Iron deficiency in pernicious anemia: Specific features of iron deficient patients and preliminary data on response to iron supplementation.

BACKGROUND & AIMS: While vitamin B12 (B12) deficiency is considered as the hallmark of pernicious anemia (PA), iron deficiency (ID) is also prevalent. Indeed, this auto immune gastritis is responsible for parietal cell atrophy and increase in gastric pH, leading to impaired iron absorption. We compared PA patients' features according to their iron status at PA diagnosis, and we assessed the iron status recovery after oral or intravenous iron supplementation. METHODS: We prospectively included patients presenting with a newly diagnosed PA in a tertiary referral hospital between November 2018 and October 2020. Iron status was assessed at PA diagnosis then regularly during a standardized follow-up. In case of ID, the decision of treatment with oral and/or intravenous iron supplementation was left to the clinician convenience. RESULTS: We included 28 patients with newly diagnosed PA. ID was observed in 21/28 (75.0%) patients: from the PA diagnosis in 13 patients, or during the follow-up in 8 patients. Iron deficient PA patients had higher plasma B12 (p = 0.04) and lower homocysteine levels (p = 0.04). Also, ID was independently associated with the 'APCA (anti-parietal cell antibodies) alone' immunological status (absence of anti-intrinsic factor antibodies) after adjustment for age, gender and B12 level (aOR 12.1 [1.1-141.8], p = 0.04). High level of APCA was associated with lower ferritin level. After 3 months of supplementation, 3/11 PA patients normalized the iron status with oral iron supplementation, versus 7/8 with intravenous iron supplementation (p = 0.02). CONCLUSION: The high frequency of iron deficiency in PA highlights the interest of regular assessment of iron status in this condition. ID was associated with a profile including APCA alone and less pronounced B12 deficiency. Intravenous iron supplementation seemed to be more efficient than an oral supplementation in these preliminary data.

A New Case of Association of Megaloblastic Anemia and Pancytopenia of Infants.

BACKGROUND: Vitamin B12, or cobalamin deficiency, an infrequent clinical entity in pediatric age, is found almost solely in breastfed infants whose mothers are purely vegetarian, non-supplemented or with pernicious anemia. Megaloblastic anemia in infants presents with generalized weakness or irritability. METHODS: Diagnosis is usually centered on complete blood count, vitamin dosing, and peripheral smear, which may show macrocytes, hypersegmented neutrophils, reticulocytopenia and a raised mean corpuscular volume (MCV ˃ 100 fL). Pancytopenia has also been noted. RESULTS: We report an exclusive breastfed nine-month-old female child who presented with irritability, developmental delay, and difficulties in introducing new foods. Her initial blood count revealed pancytopenia. Vitamin B12 levels were found to be reduced. Maternal levels of Vitamin B12 were also found to be borderline low. The child was treated as per protocols, and improvement was evidenced with the return of hematological parameters to the regular and gradual advancement of milestones. CONCLUSIONS: We aim to underscore the importance of megaloblastic anemia as an important and rare cause of anemia in infancy.

A case report: subacute combined degeneration of the spinal cord and pernicious anemia caused by autoimmune gastritis.

INTRODUCTION: Autoimmune gastritis causing both subacute combined degeneration of the spinal cord and pernicious anemia is rare in clinical practice. Here, we report a case of subacute combined degeneration of the spinal cord and pernicious anemia resulting from vitamin B12 deficiency due to autoimmune gastritis. PATIENT CONCERNS: A 66-year-old woman presented with a 2-month history of numbness in her extremities. DIAGNOSES: The diagnoses were (1) autoimmune gastritis (2) subacute combined degeneration of the spinal cord (3) pernicious anemia (4) hypergastrinemia (5) chronic lymphocytic thyroiditis. INTERVENTIONS: The patient received intramuscular methylcobalamin treatment for 5 days, followed by oral methylcobalamin daily.Outcomes: Symptoms improved, and anemia recovered in the second month after discharge. She discontinued her medication afterward, and the neurological symptoms recurred. CONCLUSIONS: Autoimmune gastritis can lead to several diseases if not intervened in the early course. Neuropathy and hematopathy recur with treatment discontinuity. Methylcobalamin and adenosylcobalamin are unlikely to be more effective than vitamin B12.

Pernicious anaemia: cause of recurrent cerebral venous thrombosis.

This case of recurrent cerebral venous thrombosis (CVT) highlights hyperhomocysteinemia in pernicious anemia due to vitamin B12 deficiency. No other risk factors such as trauma, infections, coagulation disorders or autoimmune diseases were present. The patient was cured with vitamin B12 and anticoagulation therapy. So, it is worthwhile and important to investigate levels of vitamin B12 and homocysteine in CVT.

