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

Marked weight loss with cachexia together with severe depression and pain from symmetrical peripheral neuropathy were noted in a 66-year-old man, known to have had diabetes for six years, which required insulin on admission to hospital. The patient died of bronchopneumonia after one year. The severe neuropathy was proven both neurophysiologically and at necropsy. There was no diabetic retinopathy and no histological evidence of renal glomerulosclerosis. There was no evidence of a malignant tumour either clinically or at necropsy.
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PMID:[Diabetic neuropathic cachexia (author's transl)]. 44 96

Severe weight loss in amenorrheic premenopausal women may significantly depress gonadotropin secretion. Gonadotropin leves were studied in 111 postmenopausal women to determine if weight loss and cachexia could similarly affect gonadotropin function. Thirty-three healthy ambulatory postmenopausal women and twenty-seven healthy hospitalized women admitted electively were found to have a wide range of elevated values, whose mean did not differ significantly. Mean levels for both LH and FSH were significantly suppressed (P less than .005) in severely ill postmenopausal women both with or without weight loss. (formula: see text) Recovety from illness in six patients was associated with a rapid rise in FSH levels while LH remained depressed. Two severely ill patients studied over a 6 h period revealed constant depression of both gonadotropins without the characteristic pulses seen in four normal control postmenopausal women. These results indicate that gonadotropin secretion may be suppressed in severely ill postmenopausal women whether weight loss is present of not, and the central nervous regulatory mechanism responsible for intermittant release of gonadotropins is impaired. The disparate FSH and LH recovery indicates that if separate gonadotrophs exist, the LH gonadotroph is more severely affected than the FSH gonadotroph and/or that the responsible regulatory mechanisms are different.
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PMID:The influence of severe illness on gonadotropin secretion in the postmenopausal female. 87 69

The chemotherapeutically effective 5:1 combination N1-(4,5-dimethyl-2-oxazolyl)-sulfanilamide (sulfamoxole) and 2,4-diamino-5-(3,4,5-trimethoxy-benzyl)-pyrimidine (trimethoprim) (CN 3123, Nevin, Supristol) was investigated to determine any evidence of toxicological potentiation or new toxic signs. It was found that CN 3123 had a very low acute toxicity when administered orally to mice, rats and dogs (oral LD50: mouse greater than 12 000 mg/kg; rat greater than 14 000 mg/kg; dog greater than 1000 mg/kg body weight). The combination was also tolerated by rats and dogs in repeated doses administered over a period of 4 or 26 weeks, that greatly exceeded the therapeutic dose. The only change observed occurred in the thyroid, which in all doses administered exhibited a dose-related increase in weight accompanied by histological changes indicating an activation of thyroid function and a hypersecretion of basophilic thyrotropic cells in the anterior lobe of the pituitary. Six weeks after discontinuation of treatment this condition showed a tendency to reversibility or had already returned to normal. In dogs there was a dose-related increase in iodine uptake by the thyroid and a decrease in serum thyroxine over a period of 6 months under the highest dosage of CN 3123 administered. Whereas the thyroid changes observed under the combination could be reproduced with sulfamoxole, no effect on thyroid weight was observed in rats and dogs in the subacute toxicity phase of a comparative investigation with trimethoprim. Moreover, trimethoprim did not increase the effect of sulfamoxole on the thyroid gland. The effect of sulfamoxole on the thyroid is discussed in detail with a review of the literature. It can be characterized as species-specific for sulfonamides in mice, rats, rabbits and dogs but not in monkeys or in man and appears to be caused by the inhibition of the organic binding of iodine in the thyroid, whereby the predisposing factors must vary considerably from species to species. The thyroid hypertrophy observed is due to the activation of the regulatory cycle via the anterior lobe of the pituitary. The following systemic changes occurred after 600 mg CN 3123/kg, a lethal-toxic dosage and the highest administered in the study: reduced body weight, decreased food consumption leading to cachexia, slightly increased SGPT and alkaline phosphatase, slight thrombocyte depression, enlargement and increased fatty degeneration of the liver, occurrence of necrotic areas in the liver, hemosiderin accumulation in Kupffer's cells, and an increase of reticular cells in the spleen. The acute toxicity of CN 3123 and all major functional and histological changes under repeated administration were due exclusively to sulfamoxole. The combination sulfamoxole/trimethoprim gives no indication of toxicological potentiation or new toxic signs.
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PMID:[Toxicological investigations of the combination sulfamoxole/trimethoprim, a new broad-spectrum chemotherapeutic (author's transl)]. 94 24

