The posttreatment basal GH concentration less than 2.5 microg/liter in acromegalic patients is associated with a normal lifespan. Excess mortality is confined to poorly controlled patients and possibly those who have received conventional radiotherapy.

Diabetes mellitus is a common chronic disease all over the world. Self-management plays a crucial role in diabetes management. The purpose of this systematic review was to summarize what is known about the interactions between adult persons with diabetes, their family, and diabetes self-management. MEDLINE, CINAHL, PSYCHINFO, LINDA, and MEDIC databases were searched for the years 2000 to 2011 and for English language articles, and the reference lists of the studies included were reviewed to capture additional studies. The findings indicate that family members have influence on the self-management of adult persons with diabetes. The support from family members plays a crucial role in maintaining lifestyle changes and optimizing diabetes management. Diabetes and its treatment also affect the life of family members in several ways, causing, for example, different types of psychological distress. More attention should be paid to family factors in diabetes management among adult persons.

BACKGROUND.Concerns remain about risk of cancer after radioactive iodine (RAI) treatment for hyperthyroidism, especially in organs that concentrate iodine. The objective was to assess the long‐term cancer risk from RAI treatment for hyperthyroidism.METHODS.A total of 2793 hyperthyroid patients treated with RAI at Tampere University Hospital between 1965 and 2002, and 2793 age‐ and sex‐matched reference subjects were followed for an average of 10 years through the Finnish Cancer Registry.RESULTS.Cancer incidence among hyperthyroid patients treated with RAI was higher than in the population‐based control group (118.9 vs 94.9 per 10,000 person‐years, rate ratio [RR], 1.25; 95% confidence interval [CI]: 1.08–1.46). Furthermore, incidence of stomach (RR, 1.75, 95% CI: 1.00–3.14), kidney (RR, 2.32; 95% CI: 1.06–5.09), and breast (RR, 1.53; 95% CI: 1.07–2.19) cancer was increased among RAI‐treated patients. The relative risk of cancer increased with higher RAI dose administered. The increase in cancer incidence was statistically significant in patients treated at the age of 50–59 (RR, 1.44; 95% CI: 1.05–1.97) or older than 70 years (RR, 1.39; 95% CI: 1.05–1.82). There was a 5‐year latent period after the RAI treatment before the cancer incidence began to differ between the RAI‐treated hyperthyroid patients and the control group.CONCLUSIONS.Cancer incidence, especially cancer of the stomach, kidney, and breast, was higher in patients treated with RAI for hyperthyroidism. Cancer 2007. © 2007 American Cancer Society.

RAI treatment is effective in treating hyperthyroidism in patients with Graves' disease, but hypothyroidism will develop in 82% of patients in 25 years. Because the development of hypothyroidism seems to be inevitable and unpredictable by any clinical factors, the objective of RAI treatment should be to minimize the persistence of hyperthyroidism with the simplest possible form of treatment. We recommend a fixed 7 mCi dose of RAI to be used as the first empirical dose in the treatment of hyperthyroidism, at least in Graves' disease.

Hyperthyroidism per se probably accounts for the increased cerebrovascular mortality after RAI treatment. Our results of increased cerebrovascular and cancer mortality emphasize the need for long-term vigilance concerning patients treated with RAI.

Objective: It is unclear whether mortality still is increased in acromegaly and whether there are gender-related differences. We dynamically assessed outcome during long-term follow-up in our nationwide cohort. Patients and methods: We studied standardized mortality ratios (SMRs) relative to the general population and causes of death in acromegaly (n = 333) compared with age-and gender-matched controls (n = 4995). Results: During 20 (0-33) years follow-up, 113 (34%) patients (n = 333, 52% women) and 1334 (27%) controls (n = 4995) died (P = 0.004). SMR (1.9, 95% CI: 1.53-2.34, P < 0.001) and all-cause mortality (OR 1.6, 95% CI: 1.2-2.2, P < 0.001) were increased in acromegaly. Overall distribution of causes of death (P < 0.001) differed between patients and controls but not cardiovascular (34% vs 33%) or cancer deaths (27% vs 27%). In acromegaly, but not in controls, causes of deaths shifted from 44% cardiovascular and 28% cancer deaths during the first decade, to 23% cardiovascular and 35% cancer deaths during the next two decades. In acromegaly, cancer deaths were mostly attributed to pancreatic adenocarcinoma (n = 5), breast (n = 4), lung (n = 3) and colon (n = 3) carcinoma. In acromegaly, men were younger than women at diagnosis (median 44.5 vs 50 years, P < 0.001) and death (67 vs 76 years, P = 0.0015). Compared with controls, women (36% vs 25%, P < 0.01), but not men (31% vs 28%, P = 0.44), had increased mortality. Conclusions: In acromegaly, men are younger at diagnosis and death than women. Compared with controls, mortality is increased during 20 years of follow-up, especially in women. Causes of deaths shift from predominantly cardiovascular to cancer deaths.

Differentiated thyroid cancer patients have an increased CVD morbidity, which is mostly accountable to AF and to TSH suppression below 0.1 mU/L.

The adverse effects of acute and chronic ethanol exposure on cerebellar functions have been acknowledged for decades, in terms of impaired control of movement and balance. In addition to the motor impairment, cerebellar degeneration has recently been shown to contribute to distinct neuropsychological deficits in chronic alcoholics, as well as in children with prenatal ethanol exposure. The basic mechanisms underlying these ethanol-induced functional alterations and the related neuropathology in the cerebellum have mostly been clarified only recently. These mechanisms include: (i) excitotoxicity; (ii) dietary factors, especially thiamine depletion; (iii) glial abnormalities; (iv) changes in growth factors; (v) apoptotic mechanisms; (vi) oxidative stress; and (vii) compromised energy production. Although these mechanisms widely apply not only to the mature cerebellum, but also to the developing and the aging cerebella, the developing and the aged cerebellum have some special characteristics, which may make them even more vulnerable to ethanol-induced degeneration. These special instances will be discussed along with the general mechanisms of ethanol-induced cerebellar degeneration.