SUBACUTE CUTANEOUS LUPUS SECONDARY TO TRASTUZUMAB EMTASINE
Doenças autoimunes, reumatológicas e vasculites - Caso Clínico
Congresso ID: CC002 - Resumo ID: 1224
Centro Hospitalar de Lisboa Central EPE, Serviço de Medicina Interna 2.1
Teixeira, João; Costa, Catarina; Santos, Inês; Janeiro, Claudia
There is a defined, but poorly described, relationship between Trastuzumab and
Cutaneous Lupus Erythematosus (CLE), and whether Trastuzumab causes CLE or simply leads to dermatologic manifestations of latent Lupus Erythematosus has yet to be established.
We report a case of a 77-year-old female with HER2+ breast adenocarcinoma that presented with a generalized rash and pruritus after the 9th cycle of Trastuzumab emtasine (the only medication the patient was under). The lesions presented as erythematous plaques, some with desquamative properties, mainly on the lateral side of the upper right arm, on the upper thoracic region dorsum (with a predominance of desquamative plaques in the interscapular area), malar regions and forehead.
The skin biopsy revealed Cutaneous Lupus Erythematosus (CLE), and it was associated with positive antinuclear antibodies (speckled pattern, 1:320) and positive Anti-SSA (3+), in a patient that was previously ANA negative (with no previous Anti-SSA test).
She was admitted to the Internal Medicine ward, and there were never any signs of fever, respiratory, urinary or rheumathological symptoms. Transtuzumab emtasine was suspended and a short course of Prednisolone (40mg daily, tapered off the following days) plus Hydroxicloroquine (400mg daily) was initiated. There was a complete remission of the skin lesions after two weeks, with no relapse when the medication was stopped.
CLE has been previously linked with the treatment of HER2+ breast carcinoma due to aromatase inhibitors, but rarely with the use of Trastuzumab. In the literature, the cases where it was admitted that Trastuzumab led to CLE (and not simply to skin rashes) the diagnosis was always supported by the presence of an annular pattern of eruption and positive testing for Anti-Ro/SSA.
Our case seems to support the link between the two, as it clearly shows a compatible dermatologic pattern, positive skin biopsy and positive serology for Lupus, in a patient whose only related external factor was the use of Trastuzumab emtasine.
The case, however, raises some questions; Altough the link between these lesions and trastuzumab seem undeniable, the fact that they only originated after the 9th cycle, and that the description of Trastuzumab-associated CLE seems so rare in the literature, seems to suggest that either CLE is induced by the cumulative dosage of this drug in susceptible patients, or that this is a rare and idiosyncratic drug reaction. Systemic manifestations also seem to be absent in both our case and in previously described cases, leading us to question whether Trastuzumab causes true CLE or simply causes Lupus-like skin rashes.
Cutaneous Lupus Erythematosus (CLE), and whether Trastuzumab causes CLE or simply leads to dermatologic manifestations of latent Lupus Erythematosus has yet to be established.
We report a case of a 77-year-old female with HER2+ breast adenocarcinoma that presented with a generalized rash and pruritus after the 9th cycle of Trastuzumab emtasine (the only medication the patient was under). The lesions presented as erythematous plaques, some with desquamative properties, mainly on the lateral side of the upper right arm, on the upper thoracic region dorsum (with a predominance of desquamative plaques in the interscapular area), malar regions and forehead.
The skin biopsy revealed Cutaneous Lupus Erythematosus (CLE), and it was associated with positive antinuclear antibodies (speckled pattern, 1:320) and positive Anti-SSA (3+), in a patient that was previously ANA negative (with no previous Anti-SSA test).
She was admitted to the Internal Medicine ward, and there were never any signs of fever, respiratory, urinary or rheumathological symptoms. Transtuzumab emtasine was suspended and a short course of Prednisolone (40mg daily, tapered off the following days) plus Hydroxicloroquine (400mg daily) was initiated. There was a complete remission of the skin lesions after two weeks, with no relapse when the medication was stopped.
CLE has been previously linked with the treatment of HER2+ breast carcinoma due to aromatase inhibitors, but rarely with the use of Trastuzumab. In the literature, the cases where it was admitted that Trastuzumab led to CLE (and not simply to skin rashes) the diagnosis was always supported by the presence of an annular pattern of eruption and positive testing for Anti-Ro/SSA.
Our case seems to support the link between the two, as it clearly shows a compatible dermatologic pattern, positive skin biopsy and positive serology for Lupus, in a patient whose only related external factor was the use of Trastuzumab emtasine.
The case, however, raises some questions; Altough the link between these lesions and trastuzumab seem undeniable, the fact that they only originated after the 9th cycle, and that the description of Trastuzumab-associated CLE seems so rare in the literature, seems to suggest that either CLE is induced by the cumulative dosage of this drug in susceptible patients, or that this is a rare and idiosyncratic drug reaction. Systemic manifestations also seem to be absent in both our case and in previously described cases, leading us to question whether Trastuzumab causes true CLE or simply causes Lupus-like skin rashes.