Máculas eritematosas urentes orales como manifestación inicial de deficiencia de la vitamina B12 / Burning Erythematous Oral Macules as the Presenting Manifestation of Vitamin B12 Deficiency

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Subacute combined degeneration: a case of pernicious anaemia without haematological manifestations.

Vitamin B12 deficiency can be caused by a diverse group of aetiologies. One of the less common of these is an autoimmune condition pernicious anaemia, so named after the most common physiological manifestation of B12 deficiency: anaemia. However, B12 is also necessary for nervous system function and its depletion can lead to dysfunction of the posterior columns of the spinal cord resulting in subacute combined degeneration (SCD). This disease, while debilitating in its acute phase, can usually be mostly if not fully reversed if caught early and treated appropriately. Early detection can prove challenging if there are no haematological manifestations of B12 deficiency and the only guidance is the high index of suspicion. We present a case of pernicious anaemia leading to SCD without any clinical or laboratory findings of anaemia in this report.

Toxicity induced by multiple high doses of vitamin B12 during pernicious anemia treatment: a case report.

Context: The clinical consequences of excess vitamin B12 induced by multiple oral doses of cyanocobalamin are not well-known.Case details: A young woman was treated with multiple daily doses of 1 mg of cyanocobalamin for severe pernicious anemia. After a total dose of 12 mg, she developed acne, palpitations, anxiety, akathisia, facial ruddiness, headache, and insomnia. She improved two weeks after stopping the drug. There were no sequelae nor complications.Discussion: Although these symptoms of cobalamin toxicity were unexpected and unusual, the case reminds us that the administration of any drug is not entirely safe.

Nutritional neuropathies.

Neuropathies associated with nutritional deficiencies are routinely encountered by the practicing neurologist. Although these neuropathies assume different patterns, most are length-dependent, sensory axonopathies. Cobalamin deficiency neuropathy is the exception, often presenting with a non-length-dependent sensory neuropathy. Patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy, whereas vitamin E deficiency is uniquely associated with a spinocerebellar syndrome. In contrast to those nutrients for which deficiencies produce neuropathies, pyridoxine toxicity results in a non-length-dependent sensory neuronopathy. Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss (such as with dialysis), autoimmune conditions such as pernicious anemia, and with certain drugs that inhibit nutrient absorption. When promptly identified, therapeutic nutrient supplementation may result in stabilization or improvement of these neuropathies.

Hematopoyesis extramedular pleural secundaria a anemia perniciosa grave / Pleural extramedullary hematopoiesis due to severe pernicious anemia

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Reversible dementia, psychotic symptoms and epilepsy in a patient with vitamin B12 deficiency.

Vitamin B12 deficiency is a common condition, typically associated with megaloblastic anaemia, glossitis and neuropsychiatric symptoms. We report the case of a patient presenting with progressive cognitive and functional deterioration, psychosis and seizures, later found to be secondary to pernicious anaemia. Importantly, the diagnosis of pernicious anaemia was only established 5 years after symptom onset and was overlooked even when the patient was under medical care, in part due to the lack of classic neurological and haematological signs associated with the condition. The patient had a remarkable neuropsychiatric recovery after vitamin replacement and psychopharmacological management. We discuss similar presentations of vitamin B12 deficiency found in the literature, symptom reversibility and the importance of its early recognition and treatment.

Jaundice and anaemia as presenting features of an incomplete autoimmune polyglandular syndrome type II.

The coexistence of adrenal failure with either autoimmune thyroid disease and/or type 1 diabetes is defined as autoimmune polyglandular syndrome (APS) type 2 or Schmidt's syndrome. Vitiligo, hypergonadotropic hypogonadism, chronic autoimmune hepatitis, alopecia, pernicious anaemia and seronegative arthritis may also be present. We present a case of 45-year-old Indian man with progressive jaundice and asthenia for 3 months. He was also found to have pallor, icterus, dry coarse skin and delayed relaxation of ankle jerk. Investigations showed pancytopaenia with megaloblastic changes due to pernicious anaemia, autoimmune hypothyroidism and autoimmune adrenalitis with evolving adrenal insufficiency. Upper gastrointestinal endoscopy guided biopsy showed evidence of gastric mucosal atrophy. Patient responded well to hydroxocobalamin and thyroxine replacement. Detailed workup to check for evolving APS II is prudent in a hypothyroid patient presenting with pallor and jaundice. It may alert physicians to possible adrenal crisis in the future, especially after starting levothyroxine replacement in these patients.