Adrenal Crisis Masked as Septic Shock in a Patient With Opioid Use Disorder on Buprenorphine.

Opioid-induced adrenal insufficiency is a known side effect of chronic opioid use, but opioid-induced adrenal insufficiency related to chronic buprenorphine-naloxone therapy is less well-known. We present a case of a patient with opioid use disorder on chronic buprenorphine-naloxone therapy admitted with presumed septic shock and found to be in an adrenal crisis. The patient presented to our hospital with a shock-like presentation, requiring vasopressors, intubation, empiric glucocorticoids, and antibiotics. As her steroids were weaned, she developed bradycardia and blood glucose in the 60s. A low- and high-dose cosyntropin stimulation test confirmed the presence of secondary adrenal insufficiency, presumed to be due to her chronic buprenorphine-naloxone use. She was discharged on maintenance hydrocortisone and continued buprenorphine-naloxone therapy. With the high prevalence of opioid use disorder and the common need for medication for opioid use disorder, it is important that healthcare providers properly identify opioid-induced adrenal insufficiency in order to quickly and correctly diagnose and treat adrenal crises.

A case of dry beriberi from alcohol use disorder and disordered eating.

Background: Thiamin is an essential vitamin that is involved in every organ system in the body. Thiamin deficiency can present as beriberi or Wernicke's encephalopathy. We seek to educate practitioners in developed countries to include beriberi on the differential diagnosis when a patient with alcohol use disorder, poor diet and/or disordered eating presents with ascending paralysis without albuminocytologic dissociation. Case: In this case report, a 20-year-old female with no past medical history presented with three weeks of ascending paralysis. At presentation, she could not grasp objects, walk, or rise from a seated position. She reported consuming excessive alcohol and an otherwise limited diet due to picky eating. The patient was ultimately diagnosed with acute inflammatory demyelinating polyneuropathy secondary to dry beriberi from severe protein-calorie malnutrition and alcohol use disorder. She received an aggressive thiamin replacement regimen as well as physical and occupational therapy. She was discharged to home 24 days after her initial presentation. Discussion: This patient case offers a unique presentation of ascending paralysis without albuminocytologic dissociation due to severe dry beriberi from a diet of unenriched carbohydrates and excessive alcohol in an otherwise young, healthy adult in the United States. Our goal is that in reviewing the unusual details of this case, providers will be better equipped for the timely diagnosis and treatment of similar cases in the future.

Rapid Resolution of Acute Fulminant Myocarditis after IVIG and Steroid Treatment.

We report a case of a 59-year-old woman who presented with worsening dyspnea which rapidly progressed to severe heart failure. Coronary arteries showed no obstruction. Supportive measures stabilized the patient's hemodynamics. Initially intravenous solumedrol was given, but when the patient's condition continued to deteriorate, intravenous immunoglobulin (IVIG) was added to the treatment regimen and her condition improved. Studies show no benefit to using immunosuppressive agents in viral myocarditis, but benefits have been demonstrated in other etiologies. Patients presenting with acute fulminant myocarditis with unknown etiology that continue to deteriorate with aggressive heart failure treatment may benefit from steroids and IVIG.

Vulnerabilities of ventral mesencephalic neurons projecting to the nucleus accumbens following infusions of 6-hydroxydopamine into the medial forebrain bundle in the rat.

The terminal arbors of dopaminergic projections in the nucleus accumbens (Acb) core degenerate more rapidly, completely and permanently in a variety of neurotoxic circumstances than do those in the medial shell. It is unknown if this always reflects purely losses of the distal parts of axons from the core (as proposed in methamphetamine intoxication), or whether, in some circumstances, the disproportionate loss of core axons may also stem from an intrinsic vulnerability to degeneration of core-projecting neuronal perikarya. Experiments described here addressed this issue in the following manner. Three days after Fluoro-Gold (FG), a retrogradely transported tracer, had been iontophoresed selectively into the core or medial shell of male Sprague-Dawley rats, each received an infusion of saline vehicle containing or lacking 6-hydroxydopamine (6-OHDA) in the ipsilateral medial forebrain bundle (MFB). Twenty-one days later the brains were processed to exhibit ventral mesencephalic neurons containing FG. Application of an unbiased sampling method revealed substantially greater losses of FG labeled neurons relative to controls in rats that had received 6-OHDA lesions and deposition of FG in the Acb core as compared to the medial shell. Of the few core-projecting neurons that remained in the ventral mesencephalon after these lesions, 54% did not co-localize tyrosine hydroxylase immunoreactivity (TH-ir) and, thus, were not expected to degenerate. The capacity to selectively remove core-projecting dopaminergic neurons may be useful in the determination of molecular correlates of vulnerability and resistance to neurotoxicity and to possibly test the role of the core in reinforcement paradigms.