Search PubMed⌕ Search

Biomedical subjects

G Dickstein

Publications and source records attributed to G Dickstein.

At least 19 recordsLinked to original sources

[Does hypothyroidism contribute to the etiology of primary open angle glaucoma or is it just a coincidence?].

In a prospective study 83 consecutive patients with progressive primary open angle glaucoma (research group) and 62 patients scheduled for cataract surgery (control group), were evaluated for the presence of hypothyroidism by history, blood levels of TSH and free T4 when necessary. In the research group, nine patients (10.8%) had hypothyroidism, 6 of them already known. In group 2 only one patient (1.6%) had known hypothyroidism, this difference was statistically significant (p < 0.005). The association between primary open glaucoma and hypothyroidism is discussed.

Cataract Extraction↗

The assessment of the hypothalamo-pituitary-adrenal axis in pituitary disease: are there short cuts?

The main task of the hypothalamo-pituitary-adrenal (HPA) axis is to enable sufficient cortisol release under regular and stressful situations. Therefore, to prove its being intact in pituitary disease, stimulation tests are usually needed. Cortisol level has to be shown to exceed a threshold level, which has to be defined on normal subjects in each lab, as results may differ greatly. Insulin tolerance test (ITT) is considered the "gold standard". Hypoglycemia induces a severe stress, which stimulates the HPA axis maximally. However, for regularly accepted cut-off points (18-20 microg/dl, 500-550 nmol/l), false positive results are documented, even in normal volunteers, and reproducibility is far from perfect. The metyrapone test, by blocking cortisol production, stimulates ACTH release to overcome the blockade. In this test 11-DOC levels are usually measured, and a cut-off point of 7.0 microg/dl (200 nmol/l) used. Measuring ACTH and/or cortisol + 11-DOC levels may improve the test, both in reasoning and reliability. The CRH test yields unsatisfactory results, and its use is usually saved for differential diagnosis of hypercortisolism. The ACTH test is the easiest to perform, and usually used as a screening test. Abnormal responses should be considered diagnostic, while normal responses, especially in newly onset or recent pituitary disease, should be followed by either ITT or metyrapone test. Most studies show superiority of the 1.0 microg (so called "low dose") ACTH test over the high dose (250 microg) test. The physiologic dose test should replace the pharmacologic dose test whenever ACTH test is considered. In every test there are limitations and pitfalls. Knowing them, and using best clinical judgment, will reduce and minimalize mistakes.

Adrenocorticotropic Hormone↗

False positive metaiodobenzylguanidine scan in a patient with a huge adrenocortical carcinoma.

We report a case of a 17-cm cortisol-secreting adrenocortical carcinoma in which [123I] metaiodobenzylguanidine (MIBG) scan showed accumulation of the isotope in the area of the tumor. Catecholamine levels were normal, and no chromaffin cells were found in histological examination of the tumor. A literature review of previously described cases of false positive MIBG scans in the adrenal region is offered. We conclude that MIBG scans might not be as specific as previously thought in differentiating pheochromocytoma from adrenocortical carcinoma. They should be performed only when clinical suspicion and abnormalities in catecholamines advocate the need.

3-Iodobenzylguanidine↗

A prospective trial of colchicine and methotrexate in the treatment of primary biliary cirrhosis.

BACKGROUND & AIMS: The aim of this study was to determine if colchicine or methotrexate improves blood test results, symptoms, and/or liver histology in patients with primary biliary cirrhosis. METHODS: Patients with histologically confirmed primary biliary cirrhosis whose serum alkaline phosphatase (ALP) levels were at least 2 times above normal and who were not yet candidates for liver transplantation received colchicine or methotrexate and were followed up for 2 years. RESULTS: In patients receiving colchicine (n = 43), mean pruritus score decreased from 1.63 to 1.12 (P = 0.04), ALP level from 494 to 355 U/L (P < 0.0001), and alanine aminotransferase (ALT) level from 79 to 61 U/L (P < 0.0001). In patients receiving methotrexate (n = 42), pruritus score decreased from 1.25 to 0.44 (P = 0.0001), ALP from 478 to 235 U/L (P < 0.0001), and ALT from 96 to 61 U/L (P = 0.0001). Methotrexate but not colchicine significantly improved liver histology (P = 0.005) and serum immunoglobulin G levels (P = 0.0002). Methotrexate improved most blood test results more than colchicine. Serum bilirubin levels increased slightly with each drug, and albumin levels decreased slightly. CONCLUSIONS: Both colchicine and methotrexate improved biochemical test results and symptoms in primary biliary cirrhosis, but the response to methotrexate was greater.

Alanine Transaminase↗

Is there a role for low doses of mitotane (o,p'-DDD) as adjuvant therapy in adrenocortical carcinoma?

Four patients suffering from adrenocortical carcinoma were treated with low doses (1.5-2.0 g) of mitotane (o,p'-DDD) for the complete follow-up time following surgery (21-68 months). Treatment with mitotane was started shortly after surgical removal of the tumor (three patients) or the tumor and multiple lung metastasis (one patient). No significant side effects or complications from the medication were noted. Two patients remain disease free after 57 and 21 months on treatment. A third patient died of an unrelated reason (varicose vein bleeding) after 68 months on mitotane without evidence of tumor recurrence or metastasis. In the fourth patient, two lung metastasis were successfully removed after 48 months of follow-up. The patient is doing well and is disease free 6 months later. Though our series is too small to draw final conclusions, we suggest that low doses of mitotane, which are well tolerated, might offer prolonged disease-free survival in adrenocortical carcinoma. To be beneficial treatment has to be started early after surgical removal of the tumor and metastasis, and be continued for long periods of time.

