Drug induced hepatitis mimicking Wilson's disease secondary to the use of complex naturopathic regimens: a case report.

BACKGROUND: Drug induced liver injury (DILI) is an important cause of acute liver injury and accounts for approximately 10% of all cases of acute hepatitis. Both prescription and natural health products (NHPs) have been implicated in DILI. There is a dearth of studies on NHPs induced liver injury. CASE PRESENTATION: A previously healthy 37-year-old female presented with subacute hepatitis, in the context of a previous admission to a separate institution, months prior for undiagnosed acute hepatitis. Importantly, she had disclosed taking complex regiments of natural health products (NHPs) for months. Her only other medication was rivaroxaban for her homozygous Factor V Leiden deficiency. She had an extensive work up for causes of acute and unresolving hepatitis. She discontinued several but not all of her NHPs after her initial presentation for acute hepatitis at the first institution and continued taking NHPs until shortly after admission to our institution. The predominant pathological features were that of drug induced liver injury, although an abnormal amount of copper was noted in the core liver biopsies. However, Wilson's disease was ruled out with normal serum ceruloplasmin and 24-urine copper. After 2 months of stopping all the NHPs, our patient improved significantly since discharge, although there is evidence of fibrosis on ultrasound at last available follow up. CONCLUSION: NHPs are a well-established but poorly understood etiology of DILI. The situation is exacerbated by the unregulated and unpredictable nature of many of the potential hepatotoxic effects of these agents, especially in cases of multiple potential toxic agents. This highlights the importance of acquiring a clear history of all medications regardless of prescription status.

Achieved blood pressures in the secondary prevention of small subcortical strokes (SPS3) study: challenges and lessons learned.

BACKGROUND: Lowering blood pressure (BP) after stroke remains a challenge, even in the context of clinical trials. The Secondary Prevention of Small Subcortical Strokes (SPS3) BP protocol, BP management during the study, and achieved BPs are described here. METHODS: Patients with recent symptomatic lacunar stroke were randomized to 1 of 2 levels of systolic BP (SBP) targets: lower: <130mm Hg, or higher: 130-149mm Hg. SBP management over the course of the trial was examined by race/ethnicity and other baseline conditions. RESULTS: Mean SBP decreased for both groups from baseline to the last follow-up, from 142.4 to 126.7mm Hg for the lower SBP target group and from 143.6 to 137.4mm Hg for the higher SBP target group. At baseline, participants in both groups used an average of 1.7±1.2 antihypertensive medications, which increased to a mean of 2.4±1.4 (lower group) and 1.8±1.4 (higher group) by the end-study visit. It took an average of 6 months for patients to reach their SBP target, sustained to the last follow-up. Black participants had the highest proportion of SBP ≥150mm Hg at both study entry (40%) and end-study visit (17%), as compared with whites (9%) and Hispanics (11%). CONCLUSIONS: These results show that it is possible to safely lower BP even to a SBP goal <130mm Hg in a variety of patients and settings, including private and academic centers in multiple countries. This provides further support for protocol-driven care in lowering BP and consequently reducing the burden of stroke.