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)

Depression has been identified at the most prevalent psychologic problem in patients with ESRD treated with hemodialysis (HD). Depression has been associated with mortality in HD patients; however, the similarity of the symptoms of depressive disorders to those of uremia and the difficulties in measuring depression and dissociating psychologic from physical aspects of depression in such patients render these studies difficult to evaluate. Conflicting data regarding the effects of depression on survival in HD patients may be the result of using somatic symptoms in quantifying the extent of depression. In this review, studies regarding the diagnosis of depression in HD patients, the association of depression and survival in HD patients in light of recent work on factors related to the morbidity and mortality in the ESRD population, and aspects of therapy for depression in HD patients are considered. Specifically, depression may affect immunologic function, nutrition, and compliance factors that may affect the prescription and delivery of dialysis, which may, in turn, influence outcome. Alternatively, depression may be an independent factor in influencing survival. Cognitive depression measures may be more useful in predicting outcome in HD patients than standard measures used in nonmedically ill populations. Although there are few studies of the effect of treatment of depression on outcome in HD patients, it is reasonable to hypothesize that treatment of depressive disorders in HD patients might effect outcome. Further studies on the association of depression and its treatment and mortality in ESRD patients are warranted.
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PMID:Survival in hemodialysis patients: the role of depression. 840 64

In order to clarify the mechanism underlying impaired cardiac performance in uraemia, the contractile function of isolated cardiac myocytes from chronically uraemic and control rats has been compared. Rats were made uraemic by sub-total nephrectomy in a two-stage surgical procedure, and left for 4 weeks. Sham-operated controls were prepared at the same time. Animals were pairfed, and final body weights were not significantly different between the groups. Ventricular myocytes were isolated and their contraction amplitude and velocity were measured using a video-based edge-detection system. Contraction was depressed in myocytes from uraemic animals, with contraction amplitude in maximum Ca2+ reduced from 16.3 +/- 0.6% shortening, to 13.0 +/- 0.8% (p < 0.01, n = 10 animals for each group). There was a concomitant decrease in the velocity of shortening (5.6 +/- 0.4 vs. 3.9 +/- 0.5 micron s-1 change in sarcomere length, p < 0.02) and of relaxation (4.6 +/- 0.4 vs. 3.2 +/- 0.4 micron s-1 p < 0.02). Similar depression was seen at lower perfusate Ca2+ concentrations (1-2 mM) and the EC50 for Ca2+ was unchanged. The response to beta-adrenoceptor stimulation was decreased by the same magnitude as that to Ca2+, with no change in the EC50 for isoproterenol or the ratio of maximum response to isoproterenol or to Ca2+ in the same cell (isoproterenol/Ca2+ ratio). There was no shift in the myosin isozyme composition in uraemic cells, with both groups showing a heterogeneous V1/V2/V3 pattern. We conclude that chronic uraemia is associated with a depression of contractile function in the isolated myocyte but no shift in myosin isoforms or specific beta-adrenoceptor desensitisation.
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PMID:Contractile dysfunction of isolated ventricular myocytes in experimental uraemia. 877 76

Paramagnetic centers of the blood were investigated in 75 patients with chronic uremia (Electron Spin Resonance, 77 K). The analysis of hemodialysis action on paramagnetic centers in the blood showed that this procedure provokes gradual depression of antioxidant defense.
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PMID:[Changes in the activity of the blood antioxidant enzymes during hemodialysis of patients with terminal kidney failure]. 882 55

Lithium carbonate is a widely used pharmacologic agent for acute bipolar disorder, long term prophylaxis of mania in a bipolar patient, and prevention of "manic overshoot" with an antidepressant in acute depression in a bipolar patient. Although clinical neurological associations with lithium overdose have been-established, there has been a dearth of reports of pathologic changes related to lithium toxicity. We report a case of a 52-year-old Black female with bipolar disorder who had been treated with lithium for over 5 years and who expired 24 days after presenting in a stuporous state with an elevated lithium level of 3.2 mEq/l. Postmortem neuropathologic examination revealed severe cerebellar atrophy of the internal granule and Purkinje cell layers with attendant Bergmann gliosis presumably resulting from chronic lithium use and toxicity. There was also Alzheimer type II cell change in the thalamus and lentiform nuclei possibly due to terminal uremia. In summary, this is a unique case which appears to illustrate cerebellar atrophic changes related to lithium therapy and acute lithium intoxication.
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PMID:Pathologic assessment of cerebellar atrophy following acute lithium intoxication. 902 Mar 92

