[A study concerning the nature of the optokinetic after nystagmus (report II)].
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Biomedical subjects
Publications and source records attributed to K Uchida.
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Advanced secondary (renal) hyperparathyroidism induced by chronic renal disturbance is one of the most serious complications for long-term hemodialysis patients. Parathyroidectomy is indicated in patients with severely advanced renal hyperparathyroidism refractory to medical treatment (including calcitriol pulse therapy) and the clinical effect of parathyroidectomy is striking. However, skeletal deformity, vessel calcification, and remarkable reduction of bone content is irreversible, and it is important to perform parathyroidectomy at right time. Based on histopathological and pathophysiological investigations, nodular hyperplasia is monoclonal neoplasia with abnormal parathyroid hormone (PTH) response to extracellular calcium and vitamin D. When parathyroid hyperplasia progresses to nodular hyperplasia, parathyroidectomy should be required. Total parathyroidectomy with forearm autograft is the preferable procedure for renal hyperparathyroidism, especially for patients who need to continue hemodialysis treatment after parathyroidectomy. Removal of all parathyroid glands, including supernumerary glands, at the initial operation, and proper choice of adequate parathyroid tissue for autograft, are important to prevent persistent and recurrent hyperparathyroidism. Preoperative image diagnosis is useful for localization, and routine resection of thymic tissue is necessary to remove supernumerary glands. In our series of 548 patients, graft-dependent recurrent hyperparathyroidism was not negligible and the incidence was about 20% at the 5th year postoperatively. Enlarged autografts of parathyroid tissue could be removed from forearm under local anesthesia with fewer invasions. The function of autografted parathyroid tissue is nearly satisfactory and no re-transplantation of cryopreserved parathyroid tissue was necessary. To avoid adynamic bone disease, relatively high PTH level is required-over-suppression of PTH by excess of vitamin D and calcium salts should be avoided. In our experience, total parathyroidectomy with forearm autograft is very effective and adequate treatment for advanced renal hyperparathyroidism, and parathyroid function can be controlled after parathyroidectomy.
Secondary hyperparathyroidism (2'HPT) improves after renal transplantation (RTx) along with recovered function of the renal allograft. However, normal renal function does not last long due to rejection, drug-induced nephrotoxic nepthropathy, or recurrence of post-transplant glomerulonephritis. Therefore, improved calcium and phosphate metabolism, and parathyroid function after RTx fluctuate in accordance with the function of the renal allograft. In cases with severe 2'HPT, parathyroidectomy should be performed before RTx because hypercalcemia due to secondary or tertiary hyperparathyroidism aggravates the renal allograft function. In the follow-up of mild 2'HPT after RTx, hypercalcemia and vascular calcification should be monitored carefully by serum parathyroid hormone, calcium and phosphate concentrations, alkaline phosphatase activity, and bone X-ray film. If serum calcium level exceeds 12 mg/dl, parathyroidectomy (PTx) should be performed to prevent the acceleration of vascular calcification. Total PTx with forearm allograft is a preferred surgical procedure for 2'HPT even after RTx.
In spite of recent therapeutic advances, severe overt secondary hyperparathyroidism due to chronic renal failure necessitates parathyroidectomy and recurrent hyperparathyroidism is one of the most significant problems in this patient population. In the present study, the incidence of recurrent hyperparathyroidism was evaluated in relation to the histopathological features. Image cytometric DNA analysis was performed to estimate the proliferative potential of parathyroid tissue. The study comprised 248 patients who underwent parathyroidectomy from 1973 to 1991. The frequency of recurrent hyperparathyroidism after subtotal parathyroidectomy was 4 (21.1%) of 19 patients, the rate of graft-dependent recurrence after removal of residual parathyroid tissue with forearm autograft was 2 (50%) of 4 patients. The frequency of graft-dependent recurrence after total parathyroidectomy with forearm autograft was 16 (7.5%) of 212 patients. The frequency of recurrence was significantly higher (p less than 0.01) when nodular hyperplastic parathyroid tissue was autografted (17 of 68 patients, 25%) than when diffuse-hyperplastic tissue was grafted (1 of 105 patients, less than 1%). All 58 specimens subjected to image cytometric DNA analysis showed a diploid nuclear pattern cytometrically. However, the relative number of scattered cells that displayed cytometric nuclear DNA values outside the main diploid histogram peak was significantly greater (p less than 0.01) in nodular hyperplastic tissue before being autografted and in parathyroid tissue removed at re-operation performed for recurrence than in diffuse hyperplastic tissue. These clinical findings and results of DNA analysis clearly indicated that nodular hyperplastic parathyroid tissue has a higher growth potential, and it is concluded that to prevent graft-dependent recurrence, the nodular type of hyperplastic tissue should not be autografted.
