**Acknowledgements**

*Cells of the Immune System*

atopic patients [33].

**5. Conclusions**

cytoplasmic granules.

that are not appreciated in the mild form [32, 33].

reactivation of the human herpes virus (HHV-6-7) or EBV [34].

mentioned not only by DRESS but identify an atopic patient (**Table 1**).

ies, and markers of apoptotic genes, PCM1-JAK2, Fas L, and bcl2.

The prolongation of eosinophilia can cause tissue damage, although without being clarified specifically, adding to the condition infections as another factor that preserves eosinophilia (parasitic and fungal infestations) or decreases (eosinopenia due to bacterial and viral infections). The diagnosis can be complicated because of the presence of the drug which worsens a preexisting eosinophilia, particularly in

DRESS is more common in adult patients than in children, with approximately 50 drugs being described, highlighting anticonvulsants (phenytoin, phenobarbital, and carbamazepine) and antibiotics as the main causes of the syndrome and, to a lesser extent, sulfate derivatives, antidepressants, NSAIDs, and antidiuretics [34]. There is no clear association between variability of the type of drug and the affected organ with the degree of eosinophilia, which can be mild or self-limited and severe when multisystemic complications are generated due to the presence of symptoms

Other proposals that lead to the pathogenesis of DRESS include detoxification defects at the time of the formation of reactive metabolites, slow acetylation, and

In general, the diagnostic algorithm for eosinophilia linked to SCAR can be visualized as a hypersensitivity response type IVb (SJS and NET) and type IVc (DRESS), which in some way can highlight the pathogenesis proposals previously

Eosinophils are leukocytes (white blood cells) found in the peripheral blood, hematopoietic, lymphatic organs, thymus, connective tissue, and digestive tract. They are identified and quantified by manual counting (Neubauer chamber), automated count with autoanalyzer hemocytometers (impedance, colorimetry, and differential in optical microscope), flow cytometry after the advent of monoclonal antibodies, currently the most used to identify surface markers and immunoenzymatic methods (ELISA, RAST, IMMUNOCAP) for

The classification of eosinophilic diseases "eosinophilic disorders" was revised in 2008 and confirmed in 2016; its study focused on external (extrinsic) and internal (intrinsic) causes (optimized) and optimized and failed diagnosis by precise and timely diagnosis. The algorithms are used and started with the main pillar: The clinical history (clinical criteria, anamnesis, and exploitative maneuvers leading to clinical laboratory algorithms, with initial, basic, and special tests including imaging, tomography, and X-rays to finally improve the prognosis and modify the natural history. The intrinsic and extrinsic disorder algorithm planting is different; this is due to the recognition of molecular altered T cell clones, bone marrow stud-

Some allergies to medications with symptomatology related to specific organ and severe cutaneous against antiepileptics (phenytoin, phenobarbital, carbamazepine) as well as other medications (antibiotics, NSAIDs, antidiuretics) can be related, which rethinks the proposed immunological response algorithm not only in basophil evaluation but also the search for eosinophils in flow cytometry or optical microscopy to assess not only damage but neutralization (eosinophil

Corticosteroids are considered the first line of treatment because of their potent anti-eosinophilic effect for disease control, prognosis, and prevention. So the new

**164**

histaminase).

Thanks to the headquarters and staff of the Department of Allergy and Immunology of the Juarez Hospital of Mexico, Dr. Ruben Humberto Meyer Gomez of the Angeles Hospital, and the laboratory technician Isabel Guerrero Vargas of the LCEIL Laus Deo.
