Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 212 cases of diphtheria toxica in adults 90 (42%) suffered from cardiac complications. While early clinical signs were lacking or unspecific, the diagnosis could be suspected based on changes in the ECG. The earliest signs were sinus bradycardia, AV dissociation, AV escape rhythmus, prolongation of QT interval and large U wave (U > T, T + U wave). In cases where the differential diagnosis of myocarditis and other heart diseases in adults is difficult, attention should focus in the sickle-like depression ('sagging') of the ST interval, which is a typical sign for diphtheric myocarditis. It occurs even in the presence of pre-existing left-ventricular hypertrophy or bundle branch block. The severest forms of diphtheric myocarditis are complicated by AV and intraventricular conduction disturbances and malignant ventricular tachyarrhythmias.
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PMID:[Cardiac complications in adult diphtheria: analysis of 212 cases]. 902 77

46 patients with infectious-and-allergic myocarditis (IAM) and 46 patients with myocarditic cardiosclerosis (MCS) were studied for cytochemical parameters of blood lymphocyte bioenergetics. In IAM, cellular metabolism was found out to be disturbed, with the activity of G-6-PDG in spontaneous NST-test being risen against the background of depression of NAD- and NADP-diaphorases, lowering of the endogenous cytochrome "C" content and activity of alpha-GPDG. One third of IAM patients demonstrated protracted variant of the disease course by a study into the bioenergetic status of blood lymphocytes. Examination of parameters of blood lymphocytes energy exchange permits establishing more differential and diagnostic criteria for inflammatory lesion of the myocardium.
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PMID:[The bioenergetics system of the blood lymphocytes in infectious-allergic myocarditis]. 907 68

In 45% of 212 cases of diphtheria toxica in adults heart complications were observed. The earliest ECG signs are sinus bradycardia, AV dissociation, AV escape rhythms, prolongation of QT interval, high U wave (U > T, T + U wave). In the cases where differential diagnosis of myocarditis and other heart diseases in adults is difficult, the attention must be focused on the sickle-like depression ("sagging") of ST-interval that is a typical sign in diphtheric myocarditis. The most severe forms of diphtheric myocarditis are complicated by AV and intraventricular conduction disturbances and malignant ventricular arrhythmias.
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PMID:[The characteristics of myocarditis in diphtheria in adults based on data from the 1993-1994 epidemic]. 932 96

The routine diagnosis of tuberculosis and other mycobacterial diseases based on organism identification was completed during a period of one year in 730 patients, with serological IgG, IgM and IgA determination of antibodies against antigen 60 from M. bovis , strain BCG. The analysis was performed on 10 groups of patients consisting of 1) inflammatory diseases of the respiratory tract, 2) pericarditis, myocarditis, lymphadenitis and CNS diseases, 3) chronic non-inflammatory diseases of kidneys, liver and pancreas, 4) non-inflammatory diseases of the heart, sarcoidosis and pneumoconiosis, 5) tumor, 6) healthy people with TB contact, 7) inactive TB, 8) culture-positive pulmonary and extra-pulmonary TB, 9) culture-negative TB and extra-pulmonary TB, and 10) potentially pathogenic mycobacteria. The specificity of the test (100% negative cases in Group 6, composed of healthy people) is estimated at about 90%, in accordance with determinations made in other laboratories. In non-tuberculous patients, the specificity varied according to the analysed groups. Group 1 was largely unspecific for IgM (76% positives) but the specificity was acceptable for IgG (6.2% positives ) and IgA (7.4% positives). Group 2 was similar to Group 1. Group 3 was associated with positive IgA titers. Group 4 was only exceptiony seropositive and Group 5 was positive mainly for IgA (11. 4%) associated with lower respiratory tract ailments. This unspecific seropositivity was attributed to inapparent infections by PPM whose colonisation was favored by the particular disease of the patients. The sensitivity of serological measurements applied to the diagnosis of TB patients and PPM patients was similar, regardless if the disease was pulmonary or non-pulmonary, regardless if cultures were positive or not and, in our hands, was low (positivity for IgA about 30 %, for IgM about 10% and for IgG about 30%). This poor sensitivity observed with people presenting for treatment is attributed to an immune depression occuring mainly in elderly patients. The remarkable sensitivity of the serological instrument applied to culture-negative pulmonary and non-pulmonary TB cases as well as PPM cases makes the test a good adjuvant in cases of suspicion of TB. The assessment of the serological status of people under chemotherapy is worth the analysis, a high IgG level being associated with immunocompetence while the absence of IgG antibodies and/or the presence of IgA antibodies denotes an immunologically misdirected response potentially opening the way to chronic infections.
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PMID:Serological IgG, IgM and IgA diagnosis and prognosis of mycobacterial diseases in routine practice. 936 Sep 40

