2) Recognize that patients with adult-onset recalcitrant eczema may have underlying noncutaneous lymphoproliferative disorder. CASE INFORMATION: A 38-year old male presented with history of two and a half years of insidious onset of severe itching involving his feet and gradually spreading and becoming generalized in few months. Subsequently, he developed a rash, which consisted of hard bumps', intensely pruritic in nature. He was seen by several physicians and had multiple skin biopsies demonstrating folliculitis and wound cultures growing Staphylococcus species. Numerous treatment attempts were unsuccessful. Examination revealed hundreds of equally spaced excoriated crusted pink papules measuring up to 1 cm diameters. Rest of his systemic examination was normal. Investigations revealed a normal complete blood count, hepatitis profile, and complement levels. HIV and fungal serology and PPD test were negative. Skin biopsies showed chronic dermatitis and the direct immunofluorescence was negative. Chest radiograph revealed multiple lung masses and subsequent CT scan of chest revealed extensive anterior mediastinal, bilateral hilar, right paratracheal, and subcarinal adenopathy and multiple bilateral pulmonary nodules. CT abdomen was normal. He underwent mediastinoscopy and lymph node biopsy, which revealed the diagnosis of Hodgkin's Lymphoma, Nodular Sclerosing type. He was started on combination chemotherapy with ABVD. IMPLICATIONS/DISCUSSION: Chronic unexplained eczema and pruritus of adult onset might be associated with underlying lymphoproliferative malignancy. Although pruritus has been associated with Hodgkin's disease, the reports of prurigo nodularis' association with Hodgkin's lymphoma are rare. Prurigo nodularis is also associated with other malignancies like transitional cell bladder cancer, leukemia and HIV. When an obvious cause like drugs or atopy year old Asian male presented with complaint of inability to move his arms and legs. His symptoms began one day prior to admission after walking a significant amount while shopping at a local mall. After leaving the mall, he started to experience numbness and tingling of his arms, legs and abdomen. Later that day, he started to experience generalized weakness and went to sleep early due to fatigue. When he awoke the morning of admission, he could not walk or move his body. He had to be assisted out of bed and brought to the emergency room. He had no prior medical problems and was not taking any medications, drugs or supplements. Upon further questioning, he revealed that his mother has had problems with low potassium levels. His review of symptoms prior to this episode was completely negative. Physical exam was unremarkable except for neurological exam. He was alert and oriented. His cranial nerves and sensory exam were intact. Motor strength was 0/5 in upper extremities and 1/5 in lower extremities. The patient was areflexive. Labs: Na 145, K 2.0, Cl 106, CO2 16, creatinine .7, CPK 519, Ca 7.9, Phos 1.3, Mg 1.5, TSH 0.0, T4 total 13.8, T3 total 236.4. His urinary potassium excretion was normal. EKG: low voltage t waves and u waves. Patient was diagnosed with hypokalemic periodic paralysis and treated with oral and intravenous potassium chloride. Within a few hours, his potassium improved to 5.0 and his strength was 5/5. The next day, he was discharged and told to follow up with endocrinology for his hyperthyroidism IMPLICATIONS/DISCUSSION: The diagnosis of hypokalemic periodic paralysis is made most easily when hypokalemia is documented during an attack of weakness and other secondary causes are excluded. Attacks begin during the first three decades of life and occur during the rest period following exercise, stress or high carbohydrate meal. The condition can develop in patients with a familial predisposition (autosomal dominant inheritance) or in those with thyrotoxicosis. The latter form is more common in Asian males. Although, the mechanism is not entirely understood, it is thought to be related to sudden shift of potassium into cells. Patients have normal potassium values between episodes and may have decreased magnesium and phosphorus during episodes. Treatment includes oral potassium chloride and correction of thyrotoxicosis. Prevention may include beta blockers, oral supplements, potassium sparing drugs and low carbohydrate meals. Recognition is important because the condition can lead to respiratory muscle paralysis and subsequent death. LEARNING OBJECTIVES: 1. Emphasize the importance of draining an infected galactocele and describe a less-invasive modality to achieve this. 2. Highlight follow-up measures in women with a recurrent galactocele. CASE INFORMATION: A 37 year-old lady presented with a non-tender lump in her left breast 4 weeks after