Cannabidiol may be an antagonist of GPR55, a G protein-coupled receptor and putative cannabinoid receptor that is expressed in the caudate nucleus and putamen in the brain. It also may act as an inverse agonist of GPR3, GPR6, and GPR12. CBD has been shown to act as a serotonin 5-HT1A receptor partial agonist. At higher concentrations, CBD acts as an inverse agonist of 5-HT1A receptors. It is an allosteric modulator of the μ- and δ-opioid receptors as well. The pharmacological effects of CBD may involve PPARγ agonism, inhibition of voltage-gated cation channels, and intracellular calcium release. Pharmacokinetics
The oral bioavailability of cannabidiol is approximately 6% in humans, while its bioavailability via inhalation is 11 to 45% (mean 31%). The elimination half-life of CBD is 18–32 hours. Cannabidiol is metabolized in the liver as well as in the intestines by the cytochrome P450 enzymes CYP2B6, CYP2C19, CYP2D6, CYP2J2, and CYP3A4, and by the isoenzymes UGT1A7, UGT1A9, and UGT2B7, forming a variety of metabolites such as 7-hydroxycannabidiol as well as the 6α- and 6β-hydroxy isomers and derivatives hydroxylated on the alkyl side chain, followed by glucuronidation. CYP3A4 facilitates decarbonylation of CBD to liberate carbon monoxide, a bioactive gasotransmitter and pharmaceutical candidate. CBD may have a wide margin in dosing. Pharmaceutical preparations
Nabiximols (brand name Sativex), an oromucosal spray made of a complex botanical mixture containing cannabidiol (CBD), delta-9-tetrahydrocannabinol (THC), and additional cannabinoid and non-cannabinoid constituents from cannabis sativa plants, was approved by Health Canada in 2005, to treat central neuropathic pain in multiple sclerosis, and in 2007, for cancer-related pain.
Clinical observation is considered when the mass is diagnosed pre-operatively. Surgery is often required to confirm the diagnosis and exclude a mimic of a malignant mass. Surgical approach should attempt to divide the mass and the gonad at the connecting plane for removal of the splenic tissue. Orchiectomy is generally not indicated. Causality between splenogonadal fusion and future malignant transformation has not been established, but literature has highlighted infrequent cases of testicular neoplasms and splenogonadal fusion. These cases were found in patients who also had a history of cryptorchidism, which is a known risk factor for testicular cancer. See also
Splenogonadal fusion-limb defects-micrognathia syndrome


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