Saudi Journal of Medicine and Medical Sciences

LETTER TO THE EDITOR
Year
: 2020  |  Volume : 8  |  Issue : 2  |  Page : 160--161

Methemoglobinemia secondary to herbal products


Kamal Kant Sahu1, Ahmad Daniyal Siddiqui2, Susan V George1,  
1 Department of Internal Medicine, Saint Vincent Hospital, Worcester, MA, USA
2 Department of Hemato-Oncology, Saint Vincent Hospital, Worcester, MA, USA

Correspondence Address:
Kamal Kant Sahu
Saint Vincent Hospital, 123 Summer Street, Worcester, MA 01608
USA




How to cite this article:
Sahu KK, Siddiqui AD, George SV. Methemoglobinemia secondary to herbal products.Saudi J Med Med Sci 2020;8:160-161


How to cite this URL:
Sahu KK, Siddiqui AD, George SV. Methemoglobinemia secondary to herbal products. Saudi J Med Med Sci [serial online] 2020 [cited 2020 Oct 27 ];8:160-161
Available from: https://www.sjmms.net/text.asp?2020/8/2/160/282814


Full Text



Dear Editor,

We read with interest the recent article by Al-Qahtani et al. regarding methemoglobinemia in a young boy.[1] We would like to discuss few other essential points that we believe to be important for Saudi J Med Med Sci readers to have a comprehensive understanding of this topic.[2],[3]

While there seems to be a good temporal correlation between Ferula asafoetida ingestion and the development of methemoglobinemia in the case reported, we still strongly recommend that in such cases, a comprehensive workup should be performed to rule out congenital methemoglobinemia. In young patients, we should be very cautious and always consider congenital methemoglobinemia before labeling them as a case of acquired methemoglobinemia. We recommend genetic testing for cytochrome b5 reductase deficiency and hemoglobin (Hb) M to ensure that in such cases, the child is free from any genetic perturbations that can put him/her at risk for the recurrence of methemoglobinemia in future.[4] Hb M is a special variant in which heme iron can undergo auto-oxidation, resulting in methemoglobinemia. The common Hb M variants are Hb M-Boston, Hb M-Iwate, Hb Auckland, Hb Chile, Hb M-Saskatoon and Hb M-Milwaukee.

Food products such as frozen items may have high nitrate content, and there have been reports of clusters of cases with many family members developing methemoglobinemia because of frozen food consumption.[5] In addition, it should be noted that rarely used topical agents such as eutectic mixture of local anesthetic cream, e-cigarettes, contaminated water and other herbal medicines such as choy sum can lead to methemoglobinemia.[6]

In the case reported by Al-Qahtani et al., it is unclear why the patient had anemia of 10.4 g/dl and leukocytosis of 24,000/mm. Did the authors look for hemolysis in this case and what was the likely explanation of the high white blood cell count? Getting a serum lactate dehydrogenase and other hemolytic panel such as serum haptoglobin, direct antiglobulin test and peripheral blood smear would be beneficial to rule out concomitant hemolysis that can be associated with methemoglobinemia.[7]

The family history is very relevant in this case, as rightly explained by Al-Qahtani et al.[1] As per the history provided, both the brothers of the infant had glucose-6-phosphate dehydrogenase (G6PD) deficiency. However, we recommend that the parents should also be checked for this deficiency. In case of a male boy, there is a 50% chance of having a G6PD deficiency if the mother is a carrier. Therefore, genetic testing of parents is mandatory to predict the likelihood of transmitting the condition to children.

Methylene blue (MB) is the drug of choice in the management of methemoglobinemia. In the case reported by Al-Qahtani et al., MB was not given for the fear that he may be positive for G6PD deficiency given the strong family history. This patient was critically sick and mechanically ventilated. We are not sure about the logistic resources at the author's medical center, but a rapid fluorescent spot test for G6PD deficiency is now readily available, which can confirm G6PD deficiency in as early as a few minutes.[8] This patient was not given either MB or vitamin C and instead was successfully treated with hyperoxic ventilation. This is a great learning case, but we wish to reinforce the fact to the readers that MB should be thefirst choice and all efforts should be made to check the G6PD status so that patients are not denied the standard of care. It should also be noted that in addition to MB and ascorbic acid, other drugs such as riboflavin and cimetidine can be used to treat methemoglobinemia with variable outcomes.[3]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Al-Qahtani S, Abusham S, Alhelali I. Severe methemoglobinemia secondary to ferula asafetida ingestion in an infant: A case report. Saudi J Med Med Sci 2020;8:56-9.
2Sahu KK, Mishra AK, George S, Siddiqui AD. Cetirizine: Old culprit or a new member in the family of methemoglobinemia? J Pediatr Pharmacol Ther 2020;25:167-8.
3Sahu KK, Lal A, Mishra AK, George SV. Methemoglobinemia in transplant recipient patients: Future of dapsone as Pneumocystis carinii pneumonia prophylaxis. Prog Transplant 2020;30:71-2.
4Dhibar DP, Sahu KK, Varma SC. Congenital methemoglobinemia: It is Time for National Level Registry System. J Pediatr Hematol Oncol 2017;39:629.
5Sahu KK, Mishra AK, Lal A, George SV. Acetaminophen induced methemoglobinemia. Clin Toxicol (Phila) 2019;17:1.
6Sahu KK, Brown R, Mishra AK, Lal A, George SV. Topical agents causing methemoglobinemia. Am J Emerg Med 2019; pii: S0735-6757(19)30762-4.
7Volney G, Tatusov M, Yen AC, Karamyan N. Naphthalene toxicity: Methemoglobinemia and acute intravascular hemolysis. Cureus 2018;10:e3147.
8Thielemans L, Gornsawun G, Hanboonkunupakarn B, Paw MK, Porn P, Moo PK, et al. Diagnostic performances of the fluorescent spot test for G6PD deficiency in newborns along the Thailand-Myanmar border: A cohort study. Wellcome Open Res 2018;3:1.