Directed forgetting of emotionally toned items and mental health: a meta-analytic review.

Item- and list-method directed forgetting paradigms have been used to study forgetting of emotionally toned items in clinical and control group populations for several decades. Meta-analysis of item-method studies found that clinical populations retained more remember- than forget-cued items of each valence. These effects were comparable to that shown by control populations for positive and negative items, but less than that shown by controls on neutral items. Encoding deficits may underlie clinical populations' item-method directed forgetting since those populations retained fewer remember-cued items of each valence compared to control populations. Moderator analysis indicated larger effect size variability for some clinical populations (e.g., anxiety disorders) than other populations (e.g., PTSD, schizophrenia). Meta-analysis of list-method directed forgetting among clinical populations revealed only List 1 forgetting or costs for neutral items; i.e., better memory for to-be-remembered than forgotten List 1 neutral items, but no List 2 enhancements or benefits; i.e., better memory for List 2 items among those told to forget than remember List 1 items, for any item valence. Control populations showed costs and benefits for all item valences. Results from both paradigms are discussed in terms of clinical-control population differences in executive processes. Limitations of the meta-analyses and suggestions for future research are presented.

Recognition of faces of ingroup and outgroup children and adults.

People are often more accurate in recognizing faces of ingroup members than in recognizing faces of outgroup members. Although own-group biases in face recognition are well established among adults, less attention has been given to such biases among children. This is surprising considering how often children give testimony in criminal and civil cases. In the current two studies, Euro-Canadian children attending public school and young adults enrolled in university-level classes were asked whether previously presented photographs of Euro-American and African American adults (Study 1) or photographs of Native Canadian, Euro-Canadian, and African American children (Study 2) were new or old. In both studies, own-group biases were found on measures of discrimination accuracy and response bias as well as on estimates of reaction time, confidence, and confidence-accuracy relations. Results of both studies were consistent with predictions derived from multidimensional face space theory of face recognition. Implications of the current studies for the validity of children's eyewitness testimony are also discussed.

What children remember about ingroup and outgroup peers: effects of stereotypes on children's processing of information about group members.

Three studies are reported about children's memory for stereotypic behaviors attributed to ingroup and outgroup members. According to research and theory in social cognition, cues present in the situation make cultural representations about group members accessible, and once primed, influence all phases of the information processing sequence. In Study 1, Euro Canadian and Native Canadian children (N=98) recalled stereotypic behaviors attributed to ingroup and outgroup members. In Study 2 (N=87), the influence of individual difference variables was explored. In Study 3 (N=32), the memory of Native Canadian children living on a First Nation reserve for behaviors attributed to ingroup and outgroup members was studied. Biases in recall were found in Studies 1 and 2, but in Study 3, outgroup favoritism, typically found among low status group members, was reversed among children attending a heritage school. Among the individual difference measures examined, age and level of cognitive development predicted what was remembered about group members. Older Euro Canadian children recalled more negative behaviors about outgroup members than did younger children, and more cognitively mature children recognized more information about ingroup than outgroup members. Results were discussed in terms of cognitive and situational factors influencing children's processing of group-relevant information and the challenges children in low status groups face in maintaining a sense of cultural identity.

Normal endothelial function despite insulin resistance in healthy women with the polycystic ovary syndrome.

Women with the polycystic ovarian syndrome (PCOS) carry a number of cardiovascular risk factors, including insulin resistance, lipid abnormalities, and an altered pattern of sex steroid exposure. Noninvasive measurements of endothelial function, which can demonstrate abnormalities well in advance of clinically apparent disease, have not been previously reported in this patient group. We undertook a cross-sectional evaluation of endothelium-dependent and -independent vascular function using brachial artery ultrasound. We studied healthy women with clinical and laboratory evidence of PCOS (n = 18) and age-matched controls (n = 19), not taking any antihypertensive, cholesterol-lowering, or hormonal therapies. Laboratory parameters of insulin resistance, glycemia, cholesterol status, and hormone levels were also measured. Despite marked differences in glucose/insulin ratio [6.1 +/- 1.1 mmol/pmol (PCOS) vs. 9.9 +/- 0.6 (controls)] and free androgen index [11.9 +/- 2.3 (PCOS) vs. 3.7 +/- 0.6 (controls); normal, <5], we did not find evidence of impaired endothelial function in our patients with PCOS. Both endothelium-dependent (8.7 +/- 3.1%) and endothelium-independent (23.2 +/- 3.4%) vascular responses were normal, and practically identical to the responses seen in the control group (endothelium-dependent, 9.0 +/- 0.7; endothelium-independent, 23.0 +/- 1.2%). The PCOS women were more obese, but baseline brachial arterial diameters were not different between groups. There was no correlation between degree of insulin resistance or hyperandrogenism and the brachial response. This group of healthy obese young women with insulin resistance and hyperandrogenism due to PCOS had normal endothelium-dependent and -independent vascular responses compared to age-matched controls. The factors resulting in preservation of these response are unclear and warrant further investigation.

