Is axillary botulinum toxin efficient in controlling secondary Raynaud's phenomenon? A case report.

Raynaud's phenomenon when secondary to underlying systemic disease such as systemic sclerosis occurs early in the disease course and progression can bring significant morbidity such as pain, digital ulceration, and necrosis. Standard medical therapies are aimed at promoting distal arterial vasodilation but are often inadequate in managing Raynaud's phenomenon. Options for refractory cases include surgical and chemical sympathectomy with Botulinum neurotoxin type A (BoNT/A) hand injections but the latter can be associated with transient hand weakness. We describe the case of a 35-year-old woman with undifferentiated connective tissue disease, Raynaud's phenomenon, and concomitant primary focal axillary hyperhidrosis for which she received axillary BoNT/A therapy every 6 months who noted significant improvement in her Raynaud's phenomenon and hand arthralgias for 5 months following the axillary injections. This effect remained durable after 24 months of therapy. This improvement in Raynaud's phenomenon after axillary BoNT/A has not been previously described.

Weakness Due to Anemia? Go Fish! Melena as a Red Herring in the Diagnosis of Statin-Induced Myopathy.

Statins are a ubiquitous medication class in the primary care setting where they provide effective primary and secondary prevention of coronary artery disease by lowering cholesterol. While statins are mostly safe, muscle-related adverse events are well described. Very rarely patients can actually develop elevated creatine kinase (CK) consistent with myonecrosis. We present a case of progressive anti-hydroxymethylglutaryl coenzyme A reductase (anti-HMGCR) inflammatory myopathy, which was misdiagnosed for many months. Our patient was a 67-year-old gentleman sent to the ER by the Internal Medicine Clinic for profound weakness and melena. He had recently undergone esophagogastroduodenoscopy (EGD) for evaluation of progressive dysphagia and was found to be significantly anemic. Repeat EGD demonstrated a bleeding ulcer, and his weakness was attributed to anemia; however, careful examination demonstrated objective muscle weakness which could not be attributed to anemia alone. Subsequent work-up demonstrated myositis due to HMGCR antibody. Statin cessation and treatment with steroids and intravenous immunoglobulin (IVIG) led to a nearly full recovery in strength and resolution of dysphagia over the next several months.