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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case of isolated adrenocorticotrophic hormone (ACTH) deficiency (IAD) in a late onset hypogonadism (LOH) clinic, not diagnosed by examinations in internal medicine. A 54-year-old man showed body weight loss with severe appetite loss, general malaise and hypotension. He visited our clinic for a checkup for LOH after general examinations in internal medicine. His hormonal examination showed undetectable ACTH and cortisol levels. However, the values of other pituitary hormones and testosterone were normal. A load test for anterior pituitary hormone (CRH + TRH + LHRH + GRH test) revealed that the ACTH-cortisol system showed no response although the other pituitary hormones responded. These findings confirmed the diagnosis of isolated ACTH deficiency. Administration of hydrocortisone dramatically improved his symptoms. Symptoms of IAD are similar to those of LOH syndrome and depression. Thus, we should consider IAD as one of the differential diagnoses in LOH clinics.
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PMID:[Isolated ACTH deficiency in a late onset case of hypogonadism (LOH) not diagnosed by examination in an internal medicine clinic]. 1878 51

As part of the process of developing cognitive-behavioral therapy (CBT) for medical adherence and depression (Safren, Gonzalez, & Soroudi, 2007), the authors conducted exit interviews among 14 HIV-infected patients who received the intervention, and transcribed, coded, and analyzed these data. The authors concluded that CBT was structured yet flexible, developed self-awareness emphasized social support, and involved therapist empathy and supportiveness. Limitations included the discomfort of discussing personal information and the impact of feeling ill on attendance and homework completion. Suggestions included more sessions, more flexibility in scheduling appointments, and more realistic and clear expectations regarding homework. These results provide insights about strengths and limitations of this psychotherapy with medically ill patients and may help to maximize intervention effectiveness and client acceptability.
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PMID:Participants' perspectives on cognitive-behavioral therapy for adherence and depression in HIV. 1881 79

This article will present a model for how 'depression' (i.e. depressive symptoms) can be divided into four self-diagnosed sub-types or causes which might then be self-treated using agents available without prescription. (Another, much rarer, cause of depressed symptoms is the classical illness of 'melancholia', which when severe cannot be self-treated and typically requires hospitalization.) A self-management option and alternative is now needed due to the an inappropriate emphasis of modern psychiatry on treatment of imprecise syndromal 'disorders' which may entail treating 'depression' at the cost of making the patient feel and function worse. By contrast, the basic theoretical stance of self-management is that depressed mood should be seen as a result of unpleasant symptoms - and it is the symptoms that require treatment, not the mood itself. Furthermore, drugs (or other interventions) need to be classified in terms of their potential therapeutic effects on these symptoms that may cause depressed mood. The four common causes of depressed mood considered here are the personality trait of Neuroticism; the state of malaise (fatigue, aching etc) which accompanies an illness with an activated immune system; demotivation due to lack of positive emotions (anhedonia); and the syndrome of seasonal affective disorder (SAD). Each of the four sub-types is then 'matched' with a first-line non-prescription agent. The 'stabilizing' agents such as St John's Wort and the antihistamines chlorpheniramine and diphenhydramine are used for treatment of Neuroticism; analgesics/pain killers such as aspirin, ibuprofen, paracetamol/acetaminophen and the opiates are used to treat malaise; energizing agents such as caffeine and nicotine are used for the treatment of demotivation; and bright light used in the early morning to treat SAD. Self-treatments are intended to be used after research and experimentally, on a trial-and-error basis; with self-monitoring of beneficial and harmful effects, and a willingness to stop and switch treatments. The model of S-DTM (self-diagnosis, self-treatment and self-monitoring) is suggested as potentially applicable more widely within psychiatry and medicine.
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PMID:A model for self-treatment of four sub-types of symptomatic 'depression' using non-prescription agents: neuroticism (anxiety and emotional instability); malaise (fatigue and painful symptoms); demotivation (anhedonia) and seasonal affective disorder 'SAD'. 1884 2