We report a rare case of prostatic abscess with Crohn's disease in a 21-year-old male. Computed tomography showed a typical prostatic abscess. Moreover, filling of the abscess cavities with contrast medium was demonstrated after micturition, which represented the rupturing of the abscess into the urethra. Crohn's disease should be included in the differential diagnosis of prostatic abscesses even in young males.
The bile flow and the bile acid secretion, calculated on liver weight basis, increased 12 H and 24 H after 60-70% hepatectomy and returned to the initial levels thereafter. The biliary phospholipid secretion much more increased than bile acids, but the cholesterol secretion decreased. Bile acid composition changed with an increase of the cholic acid group and a decrease of the chenodeoxycholic acid group in both bile and feces. These changes almost disappeared on Day 14. The pool size of bile acid decreased maximally on Day 4 to about 40% of the initial, but the distribution of bile acids in the enterohepatic circulation was not changed. The fecal cholesterol and coprostanol markedly decreased on Day 2 but gradually returned to the initial levels according to the recovery of diet intake. The fecal bile acids decreased on Day 2, increased on Day 4, and returned to the normal range after Day 7. In conclusion, the regenerating liver secretes more bile, bile acids and phospholipids, and less cholesterol than the normal liver. Cholic acid predominates in the bile acids. These changes restored to the initial levels by about one week after the operation.
The effects of long-term cilazapril treatment on glucose and lipid metabolism were assessed in 25 hypertensive patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients were treated with 0.5 to 1 mg of cilazapril once daily or a combination of cilazapril and other antihypertensive drugs once daily for 48 weeks. Both systolic and diastolic blood pressures were significantly reduced (P < 0.001) throughout the study with no significant changes in heart rate and no adverse effects such as cough. There were no significant changes in body mass index or serum levels of glycated hemoglobin A1c, fructosamine, total cholesterol, triglycerides, lipoproteins (high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol), or apolipoproteins (apo A-I, apo C-II, apo C-III, apo B, and apo E). Cilazapril caused a significant increase (P < 0.05) in levels of apo A-II and a significant decrease (P < 0.05) in the apo B:apo A-I ratio, an index of arteriosclerosis. These results suggest that cilazapril has favorable effects on glucose and lipid metabolism and that it may be useful as the first or second choice of antihypertensive drugs in hypertensive patients with NIDDM.
The effects of treatment with epalrestat, an aldose reductase inhibitor, on peripheral neuropathy were studied in 45 patients with non-insulin-dependent diabetes mellitus (NIDDM). Epalrestat 150 mg three times daily was given for 24 weeks. Subjective symptoms, such as spontaneous pain in the lower extremities and numbness and hypoesthesia of the extremities or trunk, were significantly (P < 0.001) relieved after 12 and 24 weeks of epalrestat treatment. Vibratory perception thresholds, as measured by using a tuning fork (C-128) and a vibrometer, were improved after 24 weeks of treatment. Furthermore, there were no adverse effects on glucose or lipid metabolism during treatment. These results suggest that long-term (24-week) epalrestat therapy can be used effectively to treat peripheral neuropathy in NIDDM patients without affecting glucose or lipid metabolism.
Cholesterol and bile acid leves were examined in young (8 weeks), middle-aged (12 months) and old (24 months) germ-free male rats, and young (8 weeks) and middle-aged (12 months) conventional male rats. The plasma cholesterol levels were higher in the aged rats, being more marked in the conventional rats. The liver cholesterol levels also increased with age and the increases were almost identical for both groups. No age-related changes were found in the biliary bile acid secretion, the pool size and distribution of bile acids in the bile, small intestine and large intestine, nor in the turnover frequency of bile acids, but the pool size in the young and middle-aged germ-free rats was much larger than that in the conventional rats. The turnover frequency was less in the germ-free rats. The bile acid synthesis presumed from the fecal bile acid excretion decreased in the aged germ-free rats but not in the conventional rats. A most remarkable age-related change was found in the bile acid composition; cholic acid increased and beta-muricholic acid derived from chenodeoxycholic acid in the rat decreased by aging, resulting in an increase of the CA/CDCA ratio (bile acids belonging to the cholic acid group/bile acids to the chenodeoxycholic acid group) in the bile, feces and pool. These results suggest that cholic acid synthesis increases while chenodeoxycholic acid synthesis is impaired by aging in rats.