Hormonal side effects in women: typical versus atypical antipsychotic treatment.

Neuroleptic-induced hyperprolactinemia can cause menstrual disorders, impaired fertility, galactorrhea, and sexual dysfunction, as well as hypoestrogenism secondary to disruption of the hypothalamic-pituitary-ovarian axis. The development of the prolactin-sparing atypical antipsychotic drugs offers prevention and resolution of these adverse reactions. Thus far, this property of the new medications has received insufficient clinical attention. The authors use case vignettes to discuss assessment and management of clinical situations that arise as a result of antipsychotic-induced endocrine changes.

Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity.

OBJECTIVE: To assess the role of insulin resistance, independent of obesity, in determining cardiovascular risk among women with the polycystic ovarian syndrome (PCOS). DESIGN: Cross-sectional study examining the relationships between hyperinsulinemia, composite cardiovascular risk scores, and prevalence of individual risk factors among lean and obese women with PCOS and healthy controls. SETTING: University-based tertiary care outpatient endocrinology clinic. PATIENT(S): 57 women with clinically defined PCOS and 45 unselected healthy age-matched controls. INTERVENTION(S): Clinical and anthropomorphic measurements and laboratory determinations of insulin and lipid levels. MAIN OUTCOME MEASURE(S): Fasting serum insulin and a cardiovascular risk score. RESULTS: Hyperinsulinemic women with PCOS carried more cardiovascular risk than their normoinsulinemic counterparts, who in turn had more risk than the control women (P=.004 by analysis of covariance). In addition to the lipid changes expected with insulin resistance (high triglyceride and low HDL cholesterol levels), there was an excess of LDL cholesterol among the women with PCOS (P=.006 by analysis of covariance). Across the range of body mass index, women with PCOS had greater insulin resistance than controls, suggesting that PCOS itself and body mass index both contribute to the observed insulin resistance. CONCLUSIONS: Our data support the hypothesis that insulin resistance in PCOS is a determinant of overall cardiovascular risk independent of obesity. The mechanism of this relationship remains uncertain and is the subject of ongoing research.

Maintenance of serum calcium by parathyroid hormone-related peptide during lactation in a hypoparathyroid patient.

We describe the changes in calcium homeostasis seen in a hypoparathyroid woman during the third trimester and with lactation following her second pregnancy. During lactation her need for supplemental calcium and calcitriol abated, and in fact she was transiently hypercalcemic and hypophosphatemic. This change was associated with a rise of serum parathyroid hormone-related peptide (PTHrP) released systemically during lactation. This is the first documentation of the time course of serum PTHrP levels from the late third trimester throughout lactation in a hypoparathyroid woman. In this context PTHrP may have sufficient biological activity to compensate for parathyroid hormone deficiency.

The natural history of the pituitary incidentaloma.

BACKGROUND: The wide availability of computed tomography and magnetic resonance imaging has resulted in the discovery of unsuspected endocrinologically silent pituitary masses (incidentalomas). Because the natural history of this entity is not known, the approach to the pituitary incidentaloma has not been established. OBJECTIVE: To determine the natural history of untreated pituitary incidentaloma, recognizing that this includes lesions of various causes. METHODS: Thirty-one adults with incidentalomas were prospectively followed up conservatively for a mean of 6.4 years (range, 3 to 11 years). Clinical and biochemical assessment, computed tomography or magnetic resonance imaging of the pituitary, and visual field testing by Goldmann perimetry at baseline, 6 months, and yearly thereafter were the outcomes assessed. RESULTS: Only patients with pituitary incidentalomas greater than 10 mm in greatest diameter developed tumor enlargement or complications. Three patients developed asymptomatic tumor enlargement. In four patients, masses decreased in size. Only two patients developed complications. One required subsequent surgery. The only permanent impairment was panhypopituitarism following surgery in this patient. CONCLUSIONS: Patients with pituitary incidentalomas of unknown causes usually follow a benign course for at least 6 years after discovery. Neurosurgical intervention is not initially required in the management of is not initially required in the management of pituitary incidentalomas, particularly those less than 10 mm, as long as clinical observation can be continued.

