Maureen C. Farrell

We describe a case of Wernicke's encephalopathy secondary to thiamine (B1) deficiency in a patient status post-bariatric sleeve gastrectomy. The presenting symptoms of new-onset weakness, diplopia, and confusion in a young female patient raised suspicion for multiple sclerosis (MS), but given a history of bariatric surgery, thiamine levels were checked, revealing significant Vitamin B1 (thiamine) deficiency. This case highlights the importance of thorough history taking, as a misdiagnosis of MS in this case could have resulted in irreversible neurological deterioration and hematological and infectious consequences associated with the inappropriate administration of disease-modifying therapies. It is also important to note that severe vitamin deficiency occurred despite medication compliance.

Purpose Neurogenic orthostatic hypotension (nOH) is the hallmark of neurodegenerative forms of autonomic failure, including pure autonomic failure, multiple system atrophy, and Parkinson’s disease. Studies have shown autonomic physiological differences in Africans Americans (AA) such as lower heart rate variability, enhanced blood pressure reactivity, and blunted sympathetic neural response compared to non-Hispanic whites. However, the clinical characteristics and neurohormonal profile of autonomic failure in AA is unknown. Methods A total of 65 patients with nOH participated in this study (9 AA and 56 non-Hispanic whites). Both groups were of similar age and comorbidity status, and they underwent standardized autonomic testing and assessment of neurohormonal levels and renin activity and aldosterone in supine and upright positions. Results There were no significant differences in baseline autonomic clinical characteristics between non-Hispanic whites and AA with nOH. Non-Hispanic whites demonstrated a significant increase in upright renin activity compared to AA (295 ± 88% vs. 13 ± 13%, respectively). AA showed a blunted increase in aldosterone compared to non-Hispanic whites (188 ± 27% vs. 59 ± 38%, respectively). These results indicated persistent suppression of the renin-angiotensin system in AA, particularly during upright posture. Conclusion Our findings demonstrate that AA with nOH have similar clinical characteristics and hemodynamic autonomic profiles, but lower upright renin activity and aldosterone levels, compared to non-Hispanic whites. Renin suppression persists in AA with severe autonomic failure and can potentially contribute to postural changes and supine hypertension.

Racial and ethnic differences in cardiovascular morbidity and mortality persist despite advances in risk factor identification and implementation of evidence-based treatment strategies. African American men and women are disproportionately affected by cardiovascular risk factors, particularly hypertension. In this context, previous studies have identified sex and racial differences in autonomic cardiovascular regulation which may contribute to the development of hypertension and its high morbidity burden among African Americans. In this review, we provide a comprehensive evaluation of the potential pathophysiological mechanisms of blood pressure control and their differences based on sex and race. These mechanisms include obesity-induced sympathetic activation, sympatho-vascular transduction, baroreflex sensitivity and adrenoreceptor vascular sensitivity, which have been the subjects of prior investigation in this field. Understanding the racial differences in the pathophysiology of hypertension and its co-morbid conditions would allow us to implement better treatment strategies tailored to African Americans, with the ultimate goal of reducing cardiovascular mortality in this population.