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Biomedical subjects

J A Rull

Publications and source records attributed to J A Rull.

At least 37 records · Page 2Linked to original sources
PubMedDate not supplied

An ectopic adrenocorticotropic hormone syndrome caused by a sacrococcygeal chordoma: report of a case with a slow progression.

OBJECTIVE: To report the first case of an ectopic adrenocorticotropic hormone (ACTH) syndrome caused by a sacrococcygeal chordoma. METHODS: We present a case report with clinical, laboratory, and histologic details. RESULTS: A 76-year-old man was admitted to the hospital because of urinary obstruction. Five years previously, a urethral mass had been detected, and transurethral prostatectomy had been performed. Annual computed tomographic (CT) scans showed no change in size of the mass. In 1995, skin hyperpigmentation, central obesity, and bilateral edema were noted. The patient was admitted to the hospital in July 1996. A CT scan of the abdomen revealed a large mass close to the sacrum and compressing the bladder and rectum. Cortisol measurements (AM and PM) were 309 and 271 ng/mL, respectively. The plasma ACTH concentration was extremely elevated (3,125 pg/mL). Although resection of the mass was attempted, complete resection was not possible because the tumor had infiltrated the sacrum. Plasma cortisol concentrations in samples obtained 7 and 8 days postoperatively were normal. Plasma ACTH was substantially decreased (180 pg/mL) but remained above normal. The histologic features of the tumor were compatible with a chordoma. Neoplastic cells stained positively for ACTH. CONCLUSION: This report describes the first case of an ectopic ACTH syndrome caused by a sacrococcygeal chordoma. A slow progression of symptoms in an ectopic ACTH syndrome had been described only for carcinoid tumors. These data add a new entry to the list of neoplasms capable of causing this syndrome.

Journal Article↗
PubMedDate not supplied

[Diagnosis of malignant and benign insulinoma. Experience of the National Institute of Nutrition].

INTRODUCTION: Insulinomas are uncommon tumors, their incidence is approximately one case for 1 million population per year. OBJECTIVE: To expose our experience in the diagnosis of these tumors at the Instituto Nacional de la Nutrición Salvador Zubirán. MATERIAL AND METHODS: All patients with histologic diagnosis of insulinoma were reviewed; the period was from 1959 to 1996. The methods used for diagnosis and localization as well as the clinical picture according to the benignity or malignity of the tumor were registered. RESULTS: Eighteen patients were included, four of them with malignant tumors. In two patients islet cell tumors occurred in association with MEN type I, one of them benign and the other malignant. The mean age of patients with benign tumor was 38.2 +/- 13.5 years, in those with malignant tumors it was 51.5 +/- 16.2 years. The median period between symptoms and diagnosis was 34.4 +/- 15 months for benign tumors and 6 +/- 1.1 months for those with malignant tumors (p = 0.02). Patients with increasing weight had benign tumors. The 24 hours fasting test was not done in patients with malignant tumors because of the severity of hypoglycemia. The insulin/glucose ratio in patients with a malignant tumor was 5.2 +/- 4.7, while in patients with a benign tumor it was 1.82 +/- 1.7. The imaging studies showed that three patients with malignant tumors had hepatic metastasis and one had lymph node metastasis. The low accuracy of localization by radiological methods is due to the size of the tumor (> 2 cm). CONCLUSIONS: Malignant insulinomas are more aggressive and the delay of diagnosis is shorter that in cases with benign tumors. Selective arteriography remains the best preoperative localization procedure.

Adenoma, Islet Cell↗
PubMedDate not supplied

[Limitations of the diagnostic criteria for type 2 diabetes and glucose intolerance].

Conflicting results have been published during the past three decades regarding the cut points for the diagnosis of diabetes and glucose intolerance. Two major consensus changed the diagnostic values; the last revision occurred in 1997. After the publication of the new criteria, the controversy grew. New evidence was published demonstrating that the new cut points were inappropriate. The purpose of this review paper is to summarize the currently available information useful to evaluate the sensibility and specificity of the diagnostic criteria and to discuss the difficulties to define properly the cut-points for the diagnosis of diabetes and glucose intolerance.

Aged↗
PubMedDate not supplied

The combination metformin/glyburide exerts its hypoglycemic effect mainly by increasing insulin secretion: a controlled, randomized, double-blind, crossover study.