Bedside assessment of skin-fold thickness. A useful measurement for distinguishing Cushing's disease from other causes of hirsutism and oligomenorrhea.

BACKGROUND: The known catabolic effects of glucocorticoid excess on protein metabolism prompted us to devise a method to assess this measure in reproductive-aged females with Cushing's disease. Since collagen protein is a major component of skin, decreased abundance of this protein should cause a reduction in skin-fold thickness. To determine whether skin-fold thickness is useful as an added tool in the diagnosis of Cushing's disease, we compared this value in female patients with Cushing's disease with those who presented with a similar set of symptoms. METHODS: This open prospective study was conducted in an endocrinology clinic at a tertiary care center. The study population consisted of 88 females in the reproductive age group who presented to the clinic with hirsutism, oligomenorrhea, and/or obesity. Measurement of skin-fold thickness, body mass index, Ferriman-Gallwey index, and serum testosterone were performed in all patients. RESULTS: Skin-fold thickness in the patients with Cushing's disease was 1.5 +/- 0.2 mm (range, 1.0 to 1.8 mm). This value was significantly (P < .01) lower than that in controls or subjects with other disorders that have a similar set of presenting symptoms. CONCLUSIONS: Bedside assessment of skin-fold thickness is an easy, low-cost, and noninvasive test for distinguishing Cushing's disease from disorders with similar presenting symptoms in females of reproductive age. Assessment of skin-fold thickness should be used as an adjunct to current physical and biochemical study of patients with symptoms suggestive of Cushing's disease.

High-dose, short-term glucocorticoids for the treatment of infertility resulting from premature ovarian failure.

OBJECTIVE: To evaluate prospectively the effects of high-dose, short-term treatment with a glucocorticoid in an attempt to normalize ovarian failure and induce pregnancy in women presenting with infertility. DESIGN: Uncontrolled, nonrandomized prospective study. SETTING: Two university-based reproductive endocrinology clinics. PATIENTS: Eleven consecutive women with premature ovarian failure (POF) who were desirous of pregnancy. INTERVENTIONS: Prednisone 25 mg four times per day for 2 weeks. MAIN OUTCOME MEASURES: Two women demonstrated normalization of their serum gonadotropins, an increase of serum E2, and ultrasonographic visualization of follicular growth, with both conceiving. The other nine demonstrated no biochemical or clinical response. CONCLUSIONS: Premature ovarian failure may not be an irreversible process and may either spontaneously resolve or may respond to therapeutic modalities such as high-dose glucocorticoids in selected patients. In this uncontrolled study, the results were best with women with concomitant autoimmune thyroid disease and POF of < 2 years' duration.

The safety of physiological estrogen plus progestin replacement therapy and with oral contraceptive therapy in women with pathological hyperprolactinemia.

In summary, E- replacement therapy may be administered to women with E deficiency, despite the presence of pathological hyperprolactinemia, with apparently no adverse effect on the underlying disease process. The concern of induction of rapid growth of an underlying pituitary adenoma was not substantiated.

PIP: 38 women aged between 23 and 42 years had secondary amenorrhea and clinical hypoesterogenism as assessed by the failure to have a withdrawal bleed in response to a progestin. All women were initially treated with up to 7.5 mg bromocriptine but it was discontinued because of failure to lower serum prolactin (PRL) or intolerance. Each woman had a basal computerized tomography (CT) scan before estrogen (E) replacement therapy, which was repeated after 6 months, and then yearly. The clinical course was monitored at 3-month intervals for the first year and the yearly. The patients were classified by CT scan as having either idiopathic hyperprolactinemia (19 patients), microadenoma (18 patients), or macroadenoma (1 patient). All patients have been followed with continuous exogenous E therapy for 2 to 6 years. The serum PRL was measured as a single random value by a double antibody homologous radioimmunoassay. 29 received physiological replacement with conjugated E (.625 mg, Premarin) from days 1 to 25 of each month, and added medroxyprogesterone acetate (10 mg, Provera) from days 16 to 25 of each month for 4.0 +or- 1.2 years. There was a significant decrease of serum PRL, and monthly withdrawal bleeding occurred in all women with alleviation of E-deficiency symptoms. 9 patients were treated with OCs for 2.0 +or- .8 years. There was a downward trend in the serum PRL without statistical significance. With abnormal CT scans, 6 patients with microadenomas had a decrease in size, whereas the remainder were unchanged. The patient with the macroadenoma (patient 29) had an onset of headaches after 4 months of therapy, but there was no change in the size of the tumor. The patients with normal CT scans did not show any change. The microadenomas in 2 of 3 women decreased in size. In summary, E-replacement therapy may be given to women with E deficiency, despite the presence of pathological hyperprolactinemia, as the induction of rapid growth of an underlying pituitary adenoma was not confirmed.