Adrenal Cortex Neoplasms↗

Late complications in remission from Cushing disease. Recurrence of tumor with reinfarction or transformation into a silent adenoma.

Two of 4 patients who underwent spontaneous remission from Cushing disease (CD) demonstrated regrowth of the pituitary adenoma 2 and 5 years later. In the first patient, the recurrent tumor also secreted corticotropin, with subsequent relapse of fulminant cushingoid features. However, after 14 more months, it again became infarcted, and the patient underwent complete clinical remission, which has persisted for about 3 years. In the second patient, the regrowth of the tumor occurred silently, as no clinical cushingoid features or rise in cortisol levels were noticed. Because of its size, the tumor was resected and found to have immunoreactivity for corticotropin (silent corticotroph adenoma). About 4 years after the first operation, a second surgical procedure was performed because of massive regrowth of the tumor. Again, there was no concomitant elevation of cortisol levels or endocrinologic symptoms. This time, the tumor did not even stain for corticotropin. While spontaneous remission in CD is rare, recurrence is even rarer. Reremission of CD and the change from a corticotropin-secreting adenoma to a silent one are described herein for the first time (to our knowledge). These cases demonstrate that patients with CD have to receive careful follow-up, even if they undergo remission, and that the long-term outcome of such remission is unpredictable.

Adenoma↗

Lithium treatment in amiodarone-induced thyrotoxicosis.

PURPOSE: Amiodarone hydrochloride is an iodine-rich drug effective in the control of various tachyarrhythmias. It is known to cause refractory to thyrotoxicosis, which usually does not respond to regular antithyroid drugs. Lithium bicarbonate is a medication used to treat psychiatric disorders; it also influences thyroid production and release of hormones. We tried it in combination with propylthiouracil (PTU) for the treatment of amiodarone-induced thyrotoxicosis. PATIENTS AND METHODS: Twenty-one patients were studied. The first group (n = 5) was treated by amiodarone withdrawal only. The second group (n = 7) received PTU (300 to 600 mg), and the third (n = 9) PTU (300 mg) and lithium (900 to 1350 mg) daily. Patient selection was not randomized. The PTU + lithium group had more severe symptoms and signs of thyrotoxicosis, as well as thyroxine levels at least 50% above the upper limit of normal. They also had been on a longer course of amiodarone treatment (34.3 +/- 11.9 months) than the PTU-only (11.4 +/- 7.5) and the no-treatment (7.8 +/- 4.2) groups. RESULTS: While there was no difference between the first two groups in time until recovery (10.6 +/- 4.0 versus 11.6 +/- 0.5 weeks, respectively), the group receiving lithium normalized their thyroid function tests in only 4.3 +/- 0.5 weeks (P < 0.01 versus both other groups). T3 levels normalized even earlier-by 3 weeks of lithium treatment. No adverse effects of lithium were encountered, and the medication was stopped 4 to 6 weeks after achieving a normal clinical and biochemical state. CONCLUSIONS: We conclude that lithium is a useful and safe medication for treatment of iodine-induced thyrotoxicosis caused by amiodarone. We would reserve this treatment for severe cases only. Further studies are needed to find out whether in patients with this troublesome complication lithium therapy could permit continuation of amiodarone treatment.

Amiodarone↗

One microgram is the lowest ACTH dose to cause a maximal cortisol response. There is no diurnal variation of cortisol response to submaximal ACTH stimulation.

There are many suggestions in the literature that the adrenal gland is more sensitive to ACTH in the evening than in the morning. However, all these studies in humans were conducted when the basal cortisol level was not suppressed, and were based on the observation that, after stimulation, the increases in cortisol differed, though the peak values were the same. To examine this, we established the lowest ACTH dose that caused a maximal cortisol stimulation even when the basal cortisol was suppressed, and used a smaller dose of ACTH for morning and evening stimulation. The lowest ACTH dose to achieve maximal stimulation was found to be 1.0 microgram, with which dose cortisol concentration increased to 607.2 +/- 182 nmol/l, compared with 612.7 +/- 140.8 nmol/l with the 250 micrograms test (P > 0.3). The use of smaller doses of ACTH (0.8 and 0.6 microgram) achieved significantly lower cortisol responses (312 +/- 179.4 and 323 +/- 157.3 nmol/l respectively; both P < 0.01 compared with the 1 microgram test). When a submaximal ACTH dose (0.6 microgram) was used to stimulate the adrenal at 0800 and 1600 h, after pretreatment with dexamethasone, no difference in response was noted at either 15 min (372.6 +/- 116 compared with 394.7 +/- 129.7 nmol/l) or 30 min (397.4 +/- 176.6 compared with 403 +/- 226.3 nmol/l; P > 0.3 for both times). These results show that 1.0 microgram ACTH, used latterly as a low-dose test, is very potent in stimulating the adrenal, even when baseline cortisol is suppressed; smaller doses cause reduction of this potency. Our data show that there is probably no diurnal variation in the response of the adrenal to ACTH, if one eliminates the influence of the basal cortisol level and uses physiologic rather than superphysiologic stimuli.

Adrenocorticotropic Hormone↗