The aim of the present study was to describe the mechanism by which the combination glyburide/metformin exerts its additive hypoglycemic effects. This is a double-blind, randomized and crossover clinical trial. Patients (n = 20) were included in a run-in period of 8 weeks in which an isocaloric diet was prescribed. If they did not achieve the treatment goals (n = 15), they received glyburide, metformin or combined treatment for 10 weeks each using three possible sequences. The dosage was adjusted to reach fasting plasma glucose (FPG) < 7.7 mmol/l. Treatment periods were separated by a 6-12 week washout period. At the beginning and the end of every treatment, insulin sensitivity and insulin secretion were measured by means of a minimal model and an oral glucose tolerance test. All treatment periods were completed by 12 cases. The glycemic goal was reached in 1 case during metformin, in 5 during glyburide and in 10 during the combination. The greatest reduction in HbA1c was achieved during the combination (HbA1c 11 +/- 1.6 vs 9.8 +/- 1.9 vs 9.0 +/- 2.1% for metformin, glyburide and the combination, p < 0.001). Increased insulin secretion was the explanation for the additive effects of the combination (percentual change in acute insulin response during the minimal model = 5.8 vs 51.5 vs 88.2% for metformin, glyburide and the combination, p < 0.05). No change in insulin sensitivity resulted from the treatments. In conclusion, the additive hypoglycemic effects of the combination glyburide/metformin was caused by increased insulin secretion.

Adult↗
PubMedDate not supplied

A controlled trial of pravastatin vs probucol in the treatment of primary hypercholesterolemia.

We compared the safety, tolerability and efficacy of the HMGCoA reductase inhibitor pravastatin and probucol in the treatment of patients with primary hypercholesterolemia using an active, drug controlled, double blind, randomized, double placebo design. Patients were included if LDL-C levels after a minimum of six weeks on an AHA phase I diet were greater than 150 mg/dL and triglycerides were less than 350 mg/dL. Included patients were randomly assigned to either pravastatin 40 mg pm or probucol 500 mg bi. They also received matching placebos for each drug. The active drug period lasted 16 weeks, during which the patients were seen at 4, 8, 12 and 16 weeks after baseline. There were no significant differences in baseline values between both treatment groups. Significantly lower values of total cholesterol and LDL-C were observed with pravastatin as compared to probucol. While a non significant increase of HDL-C was observed with pravastatin, a remarkable and statistically significant decrease was observed with probucol. A large dispersion of triglycerides levels was observed with both drugs and no statistically significant changes were demonstrated. Both pravastatin and probucol were well tolerated: only minimal clinical and laboratory changes, not considered to have been drug-related, were observed. No changes, considered drug-related, were observed in the cristalline lens. This study shows an overall superiority of pravastatin over probucol with significant larger decreases of total cholesterol and LDL-C and a better effect on HDL-C.

Double-Blind Method↗
PubMedDate not supplied

Combination daytime chlorpropamide-metformin/bedtime insulin in the treatment of secondary failures in non insulin dependent diabetes.

OBJECTIVES: To determine the effectiveness of the combination therapy with daytime chlorpropamide-metformin and bedtime NPH insulin in the treatment of secondary failures in NIDDM and to study its effects on insulin secretion. DESIGN: Non randomized open study with a duration of two months. The patients were followed six months after ending the study. INSTITUTION: Department of Diabetes and Lipid Metabolism. Instituto Nacional de la Nutrición "Salvador Zubirán", Mexico City. CHARACTERISTICS OF THE PATIENTS: Nine patients (seven women and two men) were included. All had NIDDM and secondary failure to antidiabetic oral drugs. Their fasting plasma glucose was 14.5 +/- 2 mM/L and their HbA1c 13.37 +/- 2.9%. At the entry and at the end of the study a 5h-OGTT was done with assays of plasma glucose and C-peptide. TREATMENT: Chlorpropamide (375 mg/day) plus metformin (1200 mg/day) and bedtime insulin (0.1 U/kg/day). RESULTS: After two months on combination therapy, fasting plasma glucose and HbA1c levels were remarkably improved (decreases of 7.3 +/- 0.6 and 9.1 +/- 1.02 respectively, p less than 0.002). The insulin dose was small (6.77 +/- 2.09 U/day). Side effects were minimal and infrequent. During the 5h-OGTT, the mean glucose area under the curve also decreased. The insulin secretion did not change but the C-peptide/glucose ratio increased. At the end of the study, the insulin dose was tapered off and stopped when possible. The four patients with the best glycemic control during the study were able to suspend the bedtime insulin and maintain a good control six months after the insulin suspension. CONCLUSIONS: The combination therapy is useful in the treatment of secondary failures in NIDDM: Its advantages are the very low mean daily insulin dose needed, the low incidence of side effects and, if a HbA1c less than 8.7% is achieved, the restoration of oral antidiabetic drugs efficacy. The very low insulin dose used in this study could be explained by complementary effects of metformin and bedtime insulin on hepatic glucose output and a putative decrease in peripheral resistance attributable both to sulfonylurea and metformin.

