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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 72-year-old man was found to have a 12 mm solid lesion in the pancreatic tail and an 8 mm cystic lesion in the body of the pancreas by computed tomography carried out during a routine follow-up study of his adult-onset diabetes mellitus. A distal pancreatectomy was performed revealing the pancreas to have an adenocarcinoma in the tail and a conglomeration of intraductal papillary adenoma in the body. A review of the literature disclosed similar coexistences of cystadenoma and carcinoma in four patients, none of which was documented with preoperative imaging features such as we had.
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PMID:Adenocarcinoma and concomitant intraductal papillary adenoma in the pancreas. 180 50

Cytokine effects on permanent cell lines of transformed mouse pancreatic alpha- and beta-cells were compared. The beta-tumor cell 1 (beta TC1) line (from an adenoma created in transgenic mice expressing the SV40 large T-antigen oncogene under control of the rat insulin II promoter) produced insulin predominantly, although small quantities of intracellular glucagon (100:1 insulin to glucagon) were detectable by radioimmunoassay. The alpha TC1 line (from an adenoma created in transgenic mice expressing the SV40 large T-antigen oncogene under control of the rat preproglucagon promoter) produced not only glucagon but also considerable quantities of insulin (4:1 glucagon to insulin) and preproinsulin mRNA. We therefore cloned alpha TC1 cells and obtained 12 glucagon-producing clonal cell lines that did not produce levels of insulin detectable by radioimmunoassay. Analysis by Northern blotting of total RNA from two lines, alpha TC1 clones 6 and 9, confirmed the absence of preproinsulin mRNA. No somatostatin or pancreatic polypeptide was detected by immunohistochemical staining in alpha TC1 clones 6 or 9 or beta TC1 cells. Rat recombinant gamma-interferon (IFN-gamma; 5-250 U/ml) or mouse recombinant interleukin 1 (IL-1; 1-25 U/ml) individually inhibited DNA synthesis in beta TC1 cells after 3 days of treatment. The two cytokines in combination acted synergistically to further depress DNA synthesis and increase cytotoxicity. In contrast, alpha TC1 clone 9 cells were not sensitive to inhibition of DNA synthesis by each cytokine individually, although glucagon synthesis was inhibited. The combination of these cytokines caused marked inhibition of DNA and glucagon syntheses in alpha TC1 clone 9 cells. alpha TC1 clone 9 cells were somewhat more resistant to the cytotoxic action of the combined cytokines than were beta TC1 cells. Incubation with 50 U/ml IFN-gamma induced class II MHC molecules (I-Ab, I-Ad, and I-Ed) and enhanced the constitutive expression of class I molecules (H-2Kb and H-2Kd) on the cell surfaces of beta TC1, uncloned alpha TC1, and alpha TC1 clones 6 and 9. Thus, these cell lines are heterozygous for MHC alleles derived from both parental strains used in the construction of the transgenic mice [C57BL/6J (H-2b) and DBA/2J (H-2d)]. Class II gene transcription induced by IFN-gamma was confirmed in beta TC1 and alpha TC1 clone 9 cells by Northern blot analysis with A alpha-, A beta-, E alpha, and E beta-DNA probes.(ABSTRACT TRUNCATED AT 400 WORDS)
Diabetes 1990 Apr
PMID:Comparison of cytokine effects on mouse pancreatic alpha-cell and beta-cell lines. Viability, secretory function, and MHC antigen expression. 210 69

To evaluate the long term results after operation of islet cell adenomas we analyzed our own patient material from 1.1.1967 to 30.11.1988. During this time we operated 43 patients with islet cell tumors. 36 patients had benign adenomas. After a medium time of 6.7 years we analyzed the outcome of 33 patients. Only one out of 29 patients with a solitary adenoma had a recurrence of the disease. Two patients after pancreas resection had diabetes mellitus. In contrast to this only one out of four patients with multiple adenomas was free of symptoms. One patient had diabetes mellitus. In two patients five operations were necessary up to now, nevertheless one of the patients had persistent hypoglycaemic symptoms. These results show that the most important factor in therapy of patients with islet cell tumors is the recognition and complete removal of multiple adenomas.
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PMID:[Long-term results following surgical treatment of islet cell adenoma]. 215 42

