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)

Lithium carbonate is the drug of choice for the management of bipolar disorder, but 20% to 40% of patients do not exhibit adequate response to this agent. Moreover, adjunctive therapy with tricyclic antidepressants and monoamine oxidase inhibitors (for depression) and neuroleptics (for mania) is widely prescribed in most lithium clinics. These agents, however, may precipitate or exacerbate the subsequent phase of the illness. More recently, carbamazepine, an anticonvulsant drug, has shown promise in the management of bipolar illness. Used either alone or in combination with lithium, carbamazepine has been associated with a response rate of approximately 65% in more than 500 patients enrolled in controlled and uncontrolled studies. The drug's antimanic effects have been clearly demonstrated, but its antidepressant effects must undergo further examination. Other anticonvulsants (such as valproate) appear highly effective. The high-potency benzodiazepines (such as clonazepam) and calcium channel blockers (such as verapamil) are also being evaluated in this patient population.
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PMID:Non-lithium treatment for bipolar disorder. 211 6

This study examined the possible role(s) of central acid-base stimuli in the increase in ventilation induced by hypercapnia in the skate, a response that is not due to an O2 signal (Graham et al., Respir. Physiol., 1990, 80: 251-270). Skate were sampled for cerebrospinal fluid (CSF) acid-base status, intracellular pH of the brain (14C-DMO method), and pHi in other tissues throughout 24 h of exposure to PICO2 = 7.5 Torr. CSF PCO2 rapidly equilibrated with the elevated PaCO2. Despite the much lower non-HCO3- buffer capacity in the CSF, CSF pH was not depressed to the same extent as blood pHa. CSF pH was also regulated rapidly, returning to control levels by 8-10 h, whereas pHa remained significantly depressed at 24 h. Similarly, the pHis of the weakly buffered brain and heart ventricle were initially compensated more rapidly than those of more strongly buffered white muscle and red blood cells. However, brain pHi adjustment slowed markedly after 4 h and stabilized at only 70% compensation by 20-24 h, suggesting that brain intracellular acidosis may play a role in the long-term increase in ventilation. CSF and brain were the only compartments which did not exhibit an apparent compounding metabolic acidosis during the initial stages of hypercapnic exposure. While these results illustrate the primacy of central acid-base regulation, they do not support a role for CSF pH in the long-term elevation of ventilation in response to hypercapnia. Depressions in pHa and brain pHi appear the two most likely candidates for proximate stimuli.
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PMID:Control of ventilation in the hypercapnic skate Raja ocellata: II. Cerebrospinal fluid and intracellular pH in the brain and other tissues. 212 Jul 54

In order to study the role of CO2 and acid-base status in contributing to ventilatory drive, skate were exposed to normoxic hypercapnia (PICO2 = 7.5 Torr) under conditions where the primary O2 drive would remain unaltered. Blood O2 transport was markedly insensitive to CO2, with no Root effect and only a small Bohr effect. Red blood cell pHi was not preferentially regulated, and there was no evidence of RBC swelling or nucleoside triphosphate adjustment. Although there were no changes in arterial O2 levels during hypercapnia, ventilation immediately increased 2.7-fold through large changes in stroke volume and small changes in frequency, and declined only slightly through 24-48 h. PaCO2 equilibrated rapidly with PICO2, driving down arterial pHa, which was 65% corrected through HCO3- accumulation by 24 h. In contrast, the extradural fluid outside the brain equilibrated only very slowly, and was clearly not involved in the ventilatory stimulation. Increased ventilation during hypercapnia may be related to depression in pHa.
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PMID:Control of ventilation in the hypercapnic skate Raja ocellata: I. Blood and extradural fluid. 212 Jul 53

