Secondary hypogammaglobilinemia after use of carbamazepine: case report and review

Castro, Ana Paula Beltran Moschione; Redmershi, Maria das Graças; Pastorino, Antônio Carlos; Paz, José Albino da; Fomin, Ângela B. F.; Jacob, Cristina Miuki Abe

doi:10.1590/s0041-87812001000600006

Cited by 27 publications

(32 citation statements)

References 11 publications

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“…IgG deficiency with B cell aplasia has also been reported in some patients treated with carbamazepine (3,4). According to previous case studies, the serum concentration of carbamazepine is not correlated with the occurrence of immunosuppression, and the recovery of serum immunoglobulin levels requires 4 months to 6 years after drug withdrawal (5 …”

Section: Discussionmentioning

confidence: 99%

B Cell Aplasia and Hypogammaglobulinemia after Carbamazepine Treatment

et al. 2010

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Section: Discussionmentioning

confidence: 99%

B Cell Aplasia and Hypogammaglobulinemia after Carbamazepine Treatment

et al. 2010

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“…7 A number of anticonvulsants, such as phenytoin, carbamazepine and lamotrigine, may cause reversible hypogammaglobulinaemiaparticularly IgA deficiency. 8 For all these drugs, clinically significant hypogammaglobulinaemia is rare although symptomatic panhypogammaglobulinaemia has been noted in a small number of cases requiring IgRT to prevent recurrent infections. Symptoms and immunoglobulin levels tend to normalise within several months of treatment cessation.…”

Section: Abstract: Antibody Deficiency Immunodeficiency Immunoglobumentioning

confidence: 99%

“…Symptoms and immunoglobulin levels tend to normalise within several months of treatment cessation. 8 …”

Section: Abstract: Antibody Deficiency Immunodeficiency Immunoglobumentioning

confidence: 99%

Secondary antibody deficiency – causes and approach to diagnosis

Srivastava

Wood

2016

Clinical Medicine

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AAntibody defi ciencies can occur in the context of primary disorders due to inherited genetic defects; however, secondary immune disorders are far more prevalent and can be caused by various diseases and their treatment, certain medications and surgical procedures. Immunoglobulin replacement therapy has been shown to be effective in reducing infections, morbidity and mortality in primary antibody defi ciencies but secondary antibody defi ciencies are in general poorly defi ned and there are no guidelines for the management of patients with this condition. Clinical decisions are based on experience from primary antibody defi ciencies. Both primary and secondary antibody defi ciencies can be associated with infections, immune dysregulation and end-organ damage, causing signifi cant morbidity and mortality. Therefore, it is important to diagnose and treat these patients promptly to minimise adverse effects and improve quality of life. We focus on secondary antibody defi ciency and describe the causes, diagnosis and treatment of this disorder.

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“…Carbamazepine is used in the treatment of trigeminal and glossopharyngeal nerve neuralgia, acting by reducing repetitive activation of the action potential (Solon et al, 2010). It is considered one of the best anticonvulsant, producing less psychological alterations and behavior effects (Castro et al, 2010). Previous study was conducted by Solon et al, (2010) to evaluate the physico-chemical quality control of some formulations of carbamazepine.…”

Section: Introductionmentioning

confidence: 99%

Chemical equivalence assessment of three brands of carbamazepine tablets and their anticonvulsant outcome on electrically-induced seizures in chicks

Malami¹,

Usman²,

Shehu³

et al. 2016

Bayero J. Pure App. Sci.

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Assay for content of active ingredients is a critical test of drug quality; failure to meet up the standard for content of active ingredients will result to sub therapeutic quantities. Three brands (A, B and C) of carbamazepine were assayed to determine their chemical equivalence as well as their anticonvulsant activities. This was aimed at determining the possible relation between the chemical equivalence of the brands and their anticonvulsant outcomes. The brands were randomly selected from Community Pharmacies in Zaria, Kaduna State, and assayed for chemical equivalence to establish weight uniformity and identity; percentage content of active ingredients, using UV spectrophotometric analysis. Similarly all the brands were evaluated for anticonvulsant activity using maximal electroshock seizure model in chicks at doses of 20, 10 and 5 mg/kg. All the brands passed weight uniformity test as none of the tablets deviated from the mean by more than 7.5%. Similarly, their melting points were found to conform to standard average melting point (191 o C) according to B.P. official monograph. However, the content of the active ingredients for Brands B and C did not conform to official standard of 95-105% while brand A conformed. Thus, the percentage contents for brands A, B and C were 99.49%, 76.02% and 87.59% respectively. Also, all the brands at the tested doses offered protection against seizures, ranging from 70-100%; but Brand C at 5 mg/kg offered only 40% quantal protection. The three brands of carbamazepine tablets were not chemically equivalent and their chemical equivalence indices could not be said to be the determinant of anticonvulsant effect.

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Secondary hypogammaglobilinemia after use of carbamazepine: case report and review

Cited by 27 publications

References 11 publications

B Cell Aplasia and Hypogammaglobulinemia after Carbamazepine Treatment

B Cell Aplasia and Hypogammaglobulinemia after Carbamazepine Treatment

Secondary antibody deficiency – causes and approach to diagnosis

Chemical equivalence assessment of three brands of carbamazepine tablets and their anticonvulsant outcome on electrically-induced seizures in chicks

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