To evaluate the impact of uremia and associated caloric restriction on physiologically pulsatile growth hormone (GH) release, we used deconvolution analysis of spontaneous plasma GH profiles in 5/6-nephrectomized male rats (NX, N = 9). Three different normal renal function sham-operated groups were used: rats fed a normal diet ad libitum (SAL, N = 9); NX pair-fed rats (SPF, N = 6); NX rats pair-fed for protein ingestion but calorically supplemented up to the energy intake of SAL (SPF+, N = 8). Severe renal failure was confirmed by much higher (P < 0.001) BUN in NX than sham groups. NX rats were growth retarded as shown by reduced (P < 0.01) weight and length gains as compared with sham animals. Deconvolution analysis (mean +/- SEM) of plasma samples obtained every 10 minutes over 6 hours, and 14 to 16 days after second stage nephrectomy showed that NX rats had a longer GH t(1/2) (17.0 +/- 1.8 vs. 11.6 +/- 0.8 min), less GH mass secreted per burst (48 +/- 15 vs. 95 +/- 16 ng/ml/pulse), lower secretory pulse amplitude (1.9 +/- 0.5 vs. 5.8 +/- 0.9 ng/ml/min), and a reduced total GH secretion (240 +/- 69 vs. 400 +/- 56 ng/ml/6 hr) than SAL rats. Corresponding data were not significantly different between NX and SPF, or between SAL and SPF+ groups. In summary, stunted rats with chronic renal failure exhibit a prolonged GH t(1/2) and suppression of GH secretory pattern burst mass. Control data from rats with normal renal function suggest that the amplitude-specific depression of GH secretion may be attributed, at least in part, to chronic renal failure-associated calorie deficiency.
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PMID:Impaired secretion of growth hormone in experimental uremia: relevance of caloric deficiency. 929 Nov 83

Sleep apnea is a surprisingly common disorder in end-stage renal disease (ESRD) and chronic renal failure. The symptoms of sleep apnea frequently go unreported or may be misdiagnosed as uremia, depression, chronic illness, or insomnia. A review of the literature was performed to define the prevalence, morbidity, and treatment of sleep apnea syndrome in the ESRD patient. Sleep apnea occurs in at least 60% of ESRD patients. The known complications of sleep apnea include arrhythmias, pulmonary hypertension, and systemic hypertension. In addition, sleep apnea has been implicated in coronary artery disease and strokes. The contribution of sleep apnea to the high mortality from cardiac disease and stroke in peritoneal dialysis and hemodialysis patients is unknown. The causes of the increased prevalence of sleep apnea in ESRD patients are unknown and likely differ from the general population, but the treatment is similar. The literature suggests that modality of renal replacement therapy does not matter; however, large nocturnal volume peritoneal dialysis may worsen sleep apnea. Renal transplantation may be curative. In conclusion, sleep apnea may be an under-diagnosed disease in patients on dialysis. There are significant reasons to suspect that sleep apnea may worsen the morbidity and mortality of ESRD, and there are potential successful therapies.
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PMID:Sleep apnea in renal failure. 936 Jun 57

The depression of the immune system in chronic uremia is a well-known phenomenon but the role of serum zinc (Zn) levels on both cell-mediated and humoral immunity is still controversial. The aim of this study was to investigate the effect of Zn supplementation on the immune system and on antibody response to multivalent influenza vaccine (MIV) in hemodialysis patients (HP). Twenty-six HP and 11 healthy subjects (HS) were vaccinated with MIV. Hemodialysis patients were randomly divided into two groups. Group I (13 HP) was supplemented with 120 mg ZnSO4 after each dialysis session. Group II (13 HP) and Group III (11 HS) were given placebo. In all cases, the serum Zn levels, CD3, CD4, CD8, CD19, HLA-DR+ cell percentages, CD4/CD8 ratio and CD3+ HLA-DR+ cell percentages were determined before and 30 days after vaccination. Antibody levels to subgroups of MIV were also measured. All the baseline parameters studied were not statistically different between Group I and II. However, there was a significant difference between the basal parameters of Group III and the other two groups, except for CD3 and CD4 cell percentages. Serum Zn, CD19 cell percentage and antibody levels to MIV subgroups were significantly increased in Group I at the end of the first month of the study (p<0.01, p<0.05, p<0.001, p<0.001, and p<0.01, respectively), but the other parameters showed no significant changes. The only significant change observed in Groups II and III was an increase in antibody levels to MIV subgroups one month after vaccination. Antibody levels to MIV subgroups, were not statistically different between Groups I and II, but in Group III they were strikingly higher than those of HP (p<0.001). These results led us to conclude that Zn supplementation could not restore the immune parameters and enhance antibody response to MIV in HP.
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PMID:Effects of zinc supplementation on the immune system and on antibody response to multivalent influenza vaccine in hemodialysis patients. 968 9

