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| CASE REPORT |
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| Year : 2021 | Volume
: 10
| Issue : 2 | Page : 109-111 |
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Reversible cutaneous pigmentation due to deficiency of vitamin B12
Prabhat Agarwal, Aashish Gautam, Nikhil Pursnani, Boentika Singh
Department of Medicine, Sarojini Naidu Medical College, Agra, Uttar Pradesh, India
| Date of Submission | 03-Nov-2020 |
| Date of Decision | 10-Feb-2021 |
| Date of Acceptance | 16-Mar-2021 |
| Date of Web Publication | 20-Dec-2021 |
Correspondence Address:
Ms. Boentika Singh
Department of Medicine, Sarojini Naidu Medical College, Agra, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_54_20
Vitamin B12 deficiency is rare and presents with combinations of hematological changes, discoloration of skin, hair and nails, weakness, syncope, and diarrhea. Causes of vitamin B12 deficiencies are malabsorption, pernicious anemia, gastric resection, and rarely inadequate intake. Inadequate intake occurs commonly in people having a strict vegetarian diet. Megaloblastic anemia has a slow onset when compared to that of other anemias. It results in defect in the red cell DNA synthesis and is mostly due to hypovitaminosis, specifically vitamin B12 deficiency. Hyperpigmentation of skin has been reported in medical literature as the presenting manifestation of vitamin B12 deficiency.
Keywords: Hyperpigmentation, Lactate dehydrogenase, megaloblastic anemia, vitamin B12 deficiency
How to cite this article:
Agarwal P, Gautam A, Pursnani N, Singh B. Reversible cutaneous pigmentation due to deficiency of vitamin B12. J NTR Univ Health Sci 2021;10:109-11 |
How to cite this URL:
Agarwal P, Gautam A, Pursnani N, Singh B. Reversible cutaneous pigmentation due to deficiency of vitamin B12. J NTR Univ Health Sci [serial online] 2021 [cited 2023 Mar 30];10:109-11. Available from: https://www.jdrntruhs.org/text.asp?2021/10/2/109/332854 |
| Case Report | |  |
A 25-year-old Indian male presented with chief complaint of generalised weakness, weight loss, and is easily fatigued. There was no history of type 2 diabetes mellitus, hypertension, tuberculosis. There was no history of drug intake. Patient was a non-smoker, non-alcoholic but was consumer of tobacco and betel nut on daily basis. On examination cutaneous hyper pigmentation was observed on large parts of palmar and dorsal aspects of hand involving nails, knuckles, creases. [Figure 1]. This pigmentation had progressed over to his tongue [Figure 2]. Lab tests were ordered- [Table 1] and [Table 2]. On peripheral smear macro- ovalocytes, hypersegmentated neutrophils, macrocytosis were seen. The patient was diagnosed with Megaloblastic anemia in view of peripheral blood smear and decreased vitamin B12 level. | Figure 1: Dorsum of hand showing hypercutaneous pigmentation. Ventral part of digits of both hands showing hyperpigmentation
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Increase in LDH isozymes 1 and 2 is more specific for red blood cell destruction. Lactate dehydrogenase as a biomarker of hemolysis.[1]
After treatment for vitamin B12 deficiency, improvement in clinical symptoms was noticed within weeks. His hyperpigmentation also reduced. [Figure 3] Here the patient was diagnosed to be suffering from Megaloblastic anemia due to vitamin b12 deficiency. Other causes of hyperpigmentation were also excluded like systemic cause (Hemochromatosis, Addison's, and Hyperthyroidism) and drug-induced (Amiodarone, Quinolones, NSAID's, Quinine, Methotrexate, Arsenic etc.).
| Discussion | | |
The main source of vitamin B12 for humans is the intake of meat, poultry, and dairy products. The Recommended Dietary Allowances (RDA) varies with age.[2] [Table 3] Inadequate intake of animal-source foods with pernicious anemia in young adults and food-bound cobalamin malabsorption in the gut due to gastric atrophy in older persons are the main cause of low levels of vitamin B12 and is mainly the cause in poor people worldwide.[2],[3] In this present case the cause of vitamin B12 deficiency was decrease dietary intake. Unusual high presentation of increased lactate dehydrogenase and decreased Red blood cell count which was found to be due to hemolysis of cells that is, Megaloblastic Anemia caused due to deficiency of vitamin B12, there is a defect in DNA synthesis in the rapidly dividing cells and to a lesser extent, RNA, and protein synthesis are also impaired. Therefore, unbalanced cell proliferation and impaired cell division occur as a result of arrested nuclear maturation, so the cells show nuclear-cytoplasmic asynchrony. Hyper pigmentation of skin has been reported in literature as the presenting manifestation of vitamin B12 deficiency as found in this patient.[4]
The patient was later discharged home after intramuscular Vitamin B12 according to the protocol of Vitamin B12 replacement. On subsequent follow-up, he was found to be stable with hemoglobin levels within normal range and the pigmentation was now getting lighter in color.
There have been increase in case reports with descriptions of the clinical signs of skin, hair, nail changes in patients with megaloblastic anemia.[5] Similarly other published reports too have noted an improvement or reversal of the pigmentary changes after 8 to 12 weeks of parenteral administration of cobalamin therapy.[6]
| Conclusion | | |
Megaloblastic anemia (Vitamin B12 deficiency) may be worthwhile to consider the possibility in a patient with unexplained pigmentary changes.
Early detection and adequate treatment will also prevent partially irreversible neurological manifestations.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Gregory JK, Vicki M, Roberto FM, Jane AL, James T, Claudia RM, et al. Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. Blood 2006;107(:2279-85.  |
| 2. | Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline.Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B 6, Folate, Vitamin B 12, Pantothenic Acid, Biotin, and Choline ISBN-13: 978-0-309-06411-8. |
| 3. | Allen LH. How common is vitamin B-12 deficiency? Am J Clin Nutr 2009;89:S693-6. |
| 4. | Padhi S, Sarangi RL, Ramdas A, Ravichandran K, Varghese RG, Alexander T, et al. Cutaneous hyperpigmentation in megaloblastic anemia: A five year retrospective review. Mediterr J Hematol Infect Dis 2016;8:e2016021. |
| 5. | Aaron S, Kumar S, Vijayan J, Jacob J, Alexander M, Gnanamuthu C. Clinical and laboratory features and response to treatment in patients presenting with vitamin B12 deficiency–related neurological syndromes. Neurol India 2005;53:55-8. [ PUBMED] [Full text] |
| 6. | Santra G, Paul R, Ghosh SK, Chakraborty D, Das S, Pradhan S, et al. Generalized hyperpigmentation in vitamin B12 deficiency. J Assoc Physicians India 2014;62:714-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]
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