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Mortality, cardiovascular events and risk factors in hypopituitarism
1Department of Medicine, School of Postgraduate Medicine, Keele University, Stroke on Trent, UK.
Insights
Hypopituitarism may increase all-cause mortality, but evidence linking it to vascular mortality is inconclusive. Further large-scale prospective studies are needed to clarify these risks.
Area of Science:
- Endocrinology
- Epidemiology
- Public Health
Background:
- Hypopituitarism is a complex endocrine disorder.
- Previous studies suggest a potential link between hypopituitarism and increased mortality.
- The specific relationship with vascular mortality remains unclear.
Purpose of the Study:
- To evaluate hypopituitarism as a risk factor for all-cause and vascular mortality.
- To analyze findings from four retrospective epidemiological studies.
Main Methods:
- Retrospective analysis of four studies.
- Comparison of mortality rates in hypopituitary patients versus age- and sex-matched cohorts.
- Assessment of all-cause and vascular mortality ratios.
Main Results:
- All-cause mortality was significantly increased (1.3-2.2-fold) in hypopituitary patients.
- Vascular mortality increase was significant in Swedish studies but not in UK studies.
- Studies had limitations including small sample sizes, wide confidence intervals, and incomplete diagnostic data.
Conclusions:
- Current retrospective data do not conclusively support a link between hypopituitarism, growth hormone deficiency, and vascular or all-cause mortality.
- Preliminary evidence suggests hypogonadal individuals may have a protective effect.
- A large, multicenter prospective study is recommended for definitive conclusions.
Abstract:
The issue of whether hypopituitarism is a risk factor for increased mortality from all causes, and particularly from vascular disease, has been evaluated in four retrospective analyses. In all studies, all-cause mortality was significantly increased by 1.3-2.2-fold compared to age- and sex-matched cohorts. The increase in vascular mortality was significant in the two studies from Sweden (1.8-1.9-fold) but not in the two from the UK (0.8-1.4-fold). The total number of deaths relating to all-cause and vascular mortality was relatively small, and the 95% confidence intervals on the observed to expected (O/E) mortality ratios were wide, in some instances crossing the unity line. As retrospective epidemiological studies, these trials suffer from several drawbacks. They included small numbers of patients and events (i.e. deaths), and determination of the number of deaths and their causes may be incomplete, with small additions or subtractions impacting on O/E mortality ratios. A precise diagnosis of pituitary hormone deficiency in patients recruited in the earlier years of the studies (pre-1965) often relied on historical details and not on firm biochemical values. None of the studies provided any measurement of growth hormone status for the cohorts, and in only one study was there any relationship between a particular axis deficiency and all-cause mortality. This finding suggested that hypogonadal subjects were relatively protected compared with eugonadal counterparts. However, this must be regarded as a preliminary conclusion. These retrospective studies indicate that there are no data to support a relationship between vascular or all-cause mortality in hypopituitarism and growth hormone deficiency. Nevertheless, they do provide preliminary evidence to suggest that it would be worthwhile to conduct a large, multicentre, prospective study of well-characterized and documented patients with a sufficient number of events, in order to establish definitively the relationship between various axis deficiencies and mortality.