Five adult female Eld's deer died acutely or were euthanatized because of clinical signs including anorexia, signs of depression, and uremia. On necropsy, these deer had large masses of necrotic abdominal fat constricting the ureters, causing hydroureter and hydronephrosis. The herd from which these deer originated was maintained on pastures consisting primarily of tall fescue, samples from which were subsequently confirmed to be infected with an endophytic fungus that is known to cause similar lesions in cattle. A retrospective study of deaths in this herd revealed a sharp increase in incidence of abdominal lipomatosis since 1994. Physical examinations on the herd revealed > 90% of females to be affected. Endophyte-infected tall fescue forage was concluded to be a major factor in the development of lipomatosis in these deer. Other contributing factors were considered. Lesions caused by endophyte-infected fescue can be severe, and this disease can develop in nondomestic species.
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PMID:Abdominal lipomatosis attributed to tall fescue toxicosis in deer. 986 75

Restless legs syndrome (RLS) is common in the elderly, with an estimated prevalence of 10 to 35% in individuals over 65 years of age. RLS is characterised by paraesthesias and dysaesthesias of the legs, typically occurring in the evening. The symptoms occur at rest and result in motor restlessness; movement often temporarily relieves the symptoms. Patients with poorly controlled RLS may develop related problems including insomnia (due to sleep-onset restlessness or periodic limb movements or related sleep fragmentation) and depression. RLS can be a primary disorder that develops in the young and includes familial cases. Secondary RLS occurs in association with iron-deficiency anaemia, uraemia and polyneuropathies. Typically, RLS is misdiagnosed or undiagnosed for years. In the elderly, both primary and secondary types of the disorder are common. It is thought that RLS represents lower CNS levels of, or reduced responsiveness to, dopamine. The symptoms improve with dopaminergic therapy. Ergotamine dopamine-receptor agonists such as pergolide, and the non-ergotamine dopamine-receptor agonists pramipexole and ropinirole, are becoming more commonly used to treat RLS. The dopamine precursor levodopa, in combination with carbidopa, is another effective therapeutic agent. An advantage of levodopa is lower cost than non-ergotamine and ergotamine dopamine-receptor agonists. However, the adverse effect of symptom augmentation appears to develop more frequently with levodopa than dopamine-receptor agonists; therefore, levodopa may currently be used somewhat less often as first-line therapy. Patients with painful symptoms may respond favourably to the anticonvulsants gabapentin and carbamazepine. Opioids and hypnosedatives are helpful in selected patients; however, these agents may have troubling adverse effects in the elderly. Correction of iron deficiency improves symptoms in patients with low ferritin levels. Lifestyle modification may also be helpful. Therapy is directed at symptoms, and most symptomatic patients benefit from treatment. It is important to consider RLS in the differential diagnosis of any patient with paraesthesias of the limbs.
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PMID:Restless legs syndrome in the older adult: diagnosis and management. 1239 51