The heart is a tumor necrosis factor (TNF)-producing organ. Both myocardial macrophages and cardiac myocytes themselves synthesize TNF. Accumulating evidence indicates that myocardial TNF is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischemia-reperfusion injury, sepsis, chronic heart failure, viral myocarditis, and cardiac allograft rejection. Indeed, locally (vs. systemically) produced TNF contributes to postischemic myocardial dysfunction via direct depression of contractility and induction of myocyte apoptosis. Lipopolysaccharide or ischemia-reperfusion activates myocardial P38 mitogen-activated protein (MAP) kinase and nuclear factor kappa B, which lead to TNF production. TNF depresses myocardial function by nitric oxide (NO)-dependent and NO-independent (sphingosine dependent) mechanisms. TNF activation of TNF receptor 1 or Fas may induce cardiac myocyte apoptosis. MAP kinases and TNF transcription factors are feasible targets for anti-TNF (i.e., cardioprotective) strategies. Endogenous anti-inflammatory ligands, which trigger the gp130 signaling cascade, heat shock proteins, and TNF-binding proteins, also control TNF production and activity. Thus modulation of TNF in cardiovascular disease represents a realistic goal for clinical medicine.
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PMID:Tumor necrosis factor in the heart. 953 Feb 22

This review focuses on the role of the myocardial force-frequency relation (FFR) in human ventricular performance and how changes in the FFR can reduce cardiac output and, ultimately, can contribute to altering the stability of the in-vivo cardiovascular system in a way that contributes to the progression of heart failure. Changes in the amplitude, shape, and position of the myocardial FFR occurring in various forms of heart failure are characterized in terms of maximal isometric twitch tension, slope of the ascending limb (myocardial reserve), and position of the peak of the FFR on the frequency axis (optimum stimulation frequency). All three of these parameters decline according to severity of myocardial disease in the following order: non-failing atrial septal defect, non-failing coronary artery disease, non-failing coronary artery disease with diabetes mellitus, failing mitral regurgitation, failing viral myocarditis, failing idiopathic dilated cardiomyopathy. Evidence is presented supporting a sarcoplasmic reticulum Ca-pump based mechanism for this progressive depression of the FFR. Intracellular calcium cycling and concentration and Ca-pump content all diminish in proportion to degree of depression of the FFR. Additional evidence from myocyte culture studies suggests a cause of diminished Ca-pump content is sustained, elevated levels of plasma norepinephrine. A hypothesis is presented to explain the mechanism of myocardial failure and its progression in terms of changes in the cardiovascular feedback control system that are triggered by reduced myocardial reserve. Sustained elevation of plasma norepinephrine levels depresses expression of sarcoplasmic reticulum Ca-pump protein causing depression of the FFR and this causes a compensatory further increase in norepinephrine levels and a further depression of Ca-pump protein.
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PMID:A mechanistic analysis of the force-frequency relation in non-failing and progressively failing human myocardium. 983 27

The SLE patient database at the Rheumatology Clinic, St. Luke's Hospital includes 62 patients, 58 of which have complete data. The patients were grouped according to sex (7 males vs 51 females). The presentation, clinical manifestations, ACR criteria and laboratory findings of the 2 groups were analyzed and compared. Serositis as the initial manifestation at presentation was significantly commoner in males (29% vs 2%; p < 0.05). Cardiorespiratory problems such as pleurisy, pericarditis, pericardial effusions and myocarditis were more frequent in the male subgroup. Female patients had more arthritis, myositis, neuropsychiatric manifestations (depression, psychosis and headache) anemia, leucopenia and ENA positivity than their male counterparts. All 6 mortalities recorded were in the female subgroup.
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PMID:Male SLE patients in Malta. 1059 40

During 1999 and 2000, a disease outbreak of West Nile (WN) virus occurred in humans, horses, and wild and zoological birds in the northeastern USA. In our experiments, WN virus infection of young domestic geese (Anser anser domesticus) caused depression, weight loss, torticollis, opisthotonus, and death with accompanying encephalitis and myocarditis. Based on this experimental study and a field outbreak in Israel, WN virus is a disease threat to young goslings and viremia levels are potentially sufficient to infect mosquitoes and transmit WN virus to other animal species.
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PMID:Fatal encephalitis and myocarditis in young domestic geese (Anser anser domesticus) caused by West Nile virus. 1158 45

Dilated cardiomyopathy (DCM) is a myocardial disease characterized by progressive depression of myocardial contractile function and by ventricular dilatation. Abnormalities of the cellular and humoral immune system are present in patients with myocarditis and DCM. Various circulating cardiac autoantibodies have been detected among patients suffering from DCM. The relative contribution of cardiac antibodies to cardiac malfunction in DCM remains to be elucidated. Extraction of antibodies by immunoadsorption has been successfully used for treatment of various autoimmune diseases. In this review we report recent studies, which indicate that immunoadsorption improves cardiac function of patients with DCM. The data from these studies indicate that activation of the humoral immune system, with production of cardiac autoantibodies, may play a functional role in cardiac malfunction of patients with DCM.
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PMID:Improvement of cardiac function after immunoadsorption in patients with dilated cardiomyopathy. 1190 80

We describe the case of a patient who came to our attention because of a reversible depression of myocardial contractility, probably due to myocarditis. A positron emission tomography study showed, in correspondence to the malfunctioning segments, a decreased F18-2-fluoro-2-deoxyglucose (F18-FDG) uptake in the presence of a normal perfusion as assessed by means of N13-labeled ammonia uptake. This phenomenon, called "reverse mismatch", shows that viability is not always dependent on FDG uptake and that it could be associated with the recovery of myocardial contractility. Some interpretations of the association between a reversible dysfunction and a reduced myocardial glucose metabolism are presented. The central role of nitric oxide and of cyclic guanosine monophosphate is hypothesized to explain both the mechanical and metabolic abnormalities.
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PMID:Evidence of reverse mismatch with positron emission tomography imaging in a patient with reversible myocardial dysfunction. 1247 22


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