Thalidomide for the treatment of angiodysplasia-related recurrent gastrointestinal hemorrhage: Is low dose a safe and viable option?

Thalidomide is often used for the management of refractory gastrointestinal angiodysplasia (GIAD). The tolerance, toxic profile, and compliance of thalidomide are dose-dependent. The low-dose thalidomide (50 mg) is safe and a viable option for bleeding related to GIAD.

Refractory Septic Shock due to Underlying Immunocompromised Disease: A Case of Fatal Peripheral T-Cell Lymphoma Not Otherwise Specified in a Young Hispanic Woman.

Peripheral T-cell lymphoma not otherwise specified (PTCL-NOS) is known as an unclassified group of non-Hodgkin lymphomas. PTCL-NOS is a subtype of peripheral T-cell lymphoma that accounts for 3% of all lymphomas in the United States. PTCL-NOS commonly presents as a disseminated disease, B symptoms (fever, night sweats, and weight loss), generalized lymphadenopathy, bone marrow infiltration, and extranodal involvement. Other rare and possible manifestations include peripheral eosinophilia, pruritus, or hemophagocytic syndrome. This type of lymphoma is aggressive in nature and carries a high mortality rate. There is no established standard-of-care treatment protocol for PTCL-NOS, several chemotherapy drug combinations are frequently used as a frontline treatment with an overall 5-year survival rate of 25%. We present a case of a 35-year old Hispanic woman who initially presented with a chief complaint of bilateral lower extremity swelling due to hypoalbuminemia and new-onset hyperkeratotic skin of the palms and soles.

Critical Management of Severe Hypotension Caused by Amlodipine Toxicity Managed With Hyperinsulinemia/Euglycemia Therapy Supplemented With Calcium Gluconate, Intravenous Glucagon and Other Vasopressor Support: Review of Literature.

Calcium channel blocker (CCB ) overdose, whether intentional or accidental, is a common clinical scenario and can be very lethal. Conventional treatments for CCB overdose include intravenous (IV) fluids, calcium salts, dopamine, dobutamine, norepinephrine, phosphodiesterase inhibitors, and glucagon. However, the conventional therapies are unsuccessful in reversing the cardiovascular toxicity of CCB, so they commonly fail to improve the hemodynamic condition of the patient. Blockade of the L-type calcium channels that mediate the antihypertensive effect of CCBs also decreases the release of insulin from pancreatic ß-islet cells and reduces glucose uptake by tissues (insulin resistance). By targeting this insulin-mediated pathway, hyperinsulinemia/euglycemia therapy (HIET) appears to have a distinct role, and its clinical potential is underrecognized in the management of severe CCB toxicity. We present a case of young man with amlodipine toxicity successfully managed with high dose of IV insulin therapy.