Eighteen patients who developed cutaneous reactions to red tattoos were studied to identify the chemicals responsible for the reactions to modern red tattoo pigments. Biopsies from the tattoos were examined histologically and the chemical composition of the red pigments was analysed by X-ray microanalysis. A variety of metallic elements including aluminium, iron, calcium, titanium, silicon, mercury and cadmium were detected. Patch tests were performed to the relevant chemicals in nine cases, and only one patient reacted to mercury. This study demonstrates that although reactions to mercury still occur, other red dyes containing a variety of inorganic pigments may provoke a cutaneous inflammatory response.
A patient with sarcoidosis who presented with a granulomatous tattoo reaction is described. Although tattoo granulomata usually represent a local hypersensitivity reaction to tattoo pigments, they can be a manifestation of systemic sarcoidosis. In this case the lesions were confined to the red areas of tattoos suggesting that tattoo sarcoid may be more than just an example of the Koebner response.
INTRODUCTION: Sporadic Lymphangioleiomyomatosis (LAM) is a benign neoplastic disorder which primarily affects premenopausal women. It is characterized by abnormal proliferation of smooth muscle cells with a predilection for the lungs and lymphatics, and diffuse pulmonary cysts on chest CT [1,2]. A review of the literature identified two translational studies and three other case reports which have linked hyperprolactinemia to LAM [1-3]. We discuss a case of a 40-year-old woman with a known prolactinoma, who presented with pleuritic chest pain, chylothorax, and was subsequently diagnosed with sporadic LAM. CASE PRESENTATION:A 40-year-old female presented to the Emergency Department for a 3-week history of pleuritic chest pain and dry cough. She had a known prolactinoma discovered at the age of 26 after reporting galactorrhea. Upon diagnosis, serum prolactin was 90 ng/ml, and cabergoline was initiated. Physical exam was remarkable for decreased breath sounds in the right basilar region. A CXR revealed a moderate right-sided pleural effusion (Image 1). Chest CT angiography found a large rightsided pleural effusion, and bilateral, diffuse, uniform, thin-walled pulmonary cysts (Image 2). An ultrasound-guided thoracentesis drained 1.4L of milky appearing fluid. The pleural fluid sample was transudative, and the cell count revealed >10,000 leukocytes with 99% lymphocytes. Further analysis found triglycerides 3147 mg/dL, and cholesterol 108 mg/dL, consistent with a chylous effusion. Pleural cultures were negative and cytology revealed chronic inflammation without malignant cells. A clinical diagnosis of sporadic LAM was made. The patient was referred to a LAM center, an indwelling pleural catheter was placed, and treatment with Sirolimus was initiated. At 6 month follow up, the patient reported moderate improvement of her symptoms. DISCUSSION:The pathogenesis of sporadic LAM is most commonly a somatic mutation of TSC2. The mTOR pathway is subsequently disinhibited resulting in infiltrative peribronchial and perilymphatic smooth muscle cell proliferation and pulmonary cysts. Typical clinical findings are dyspnea, spontaneous pneumothorax, and chylous effusion. Sirolimus is first line treatment for patients with FEV1 <70% predicted [1,2]. Translational studies have found pulmonary LAM lesions containing elevated prolactin mRNA levels and increased expression of the prolactin receptor. In murine TSC2 knockdown models, prolactin was observed to increase activation of intracellular signaling pathways and cellular proliferation versus controls. Hyperprolactinemia has also been associated with a faster rate of decline of FEV1 [1,2]. To our knowledge, this is the fourth case of LAM occurring in the setting of hyperprolactinemia [3].CONCLUSIONS: LAM cells may have an elevated sensitivity to prolactin. Future studies are required to further elucidate the potential connection between these two entities.
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