Adult↗
PubMedDate not supplied

[Efficacy and tolerance to acarbose in non-insulin-dependent diabetics].

Oral acarbose, a competitive inhibitor of alpha-glucosidase, has been shown to be effective in decreasing the postprandial rise in blood glucose and insulin. A double blind, cross-over, placebo controlled, randomized study in poorly controlled, non-insulin dependent diabetic patients under treatment with sulfonylureas was carried out. The patients continued receiving sulfonylureas throughout the study period and were randomly allocated into two sequences. In sequence A they received 100 mg tablets tid during 12 weeks; placebo tid during 2 weeks (wash-out period) and finally they were crossed over to placebo tid during 12 weeks. In sequence B, they received placebo tid 12 weeks, placebo tid during 2 weeks and finally acarbose 100 mg tid during 12 weeks. Sixteen patients were included in each sequence; three were excluded from sequence A, one because of side effects, one because of severe neuropathy and one because of change of address. One was excluded from sequence B because of failure to take the sulfonylurea. A slight but statistically significant decrease in weight was observed with acarbose as compared with placebo in both sequences. Significant reductions in postprandial glucose were observed in both sequences with acarbose. Significant reductions in fasting blood glucose were also observed in some visits. Although lower mean values of triglycerides and HbA1c were observed with acarbose, they were not statistically significant. Acarbose had side effects almost in all patients, but decreased on continued therapy. Only one patient had to be excluded for this cause. Acarbose is a useful therapeutic resource in poorly controlled non-insulin dependent diabetic patients in combination with sulfonylureas.

Acarbose↗
PubMedDate not supplied

[Metabolic disorders in survivors of myocardial infarct].

Several lines of evidence have clearly established the role of lipoproteins as risk factors for the development of atherosclerosis. Epidemiologic studies from different countries have found that about one third of myocardial infarction survivors under 60 years of age are hyperlipidemic. The acute stress reaction occurring in the first hours following an acute myocardial infarction causes distinct changes in the patient's metabolic profile, these changes include a significant reduction of total cholesterol and cholesterol associated with low density lipoproteins and a usually mild elevation of blood glucose. With the purpose of establishing the prevalence and severity of lipoprotein disorders found in myocardial infarction survivors living in Mexico city we conducted a prospective study of 106 consecutive admissions to the coronary care unit at the National Institute of Cardiology with the fully proven diagnosis of acute myocardial infarction, we included only patients younger than 60 years of age that could be sampled within the first 72 hours of the appearance of typical symptoms, at this time the coronary risk factor profile was assessed and blood samples were drawn (acute sample). After three months of the diagnosis we sampled 81 of the original 106 patients (chronic sample). The comparison of these 81 patients showed remarkable differences in the lipid values obtained on each sample. The mean value for total cholesterol in the acute sample was 225 mg/dl whereas the corresponding value for the chronic sample was 240.5 mg/dl (p less than 0.005). This difference was also highly significant for the low density fraction. On the basis of the chronic sample analysis we estimated a prevalence of hyperlipoproteinemia of 35.8%. (II: 18.5%, III: 2.5%, IV: 14.8%), an additional subgroup of 10 patients (12.3%) had the hypo-HDL phenotype raising the number of subjects at risk for atherosclerosis to as high as 48.1% considering only the lipoproteins. The prevalence figures for the rest of the risk factors were as follows: 70.3% for tobacco smoking, 35.8% for Systemic Arterial Hypertension, 33.4% for Obesity and 30.8% for Diabetes Mellitus. Among the group of 81 patients, 17 were known diabetics, eight additional cases of Diabetes Mellitus were diagnosed at the chronic phase (two with fasting hyperglycemia and six with diagnostic oral glucose tolerance tests). The "acute plase" glycemia for these eight subjects was significantly higher (mean: 98.4 mg/dl) than the corresponding value for the non diabetic patients (mean: 83.4 mg/dl p less than 0.002), the seventeen known diabetics had a mean glycemia of 150.6 mg/dl in the acute sample.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