An open clinical study with 20 consecutive outpatients suffering from major depression with melancholia (DSM-III) was carried out. All patients were resistant to desipramine after at least six weeks of treatment. A significant improvement was found in 13 of the 20 patients when lithium carbonate was added. Among the responder patients, five improved in the first week of lithium augmentation, while eight others improved after one week of lithium. The mechanism of action of the lithium augmentation effect in tricyclic-resistant depressed patients is discussed in view of our findings. We suggest that the unified 5-HT/NE hypothesis used in affective disorder could be applied in drug refractory depression.
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PMID:Lithium carbonate augmentation of desipramine in refractory depression. 212 37

Elevation of total protein is the most frequent pathologic finding in the cerebrospinal fluid (CSF) examination. It occurs in a variety of situations, such as inflammation or tumors of the central nervous system (CNS), degenerative disorders, and subarachnoid hemorrhage, or as a result of traumatic taps. It has also been reported, for unknown reasons, in patients with psychiatric disease. In a study of hormone changes in depression, 9 of 24 (38%) patients (13 male, 11 female) were found to have elevated CSF protein levels (greater than 45 mg/dl), whereas no elevations were found in healthy controls (8 male, 9 female). Eight of the patients with the elevated CSF protein levels were male (62%) and one was female (9%). Depressed patients had significantly higher CSF protein levels (44.7 +/- 18.0 mg/dl) than controls (31.5 +/- 6.0 mg/dl) (t = 3.32, df = 30.37, p = 0.002). No relationship was found between CSF protein levels and (1) the use of medication (tricyclic antidepressants, lithium carbonate, or monoamine oxidase inhibitors) or (2) post-dexamethasone suppression test cortisol levels. Female controls, however, tended to have lower protein levels than male controls, whereas female patients had significantly lower levels than male patients. Protein electrophoresis was performed on 21 of the 41 subjects (13 patients, 8 controls). Male patients had nonsignificantly higher absolute concentrations of CSF albumin and the globulin fractions when compared to male controls. These differences in CSF protein do not suggest monoclonal CSF protein production, nor are they the result of this elevated peripheral protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated CSF protein in male patients with depression. 222 29

Bicarbonate and sodium fluxes were measured across the isolated rabbit corneal endothelium under the influence of several inhibitors. Depression of PO2 in the bathing medium decreased net sodium movement but increased bicarbonate movement. Furosemide did not alter bicarbonate fluxes at either 10(-4) or 10(-5) M, but increased passive sodium flux leading to a decrease in net flux. Thiocyanate, at 5 x 10(-3) or 5 x 10(-2) M, decreased active bicarbonate flux and hence net flux, but had no effect on sodium fluxes. Dinitrophenol increased only the passive bicarbonate flux while decreasing both active and passive sodium fluxes, albeit unequally, leading to a decreased net flux. Ethacrynic acid affected only passive bicarbonate flux, while decreasing net sodium flux. The stilbene derivatives, SITS and DIDS caused opposite effects on both sodium and bicarbonate fluxes. SITS decreased net bicarbonate flux by decreasing active and increasing passive flux, yet increased net sodium flux. DIDS, however, increased net bicarbonate flux but decreased net sodium flux. The results may be explained by current models for endothelial ion transport that include a Na+/H+ antiport and a HCO3-/Na+ symport system in parallel with an independent pathway for HCO3- exit from the endothelial cells. When compared with prior corneal swelling data using these same inhibitors, the maintenance of corneal thickness appears to be dependent on the variation of ion fluxes from normal values, and the dissociation of the two active ion fluxes. In addition, there appears to be a significant ability of ion transport systems to compensate for disturbances to other ion exchange or transport mechanisms.
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PMID:Effect of PO2 and metabolic inhibitors on ionic fluxes across the isolated rabbit corneal endothelium. 227 27

