About 20% of pregnant women experience clinical depression. Inadequate treatment of depression has been associated with adverse outcomes in the mother as well as the newborn. Clinicians are often uncertain about pharmacological interventions to treat depressed pregnant women due to concerns regarding fetal exposure to medications. Moreover newer antidepressants with different pharmacological profiles and little data on fetal risk continue to be introduced at a brisk pace. Accumulating data from pharmaceutical registries, cohort studies, toxicology centers, some prospective studies, and case series have permitted certain guidelines for antidepressant use during pregnancy. We review the safety profiles of commonly used antidepressants, discuss clinical decision making based on risk-benefit considerations and make recommendations for pharmacological treatment of depressed women during pregnancy.

Fibromyalgia is characterized by widespread pain, persistent fatigue, nonrestorative sleep, and generalized morning stiffness. The diagnosis is based on patients' reports of pain and fatigue, clinical findings of multiple tender points, and exclusion of a range of connective tissue and other medical disorders. Treatment of fibromyalgia is multidisciplinary with an emphasis on active patient participation, medications, cognitive behavioral therapy, and physical modalities. No single medication has been found to effectively control all the symptoms, and a rational combination of different medications is often necessary. Currently available medication classes include the selective serotonin uptake inhibitors, the serotonin and norepinephrine reuptake inhibitors, tricyclic antidepressants, analgesics, hypnotic agents, and anticonvulsants. Treatment modalities should be individualized for patients based on target symptoms and impairment in functioning. As is the case with several chronic disorders, the treatment is often prolonged and improvement may occur slowly. Patience and positive attitude on part of the physician and active involvement of patients and their families in treatment are likely to enhance improvement.

Alterations in the serotonin transporter (5-HTT) have been implicated in a variety of psychiatric disorders including cocaine dependence. A polymorphism in the promoter region of the serotonin transporter gene (5-HTTLPR) appears to influence the expression of 5-HTT in human cell lines. We investigated whether 5-HTTLPR variants were related to differences in measures of platelet 5-HTT sites in cocaine-dependent patients and healthy volunteers (controls). Polymerase chain reaction-based genotyping of a 44 base pair insertion/deletion polymorphism in 5-HTTLPR was performed in 138 cocaine-dependent African-American subjects and 60 African-American controls. This yielded a short (S) and a long (L) allele. Platelet 5-HTT sites were measured using the tritiated paroxetine binding assay. Relationships of 5-HTTLPR genotypes with Bmax (density of serotonin transporter) and Kd (affinity constant) were examined. Bmax values were significantly lower in cocaine-dependent patients (640 +/- 233) than controls (906 +/- 225) (P < 0.001); however, 5-HTTLPR genotype distributions or allele frequencies did not differ between the two groups. There were no significant differences in Bmax between the three genotypes among cocaine-dependent patients (LL = 690 +/- 246, LS = 620 +/- 235, SS = 587 +/- 183; P = 0.14) or controls (LL = 909 +/- 233, LS = 938 +/- 279, SS = 866 +/- 143; P = 0.65). All three genotypes in cocaine-dependent patients showed comparable reductions in Bmax from the corresponding genotypes in controls. Demographic variables, severity of substance use or depression were unrelated to Bmax or 5-HTTLPR genotypes. Although platelet 5-HTT densities are reduced in patients with cocaine dependence compared with healthy volunteers, these genotypic variations in the serotonin transporter do not seem to influence levels of platelet 5-HTT in cocaine-dependent patients or healthy volunteers.

No abstract

No abstract