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)

The 'missing peptidase' hypothesis to explain the aetiology of coeliac disease has never been satisfactorily resolved and recent reports suggest that coeliac brush borders may have depressed levels of specific peptidase enzymes. It has been inferred from these studies that the subsequent brush border digestion of gliadin peptides may therefore be defective. In this present study a sensitive fluorometric assay was used to measure the hydrolysis of a peptic-tryptic digest of gliadin by both normal and coeliac brush borders. The coeliac brush borders were as efficient as the normals in hydrolysing gliadin peptides and showed no depression of any specific peptidase activity.
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PMID:Breakdown of gliadin peptides by intestinal brush borders from coeliac patients. 638 Dec 46

The activities of microvillus aminopeptidase (microsomal, EC 3.4.11.2), dipeptidyl peptidase IV (EC 3.4.14.-), glycyl-leucine dipeptidase (EC 3.4.13.11), proline dipeptidase (EC 3.4.13.9), sucrase (EC 3.2.1.48) and gamma-glutamyl transpeptidase (EC 2.3.2.2) were measured in peroral intestinal biopsies taken from patients with coeliac disease in the acute phase and in remission. A comparison with the amounts of corresponding activities from a reference group showed that all the measured activities were significantly decreased in the acute phase of the disease. In patients in remission only microvillus aminopeptidase and dipeptidyl dipeptidase IV displayed a substantial depression as compared to the reference group. It is suggested that a primary mucosal digestion defect will result in lack of substrate for other intestinal enzymes. This is a situation comparable to starvation and may explain the variation in the grade of restitution for the different enzymes.
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PMID:Intestinal peptidases and sucrase in coeliac disease. 700 82

Adult coeliac patients living in a defined area of Sweden were examined for a history of major psychiatric illness occurring before the coeliac disease had been diagnosed. Eight of 42 patients without dermatitis herpetiformis (19%) and one medical control subject had attended a psychiatric clinic over a 10-year period for neurotic disorders (p less than 0.05), mostly depression. Our study shows that psychiatric illness may be severe in undiagnosed adult coeliac patients. It was found to be the commonest reason for granting disability pension in our series, having occurred in altogether six patients.
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PMID:Psychic disturbances in adult coeliac disease. I. Clinical observations. 713 33

Psychiatric illness has been observed to be a main cause of disability in undiagnosed adult coeliac disease. A consecutive series of 16 patients with newly detected adult coeliac disease underwent assessment of personality by means of the MMPI. The coeliacs scored high, 70.3 +/- 12.5, only on MMPI scale 2 ('depression'), which was the only significant difference from matched surgical controls. The score correlated 0.66 with daily fat excretion (p less than 0.05) but was unrelated to abdominal complaints. The general intellectual level, assessed by the SRB test, was similar in coeliacs and controls. Our results suggest that depressive psychopathology is a feature of adult coeliac disease and may be a consequence of malabsorption.
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PMID:Psychic disturbances in adult coeliac disease. II. Psychological findings. 713 34

Adults with untreated coeliac disease show signs of reduced central monoamine metabolism. The reason is obscure, and in the present study we investigated the brain availability of the monoamine precursors tryptophan and tyrosine in 11 untreated coeliac patients. The brain availability appeared to be unaffected in most of the patients, and the rise in serum tryptophan levels after oral casein administration was similar in coeliac and control subjects. Four of the 11 coeliac patients showed impaired brain availability with respect to tryptophan. Since they comprised all with a history of major psychiatric illness, this observation may have therapeutical implications for the management of depression in adult coeliac patients.
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PMID:Brain availability of monoamine precursors in adult coeliac disease. 713 41

