[Classification of secretory breast disease].
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Sodium lactate infusion provokes more physiological and psychological symptoms of panic in patients with panic attacks than in normal controls. The relationship between response to sodium lactate infusion and presenting clinical characteristics was examined in 50 patients with panic disorder or agoraphobia with panic attacks. Lactate-induced panic was significantly related only to a patient-reported family history of panic. Rating of physical symptoms during lactate infusion, but not overall response to lactate, was significantly correlated with Symptom Checklist-90 somatization scores. In general, lactate response does not identify clinically distinct subpopulations of patients with panic disorder.
A sodium lactate test was performed during the premenstrual phase in 35 women suffering from prospectively confirmed premenstrual syndrome (PMS) and in 16 controls in order to assess whether these patients were sensitive to this test and whether this sensitivity was accounted for primarily by the presence of concomitant panic disorder. Patients with PMS also underwent the Structured Clinical Interview for the DSM-III-R (SCID) to determine the presence of co-morbid anxiety and/or mood disorders. Only 31% of the PMS patients were free from a depressive/anxiety disorder, while nine patients met criteria for panic disorder, and the remaining 15 subjects were diagnosed as having anxiety and/or mood disorders. Lactate infusion induced panic attacks in 22 subjects (62.9%) and two controls (12.5%). Panickers were equally distributed among PMS patients with or without a concurrent anxiety/mood disorder. Although cardiovascular responses to lactate were similar among PMS patients regardless of the presence of concomitant anxiety/mood disorders, both plasma cortisol levels and panic and mood scores were higher during the test in those patients with concomitant panic disorder. These results suggest that PMS patients display an increased sensitivity to lactate, which is not primarily accounted for by the presence of co-morbid panic disorder.
Members of the workgroup on female reproductive disorders discussed methods to evaluate five principal functions: menstrual dysfunction, infertility, pregnancy loss, lactation disorders, and pregnancy complications. To test each function, a nested strategy was considered, based on progressive levels of effort available to conduct field investigations. This strategy was analogous to the three-tier classification of biomarkers used by other workshops. The lowest level of effort, corresponding to Tier 1, consists only of questionnaires, diaries, and reviews of maternal and infant medical records. The medium level of effort (Tier 2) collects data from questionnaires and diaries, and some biologic specimens. Suggested laboratory analyses included measurement of progesterone in saliva and several glycoprotein hormones in urine that evaluate menstrual dysfunction, infertility, and pregnancy loss. The highest level of effort (Tier 3) involves prospective collection of diary information and simultaneous collection of biological specimens.
Intravenous sodium lactate infusion provokes symptoms of panic in patients with panic disorder at a significantly higher rate than in normal controls. Lactate sensitivity has been postulated to be specific for patients with panic attacks regardless of frequency of attacks or coexisting diagnoses. The authors present results of a pilot study of lactate infusions in patients with generalized anxiety disorder (GAD) without any history of panic attacks. Patients with GAD reacted more like panic disorder patients than like normal controls in anxiety and symptom scores during lactate infusion and in the rate of positive responses to lactate. Although preliminary, these findings raise questions regarding the specificity of lactate sensitivity and the relationship of GAD to panic disorder.
The treatment of panic disorder during pregnancy and lactation poses special problems. It is important that both the practitioner and patient consider a number of issues to find the most appropriate treatment for the patient. New cognitive-behavioural treatment options often circumvent the problems of pharmacotherapy for pregnant or lactating women while providing therapeutic benefits which are at least equivalent.
Seventy five mothers with lactation failure were studied, whose less than 4-month-old babies were admitted to the hospital. Partial lactational failure (94.7%) was noted more often than complete lactational failure (5.3%). Initiation of breastfeeding was delayed for 2 to 5 days usually for traditional reasons (77.3%) and because the mothers felt that the milk output was inadequate (92%). The various causes of lactation failure were determined and the relationship to various factors was analyzed. The commonest cause of lactation failure was insufficient milk or no milk (80%). The age, parity, education, socio-economic status, religion, family structure and urban vs rural status of mother--all had a bearing on the occurrence of lactation failure. An attempt was made to relactate all these mothers. The outcome was successful in 69.3 cases and failed in only 4% cases. In 26.7% cases, we cannot predict the outcome as the mothers hospital stay was very brief with no follow up.
