Growth hormone deficiency in the adult: only an endocrinologic problem?

In the literature published during the last decade an increased risk of death due to cerebrovascular and cardiovascular events in growth hormone deficient adults has been reported. A partial reversibility of the syndrome following recombinant growth hormone treatment has also been described. Both these factors have contributed to the proposal of growth hormone therapy not only for children but also for adults. Following the initial enthusiasm, the scientific community is now evaluating various clinical experiences held over recent years and weighing up the results. Present day medicine has to take the economic impact of prescribed therapeutic regimens into consideration; in other words the ratio between cost and benefits must be calculated. The relatively recent issuance of the license for the treatment of growth hormone deficiency in adults using recombinant growth hormone does not allow us to evaluate a possible reduction in the risk of death due to cerebrovascular and cardiovascular events in treated subjects. A much longer observational period will be required. Besides the partial reversibility of the syndrome as a consequence of treatment, it is necessary to single out the selection criteria for the choice of treatment. These could also be useful as indicators of the efficacy of the same treatment.     

Growth hormone deficiency in adulthood: how to diagnose and when to treat?

Adult growth hormone deficiency (AGHD) is a well-established clinical entity with heterogeneous characteristics, in which the main causes are hypothalamus-pituitary tumors and/or their treatment. The diagnosis of ADGH should be considered in patients with a prior history of childhood-onset GH deficiency or a history of organic hypothalamus-pituitary disease. In these patients diagnosis is performed biochemically by provocative tests of GH secretion, once the measurement of the biological markers for GH action:IGF-l and IGFBP-3 levels, can be in the normal range in an important percentage of AGHD patients. The current treatment using an initial low dose of hrGH followed by individualised dose titration adjusted according to serum IGF-1 levels, leads to similar beneficial effects with less incidence of side effects, improved tolerance to treatment and a lower stable GH dose as compared to hrGH replacement therapy based on body weight or body surface area. As some patients might not profit from hrGH therapy, the potential beneficial effects of hrGH replacement therapy should be analyzed on individualized basis. Alternative available therapies with similar efficacy should be taken into consideration. Physical activity may improve body compostion, cardiovascular perfomance and well being in ADGH subjects not submitted to hrGH treatment. An important target of hrGH replacement therapy is its impact on quality of life, leading to social and professional improvement. Epidemiological evidence points to a decreasing life expectancy in ADGH patients but data regarding the impact of hrGH replacement on life expectancy are still lacking.     

Alzheimer's disease and chronic periodontitis: Is there an association?

Alzheimer's disease, an affliction of old age, is one of the leading causes for dementia worldwide. Various risk factors including family history, genetics and infections have been implicated in its pathogenesis. The cognitive decline in this condition is mainly a result of the formation of amyloid deposits that provoke neuroinflammation, ultimately resulting in cell death. Recently, an association between peripheral inflammation and Alzheimer's disease was hypothesized. It was suggested that chronic systemic inflammation worsened the inflammatory processes in the brain. This was mainly attributed to increased levels of pro‐inflammatory mediators, such as interleukin‐1, interleukin ‐6 and tumor necrosis factor‐α in the plasma. As chronic periodontitis is a widespread peripheral immunoinflammatory condition, it has been proposed to play a significant role in the aggravation of Alzheimer's disease. With this background, the current review focuses on the relationship between Alzheimer's disease and chronic periodontitis, and its therapeutic implications. Geriatr Gerontol Int 2015; 15: 391–404.     

Alpha-1 antitrypsin deficiency and splenic artery aneurysm rupture: an association?

OBJECTIVE: Theoretically, patients with alpha 1-antitrypsin deficiency may be vulnerable to the development of splenic artery aneurysms. alpha-1 antitrypsin deficiency can induce cirrhosis with portal hypertension, and resulting protease-antiprotease imbalances may exaggerate arterial wall weakness due to proteolysis of arterial structural proteins. A splenic artery aneurysm rupture 7 days after liver transplantation provoked a reassessment of the incidence of this phenomenon in a liver transplant population. METHODS: Case records from three institutions and the results of a survey sent to 126 liver transplantation programs in the United Network for Organ Sharing database were reviewed. The incidence of splenic artery aneurysm rupture in the peritransplantation period, etiology of liver disease associated with this phenomenon, and recommendations regarding management of splenic artery aneurysms was assessed. RESULTS: Twenty-one cases of splenic artery aneurysm rupture were identified. alpha-1 antitrypsin deficiency was the most common cause of cirrhosis in the majority of identified patients who presented with splenic artery aneurysm rupture, which was associated with a mortality rate of 57%. Respondents to the survey indicated that a preoperative evaluation was warranted if a splenic artery aneurysm was suspected; however, no consensus regarding management exists. CONCLUSIONS: The presence and risk of rupture of splenic artery aneurysms may be greater in patients with alpha-1 antitrypsin deficiency. If identified before rupture, an aggressive approach to diagnosing and treating these aneurysms should be initiated. At present, no consensus exists regarding the management of splenic artery aneurysms.     