Subcutaneous injection of acetazolamide (50 or 200 mg/kg) markedly increased the blood H+ and lowered the HCO3- concentrations in a dose-related manner. The urinary pH and HCO3- excretion were elevated. Restraint stress normalized the blood HCO3- levels but not the H+ concentrations; the high levels of urinary pH and the HCO3- content were unaffected in the acetazolamide-treated animals. These findings suggest that acetazolamide induces metabolic acidosis which appears not to be caused by depletion of blood HCO3- through increased urinary HCO3- excretion. Instead, an extra-renal mechanism could be responsible for the increased blood H+ concentration. Restraint stress significantly decreased the respiratory rate, which was prevented by acetazolamide pretreatment. The reversal of restraint-stress-induced respiratory depression by acetazolamide is probably due to the activation of both peripheral and medullary chemoreceptor sites by acidosis.
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PMID:Dissociation between the renal and blood acid-base actions of acetazolamide in restraint-stressed rats. 227 2

We assessed the efficacy of lithium carbonate in the treatment of 457 male alcoholics in a double-blind, placebo-controlled Department of Veterans Affairs Cooperative Study. Alcoholics either without depression or with a history of major depression, current major depression, or dysthymic disorder were studied. Two hundred eighty-six alcoholics without depression and 171 alcoholics with depression began the 52-week outpatient study; 172 alcoholics (60.1%) without depression and 108 alcoholics (63.2%) with depression completed the study. Among both all alcoholics who began the study and a subgroup who completed the study, no significant differences between alcoholics who took lithium and those who took placebo were found for the following outcome measures:number of alcoholics abstinent, number of days of drinking, number of alcohol-related hospitalizations, changes in rating of severity of alcoholism, and change in severity of depression. Similarly, no significant differences were found when only the 82 alcoholics compliant in taking lithium and the 89 alcoholics compliant in taking placebo were considered. In our study, lithium treatment did not affect the course of alcoholism in either depressed or nondepressed alcoholics.
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PMID:Lithium treatment of depressed and nondepressed alcoholics. 276 23

The addition of lithium carbonate to various antidepressant agents, including heterocyclics and monoamine oxidase inhibitors, has been reported to rapidly effect an antidepressant response in otherwise treatment-unresponsive depressed patients. Fifteen depressed patients diagnosed by DSM-III criteria who had not responded to double-blind treatment with carbamazepine were treated with the blind addition of lithium to carbamazepine. Eight patients (53%) responded with a moderate to marked improvement. The time to onset of substantial clinical improvement was rapid; ie, the mean (+/- SD) was 4.1 +/- 2.4 days for lithium potentiation compared with 9.7 +/- 4.1 days in a separate group of depressed patients responding to lithium alone. Side effects during carbamazepine-lithium combination therapy were minimal. The mechanisms by which lithium appears to rapidly potentiate the effects of carbamazepine in treatment-resistant depression are discussed.
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PMID:The addition of lithium to carbamazepine. Antidepressant efficacy in treatment-resistant depression. 250 30

Leukopenia is a common complication noted in patients receiving radiotherapy and/or chemotherapy but no effective method has been reported so far to correct this complication. In the field of psychiatry, lithium carbonate used in treating depression has been noted to have induced leukocytosis as a side effect. From July 1985 to December 1987, a total of 111 patients receiving radiotherapy and/or chemotherapy with leukopenia were included in this study. There were sixty nine patients who received lithium carbonate and the remaining forty two patients served as control group were allowed to stop their primary treatment temporarily without medication during their period of leukopenia. For the group given lithium carbonate, 79% of the patients were able to recover their white blood count (WBC) above 3,000/cu.mm. within 5 days and finished their primary treatment smoothly. For the control group, it took them on the average about 11.8 days of rest in order to recover their WBC level to 3,000/cu.mm. and above. Reports in the recent literature indicates that the average toxic level is around 1.5 mEq/l to 2.0 mEq/l. In our study, the average serum lithium level before administration is 0.44 mEq/l, it reached 0.59 mEq/l and 1.08 mEq/l after the fifth and the 10th day of intake respectively. From this laboratory data, obviously no patient reached the toxic level and no side effects were noted clinically. Based on these figures, we can see clearly that lithium carbonate can shorten the period of leukopenia in comparison to the control group which was not given any medication.
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PMID:The use of lithium carbonate to correct leukopenia during cancer treatment. 250 18


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