Background Buprenorphine–naloxone has a very high affinity for the mu-receptor and can cause precipitated opioid withdrawal, typically more severe than withdrawal that occurs naturally, when administered while a full mu-opioid receptor agonist remains in a person’s system. To avoid precipitated withdrawal, one needs to be in mild to moderate opioid withdrawal at the time of buprenorphine-naloxone induction. Recently, there have been reported cases of precipitated withdrawal occurring in patients taking fentanyl knowingly or unknowingly, despite them being in adequate opioid withdrawal at the time of induction. When this occurs, the current recommendation is to provide 2 mg of buprenorphine–naloxone every 1–2 hours. Objectives Describe a case of successful management of buprenorphine-precipitated withdrawal with escalation of the dose of buprenorphine and highlight implications for future management. Methods We present a case of a patient with a history of opioid use disorder who was in moderate opioid withdrawal at the time of buprenorphine–naloxone induction and experienced precipitated withdrawal after buprenorphine–naloxone administration. Results High-dose buprenorphine–naloxone was given to the patient and precipitated withdrawal subsided after receiving a total of 20 mg. On the next day, the patient had no symptoms of opioid withdrawal and is currently maintained on 16 mg/day. Conclusion With the rising prevalence of fentanyl-laced drugs, increased instances of precipitated withdrawal are likely to be encountered. In cases of precipitated withdrawal, giving a high dose of buprenorphine–naloxone rapidly is safe and will allow rapid reversal of withdrawal symptoms.

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Opioids are strong analgesics widely employed to treat various types of pain. In 2018, an estimated 168 million opioid prescriptions were dispensed in the United States. Opioids carry a number of side effects and up to 80% of patients treated with opioids experience a minimum of one adverse event. Although uncommon, hallucinosis is an effect experienced with opioids, which may be under-reported and attributed to underlying psychiatric disease rather than to the side effects of the opioid itself. Most of the opioidinduced hallucinoses reported are auditory and visual, and rarely tactile. Although opioid medication prescribing is decreasing in the United States, considering the continued opioid epidemic and deaths related to overdose, it is important for physicians to be aware of this potential adverse effect of opioids in isolation. We present a case of oral hydromorphone causing visual and tactile hallucinations. Discontinuing hydromorphone led to immediate cessation of the patient's psychotic signs and symptoms. To our knowledge, this is the first description of the use of hydromorphone resulting in tactile hallucinations.

Ependymin (EPN) is a brain glycoprotein that functions as a neurotrophic factor in optic nerve regeneration and long-term memory consolidation in goldfish. To date, true epn genes have been characterized in one order of teleost fish, Cypriniformes. In the study presented here, polymerase chain reactions were used to analyze the complete epn genes, gd (1480 bp), and sh (2071 bp), from Cypriniformes giant danio and shiner, respectively. Southern hybridizations demonstrated the existence of one copy of each gene per corresponding haploid genome. Each gene was found to contain six exons and five introns. Gene gd encodes a predicted 218-amino acid (aa) protein GD 93 percent conserved to goldfish EPN, while sh encodes a predicted 214-aa protein SH 91 percent homologous to goldfish. Evidence is presented classifying proteins previously termed "EPNs" into two major categories: true EPNs and non-EPN cerebrospinal fluid glycoproteins. Proteins GD and SH contain all the hallmark, features of true EPNs.