Recurrent hypoglycemia secondary to drug-dispensing error.

We present three patients who developed hypoglycemia due to inadvertent dispensing of sulfonylurea drugs. Each patient had a similar clinical course characterized by hypoglycemia that remitted during hospitalization and recurred after discharge. The cause of the hypoglycemia was determined only after close inspection of the patients' medications, not the label on the container. Our experience suggests that hypoglycemia due to drug-dispensing error may be more common than is generally recognized.

Medical therapy for the syndrome of familial virilization, insulin resistance, and acanthosis nigricans.

UNLABELLED: In the syndrome of familial virilization, insulin resistance, and acanthosis nigricans, the interrelationships are not understood. Twin sisters were studied, along with a lesser affected sister and mother. They manifested amenorrhea, hirsutism, masculinization, hypertension, hyperinsulinemia, hypertriglyceridemia, and hyperprolactinemia. Medical therapy with a gonadotropin-releasing hormone agonist plus an antiandrogen resulted in reversal of the hirsutism, yet with preservation of potential fertility. In response to luteinizing hormone (LH) and follicle-stimulating hormone suppression, there was normalization of the serum androgens, but not of the hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, hypertension, or acanthosis nigricans. CONCLUSIONS: (1) This syndrome may be familial. (2) Medical therapy for the virilization is successful. (3) The hyperandrogenemia is primarily LH dependent and not primarily insulin dependent, although insulin may have an amplification effect. (4) Hyperinsulinemia, hypertriglyceridemia, hyperprolactinemia, and the hypertension are not androgen dependent.

Asymptomatic hyperprolactinemia resulting from macroprolactinemia.

Five patients are presented who had moderate hyperprolactinemia as measured by RIA. The patients did not have any symptoms or signs that result from hyperprolactinemia, nor evidence of any underlying cause of hyperprolactinemia. Because of the lack of clinical features, laboratory search for macroprolactinemia was undertaken. In these patients no further investigation or therapy is indicated.

Hyperprolactinemia in hepatic encephalopathy may result from impaired central dopaminergic neurotransmission.

Ten patients with liver disease and hepatic encephalopathy (HE) and eight normal controls were studied. Five of the 10 HE patients had hyperprolactinemia. The administration of L-dopa produced a decrease of serum prolactin in all. Prior administration of Carbidopa, a peripheral decarboxylase inhibitor, did not change the prolactin suppression by L-dopa in the normal controls or in the patients with normal baseline prolactin levels. In the hyperprolactinemic group, Carbidopa significantly inhibited the response to L-dopa. Impaired central neurotransmission, at least involving the hypothalamic-pituitary dopaminergic system, may underlie the hyperprolactinemia in HE.

Drug treatment of infertility.

Diagnosis and treatment of infertility, once a purely empirical process, can now be based on rational exclusion of alternatives. The author reviews the drug treatment of infertility, emphasizing ovulation induction. He also discusses the endocrine treatment of men, drug treatment of endometriosis, and antibiotic treatment of infections. The author recommends referral to a specialist when more invasive drugs, such as gonadotrophins or gonadotrophin-releasing hormone or analogue, are indicated, if the couple continues to be infertile, or when the physician suspects endometriosis.

Induction of ovulation with luprolide acetate and human menopausal gonadotropin.

Four women with unexplained infertility and two anovulatory oligomenorrheic women who experienced repeated premature luteinization when treated with human menopausal gonadotropin (hMG) or gonadotropin-releasing hormone (GnRH) were given the gonadotropin-releasing hormone agonist (GnRHa), luprolide acetate, in order to effect medical hypophysectomy. This was followed by hMG for induction of ovulation. Four of the six patients had hMG-only cycles, which were compared with the luprolide acetate/hMG cycles. The luprolide acetate/hMG cycles resulted in normal folliculogenesis with presumptive ovulation. In luprolide/hMG cycles, significantly more hMG was needed for induction of ovulation than in hMG-only cycles. Premature luteinization was abolished with luprolide acetate treatment.