The interval between flexible sigmoidoscopy screening examinations can be expanded beyond five years.

BACKGROUND/AIMS: As one of the methods for colorectal cancer screening, asymptomatic average-risk persons aged > or = 50 years are recommended to undergo flexible sigmoidoscopy screening every 5 years. We evaluate whether the interval between examinations can be extended beyond 5 years. METHODOLOGY: A total of 192 asymptomatic average-risk subjects were studied, all of whom had undergone a initial negative examination on a flexible sigmoidoscopy screening at age > or = 50 years and a second examination at least 3 years later. The study population was divided into three groups according to the interval between examinations, which was 3-5 years in Group A, 5-6 years in Group B, and 6-8 years in Group C. RESULTS: The incidence of neoplasms was compared among the three subjects groups, and it was found to be similar: 11/96 (11.5%) in group A, 4/55 (7.3%) in group B, and 5/41 (12.2%) in group C. All detected adenomas were less than 10 mm in diameter, and none contained a villous component or high-grade dysplasia. No cancers were found in the study. CONCLUSIONS: The results suggest that the interval for screening sigmoidoscopy may be extended beyond 5 years in persons showing negative results on an initial examination.

Angiotropic B-cell lymphoma with hemophagocytic syndrome associated with syndrome of inappropriate secretion of antidiuretic hormone.

A case of angiotropic B-cell lymphoma associated with hemophagocytic syndrome (HPS) has been reported. In addition to fever, pancytopenia, hepatosplenomegaly, and lack of lymphadenopathy, unique clinical features, such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and pulmonary infarction, were manifested. Both soluble interleukin-2 receptor (sIL-2R) and IL-6 were elevated in the patient's sera in addition to an increase of serum lactate dehydrogenase and ferritin. In contrast, tumor necrosis factor-alpha and interferon-gamma were within normal ranges. Serum antibodies against Epstein-Barr virus and cytomegalovirus showed a past infection pattern. An autopsy examination revealed systemic intravascular proliferation of lymphoma cells with a B-cell phenotype, confirming the diagnosis of angiotropic B-cell lymphoma. Moreover, SIADH was suggested to result from the infiltration of tumor cells into the pituitary gland. Triple association of angiotropic B-cell lymphoma, HPS and SIADH is quite rare. Therefore, the present case seems to be helpful for clarifying the mechanism for HPS of non-Hodgkin's lymphoma with B-cell origin.

Venous response after lidocaine administration in arm veins.

We previously reported that cubital venous pressure (Pv) tended to increase initially, but this was followed by a drop in a dose-dependent response after intravenous lidocaine administration in subjects with various diseases. In this study we examined whether Pv responses after small-dose intravenous lidocaine administrations are related to the stimulating effect of lidocaine on vascular smooth muscle (VSM). In 5 subjects free of cardiovascular disease, Pv increased slightly with decreased pulsations after a 10 mg dose (p<0.01) with no change in central venous pressure. In the cinephlebographic test performed on 2 healthy volunteers, Pv increased during recovery from proximal venoconstriction caused by an injection of contrast medium mixed with 10 mg lidocaine. In 9 subjects with cardiovascular disease, deltaPv spread in the same directions (+ or -) after 5 and 10 mg drug administrations. In 6 of those tested with both drug doses, deltaPv had positive means and no significant difference was observed. Thus, Pv responses after small-dose lidocaine administrations are consistent with neither the stimulating effect of lidocaine nor with a dose-dependent response. They could be attributed to the spasmolytic effect of lidocaine on the basal tone of VSM, which could be modulated by disease conditions.

Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome.

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.