The sulphonylureas and the biguanides are widely used as adjuncts to dietary measures in the treatment of non-insulin-dependent (type 2) diabetes mellitus (NIDDM). Adverse effect profiles differ markedly between the sulphonylureas and biguanides, reflecting differences in chemical structure and mode of action. Sulphonylureas are generally well tolerated, although pharmacokinetic differences between these agents have important clinical implications. The main adverse effect associated with sulphonylureas is hypoglycaemia. This effect is a predictable consequence of the principal pharmacological effect of these drugs, i.e. sensitisation of the islet beta-cell to glucose, resulting in enhanced endogenous insulin secretion. Sulphonylurea-induced suppression of hepatic glucose production may cause profound and protracted hypoglycaemia, especially in elderly patients, in individuals with intercurrent illnesses and reduced caloric intake, or when taken in combination with other compounds with hypoglycaemic potential, e.g. alcohol (ethanol). Sulphonylureas with a longer duration of action, notably chlorpropamide and glibenclamide (glyburide), are more liable to induce serious hypoglycaemia, particularly when drug elimination is reduced by renal impairment. Other drugs such as salicylates may potentiate the actions of sulphonylureas, thereby increasing the risk of hypoglycaemia. Biguanide therapy is associated with alterations in lactate homeostasis which under certain clinical circumstances may result in fatal lactic acidosis. Phenformin is associated with a markedly greater risk of lactic acidosis than metformin. Phenformin has been withdrawn in many countries for this reason. All biguanides must be avoided in patients with renal impairment, hepatic dysfunction and cardiac failure--conditions where drug accumulation or disordered lactate metabolism may predispose to lactic acidosis. Phenformin should not be given to individuals who exhibit a severe, genetically conferred hepatic defect of hydroxylation which impedes metabolism of this drug. Less seriously, the biguanides are associated with a relatively high incidence of gastrointestinal adverse effects which limit compliance. Acarbose, a competitive inhibitor of intestinal alpha-glucosidases, has recently been introduced. In contrast to the sulphonylureas and biguanides, acarbose has not been associated with life-threatening adverse effects. This reflects the low systemic absorption of the drug and, predictably, its principal unwanted effects are gastrointestinal disturbances resulting from iatrogenic carbohydrate malabsorption.
Six patients with panic disorder who had panicked during sodium lactate infusion were given cognitive-behavioral treatment for 12-24 weeks. After treatment they underwent another lactate infusion, and four patients were rates as having no panic, suggesting that reduced vulnerability to lactate accompanies remission of panic. Controlled trials of cognitive-behavioral therapy and use of lactate infusion as a measure of remission are recommended.
We wanted to test the tolerance of intensive exercise and corresponding high levels of lactate in patients with panic disorder. Thirty-five consecutive patients with DSM-III-R panic disorder completed submaximal tests, and 24 completed additional supramaximal exercise tests. All experienced high values of lactate during the supramaximal test (M = 10.7 mmol/L, SD = 2.9), but only 1 patient experienced a panic attack. The blood lactate values in the present study were higher than the usually achieved values of 5 to 6 mmol/L during infusion. In general, 67% of patients panic during infusion, compared to 4% in the present study. This discrepancy in frequency of panic following exposure to endogenous and exogenous lactate is discussed on the basis of various hypotheses of panic disorder, with an emphasis on cognitive theory of panic. The study indicates that patients with panic disorder can safely undergo vigorous exercise of such intensity to result in significant lactate production, with the chances of panic being small.
The mammary gland, which primarily develops postnatally, undergoes significant changes during pregnancy and lactation to facilitate milk production. Through the generation and analysis of 480 transcriptomes, we provide the most detailed allelic expression map of the mammary gland, cataloguing cell-type-specific expression from ex-vivo purified cell populations over 10 developmental stages, enabling comparative analysis. The work identifies genes involved in the mammary gland cycle, parental-origin-specific and genetic background-specific expression at cellular and temporal resolution, genes associated with human lactation disorders and breast cancer. Genomic imprinting, a mechanism regulating gene expression based on parental origin, is crucial for controlling gene dosage and stem cell potential throughout development. The analysis identified 25 imprinted genes monoallelically expressed in the mammary gland, with several showing allele-specific expression in distinct cell types. No novel imprinted genes were identified and the absence of biallelically expressed imprinted genes suggests that, unlike in brain, selective absence of imprinting does not regulate gene dosage in the mammary gland. This research highlights transcriptional dynamics within mammary gland cells and identifies novel candidate genes potentially significant in the tissue during pregnancy and lactation. Overall, this comprehensive atlas represents a valuable resource for future studies on expression and transcriptional dynamics in mammary cells.
Untreated anxiety disorders during pregnancy and the postpartum period may pose significant risks to the unborn fetus and interfere with a mother's ability to properly care for her newborn child. As the symptoms of anxiety disorders are often similar to those found in pregnancy, careful screening for anxiety disorders in pregnant women is essential. For women suffering from anxiety disorders during or after pregnancy, safe and effective treatment is needed. In this article, suggestions are offered for thorough assessment of anxiety disorders in pregnant and breastfeeding women. Treatment options are discussed with an emphasis on pharmacologic and cognitive-behavioral treatment.