Bile acid synthesis from orally administered (14)C-cholesterol or from (14)C-mevalonic acid administered intravenously were examined in male and female 2-, 12- and 24-month-old rats. About 5-9% of the '4C-cholesterol administered was recovered as bile acids from the small intestine 3 days after administration. The value in the case of (14)C-mevalonic acid was about 1/10 that of (14)C-cholesterol. Major bile acids were cholic acid and beta-muricholic acid, and the formation ratio of cholic acid increased in aged rats, although no further difference was found between 12- and 24-month-old animals of either sex. Male rats formed more beta-muricholic acid than females at all ages examined. In addition, no significant difference was found in the bile acid composition between both precursors, (14)C-cholesterol and (14)C-mevalonic acid.
The influence of alacepril (50 mg/day) on arterial blood pressure and microproteinuria in 26 hypertensive non-insulin-dependent diabetic patients was studied for 16 weeks. Alacepril reduced blood pressure gradually from 175/88 (standard error of mean [SEM] 2.6/1.7) to 152/81 (3.3/2.0) mm Hg (P less than .005) and albuminuria from 160.6 (SEM 29.1) to 98.1 (14.1) mg/g Cr (P less than .05), while serum blood urea nitrogen, creatinine, HbA1c, and fructosamine (FRA) remained stable. No significant changes occurred in the urinary beta 2 microglobulin and N-acetyl-beta-D-glucosaminidase levels. As compared with the effects of a calcium antagonist (nicardipine, 60 mg/day) that reduced blood pressure from 170/92 (SEM 2.5/1.4) to 154/84 (2.5/1.5) mm Hg (P less than .001) and albuminuria from 162.2 (SEM 33.9) to 95.4 (25.0) mg/g Cr (not significant), it is suggested that the angiotensin-converting enzyme inhibitor (alacepril) may have an advantageous renal effect in spite of its mild antihypertensive effect.
The effects of posture on the plasma hormonal and renal water-electrolyte excretory responses to acute water loading (20 mL/kg BW, orally) were studied in six non-insulin-dependent diabetes mellitus (NIDDM) subjects with hypoadrenergic orthostatic hypotension (HOH), eight NIDDM subjects without HOH, and seven nondiabetic subjects. The three groups were similar with respect to basal levels of mean blood pressure (MBP), serum sodium and osmolality, plasma renin activity (PRA), the plasma volume regulatory hormones alpha-atrial natriuretic peptide (ANP), arginine vasopressin (AVP) and aldosterone, and urinary water and sodium excretion. In the supine state, while allowing the subjects to stand only to void, water loading resulted in no changes in MBP and similar responses of these plasma and urinary parameters in the three groups. In the standing state, water loading produced responses of MBP, and plasma and urinary parameters comparable to those in the supine state in the diabetic group without HOH and the nondiabetic group. In the diabetic group with HOH, however, MBP and hourly urinary water and sodium excretion rates were low compared to those in the other two groups. During water loading, plasma ANP decreased, and, despite the fall of MBP, plasma AVP remained unchanged, and PRA and plasma aldosterone increased normally in the diabetic group with HOH. These results demonstrate that, in NIDDM subjects with HOH, changing from lying to standing induces deranged renal water and sodium handling after water loading, accompained by a decrease in plasma ANP, and inadequate responses of plasma AVP, PRA, and plasma aldosterone to hypotension.
BACKGROUND: Sarcoid uveitis is occasionally accompanied by proliferative changes, such as retinal neovascularization and vitreous hemorrhage. Steroid administration, retinal photocoagulation, and vitrectomy may be indicated in such proliferative cases. CASE: A 19-year-old woman presented with proliferative sarcoid uveitis accompanied by recurrent vitreous hemorrhage. OBSERVATIONS: At the initial examination, bilateral vitreous opacity, retinal exudates, mild vitreous hemorrhage, retinal vasculitis, and neovascularization of the retina and optic disc were observed. Although prednisolone was administered and panretinal photocoagulation was performed several times, recurrent vitreous hemorrhage continued. Since the vitreous hemorrhage was not absorbed, pars plana vitrectomy and lensectomy were performed. After surgery, neovascularization and intraocular inflammation decreased, and the corrected visual acuity in the right eye improved to 20/50. Histopathologic analysis of the proliferative membrane removed during surgery revealed substantial neovascularization and numerous neutrophils in the vessels. CONCLUSIONS: Based on these findings, an inflammatory reaction as well as retinal ischemia were thought to be involved in the proliferative changes in this patient.
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