Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The discussion reports on the history, etiology, and the relationship of prostaglandins to primary dysmenorrhea, reviews old and new drugs used in the treatment; and considers future research. The history of dysmenorrhea dates back to the Greeks who defined the word as "painful menstrual flow." In 1865 the 1st surgical approach was used, consisting of a bilateral oophorectomy followed by other procedures. The relationship of dysmenorrhea and ovulation was discovered in 1938 and was treated by ovulatory suppression with estrogen. The psychogenic theory was advanced in the 1940s and many feel it still remains part of the etiology of dysmenorrhea. Until the discovery of prostaglandins and the subsequent relationship of them to dysmenorrhea, the known therapies were oral contraceptives (OCs), childbirth, sedation, narcotic analgesics, other hormones to suppress ovulation, and bed rest. The relationship of prostaglandins to primary dysmenorrhea is most likely the best explanation medical science can offer. Prostaglandins are thought by many as the etiologic agent of disease. The newest link of research deals with the implication of arginine vasopressin (AVP) as another possible integrated factor in the etiology of primary dysmenorrhea. AVP has been shown to be elevated in women with dysmenorrhea, but how AVP integrates into the sequence of events surrounding painful uterine contractions is unknown. The 2 main modes of therapy are OCs and nonsteroidal anti-inflammatory drugs (NSAIDS). Each has separate indications for use. It is recommended that when relief is not found in 6-12 months that causes of secondary dysmenorrhea be ruled out. OCs have been shown to be quite effective in all groups of women with dysmenorrhea, significantly reducing symptoms in 80-98% of the population. The use of OC in dysmenorrhea is recommended in women who are young, sexually active and who seek contraception, and relief of symptoms related to dysmenorrhea where secondary dysmenorrhea and premenstrual tension syndrome has been ruled out. NSAIDs have come to surface as the mainstay of therapy for dysmenorrhea. The major effect is that they inhibit cyclo-oxygenase. The NSAIDs are recommended for use in any woman with primary dysmenorrhea who may not want therapy with OCs and who does not have a history of peptic ulcer, dyspepsia, hepatic or renal disease, aspirin allergy, asthma, or a bleeding diathesis. At times, short term use can be permissible with some of the contraindications. Guidelines for the use of anti-PGs prophylactically are somewhat nuclear at this time.
 ...
PMID:Primary dysmenorrhea: current concepts. 646 99

Despite much debate over a presumptively somatic vs psychological etiology of nonatopic food and chemical sensitivities, little systematic research has addressed the issues. The present study investigated self-reported illness from several common foods (wheat, dairy, eggs) and chemicals (pesticide, car exhaust, paint, perfume, new carpet), symptom patterns, and psychological profiles of a sample of young adult college students (n = 490, age 19.4 +/- 2.4, 52% female/48% male). Subjects were divided into 4 groups on the basis of sample medians for frequency of illness from the foods (FI) and chemicals (CI); high FI with high CI (FI/CI), high FI alone, high CI alone, and NOILL (low FI and CI). FI was associated with more defensiveness (denial of negativity) while CI was linked with more shyness (avoidance of novelty). Women outnumbered men in all groups (FI/CI: 61%; FI: 80% CI: 55%) except the NOILL (40% women). Nevertheless, the FI/CI, FI, and/or CI groups still had significantly higher total symptom scores as well as more indigestion, headache, and memory trouble than did the NOILL group, even after depression, anxiety, shyness, defensiveness, and gender were covaried. The illness groups reported significantly more limitation of foods that mobilize endogenous opioids or generate exogenous opioids (sweets, fats, bread) as well as more illness from opiate drugs, small amounts of beverage alcohol, and late meals. Nasal symptoms from pollens or animals were more common in the FI/CI (42%) and CI (42%) than in FI (26%) or NOILL (28%) groups. Premenstrual tension syndrome and irritable bowel were also more common in the FI/CI group. The findings indicate that young adults outside the clinical setting who are relatively higher in FI and/or CI have distinctive symptom and psychological patterns. Covariate analyses suggest that important symptoms in FI and CI individuals such as indigestion, headache, and memory problems may occur in addition to rather than as simply part of emotional distress. The data are consistent with a previously hypothesized role of olfactory-limbic and hypothalamic pathways and with a time-dependent sensitization model for illness from foods and chemicals.
 ...
PMID:Symptom and personality profiles of young adults from a college student population with self-reported illness from foods and chemicals. 829 25

Pregnancy and delivery are associated with activation of immune-inflammatory pathways which may prime parturients to develop postnatal depression. There are, however, few data on the associations between immune-inflammatory pathways and prenatal depression and physio-somatic symptoms. This study examined the associations between serum zinc, C-reactive protein (CRP), and haptoglobin at the end of term and prenatal physio-somatic symptoms (fatigue, back pain, muscle pain, dyspepsia, obstipation) and prenatal and postnatal depressive and anxiety symptoms as measured using the Edinburgh Postnatal Depression Scale (EPDS), Beck Depression Inventory (BDI), Hamilton Depression Rating Scale (HAMD), and Spielberger's State Anxiety Inventory (STAI). Zinc and haptoglobin were significantly lower and CRP increased at the end of term as compared with non-pregnant women. Prenatal depression was predicted by lower zinc and lifetime history of depression, anxiety, and premenstrual tension syndrome (PMS). The latter histories were also significantly and inversely related to lower zinc. The severity of prenatal EDPS, HAMD, BDI, STAI, and physio-somatic symptoms was predicted by fatigue in the first and second trimesters, a positive life history of depression, anxiety, and PMS, and lower zinc and higher CRP. Postnatal depressive symptoms are predicted by prenatal depression, physio-somatic symptoms, zinc and CRP. Prenatal depressive and physio-somatic symptoms have an immune-inflammatory pathophysiology, while postnatal depressive symptoms are highly predicted by prenatal immune activation, prenatal depression, and a lifetime history of depression and PMS. Previous episodes of depression, anxiety disorders, and PMS may prime pregnant females to develop prenatal and postnatal depressive symptoms via activated immune pathways.
 ...
PMID:Lower Serum Zinc and Higher CRP Strongly Predict Prenatal Depression and Physio-somatic Symptoms, Which All Together Predict Postnatal Depressive Symptoms. 2684 64