Giant cell arteritis (GCA) frequently appears as cranial arteritis (eg. temporal arteritis) with headache, pain on chewing and visual disturbances. In addition, extracranial manifestations are often observed leading to aneurysmatic dilatations and dissections of the aorta as well as stenoses of large thoracic, abdominal or limb arteries. The vascular signs are accompanied by general disease symptoms, e.g. malaise, elevated temperatures, weight loss and depression. Polymyalgia rheumatica (PMR) is the most frequent rheumatic manifestation of GCA but also occurs independently from GCA. The structural correlate for the PMR symptoms is first and foremost extra-articular inflammation (tenosynovitis, bursitis) of large joints and the vertebral column (interspinal bursitis). In addition, vasculitis of large arteries in PMR must be considered particularly in the presence of high inflammatory activity. While specific laboratory markers for GCA and PMR are lacking elevated values for the erythrocyte sedimentation rate and C-reactive protein are present in almost all patients at disease onset. Besides the clinical evaluation, the serological acute phase reaction represents the main parameter for the course during therapy of this relatively frequent disease in elderly people.
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PMID:[Clinical and serological findings of giant-cell arteritis]. 1915 39

Few studies have evaluated age and racial/ethnic differences in the prevalence of symptoms in human immunodeficiency virus (HIV)-infected persons. Thus, the objective of this study was to compare the prevalence of gastrointestinal, metabolic, general malaise, neurologic, or other self-reported symptoms by age and race/ethnicity among 1574 HIV-infected women enrolled in the Women's Interagency HIV Study and 955 HIV-infected men who have sex with men (MSM) enrolled in the Multicenter AIDS Cohort Study. All patients had known dates of initiation of highly active antiretroviral therapy. It was observed that women aged 50 years or more were less likely to experience gastrointestinal symptoms (24% vs. 27%; multivariable P=0.024), but more likely to experience general malaise (47% vs. 37%; multivariable P=0.004), neurologic (44% vs. 38%; multivariable P=0.048), or other symptoms (40% vs. 28%; multivariable P<0.001) compared with women less than 40 years of age. Only neurologic symptoms had a higher prevalence among older MSM (52% vs. 37%; multivariable P=0.002), largely driven by paresthesias (48% vs. 31%; multivariable P=0.004), the most common individual symptom reported by men. Caucasian women generally had the highest prevalence of symptoms, and African American women had the lowest prevalence. Few racial/ethnic differences were noted for MSM. Depression and a prior diagnosis of acquired immunodeficiency syndrome were the strongest and most consistent predictors of clinical symptoms in both cohorts. In summary, the prevalence of reported symptoms varies with patient race/ethnicity, age, and modifiable factors, such as depression and HIV disease stage. Clinicians should consider these factors when counseling patients regarding potential adverse effects of antiretrovirals or symptoms associated with HIV disease.
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PMID:Age and racial/ethnic differences in the prevalence of reported symptoms in human immunodeficiency virus-infected persons on antiretroviral therapy. 1932 74

Activation of the inflammatory immune system has been associated with the development of psychological disorders such as major depressive disorder (MDD). In this regard, the release of pro-inflammatory cytokines (signaling molecules of the immune system) provokes a constellation of neurochemical and behavioral alterations, reminiscent of the effects of traditional stressors, which if sustained could influence psychological functioning. In animal models, exogenously administered cytokines, as well as bacterial endotoxins and viral analogues, induce a variety of behavioral disturbances collectively known as sickness behavior. Although it is difficult to differentiate the general malaise of sickness engendered by cytokines from the depressogenic effects, clinical studies have revealed increased levels of circulating cytokines and acute phase proteins in patients diagnosed with MDD. Furthermore, the incidence of MDD is increased in patients suffering from chronic inflammatory conditions, and immunotherapy used to treat chronic illnesses such as Hepatitis C was related to high levels of depression that could be attenuated by antidepressant treatment. Together, these findings indicate that activation of the inflammatory immune system may favor the evolution of psychological disturbances.
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PMID:Neurochemical and behavioral responses to inflammatory immune stressors. 1948 2

