Case report: MELAS and concomitant presumed antiphospholipid antibody syndrome in an adult woman.

Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes, and other features (short stature, headaches, seizures, and sensorineural hearing loss) constitute characteristics of MELAS syndrome. MELAS is a rare condition due to mutations in maternally inherited mitochondrial DNA with levels of heteroplasmy possibly related to late adulthood presentation. A previously reported MELAS case coexisted with presumed Antiphospholipid Antibody Syndrome (APLAS), but the connection between MELAS and a potential APLAS is unclear. A 29-year-old woman presented with mild right-sided sensorimotor symptoms and mixed aphasia in November 2021. She presented again in May 2022 for unrelenting headaches and was found to have a new right hemisphere syndrome with mild left-sided sensorimotor symptoms, hemineglect, and anosognosia. Characteristic lab and imaging studies were obtained. During the first presentation (October 2021), the discovery of anticardiolipin IgM antibodies (aCL) (and their replication 3 months later) led to a diagnosis of APLAS, and Warfarin was initiated. During the second admission (May 2022), a new stroke-like lesion on the right hemisphere with characteristic features not suggestive of ischemia was detected, which led to a diagnosis of MELAS (m3243A > G mutation). Although MELAS and APLAS could co-exist, alternatively, it is possible that antiphospholipid antibodies might be generated when the strongly anionic Cardiolipin-Hydroperoxide from the inner mitochondrial membrane is exposed to immune component cells upon cell lysis. Thus, the presence of aCL in patients with stroke-like lesions might masquerade as an APLAS, but should probably be questioned if only aCL are repeatedly found and imaging findings are not characteristic for ischemic lesions.

Antiplatelet agents and proton pump inhibitors - personalizing treatment.

INTRODUCTION: Antiplatelet therapy remains one of the cornerstones in the management of non-cardioembolic ischemic stroke. However, a significant percentage of patients have concomitant gastroesophageal reflux or peptic ulcer disease that requires acid-reducing medications, the most powerful and effective being the proton pump inhibitors (PPIs). Antiplatelet efficacy, at least in vivo, and particularly for clopidogrel, has been shown to be reduced with concomitant proton pump inhibitor use. Whether this is clinically relevant is not clear from the limited studies available. METHODS: We conducted an extensive review of studies available on Medline related to pharmacodynamic interactions between the antiplatelet medications and proton pump inhibitors as well as clinical studies that addressed this potential interaction. RESULTS: Based on the present pharmacodynamic and clinical studies we did not find a significant interaction that would reduce the efficacy of antiplatelet agents with concomitant user of proton pump inhibitors. CONCLUSIONS: Patients on antiplatelet agents after a transient ischemic attack or ischemic stroke can safely use aspirin, and extended release dipyridamole/aspirin with proton pump inhibitors. Patients on clopidogrel may use other acid-reducing drugs besides proton pump inhibitors. In rare cases where proton pump inhibitors and clopidogrel have to be used concurrently, careful close monitoring for recurrent vascular events is required.

Coated-platelet levels are low in patients with spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Coated-platelets are a subset of platelets with high procoagulant potential observed on dual agonist stimulation with collagen and thrombin. Failure to produce coated-platelets in animals results in a bleeding diathesis. With this background, we undertook a pilot study to investigate coated-platelet production in patients with spontaneous intracerebral hemorrhage (SICH). METHODS: Coated-platelet levels were determined in 26 patients with a diagnosis of SICH and 52 controls. RESULTS: The patient population had significantly lower coated-platelet levels than the controls (mean+/-SD, 24.8+/-9.7% versus 32.9+/-12.6%, P=0.0035). CONCLUSIONS: Decreased coated-platelet synthesis may be linked to the mechanisms involved in the events leading to SICH.