Vitamin B(12) deficiency and incontinence: is there an association?

BACKGROUND: This study investigated the relationship between B(12) (cobalamin) levels and incontinence in older outpatients using secondary data analysis. METHODS: Between 1991 and 1999, there were 929 patients (258 men and 671 women) for whom urinary incontinence (UI), fecal incontinence (FI), and B(12) were prospectively recorded. Covariates included race, gender, age, medications, Mini-Mental State Examination, modified illness rating, and instrumental activities of daily living (IADLs). RESULTS: Some form of incontinence (UI or FI or both) was found in 41% of subjects, isolated UI in 34%, double incontinence (DI) in 12%, and isolated FI in 4%. Having UI increased the risk of also having FI (p <.0001). Serum B(12) levels of 300 pg/ml or less were not predictive of isolated UI or isolated FI. However, in logistic regression, DI was predicted by B(12) (odds ratio [OR] = 2.113, p =.0094), IADLs (OR = 0.810, p <.0001), cathartics/laxative use (OR = 1.902, p =.126), and diuretic use (OR = 2.226, p =.006). Considering isolated UI in women, higher IADLs reduced risk of UI (OR = 0.956, p =.002), while diuretics (OR = 1.481, p =.041) and antihistamines (OR = 1.909, p =.046) both increased risk of UI. In men, only use of anticonvulsant medications (OR = 4.529, p =.023) increased risk of isolated UI. Greater physical illness in both genders increased risk of isolated FI (OR = 1.204, p =.006). CONCLUSIONS: These findings suggest that serum B(12) at levels of 300 pg/ml or less are not associated with isolated UI or isolated FI but may play a role in DI. A possible association of low B(12) levels with DI is intriguing because of the implications for treatment and prevention. More immediately, medication side effects should be considered when evaluating this problem.     

Dietary fiber and coronary disease: Does the evidence support an association?

Large, prospective, epidemiologic studies show a protective effect of dietary fiber against coronary heart disease (CHD) and form the basis for new recommendations from the National Academy of Science for fiber intake (38 and 25 g/d for young men and women, respectively, based on an intake of 14 g of fiber per 1000 kcal). Mechanisms by which fibers may protect against CHD include lowering blood cholesterol (soluble fibers), attenuating blood triglyceride levels (mostly soluble fibers), decreasing hypertension (all fibers), and normalizing postprandial blood glucose levels (all fibers). An important consideration in making diet recommendations to protect against CHD is that the total amount of fiber from fiber-containing foods is important, and individuals should not just be counseled to focus on soluble fiber.     

Acalculous cholecystitis and tamponade: an unusual combination?

Although pericardial effusion is a well-known feature of Churg-Strauss syndrome, cardiac tamponade has rarely been encountered. The present report describes a case of Churg-Strauss syndrome that presented as an acute cholecystitis and was complicated by tamponade. Histopathological exam of both pericardium and gall bladder was conclusive for Churg-Strauss syndrome.     

Is there an association between Kawasaki disease and Chlamydia pneumoniae?

The clinical and epidemiological features of Kawasaki disease (KD) are consistent with an infectious cause. Because chronic infection with Chlamydia pneumoniae has been implicated in the pathogenesis of atherosclerosis, it has been suggested that it may also be involved in the pathogenesis of KD. Paired sera (baseline pretreatment and 1 year after treatment with intravenous immunoglobulin [IVIG]) from 26 children with KD and 29 age-matched controls were examined by microimmunofluorescence (MIF) serology and immunoblotting. There were no significant differences in the prevalence of anti-C. pneumoniae IgG, IgA, or IgM between cases and controls; however, 73%-85% of sera from cases and controls reacted with C. pneumoniae proteins by immunoblotting. There was significantly more reactivity in the pre-IVIG, but not post-IVIG, KD sera compared with sera from controls to proteins at 72-74 kDa and 74-76 kDa. They may be heat shock proteins. The results of this study do not support an association between KD and C. pneumoniae on the basis of MIF and immunoblot analysis.