A 36-year-old male with a history of lumbar radiculopathy and depressive disorder treated with carbamazepine and clomipramine started six weeks before admission.
The patient was admitted to the hospital for a seven-day period characterized by fever up to 39 °C associated with chills, severe headache, malaise and abdominal pain, especially in the right hypochondrium.
On admission she was wet, febrile, tachycardic and hypertensive.
Physical examination revealed an increase in facial volume, without involvement of the oral mucosa, associated with a non-palpable purpura in the upper part of the thorax, with sensitivity to inguinal or peritoneal irritation without palpable neck or hypochondrium.
A complete blood count with a slight increase in eosinophils (6% of 3,300 leukocytes) and few atypical lymphocytes (less than 1%), creatinine 1 mg/dL, LDH 172 U/L liver test abnormal AST: UGT
An abdominal ultrasound showed hepatomegaly associated with hyperechogenicity of portal spaces.
A computed axial tomography of the abdomen and pelvis corroborated the hepatomegaly and showed periportal adenopathies.
He was admitted with the diagnosis of hepatitis under study; probably secondary to drugs or infectious etiology.
An extensive etiologic study was requested.
Blood cultures and urine cultures were negative.
IgM serology for hepatitis A virus, surface antigen for hepatitis B virus, hepatitis C virus antibodies, IgM VCA Epstein (VEB) virus, cytomegalovirus and HIV were negative.
The study was complemented with RPR, IgM Toxoplasma gondii, IgM and IgG Leptospira spp., IgM measles, agglutination reaction for Brucella abortus/melitensis, IgG harbor
A molecular panel of respiratory viruses was also performed, which was negative.
Tissue necrosis revealed normal antinuclear antibodies, anti-cytoplasmic, anti smooth muscle, anti-mitochondrial, anti-endomysium, rheumatoid factor, and anti-transglutamine.
The thorax was palpable with clinical stability, without signs of hepatic insufficiency, but with persistent fever and appearance of headache and a maculo-pular rash morbilliform with perifollicular predominance in the face and neck,
Since headache was intensified during its evolution, it was decided to perform a lumbar puncture, which gave way to a colorless, transparent white cephalospinal fluid (CSF) without latex gram-negative bacteria, 100% glucose mononuclear cells were found.
Current culture was also negative.
A polymerase chain reaction (PCR) was performed in CSF for enterovirus, herpes simplex virus 1-2 and varicella zoster virus that were negative.
With these findings it was decided to perform a study with qualitative PCR for VHH-6 in blood and CSF, both of which were positive for VHH-6.
Biopsies of the skin lesions were taken to complete the study.
Histopathology showed superficial perivascular and liquenoid perifollicular dermatitis with the presence of eosinophils, compatible with an adverse drug reaction.
Given the clinical presentation, laboratory findings and the recent use of carbamazepine, a drug frequently associated with hypersensitivity, the diagnosis of DRESS syndrome was established in concomitance with an acute meningoencephalitis V.
In this case, a definitive diagnosis of DRESS was established according to the JSCAR criteria and atypical DRESS.
After drug withdrawal, the patient spontaneously recovered and headache disappeared.
Cutaneous involvement decreased with topical hydrocytisone but did not require systemic corticosteroids.
Laboratory tests gradually improved and liver tests were normal one and a half months after the onset of symptoms.
No lymphocytic colitis was found > 5%.
Due to its good evolution and being immunocompetent it was decided not to give antiviral treatment, being discharged after nine days of hospitalization to be observed on an outpatient basis.
Two months after discharge, the patient was stable, with no recurrence of symptoms.