Diabetic neuropathic cachexia is characterized by neuropathic pain and severe weight loss of unknown aetiology. We describe four patients with diabetic neuropathic cachexia who were found to have malabsorption. Four diabetic patients presented with neuropathic pain, anorexia, depression and weight loss of 16 (range 10-21) kg. None complained of diarrhoea. There were three males and one female, median age 54 (46-67) years. A butterfat test showed a serum turbidity difference of 9 (6-10) light scattering units (normal greater than 60 units). The median serum xylose was low and there was delayed urinary xylose excretion. Urinary indicans, small bowel histology, liver function tests, and thyroid and renal function were normal. Ultrasound scans of liver, gall bladder and pancreas, and endoscopic retrograde cholangiopancreatogram were normal. The patients were treated with pancreatic supplements and a high calorie diet. Three have completely recovered and the other patient is improving. Thus these cases of diabetic neuropathic cachexia appeared to be associated with malabsorption which may be due to pancreatic dysfunction. It is suggested that the management of diabetic neuropathic cachexia should include the investigation and treatment of malabsorption.
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PMID:Diabetic neuropathic cachexia associated with malabsorption. 156 56

Two adult Hampshire rams, unrelated and from separate farms, were examined for the cause of intermittent bloat and, or anorexia which lasted for three to six weeks and caused depression and cachexia. The rumen of each ram was hypermotile and ballottement of the ventral abdomen of each animal revealed an enlarged doughy viscus. Mild prerenal azotaemia, hypokalaemia with metabolic alkalosis, and high rumen chloride concentrations were evident. One ram died during the induction of anaesthesia for an abomasotomy and the other was euthanased after unsuccessful medical therapy. The abomasum of each ram was four to six times larger than that of a normal adult ram and filled with coarse, semi-moist, impacted ingesta. This abnormality was clinically identical to the abomasal emptying syndrome which has been described only in the Suffolk breed.
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PMID:Abomasal dilatation and impaction in two Hampshire rams. 162 57

The haemolytic activity of the total Complement (CH50) and the fractions C3 and C4 were assayed in rats transplanted with Yoshida's tumor and then treated with hCG, LH-FSH and PGE2. A relevant increase, only concerning the values of the CH50 and C3 fraction, was observed in all animals in the early days after the transplantation, probably due to a sort of stress "by transplantation". Afterwards, hCG and PGE2 induced an increase in CH50 and C3 values, but not in the C4 fraction. Treatment with LH and FSH led to a very slight increase in the CH50 and C3. In the following days, as a consequence of the cachexia, a progressive reduction of the values of the Complement was observed in all animals. Those treated with hCG also showed a little increase of survival. The authors suggest that the increase in CH50 and C3 fraction induced by the treatment with hCG and PGE2 could be an expression of increase of the aspecific humoral immunity, as a compensatory mechanism of the cell-mediated immunological depression which occurs during neoplasias.
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PMID:[Complement behavior in rats bearing Yoshida tumors subjected to treatment with gonadotropin and PGE2]. 193 Sep 5

This double-blind, cross-over trial was designed to assess the effects of megestrol acetate (MA) on cancer-induced cachexia. Forty consecutive malnourished patients with advanced non-hormone-responsive tumors receiving no antineoplastic treatment were randomized to receive MA 480 mg/day versus placebo for 7 days. During day 8, a cross-over was made until day 15. Appetite, pain, nausea, depression, energy, and well-being were assessed with a visual analog scale (0 to 100 mm) at 9:00 AM and 4:00 PM during days 6, 7, 13, and 14. Weight (W;kg), tricep skinfold (TS; mm), arm circumference (AC; cm), and calf circumference (CC; cm) were measured at days 1, 8, and 15. Caloric intake (CI; Kcal/day) was determined during days 6, 7, 13, and 14. In 31 evaluable patients, the percentual difference in appetite at 9:00 AM, appetite at 4:00 PM, energy, and well-being after MA was +15.1, +14, +3.2, and +5.2, versus -12 (P = 0.03), -5.1 (P = 0.015), -10 (P = 0.024), and -8.3 (not significant) after placebo. Percentual difference in W, TS, AC, and CC after MA was +0.2, +1, -0.1, and +0.4 versus -0.8 (P = 0.03), -0.8 (P = 0.001), -0.3 (not significant), and -0.5 (P = 0.04) after placebo. CI during MA was 3480 +/- 1574 (48-hour intake), versus 2793 +/- 1542 (P less than 0.001) during placebo. Patients and investigators blindly chose MA in 20 (66%, P = 0.023) and 28 cases (92%, P less than 0.001), placebo in eight and two cases, and made no choice in three and one cases, respectively. Toxicity consisted of mild edema and nausea in three and two cases, respectively. After mean follow-up of 27 +/- 13 days, on an open basis, an average increase in W and AC of 4.8 +/- 1.7 kg and 2.8 +/- 1.7 cm was observed, respectively. The authors conclude that MA is a powerful appetite stimulant with subjective and objective effects on nutritional status.
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PMID:A controlled trial of megestrol acetate on appetite, caloric intake, nutritional status, and other symptoms in patients with advanced cancer. 220 58

