Background25(OH) vitamin D levels may be low in patients with moderately or severely active inflammatory bowel diseases (IBD: Crohn’s disease and Idiopathic Ulcerative Colitis) but this is less clear in patients with mild or inactive IBD. Furthermore there is limited information of any family influence on 25(OH) vitamin D levels in IBD. As a possible risk factor we hypothesize that vitamin D levels may also be low in families of IBD patients.ObjectivesTo evaluate 25[OH] vitamin D levels in patients with IBD in remission or with mild activity. A second objective is to evaluate whether there are relationships within IBD family units of 25[OH] vitamin D and what are the influences associated with these levels.MethodsParticipants underwent medical history, physical examination and a 114 item diet questionnaire. Serum 25[OH] vitamin D was measured, using a radioimmunoassay kit, (replete ≥ 75, insufficient 50–74, deficient < 25–50, or severely deficient < 25 nmol/L). Associations between 25[OH] vitamin D and twenty variables were evaluated using univariate regression. Multivariable analysis was also applied and intrafamilial dynamics were assessed.Results55 patients and 48 controls with their respective families participated (N206). 25[OH] vitamin D levels between patients and controls were similar (71.2 ± 32.8 vs. 68.3 ±26.2 nmol/L). Vitamin D supplements significantly increased intake but correlation with serum 25[OH] vitamin D was significant only during non sunny months among patients. Within family units, patients’ families had mean replete levels (82.3 ± 34.2 nmol/L) and a modest correlation emerged during sunny months between patients and family (r2 =0.209 p = 0.032). These relationships were less robust and non significant in controls and their families.ConclusionsIn patients with mild or inactive IBD 25[OH] vitamin D levels are less than ideal but are similar to controls. Taken together collectively, the results of this study suggest that patient family dynamics may be different in IBD units from that in control family units. However contrary to the hypothesis, intra familial vitamin D dynamics do not pose additional risks for development of IBD.

SUMMARY The influx of 22Na into the smooth muscle cells of incubated rat tail arteries was measured directly, in the presence and absence of 2.8 x 10" 7 M D-aldosterone. During the analysis, extracellular 22 Na and 23 Na were removed by incubation of the tissue in sodium-free lithium-substituted physiological salt solution at less than 3 °C. Aldosterone increased the influx rate coefficient by 10% (0.104 ± 0.004 [SE] min" 1 , n = 13, vs 0.095 ± 0.003 [SE] min" 1 , n = 13 without aldosterone; p < 0.01) but did not significantly reduce the sodium content. We conclude from direct measurements that aldosterone acts to increase the influx of sodium in incubated tail arteries from normal rats; we conclude from measurements of the sodium influx and sodium content that aldosterone also acts to increase the efflux of sodium in this preparation. (Hypertension 7: 873-878, 1985) KEY WORDS • sodium transport • sodium permeability • corticosterone

In single striated muscle cells of the giant barnacle Balanus nubilus, the sodium content of the myoplasm was measured with an intracellular microelectrode, and the total sodium content of the cell was measured by flame photometry, during immersion of the cells in sodium-free solution. The sodium content of the myoplasm declined slowly but steadily from ca. 10 mmol/kg water to ca. 4 mmol/kg water during immersions lasting up to 16 h. The "nonmyoplasmic" sodium content of the cells, defined as the sodium content after subtraction of the sodium in the extracellular (sorbitol) space and in the myoplasm, declined rapidly from ca. 15 mmol/kg water to ca. 3 mmol/kg water during the first 30 min of immersion in sodium-free solution, but remained constant thereafter. The rapidly lost portion of the nonmyoplasmic sodium (ca. 123 mmol/kg water) was ascribed to the extracellular space but the location of the inexchangeable portion was not discovered. The behavior of the efflux of 22Na which was loaded into the myoplasm by microinjection was consistent with this interpretation. It was concluded that the nonmyoplasmic sodium does not have an appreciable influence on the measured value of the sodium efflux from the myoplasm of barnacle muscle cells.

In the sartorius of the frog (Rana pipiens), it was found that 10-15% of the tissue sodium was not lost in sodium-free lithium-substituted solution, and was not exchanged with radiosodium in normal frog Ringer's solution, after 4 h. This sodium is not detected by an intracellular sodium-selective glass microelectrode. Detergent or freezing and thawing, in sodium-free solution, cause the loss of all but about 2% of the tissue sodium. The ionophore monensin causes a similar loss but does not disrupt cellular membranes. It was concluded that the slowly exchanging sodium exists in solution inside an organelle whose membrane has a low sodium permeability relative to the sarcolemma, and that this organelle probably is the sarcoplasmic reticulum.

The influence of diversity in the size of the cells of the frog's sartorius on the radiosodium efflux from the muscle was investigated. Morphometric analyses of light micrographs of complete cross sections of the muscle were done in the proximal and distal regions. The results were used to predict the shape of the radiosodium washout curve under the following assumptions: the cells differ in size and shape, but each has a single internal pool of exchangeable sodium; the sodium exchange properties of the limiting membranes are the same for all cells; and the diversity of the true areas of the limiting membranes is reflected by the diversity of the apparent areas measured at the light microscopic level. Radiosodium efflux measurements were performed on similar muscles. The model correctly predicted the occurrence of a continuous decline of the fractional loss of radiosodium, which was not due to diffusional delay and which would be interpreted as a second internal compartment in a compartmental analysis, and an effect of short versus long isotope loading intervals on the efflux. It was concluded that the existence of cell size diversity satisfactorily explains the flux data. No "special region" must be postulated.