Manganese is the 12th most abundant element in the earth's crust. The base metal does not occur naturally, but is a component of more than 100 minerals, including sulfides, oxides, carbonates, silicates, phosphates, and borates. In addition to occurring in foods and drinking water, manganese occurs in the atmosphere from dust, volcanic activity, forest fires, and industrial emissions. Manganese (II) sulfate monohydrate was chosen for study because of its stability, solubility, and availability. Toxicology and carcinogenesis studies were conducted by administering manganese (II) sulfate monohydrate (97% pure) in feed to groups of male and female F344/N rats and B6C3F1 mice for 14 days, 13 weeks, and 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, germ cells of Drosophila melanogaster, and cultured Chinese hamster ovary cells. 14-DAY STUDY IN RATS: Groups of five male and five female rats received diets containing 0, 3,130, 6,250, 12,500, 25,000, or 50,000 ppm manganese (II) sulfate monohydrate. All rats survived to the end of the study. Male rats exposed to 50,000 ppm had a mean body weight gain 57% lower and a final mean body weight 13% lower than those of the controls. The mean body weight gain of 50,000 ppm females was 20% lower and the final mean body weight was 7% lower than those of the controls. During the second week, 50,000 ppm males and females exhibited diarrhea. 14-DAY STUDY IN MICE: Groups of five male and five female mice received diets containing 0, 3,130, 6,250, 12,500, 25,000, or 50,000 ppm manganese (II) sulfate monohydrate. One female mouse in the 25,000 ppm group died on day 1 of unknown causes; all other mice survived to the end of the study. Differences in body weights between exposed and control mice could not be attributed to chemical administration. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats received diets containing 0, 1,600, 3,130, 6,250, 12,500, or 25,000 ppm manganese (II) sulfate monohydrate. Mean daily ingestion of manganese (II) sulfate monohydrate ranged from 110 to 1,700 mg/kg body weight in males and 115 to 2,000 mg/kg in females. All rats survived to the end of the study. Mean body weight gains were marginally lower than that of controls in males exposed to 3,130 ppm or more; mean body weight gains were significantly lower than that of the controls in females exposed to 6,250,12,500, or 25,000 ppm. At the end of the study, absolute and relative liver weights of all exposed male rats and of 25,000 ppm female rats were significantly lower than those of controls. The total leukocyte count in males was similar between exposed and control rats; however, neutrophil counts of all exposed groups were greater than those of the controls, whereas lymphocyte counts of the 6,250, 12,500, and 25,000 ppm groups were significantly lower than those of the controls. Total leukocyte counts in 6,250,12,500, and 25,000 ppm females were significantly decreased because of a decrease in lymphocytes. Male rats also demonstrated marginal but significant increases in percent hematocrit and erythrocyte count in the 6,250,12,500, and 25,000 ppm groups. No clinical or histopathologic findings in rats were chemical related. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice received diets containing 0, 3,130, 6,250, 12,500, 25,000, or 50,000 ppm manganese (II) sulfate monohydrate. Mean daily ingestion of manganese (II) sulfate monohydrate ranged from 330 to 7,400 mg/kg body weight in males and 390 to 6,900 mg/kg body weight in females. No deaths were chemical related. The mean body weight gains of exposed male mice and of 50,000 ppm female mice were significantly lower than those of controls. The absolute and relative liver weights of 50,000 ppm males were significantly lower than those of controls. The percent hematocrit and hemoglobin concentration of males and females exposed to 50,000 ppm were lower than those of the controls, and the mean erythrocyte volumes were significantly lower than those of the controls. The total leukocyte counts of males in the 25,eukocyte counts of males in the 25,000 and 50,000 ppm groups were significantly lower than that of the controls. No clinical findings were attributed to manganese (II) sulfate monohydrate ingestion. Epithelial hyperplasia and hyperkeratosis of the forestomach occurred in three 50,000 ppm males. 2-YEAR STUDY IN RATS: Groups of 70 male and 70 female rats were fed diets containing 0, 1,500, 5,000, or 15,000 ppm manganese (II) sulfate monohydrate. Based on average daily feed consumption, these doses resulted in the daily ingestion of 60, 200, or 615 mg/kg body weight (males) or 70, 230, or 715 mg/kg (females). Eight to 10 rats from each group were evaluated at 9 and 15 months. Survival, Body Weights, Feed Consumption, and Clinical Findings: Survival of 15,000 ppm male rats in the 2-year study was significantly lower than that of the control group. The deaths of males in the control and exposure groups were attributed to a variety of spontaneous neoplastic and nonneoplastic lesions; however, the greater number of deaths in the 15,000 ppm group resulted from increased incidences of advanced renal disease related to ingestion of manganese (II) sulfate monohydrate. The decreased survival of the 15,000 ppm males did not occur until approximately week 93 of the study; before week 93, survival was similar in all groups. Survival of exposed females was similar to that of the controls. The mean body weight of 15,000 ppm male rats was within 5&percnt; of the control group until week 89, by week 104, the mean body weight of 15,000 ppm males was 10&percnt; lower than that of the control group. The mean body weights of 1,500 and 5,000 ppm male rats and all exposed female groups were similar to those of the controls throughout the study. Feed consumption by all exposure