Urinary excretion of piperidine, a heterocyclic pressor amine of gut bacterial origin and nicotine-like activity in the brain, has been estimated by a gas chromatography method in healthy men and women, in normal breast-fed and formula-fed infants and in infants with untreated coeliac disease. The excretion of piperidine cannot usually be detected during the first week of life. The amount present in urine increases upon weaning with higher excretion in formula-fed than in breast-fed infants at four to six months of age. When premature infants fed on human milk are weaned, the urinary content of piperidine rises from undetectable amounts to normal for age. The high content present in untreated coeliac disease may be responsible for the initial mental depression commonly seen in this disease and suggests that piperidine is one of the "auto-intoxicating" substances arising from the bacterial decomposition of protein postulated by Metchnikoff in 1903 but hitherto unidentified.
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PMID:Increased excretion of a brain depressor amine in infantile coeliac disease and in healthy infants on a high protein milk diet. 723 85

This study was carried out to determine if an RE depressing substance is present following intestinal ischemia or thermal injury. Intestinal ischemia consisted of occluding the celiac and mesenteric arteries for 3 hr, and thermal injury was a 30% body-surface-area scald (30 sec in 90 degrees C water) in dogs anesthetized with sodium pentobarbital. Immediately following release of the arterial occlusions or 3 hr after thermal injury, portal vein blood was collected and plasma extracts prepared. RE depressing substance activity was assayed by measuring the colloidal carbon clearance rate in rats following the IV injection of the plasma extracts or saline. Plasma extracts from control animals never had detectable RE depressing substance activity. Following intestinal ischemia RE depressing activity was consistently detected in 6 assays on plasma extracts from 12 animals. Thermal injury was associated with the presence of RE depressing activity in each of the 4 animals studied. Neither intestinal ischemia or thermal injury was associated with a significant decrease in mean arterial blood pressure. These results indicate that RE depressing substance may contribute to the RES depression and impaired host-defense seen following intestinal ischemia and thermal injury.
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PMID:Presence of a reticuloendothelial depressing substance in portal vein blood following intestinal ischemia and thermal injury. 730 32

One of the ulcerogenic mechanisms by which ethanol induces mucosal lesions in the stomach is the depression of gastric mucosal blood flow (GMBF). The goal of this study was to determine whether lesion formation is the result of vascular ischemia alone or ischemia combined with congestion. The aims of this study were to answer this question by evaluating the relationship between GMBF, oxygen saturation (ISO2) and hemoglobin volume (IHb) in the gastric mucosa under the influences of ethanol and prostaglandin E2 (PGE2) in the ischemic and congestive states, using a laser Doppler flowmeter and tissue spectrum analyzer. Ligation of the gastric celiac artery or vein markedly decreased the GMBF and the ISO2 level. The former procedure also reduced but the latter increased the IHb level. Ethanol administration produced effects similar to venous ligation, i.e. vascular stasis with ischemia. There was a negative correlation between GMBF and severity of lesion formation after ethanol administration. However, at the lesion site all the hemodynamic parameters were significantly reduced, indicating that a necrotic condition had occurred. PGE2 preincubation (25 micrograms) elevated GMBF, ISO2 and IHb levels. It also alleviated the reduction of blood flow induced by ethanol and increased the recovery rate of GMBF and ISO2 after the release of arterial or venous ligation. It is concluded that the decrease in blood flow due to ethanol is probably caused by constriction of venules rather than arterioles inside the mucosa, and this effect could lead to vascular congestion. PGE2 probably dilates both arterioles and venules in the gastric mucosa and thereby increases the blood flow in the gastric mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of hemodynamic changes in rat stomachs by laser Doppler velocimetry and reflectance spectrophotometry. Effects of ethanol and prostaglandin E2 under ischemic and congestive conditions. 770 51

The present paper relates the case of a young female patient who suffers from epilepsy and depressive disorder. The discovery of digestive disturbances associated to an anaemia and various tests induces a diagnosis of a coeliac disease. Such relationship is unusual with depression and epilepsy. The author insists on the fact that a diagnostic cannot fix a person in a unique mode of attendance because a disease can mask another one.
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PMID:[A misleading depression]. 782 17

We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals. Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.
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PMID:Spinal cord infarction: etiology and outcome. 915 13


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