There is a significant 'comorbidity' between depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Depressive symptoms frequently occur during the course of ME/CFS. Fatigue and somatic symptoms (F&S), like pain, muscle tension, and a flu-like malaise, are key components of depression. At the same time, depression and ME/CFS show major clinical differences, which allow to discriminate them with a 100% accuracy. This paper aims to review the shared pathways that underpin both disorders and the pathways that discriminate them. Numerous studies have shown that depression and ME/CFS are characterized by shared aberrations in inflammatory, oxidative and nitrosative (IO&NS) pathways, like systemic inflammation and its long-term sequels, including O&NS-induced damage to fatty acids, proteins and DNA; dysfunctional mitochondria; lowered antioxidant levels, like zinc and coenzyme Q10; autoimmune responses to neoepitopes formed by O&NS; lowered omega-3 polyunsaturated fatty acid levels; and increased translocation of gram-negative bacteria. Some IO&NS-related pathways, like the induction of indoleamine 2-3-dioxygenase, neurodegeneration and decreased neurogenesis, are more specific to depression, whereas other pathways, like the 2'-5' oligoadenylate synthetase/RNase L pathway, are specific to ME/CFS. Most current animal models of depression, e.g. those induced by cytokines, are not reminiscent of human depression but reflect a mixture of depressive and F&S symptoms. The latter symptoms, sometimes called sickness behavior, differ from depression and ME/CFS because the former is a (sub)acute response to infection-induced pro-inflammatory cytokines that aims to enhance recovery, whereas the latter are characterized by long-term sequels in multiple IO&NS pathways. Depression and ME/CFS are not 'comorbid' disorders, but should be regarded as 'co-associated disorders' that are clinical manifestations of shared pathways.
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PMID:An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. 2060 77

Drugs that interfere with cannabinoid CB1 transmission suppress food-motivated behaviors, and may be useful clinically as appetite suppressants. However, there may also be undesirable side effects (e.g., nausea, malaise, anxiety, and depression) that are produced by the current generation of CB1 inverse agonists such as rimonabant and taranabant. For that reason, it is important to continue research on novel cannabinoid antagonists. The present studies examined the effects of the novel compound AM6545, which is a neutral antagonist of CB1 receptors that is thought to have relatively poor penetrability into the central nervous system. Intraperitoneal administration of AM6545 significantly reduced food-reinforced operant responding at doses of 4.0, 8.0 and 16.0 mg/kg. AM6545 also produced a strong suppression of the intake of high-carbohydrate and high-fat diets in the same dose range, but only produced a mild suppression of lab chow intake at the highest dose (16.0 mg/kg). Although AM6545 did not affect food handling, it did reduce time spent feeding and feeding rate. Taken together, these results suggest that AM6545 is a compound that warrants further study as a potential appetite suppressant drug.
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PMID:The novel cannabinoid CB1 antagonist AM6545 suppresses food intake and food-reinforced behavior. 2071 79

This study sought to translate, using a back-translation procedure, and evaluate the psychometric characteristics of Depression in the Medically Ill questionnaire (DMI-18) and its short version (DMI-10) in a Spanish population. Patients with somatic disorders (N = 366) completed the translated DMI-18 and another depression questionnaire. Among these, 167 were also assessed by a mental health professional (gold standard) to test criterion validity. Furthermore, coefficient alpha for both the versions were high (>.90), and convergent validity assessed against the Beck Depression Inventory for Primary Care, the Hospital Anxiety and Depression Scale, and the Patient Health Questionnaire-9 was satisfactory (r > .74). Confirmatory factor analysis results supported the one-factor model. When compared with the gold standard, sensitivity and specificity were 93% and 73% for DMI-18 and 87% and 74% for DMI-10, respectively. Thus, both the versions are acceptable measures that can be used by nonpsychiatric professionals to detect affective comorbidities in their patients.
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PMID:Use of the long and short forms of the depression in the medically ill questionnaire in a Spanish population. 2124 50

There is evidence of a long-term rise in the prevalence of adolescent emotional problems in the U.K. and in other countries. The aim of this study was to test whether time trends in parents' emotional difficulties contributed to these increases using data from two national surveys of English teenagers and parents studied twenty years apart (1986 and 2006). The 1986 sample is the age 16 follow-up of the 1970 British Cohort Study (N = 4524 adolescents, N = 7169 parents). The 2006 sample included 16/17-year-olds and their parents drawn from the 2002 and 2003 Health Surveys for England (N = 711). Both studies used identical self-complete questionnaire assessments of adolescent (GHQ-12 and Malaise Inventory) and parent (Malaise) symptoms of depression and anxiety. Follow-up data on emotional problems and psychiatric service use at age 30 years (N = 2785) for adolescents in the first cohort was used to validate the role of parent emotional problems as risk factors for offspring mental health. We found that maternal emotional problems increased across all socio-demographic groups between 1986 and 2006, mirroring increases in adolescent emotional problems over this period. They were cross-sectionally and prospectively associated with adolescent emotional problems. Cohort differences in adolescent emotional problems were attenuated when accounting for the increase in maternal emotional problems. Rising rates of maternal emotional problems have likely contributed to, but do not fully explain, recent time trends in adolescent emotional problems.
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PMID:Do changes in parent mental health explain trends in youth emotional problems? 2168 90


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