 15 IU/ml Thrombin reagent (and a normal curve). With an electromechanical clot detection method, PT-INR and aPTT-Ratio were normal (0.88 and 0.96 respectively), Fibrinogen-Clauss was normal (400 mg/dL) but unsteady. However in a few days our patient healed up perfectly; she declared that her sister had the same performance when she was referred to another Hospital for a check-up, nonetheless they never had any severe bleeding in their life. Samples from our patient\u2019s son and daughter were taken and resulted completely normal for coagulation tests. We hypothetized: 1) a too fast Thrombin formation and/or Fibrinogen consumption, as shown by steep coagulation curves without a stable plateau; 2) an excessive thrombin formation, (in preliminary studies, however, G20210A mutation was absent and F1+2 were normal); 3) a dysfibrinogenemia, (to be studied). Further studies for Endogenous Thrombin Potential about thrombin ipothesis and for genetical pattern about fibrinogen molecule are needed to clarify this case
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