Comorbidity of

anxiety with other psychiatric disorders The comorbidity of anxiety disorders with each other and with other psychiatric disorders,11 particularly mood12, has been observed and accepted for many decades. It is known that patients with major depression invariably show either syndromal comorbidity of one or Inhibitors,research,lifescience,medical another anxiety disorder or clinically significant severity of anxiety symptoms.13 Also, the efficacy of many major psychotropic drugs in the treatment of depression and a broad spectrum of anxiety disorders, eg, GAD, PD, social anxiety disorder, and posttraumatic stress disorder (PTSD), is well established. However, wherever possible, mood and anxiety have been separated and delineated into different disorders. Evidence for a common genetic PI 103 etiology for bipolar disorder and PD came from a family study14 in which an unusually high prevalence of PD in 57 families with high rates of bipolar disorder was reported. Families at high risk Inhibitors,research,lifescience,medical of PD showed linkage to markers on the long arm of chromosome 18 (18q), whereas families of probands without

PD did not. This led the Inhibitors,research,lifescience,medical authors to conclude that there may be a genetic subset of patients with bipolar disorder who had comorbid PD. These results were Inhibitors,research,lifescience,medical very recently extended and confirmed by the same group in an independent group of bipolar disorder families.15 In the same recent

issue of the American Journal of Psychiatry, Rotondo and colleagues16 conducted a casecontrol association study of the genetic polymorphisms of three monoamine neurotransmitter system candidate genes, catechol-O-methyltransferase (COMT), serotonin (5-hydroxytryptamine or 5-HT) transporter (5-HTT), and tryptophan hydroxylase (TPH), in patients with bipolar disorder with and without lifetime Inhibitors,research,lifescience,medical PD. Remarkably, the patients with bipolar disorder without PD showed significantly higher frequencies of the COMT Met158 and the short 5-HTTLPR alleles and genotypes. These results suggest Ribonucleotide reductase that bipolar disorder with and without comorbid PD represent distinct genetic forms, although no single genetic model could be applied to the subset of families with PD. The boundaries between the bipolar/panic phenotype remain obscure, and the question arises as to whether the bipolar/panic phenotype includes individuals with panic attacks below the threshold for a diagnosis of PD.15 Thus, it is still not clear whether panic vulnerability in families with a high prevalence of bipolar disorder is the result of general nongcnctic activation of anxiety mechanisms, a specific, partially penetrant gene, or a combination of genes.