Serum ferritin, transferrin and soluble transferrin receptor levels in multiple sclerosis patients
Over the last few years, increased evidence has supported the role of iron dysregulation [jl note: not overload) in the pathogenesis of multiple sclerosis (MS), as iron is essential for myelin formation and oxidative phosphorylation. We studied indices of iron metabolism, such as serum iron, ferritin, transferrin and soluble transferrin receptor (sTFR) levels in 27 MS patients. Seven patients had chronic progressive active disease (CP-A), six had chronic progressive stable (CP-S), ten had relapsing—remitting active (RR-A) and four had relapsing—remitting stable (RR-S) disease. sTFR levels were found to be significantly higher in CP-A (P=0.021) and RR-A (P= 0.004) patients than in controls. sTFR levels were also elevated in CP-S patients but did not reach significance (P=0.064). sTFR values in RR-S patients were comparable to those found in controls (P=0.31). Ferritin levels were significantly elevated only in CP-A patients (P= 0.002). Patients of the CP group had significantly higher ferritin values than the RR patients (P= 0.004). Haemoglobin values as well as iron and transferrin levels were within normal limits in all patients. In conclusion, the increased serum sTFR and ferritin levels in nonanaemic MS patients with active disease reflect the increased iron turnover. The mild elevation of sTFR levels in CP-S patients may indicate active inflammation with ongoing oxidative damage that is not detectable by history or examination.
Interferon β therapy increases serum ferritin levels in patients with relapsing-remitting multiple sclerosis
Serum ferritin levels have been found to be increased in patients with active progressive multiple sclerosis (MS). However, its levels are reported to be unchanged in stable and in active relapsing-remitting (RR) form of the disease. No research to date has assessed the influence of interferon β (IFN-β) on ferritin concentrations. In this study, serum ferritin levels were measured in 43 individuals with RR-MS and 38 age- and sex-matched control volunteers. There were no significant differences between controls and patients under stable and untreated conditions. In patients at 12 months after the beginning of IFN-β therapy, ferritin levels were higher in women and in men, in comparison with baseline (71.4 ± 58.6 vs 43.4 ± 29.9 ng/mL, P = 0.0006 and 216.0 ± 124.3 vs 127.8 ± 74.9 ng/mL, P = 0.0022, respectively). These results suggest that larger prospective studies are required to evaluate the role of serum ferritin in MS and its potential usefulness in monitoring responses to immunomodulatory therapies.
These results suggest that larger prospective studies are required to evaluate the role of serum ferritin in MS and its potential usefulness in monitoring responses to immunomodulatory therapies
Interestingly people with HH genes actually absorb a lot more zinc and other non-ferrous metals, the zinc accumulates in their livers with the iron, so people with HH are advised against taking these supplements.
A study reported in the British journal Gut indicates that drinking black tea rich in tannin with meals can reduce iron absorption. The control group drank water with meals; the study group drank tea with meals. Intestinal iron absorption was measured by studying serum iron-binding capacity and serum ferritin. Results showed a significant reduction of iron in the study group as opposed to the control group. Thus, drinking black tea may reduce phlebotomy frequency in the management of patients with hemochromatosis (Kaltwasser JP et al 1998).
Vitamin and Mineral Supplements
Vitamin C (ascorbic acid) increases the intestinal absorption of inorganic iron . However, vitamin C deficiency sometimes occurs in untreated patients with hemochromatosis but resolves after iron depletion . Rarely, ingestion of large quantities of vitamin C has been associated with fatal cardiac arrhythmias in persons with iron overload, presumably as a result of oxidative injury caused by mobilization of stored iron . There is no rationale for discouraging patients with hemochromatosis from consuming fresh fruits and vegetables containing vitamin C, but it seems prudent to advise them to limit ingestion of vitamin C in supplements to 500 mg/d (Table 4).
In patients with hemochromatosis, absorption of inorganic forms of some nonferrous metals, including cobalt, manganese, zinc, and lead, is increased [76-82]. Excess inorganic cobalt is rapidly excreted . Manganese and zinc, however, are deposited in the liver and other tissues [80, 82]. Lead, which is toxic in small amounts, is retained for prolonged periods . The role of these metals in the pathogenesis of symptoms and tissue injury associated with hemochromatosis has not been elucidated, but we suggest that persons with hemochromatosis use dietary supplements containing these metals only if a specific nutritional deficiency has been shown (Table 4) . Because blood concentrations of zinc, manganese, and lead are low, therapeutic phlebotomy is not effective in reducing retention of these metals [76, 77].
forgot to post this on phleb anyone thread--since you are here, here it is:
this is from Life Estension:A study reported in the British journal Gut indicates that drinking black tea rich in tannin with meals can reduce iron absorption. The control group drank water with meals; the study group drank tea with meals. Intestinal iron absorption was measured by studying serum iron-binding capacity and serum ferritin. Results showed a significant reduction of iron in the study group as opposed to the control group. Thus, drinking black tea may reduce phlebotomy frequency in the management of patients with hemochromatosis (Kaltwasser JP et al 1998).
I have read about the tea's effect before, but not that it was significant.
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