birth of her fourth child. She was lactating without difficulty and denied redness of the overlying skin or fever. Following clinical examination, she had an ultrasound of the breast revealing a 3.7cm cystic mass with internal echoes. Ultrasound-guided aspiration was performed and 30cc of milky fluid aspirated with complete resolution of the mass. However, the galactocele recurred within 24 hours but remained asymptomatic otherwise. Three weeks later, the patient presented with evidence of mastitis, was started on antibiotics, and the galactocele re-aspirated. With persistent signs of infection, galactocele-fluid cultures revealing Streptococcus viridans, and re-accumulation of the milk in the galactocele, incision and drainage was contemplated. This was subverted with a less invasive means by inserting an 8 french multiple side-hole pigtail catheter into the galactocele enabling complete drainage and healing of the underlying infection. The catheter was removed in 10 days and antibiotics given for a total of 2 weeks. To prevent development of a milk fistula through the drain site, fluid reaccumulation was monitored with ultrasound and re-aspiration performed at 4 and 16 days after drain removal. The patient recovered with complete healing of the catheter tract. The galactocele persisted even after cessation of breast-feeding. A mammogram was then performed which revealed no findings of underlying malignancy. IMPLICATIONS/DISCUSSION: A galactocele most commonly presents as a breast mass soon after the cessation of lactation, and an ultrasound evaluation is usually confirmatory. These masses usually disappear in few weeks to months. However, the persistence of a galactocele, particularly after repeated aspirations, necessitates further work-up to rule out ductal obstruction from an underlying malignant process. Our patient had another infrequent complication Ð an infected galactocele. The concern of incision and drainage of a galactocele was that of a high likelihood of milk fistula. On the other hand, if not drained, infection was likely to persist and progress to a breast abscess. An alternative was therefore considered of introducing a pigtail catheter into the galactocele to enable complete drainage while instituting appropriate antibiotic coverage. Catheter drainage of breast abscess has been described in the literature, but this is the first report, to our knowledge, of catheter drainage of an infected galactocele. A 78 year-old lady reported a``whitehead like'', non-irritating lesion on her right nipple. Watchful waiting was recommended and over the course of the next 3 weeks, this lesion progressed into a rash involving the nipple and areola with a painful central abrasion and crusting. With the use of antibiotic cream, the rash improved in 3±4 days but mild flaking of the skin persisted. Three months later, the patient presented to the Breast Clinic for evaluation of a mild, but persistent nipple rash. She denied breast lumps, pain or nipple discharge. Breast cancer risks included nulliparity, and use of hormone replacement therapy for nearly 40 years. On examination, there was mild scaling of the skin over the right nipple with no associated induration, erythema or excoriation. On palpation, no dominant mass, nipple discharge, axillary or supraclavicular lymphadenopathy was identified. Mammograms revealed increasing microcalcifications in the sub-areolar region of the right breast. Stereotactic biopsy of these calcifications was performed and demonstrated high-grade ductal carcinoma in situ (DCIS). Skin biopsy of the scaly region revealed Paget disease of the nipple characterized by tumor cells with large nucleoli distributed singly in the superficial epidermal layers with clusters in the basal portion of the epidermis. These tumor cells were immunoreactive to anti-cytokeratin 7 and carcinoembryonic antigen (CEA) antibodies confirming the diagnosis of Paget disease. In compliance with the patient's wishes, right mastectomy was performed and on pathologic evaluation, residual DCIS was noted around the biopsy site along with Paget disease of the nipple. IMPLICATIONS/DISCUSSION: Paget disease, with an incidence ranging from 0.5 to 2.6%, presents as a scaly persistent rash, and often mimics eczema, or contact dermatitis of the nippleareolar complex. It may or may not be associated with a breast mass. Diagnosis is established by a skin biopsy, revealing characteristic Paget cells. Delay in diagnosis may result when the rash is mild in intensity and if unassociated with a breast mass. Clinical management of a patient with a nipple, or areolar rash mandates continued follow-up. If the rash fails to resolve, a high index of suspicion for Paget disease of the nipple will enable appropriate work-up and optimal outcome.