Anorexia with its associated decreased food intake and weight loss is a common and profoundly important symptom in cancer, and one which has at times a psychological as well as physical component. When it is physical in origin it may be caused directly or indirectly by the disease process or treatment. Most poorly understood is the anorexia-cachexia syndrome of advanced disease. Psychological causes often reflect anxiety about cancer, its possible progression, depression, anticipatory phenomena, and learned food adversions. Pre-existing psychiatric disorders, especially anorexia nervosa or paranoid states, can substantially complicate cancer treatment. Learned food aversions, which can further restrict limited intake, have been demonstrated in children receiving chemotherapy and may also contribute to aversions of specific foods seen among adult patients after chemotherapy or radiation. Regardless of etiology, psychological management of the anorexia is often helpful. Optimal management often involves use of a combination of modalities: psychotherapeutic, behavioral and/or pharmacologic supplemented by education, counseling and support. Behavioral techniques such as relaxation exercises are useful tools to alter this response as well as to relieve the anxiety precipitated by the patient's concerns about anorexia and weight loss. Environmental interventions and nutritional advice can also be of considerable value in reversing the negative effects of this distressing symptom in cancer.
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PMID:Psychosocial issues in the diagnosis and management of cancer cachexia and anorexia. 252 Feb 68

Cachectin/tumor necrosis factor-alpha (TNF), a protein produced by macrophages upon stimulation, has been implicated as an important mediator of inflammatory processes and of clinical manifestations in chronic infectious diseases. In order to study further the potential role of TNF in infectious diseases, a homologous system was employed in which recombinant Escherichia coli (E. coli) derived bovine TNF (rBoTNF) was injected in cattle, either as a single bolus or in a repetitive treatment-regime. No clinical signs were observed, although changes occurred in hematologic and immunologic parameters when less than 0.5 mg of TNF/100 kg body weight was administered twice daily for 18 days. Prolonged treatment with 0.05-0.5 mg/100 kg induced histologic but no gross changes in the kidneys and liver. When doses were increased above 0.5 mg/100 kg, depression, anorexia, cachexia, and diarrhea appeared rapidly. Pathologic changes were apparent in various tissues including liver, kidneys, and lymphoid organs; body fat depots were depleted. Most of these changes appeared to be reversible; return to normal tissue-morphology occurred within 3 weeks of withdrawal of rBoTNF. The clinical and pathologic changes induced by prolonged rBoTNF administration resembled those observed in some chronic parasitic and viral infections of cattle in which macrophage-activation characteristically occur. Our finding may be relevant to the elucidation of the pathogenesis of these and other chronic infections.
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PMID:Effect of chronic administration of recombinant bovine tumor necrosis factor to cattle. 260 27

Relapsing polychondritis (RP) is an uncommon systemic disorder with a highly variable course. A 17-year-old woman recently presented with a 1-month history of depression, weight loss, chest wall tenderness, hoarseness, and dysphagia. Physical examination revealed cachexia, low-grade fever, pharyngeal erythema, and tenderness of the right auricle, anterior chest, cricothyroid cartilage, and both knees. Laboratory studies included a hematocrit of 34% and a sedimentation rate of 50 mm/hr. Initial improvement on oral corticosteroids was followed by respiratory distress. At that time calcified tracheal cartilage, subglottic stricture, and a saddle nose deformity were present. Despite therapy with steroids, dapsone, and pulse cyclophosphamide, the respiratory distress reoccurred, eventually necessitating tracheostomy. Tracheal cartilage biopsy confirmed the presumptive diagnosis of RP. Bilateral auricular chondritis developed after initial presentation, as did acute vertigo. Although seen in all age groups, less than 10% of cases of RP are seen in children and adolescents. Auricular chondritis (89% of all cases), inflammatory asymetric arthritis (81% of all cases), nasal chondritis (72% of all cases), respiratory tract chondritis (56% of all cases), and audiovestibular abnormalities (46% of all cases) were present in our patient. Relapsing polychondritis may follow a slowly evolving or rapidly progressive course. Appropriate diagnosis and aggressive therapy are recommended to lessen the morbidity and mortality.
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PMID:Relapsing polychondritis in an adolescent. 260 58


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