pattismith
Senior Member
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I am desesperately looking for studies about patients with inflammation associated with low ferritin and can't find it..... (gastrointestinal inflammation exclude).
But here I found one that caught my eye...
Ferritin is an acute phase response protein, which may not rise as expected in acute bacterial infections.
This could be due to the time required for its production or to a lack of response of ferritin to the bacterial inflammatory process.
Medical records of hospitalized patients with acute hyper inflammation were retrieved and studied, looking closely at two acute phase proteins: C-reactive protein (CRP) and ferritin.
The estimated time between symptom onset and the procurement of blood tests was also measured. 225 patients had a median ferritin level of 109.9 ng/mL [IQR 85.1, 131.7] and a median CRP level of 248.4 mg/L [IQR 221, 277.5].
An infectious inflammatory process was identified in 195 patients.
Ferritin levels were relatively low in comparison with the CRP in each group, divided according to time from symptom onset until the procurement of blood tests.
The discrepancy between high CRP and low ferritin suggests that these two acute phase response proteins utilize different pathways, resulting in a failure to increase ferritin concentrations in a documented state of hyperinflammation.
A new entity of normoferremic inflammation accounts for a significant percentage of patients with acute bacterial infections, which enables bacteria to better survive the inflammation and serves as a new “inflammatory stamp”.
....
Discussion
....
A different, though opposite, response of these two biomarkers has been recently reported in patients with hemophagocytic lymphohistiocystosis (HLH), in whom hyperferritinemia has been observed in the presence of relatively low CRP concentrations [15].
Such a dichotomy might be clinically useful as these findings could be revealing a unique “inflammatory stamp”. This study describes the opposite situation, in which normoferremia exists in patients with very high concentrations of CRP, which confirms the presence of a significant inflammatory response. Furthermore, ferritin regulation is influenced by multiple factors involved in the inflammatory cascade: the inflammatory stimulus of reactive oxygen species, pro-inflammatory cytokines tumor necrosis factor α, IFN-γ, IL-6 and the anti-inflammatory IL-10. These all contribute to ferritin expression.
....
Even though ferritin is traditionally regarded as a mechanism of the host for withholding iron from infecting bacteria, several studies have demonstrated the ability of certain bacteria to use ferritin as a source of iron.
....
A possible advantage of normoferremia in hosts infected with the above-described bacteria might be to reduce their ability to acquire iron from ferritin; however, this assumption should be further studied.
But here I found one that caught my eye...
Normoferremia in Patients with Acute Bacterial Infections—A Hitherto Unexplored Field of the Dichotomy between CRP and Ferritin Expression in Patients with Hyper Inflammation and Failure to Increase Ferritin
Abstract
Ferritin is an acute phase response protein, which may not rise as expected in acute bacterial infections.
This could be due to the time required for its production or to a lack of response of ferritin to the bacterial inflammatory process.
Medical records of hospitalized patients with acute hyper inflammation were retrieved and studied, looking closely at two acute phase proteins: C-reactive protein (CRP) and ferritin.
The estimated time between symptom onset and the procurement of blood tests was also measured. 225 patients had a median ferritin level of 109.9 ng/mL [IQR 85.1, 131.7] and a median CRP level of 248.4 mg/L [IQR 221, 277.5].
An infectious inflammatory process was identified in 195 patients.
Ferritin levels were relatively low in comparison with the CRP in each group, divided according to time from symptom onset until the procurement of blood tests.
The discrepancy between high CRP and low ferritin suggests that these two acute phase response proteins utilize different pathways, resulting in a failure to increase ferritin concentrations in a documented state of hyperinflammation.
A new entity of normoferremic inflammation accounts for a significant percentage of patients with acute bacterial infections, which enables bacteria to better survive the inflammation and serves as a new “inflammatory stamp”.
....
Discussion
....
A different, though opposite, response of these two biomarkers has been recently reported in patients with hemophagocytic lymphohistiocystosis (HLH), in whom hyperferritinemia has been observed in the presence of relatively low CRP concentrations [15].
Such a dichotomy might be clinically useful as these findings could be revealing a unique “inflammatory stamp”. This study describes the opposite situation, in which normoferremia exists in patients with very high concentrations of CRP, which confirms the presence of a significant inflammatory response. Furthermore, ferritin regulation is influenced by multiple factors involved in the inflammatory cascade: the inflammatory stimulus of reactive oxygen species, pro-inflammatory cytokines tumor necrosis factor α, IFN-γ, IL-6 and the anti-inflammatory IL-10. These all contribute to ferritin expression.
....
Even though ferritin is traditionally regarded as a mechanism of the host for withholding iron from infecting bacteria, several studies have demonstrated the ability of certain bacteria to use ferritin as a source of iron.
....
A possible advantage of normoferremia in hosts infected with the above-described bacteria might be to reduce their ability to acquire iron from ferritin; however, this assumption should be further studied.