P. Carpenter (1986) used the term "incidentalomas" in connection with all incidentally discovered adrenal masses. Previously these masses were frequent incidental discoveries at autopsies, but now, with the increasing use of abdominal computed tomography. In the last 10 years 5 patients with incidentally diseases, significant number of them have been detected. In the last 10 years 5 patients with incidentally discovered adrenal masses (4 males and 1 female, aged from 37 to 66 years) were examined and treated in our Department. Long-lasting arterial hypertension was found in all of them, and in one patient here was impaired glucose tolerance with further evolution of diabetes. A possible excessive secretion of glucocorticoids, mineralocorticoids, androgenes and catecholamines was excluded. However, markedly elevated urinary excretion of pregnanediol, proved in all patients, indicated to a possible preservation of the first reaction in the biosynthesis of cortisol, at least synthesis of pregnenolone from cholesterol. One patient, submitted to a regular functional and morphological evaluation of previously discovered 'incidentaloma', showed no sign of expansion or pathological hormonal activity. Four patients were operated because of the suspected expansion and malignant alteration of the adrenal nodus. The histological proof of adrenocortical adenoma or hyperplasia, composed of the 'fasciculata-like' cells, postoperatively maintained elevated values of steroid precursors in urine, and also a finding of adrenocortical noduses in remained adrenal noduses, confirmed the presumption that such masses could be the non-essential finding in long-lasting arterial hypertension and degenerative changes during aging.
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PMID:[Adrenocortical "incidentalomas" as a diagnostic and therapeutic problem]. 221 35

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

150 patients dying from renal cell carcinoma are studied in order to reveal the background disease, incidence and character of the nephrosclerosis and the possible morphogenetic link between nephrosclerosis and carcinoma. Renal cell carcinoma is found to develop in 82.7% of cases in the kidneys with signs of nephrosclerosis. The diffuse nephrosclerosis developing in connection with the hypertension disease, atherosclerosis, diabetes mellitus, chronic pyelonephritis, nephrolithiasis is the most important. Proliferation of the canaliculi epithelium with the appearance of undifferentiated cells are regularly found in the nephrosclerotic areas. The disturbance of the epithelium differentiation is followed by the development of dysplasia the phenotypical variants of which are similar to those of renal cell carcinoma. Adenomas are found in 11.3% of cases of renal cell carcinoma which may originate from the adenomas developing against the background of nephrosclerosis.
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PMID:[Background and precancerous processes in renal cell carcinoma]. 280 41

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.
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PMID:Hyperadrenocorticism in cats: seven cases (1978-1987). 284 Dec 69

SMS 201-995 (Sandostatin) was studied using low doses (50 to 100 micrograms) administered subcutaneously every 12 hours. A single 50-micrograms dose of SMS 201-995 effectively controlled gastric acid and blood gastrin levels for 12 hours in three patients with benign gastrinomas and was useful in their perioperative management. Higher doses of the agent (500 to 800 micrograms per day) had no effect on metastases in one of two patients with metastatic gastrinoma. In the other patient, one tumor shrank but the other continued to grow after three months of treatment while serum gastrin levels did not change. Cultured metastatic tumor tissue from this patient released different forms of gastrin; growth rates varied, independent of uptake of SMS 201-995, and gastrin release increased. A neonate with nesidioblastosis maintained normal blood glucose levels while receiving SMS 201-995 therapy following a 95 percent pancreatic resection. In two elderly patients with organic hypoglycemia--one with a single benign adenoma and one with multiple adenomatosis--the somatostatin analogue did not prolong the hypoglycemia-free interval. In nine patients with carcinoid syndrome, flushing was uniformly controlled with 50 micrograms of SMS 201-995 administered every eight to 12 hours. One of the nine required exocrine pancreatic replacement. After six months of treatment, three of the nine had no change in tumor size and one had remission of symptoms and stopped treatment. In two patients with vipoma, SMS 201-995 controlled diarrhea and reduced levels of vasoactive intestinal peptide; tumor necrosis occurred in one patient. In a patient with diabetic diarrhea unresponsive to all treatments, SMS 201-995 therapy controlled the diarrhea but did not interfere with control of the diabetes.
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PMID:Somatostatin analogue (SMS 201-995) in the management of gastroenteropancreatic tumors and diarrhea syndromes. 287 47

Two patients with neurofibromatosis and somatostatinoma are described, one patient in addition having a parathyroid adenoma diagnosed post mortem. The other patient had a partial somatostatinoma syndrome with diabetes, abdominal pain and cholelithiasis. The tumour was diagnosed preoperatively and metabolic studies demonstrated mild diabetes mellitus apparently due to suppression of insulin secretion by somatostatin, since oral glucose tolerance returned to normal post-operatively despite hemipancreatectomy. The tumour also secreted gastrin. There are now 18 reported cases of neurofibromatosis and duodenal carcinoid tumours which makes a genuine association between these two conditions very likely. With the present two cases, seven of the carcinoid tumours in this group have been positively identified as somatostatinomas. The histological finding of psammoma bodies is important in the diagnosis of duodenal somatostatinomas.
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PMID:Neurofibromatosis associated with somatostatinoma: a report of two patients. 290 5

A case of microcystic adenoma (glycogen-rich cystadenoma) of the exocrine pancreas in a 62-year-old white female presenting with adult-onset diabetes mellitus is reported. Clinical, histopathologic, and ultrastructural findings are discussed with particular emphasis on the presence of myoepithelial cells, a morphologic feature not seen in this tumor previously. The controversy over diabetes mellitus as a significant related factor is also discussed.
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PMID:Microcystic adenoma of the pancreas with myoepithelial cells. A hitherto undescribed morphologic feature. 299 Jan 90


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