In the case of the DSM, the first and second versions listed hypochondriasis as a neurosis, whereas the third and fourth versions listed hypochondriasis as a somatoform disorder. The current version of the DSM (DSM-5) lists somatic symptom disorder (SSD) under the heading of "somatic symptom and related disorders", and illness anxiety disorder (IAD) under both this heading and as an anxiety disorder. The ICD-10, like the third and fourth versions of the DSM, lists hypochondriasis as a somatoform disorder. The ICD-11, however, lists hypochondriasis under the heading of "obsessive-compulsive or related disorders". There are also numerous influential scientific publications that have argued for other classifications of hypochondriasis. Notably, since the early 1990s, it has become increasingly common to regard hypochondriasis as an anxiety disorder, and to refer to the condition as "health anxiety" or "severe health anxiety". Treatment
Approximately 20 randomized controlled trials and numerous observational studies indicate that cognitive behavioral therapy (CBT) is an effective treatment for hypochondriasis. Typically, about two-thirds of patients respond to treatment, and about 50% of patients achieve remission, i.e., no longer have hypochondriasis after treatment. CBT for hypochondriasis and health anxiety may be offered in various formats, including as face-to-face individual or group therapy, via telephone, or as guided self-help with information conveyed via a self-help book or online treatment platform. Effects are typically sustained over time.There is also evidence that antidepressant medications such as selective serotonin reuptake inhibitors can reduce symptoms. In some cases, hypochondriasis responds well to antipsychotics, particularly the newer atypical antipsychotic medications.
The compound looked promising and passed initial screening in which rodents were given opioids along with charcoal meals to track GI transit, and were tested for analgesia. In a 1982 paper by Russell et al., it was first reported that the GI effects of the opioids could be prevented without affecting centrally mediated analgesia in this model. Subsequent preclinical studies also demonstrated this separation of central and peripherally mediated opioid effects for other smooth muscles of the GI tract and the cough reflex. Interest also developed in the potential for MNTX to act at the chemoreceptor trigger zone and block the emetic effect of opioids. This blockade of opioid-induced emesis was demonstrated in a canine model. Goldberg died before he could see the core of this idea come into clinical practice. Research on methylnaltrexone continued in the Department of Anesthesiology and Critical Care at the University of Chicago through the 1990s. More recent investigations, however, discovered opioid receptors on peripheral sensory neurons.In December 2005, Wyeth and Progenics entered into an exclusive, worldwide agreement for the joint development and commercialization of methylnaltrexone for the treatment of opioid-induced side effects, including constipation and post-operative ileus (POI), a prolonged dysfunction of the gastrointestinal tract following surgery. Under the terms of the agreement, the companies are collaborating on worldwide development. Wyeth received worldwide rights to commercialize methylnaltrexone, and Progenics retained an option to co-promote the product in the United States. Wyeth will pay Progenics royalties on worldwide sales and co-promotion fees within the United States.