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Biomedical subjects

M Ligumsky

Publications and source records attributed to M Ligumsky.

70 records · Page 4Linked to original sources
PubMed1981

Enhanced thromboxane A2 and prostacyclin production by cultured rectal mucosa in ulcerative colitis and its inhibition by steroids and sulfasalazine.

Accumulation of 6-ketoprostaglandin F1 alpha and thromboxane B2, the stable metabolites of prostacyclin I2 and thromboxane A2 respectively, by cultured rectal mucosa obtained from patients with active ulcerative colitis was significantly higher than their respective accumulation by cultured biopsy specimens obtained from normal subjects. Accumulation of prostacyclin I2 and thromboxane A2 by rectal mucosa obtained from ulcerative colitis patients in remission was not enhanced. Prostacyclin I2, thromboxane A2, and prostaglandin E2 accumulation was significantly inhibited by the addition to the culture medium of 5-aminosalicylic acid, flufenamic acid, aspirin, azathioprine, and methylprednisolone. Sulfapyridine inhibited significantly only prostaglandin E2 and prostacyclin I2 while sulfasalazine inhibited thromboxane A2, prostaglandin E2, and prostacyclin I2 accumulation. Flufenamic acid potentiated the inhibition of prostaglandin E2 accumulation induced by methylprednisolone when administered alone. These results suggest that in addition to the mediation by prostaglandin E2, thromboxane A2 and prostacylin I2 may also be involved in the inflammatory response in ulcerative colitis. Moreover, the therapeutic effects of steroid hormones and sulfasalazine may be partially related to their inhibition of colonic prostaglandin E2, prostacyclin I2, and thromboxane A2 synthesis.

Colitis, Ulcerative↗
PubMed1980

Glycogenic acanthosis of the esophagus. A benign but confusing endoscopic lesion.

During 160 consecutive fiberoptic endoscopic examinations, glycogenic acanthosis was diagnosed in 24 patients. The endoscopic diagnosis was confirmed histologically in the first 14 patients from whom biopsies were obtained. No correlation with any other disease affecting the gastrointestinal tract was found including reflux esophagitis. This common benign condition must be differentiated from lesions of similar appearance and more important prognostic significance.

Biopsy↗
PubMed1979

Papaverine stimulation of prostaglandin E2 production by cultured rabbit gastric mucosa.

Prostaglandins (PGs) are synthesised by gastric mucosa, and have been shown to inhibit gastric acid secretion and ulcer formation in man and experimental animals. Recently exogenous PGs, mainly of the E group, have been used for the treatment of peptic ulcer disease. We therefore searched for a drug that would stimulate endogenous gastric prostaglandin E(2) (PGE(2)) synthesis. Rabbit gastric mucosa slices were cultured for 22 hours at 77 degrees C. PGE(2), measured by radioimmunoassay, was found to be linearly secreted into the culture medium. PGE(2) accumulation in the medium during 22 hours of culture was 7.9+/-0.5 (SE) ng/mg tissue (N=20). Addition of papaverine (100 mu/ml), a cyclic nucleotide phosphodiesterase inhibitor, resulted in a significant increase (250% of control) in PGE(2) accumulation in the medium: 24.3+/-1.8 ng/mg tissue (N=25). Isobutylmethylxanthine (IBMX 100 mug/ml), another phosphodiesterase inhibitor, only slightly increased PGE(2) accumulation, while 8 bromo-cyclic AMP (1 mM) had no effect. Under these conditions IBMX increased by 20-fold mucosal cyclic AMP levels: 3.9+/-0.3 pmol/mg tissue (N=8) as compared with control levels: 0.2+/-0.03 pmol/mg tissue (N=8). Papaverine, however, did not alter mucosal cyclic AMP accumulation. These results indicate that papaverine stimulates PGE(2) production by cultured rabbit gastric mucosa and that this stimulation is not related to the inhibition of phosphodiesterase activity and accumulation of mucosal cyclic AMP. Papaverine induced stimulation of PGE(2) production should be further evaluated regarding its possible beneficial effects in protecting gastric mucosa and in reducing acid secretion in peptic ulcer patients.