groups was similar to that by the control groups. No clinical findings were attributed to manganese (II) sulfate monohydrate ingestion. Hematology, Clinical Chemistry, and Tissue Metal Concentration Analyses No differences in hematology and clinical chemistry parameters attributable to the ingestion of manganese (II) sulfate monohydrate occurred between exposed and control groups. At both the 9- and 15-month interim evaluations, tissue concentrations of manganese were significantly elevated in the livers of 5,000 and 15,000 ppm male and female rats, with an accompanying depression of hepatic iron. Pathology Findings: The ingestion of diets containing 15,000 ppm manganese (II) sulfate monohydrate was associated with a marginal increase in the average severity of nephropathy in male rats (0 ppm, 2.9; 1,500 ppm, 3.0; 5,000 ppm, 3.0; 15,000 ppm, 3.2). The increased severity of nephropathy in the 15,000 ppm male rats was accompanied by significantly increased incidences of mineralization of the blood vessels (4/52, 10/51, 6/51,17/52) and glandular stomach (8/52,13/51, 9/51, 23/52), parathyroid gland hyperplasia (14/51, 14/46, 12/49, 23/50), and fibrous osteodystrophy of the femur (12/52,14/51,12/51, 24/52). These lesions are manifestations of renal failure, uremia, and secondary hyperparathyroidism. The increased incidence of advanced renal disease caused reduced survival of the high-dose male rats. No increase in the incidence of neoplasms in male or female rats was attributed to the ingestion of diets containing manganese (II) sulfate monohydrate. 2-YEAR STUDY IN MICE: Groups of 70 male and 70 female mice received diets containing 0, 1,500, 5,000, or 15,000 ppm manganese (II) sulfate monohydrate. These levels resulted in an average daily ingestion of 160, 540, or 1,800 mg/kg body weight (males) or 200, 700, or 2,250 mg/kg (females). Nine or 10 mice from each group were evaluated at the 9-month and 15-month interim evaluations. Survival, Body Weights, Feed Consumption, and Clinical Findings: Survival rates of exposed male and female mice in the 2-year study were similar to those of the control groups. The mean body weights of exposed male mice were similar to that of the control group. Compared to controls, female mice had exposure related lower mean body weights after week 37, and the final mean body weights for the 1,500, 5,000, and 15,000 ppm groups were 6&percnt;, 9&percnt;, and 13&percnt; lower than that of the control group. Feed consumption by all exposure groups was similar to that by the control groups. No clinical findings were attributed to the administration of manganese (II) sulfate monohydrate. Hematology, Clinical Chemistry, and Tissue Metal Concentration Analyses No chemical-related differences between exposed and control groups occurred in hematology or clinical chemistry parameters. At the 9- and 15-month interim evaluations, tissue concentrations of manganese were significantly elevated in the livers of the 5,000 and 15,000 ppm groups. Hepatic iron levels were significantly lower in exposed females at the 9-month interim evaluation and in 5,000 and 15,000 males and all exposed females at the 15-month interim evaluation. Pathology Findings: Incidences of thyroid follicular dilatation and hyperplasia were significantly greater in 15,000 ppm male and female mice than in controls. Follicular cell adenomas occurred in one 15,000 ppm male at the 15-month interim evaluation and in three 15,000 ppm males at the end of the study but not in the lower exposure groups or the control group. Follicular cell adenomas also occurred in two control, one 1,500, and five 15,000 ppm female mice at the end of the study. It is uncertain if the slightly increased incidence of follicular cell adenoma is related to the ingestion of manganese (II) sulfate monohydrate. The incidences of focal hyperplasia of the forestomach epithelium were significantly greater in the 15,000 ppm male and exposed female groups. The hyperplasia was associated with ulcers and inflammation in some mice, particularly males. GENETIC TOXICOLOGY: Manganese (II) sulfate monohydrate was not mutagenic in Salmonella typhimurium strains TA97, TA98, TA100, TA1535, or TA1537, with or without exogenous metabolic activation (S9), and did not induce sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster. Tests for induction of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells treated without S9 were positive; with S9, only the sister chromatid exchange test with manganese (11) sulfate monohydrate was positive. CONCLUSIONS: Under the conditions of these 2-year feed studies, there was no evidence of carcinogenic activity of manganese (II) sulfate monohydrate in male or female F344/N rats receiving 1,500, 5,000, or 15,000 ppm. There was equivocal evidence of carcinogenic activity of manganese (II) sulfate monohydrate in male and female B6C3F1 mice, based on the marginally increased incidences of thyroid gland follicular cell adenoma and the significantly increased incidences of follicular cell hyperplasia. The ingestion of diets containing manganese (II) sulfate monohydrate was associated with an increased severity of nephropathy in male rats, focal squamous hyperplasia of the forestomach in male and female mice, and ulcers and inflammation of the forestomach in male mice. These studies were not designed to assess any neurotoxicity that might have been expected with chronic exposure to sufficiently high doses of manganese. Synonyms: Manganese sulfate; manganous sulfate; sulfuric acid. manganese2+ salt (1:1), monohydrate
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PMID:NTP Toxicology and Carcinogenesis Studies of Manganese (II) Sulfate Monohydrate (CAS No. 10034-96-5) in F344/N Rats and B6C3F1 Mice (Feed Studies). 1261 3


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