Animals↗
PubMed1978

Effect of co-trimoxazole on normal creatinine clearance.

The effect of co-trimoxazole on creatinine clearance was studied in six individuals with normal kidney function. The mean decrease in creatinine clearance during treatment was 47 ml/min and the mean increase in plasma-creatinine was 0.27 mg/dl (P less than 0.01). Although creatinine clearance decreased by 29%, sodium excretion increased by 22%. Discontinuation of co-trimoxazole resulted in a prompt return of creatinine clearance to pretreatment values, and a consistent antinatriuresis.

Adult↗
PubMed1978

Role of prostaglandins in ulcerative colitis. Enhanced production during active disease and inhibition by sulfasalazine.

Prostaglandin E2 (PGE2) level in rectal mucosa excised from 17 patients suffering from ulcerative colitis was 2-fold higher than that found in rectal mucosa of 17 normal subjects: 2.0 +/- 0.4 and 0.9 +/- 0.2 ng per mg of wet tissue, respectively. Accumulation of PGE 2 in 24-hr cultures of rectal mucosa specimens obtained from patients with ulcerative colitis was 112% higher than that observed in cultures from control subjects. Addition of sulfasalazine, sulfapyridine, and 5-aminosalicylic, acid to the culture medium of ulcerative colitis mucosa resulted in inhibition of PGE2 production by 34, 32, and 62%, respectively, compared to rectal specimens cultured in drug-free medium. These results suggest that PGE may mediate the inflammatory response in ulcerative colitis and that some of the therapeutic effect of sulfasalazine and its constituents are related to the inhibition of PGE synthesis.

Aminosalicylic Acids↗
PubMedDate not supplied

Indomethacin-induced colonic ulceration and bleeding.

OBJECTIVE: To report a case of nonsteroidal antiinflammatory drug (NSAID)-induced lower gastrointestinal (GI) bleeding. CASE SUMMARY: A patient in whom short-term ingestion of indomethacin was associated with colonic ulceration and significant gastrointestinal bleeding is described. DISCUSSION: The bleeding ulceration of the ascending colon, associated in our patient with short-term indomethacin intake, confirms previous reports of the drug's deleterious effect on the lower GI tract. The incidence of NSAID injury of the small intestinal colon may be higher than that previously reported. CONCLUSIONS: A prospective study of NSAID users could assess the magnitude of lower GI lesions, concomitant with upper GI evaluation, and help determine limitations in the use of this drug class.

Aged↗
PubMedDate not supplied

Functional and morphological alterations following isolated rat stomach irradiation. A model for estimation of radiation injury.

Exposure of the stomach to tumoricidal doses of radiation is associated with functional and morphological changes. The experimental data have been mainly obtained from studies of whole body irradiation of the stomach. We investigated the separate effect of irradiation on the surgically exposed stomach with doses of between 3 and 30 Gy. A dose-dependent decrease in free and total acidity was observed with relatively low doses (5-9 Gy). Serum pepsinogen and serum gastrin levels increased following irradiation with doses ranging from 5 to 15 Gy. Two phases of increased regenerative activity were documented (between the 1st and 3rd weeks and between the 4th and 8th weeks). No radioprotective effect was observed when sucralfate or misoprostol were utilized. Further investigations are mandatory in order to find an effective radioprotector for the irradiated stomach.

Animals↗
PubMedDate not supplied

Spontaneous midesophageal rupture.

Spontaneous rupture of the esophagus is rare. To date, 17 such cases, including our patient, have been reported in the literature. We present a case of true spontaneous rupture that occurred during sleep. Because the correct diagnosis was made 36 h after the rupture, treatment consisted of surgical drainage only. The drainage was extrapleural, though a posterior mediastinal approach, thereby avoiding the complication of empyema. The paraesophageal abscess was repeatedly irrigated with povidone-iodine solution. The patient recovered after a long period--56 days--of hospitalization. The report includes a review of the signs and symptoms of esophageal perforation, the current mode of therapy, and some speculation on the pathogenesis of true spontaneous perforation.

Drainage↗