On October, 2010, a 35-year-old male presented to our outpatient department complaining of multiple swellings on left calf, headache, and weakness of left upper limb followed by both lower limb for the past 4 months. He complained of blurring of vision for last 15 days, but there was no diplopia. Patient developed gradually progressive swellings over left calf involving the whole of leg below knee joint up to the ankle, with reddish brown discoloration of overlying skin (Figure 1). Swellings were not painful, nonitchy with no discharging sinus or ulceration. He denied history of fever, tinnitus and vertigo, or hearing impairment. There was a positive history of previous treatment for pulmonary tuberculosis 4 years back. Patient was an alcoholic and heavy smoker for the past 15 years. 
On examination, our patient was severely pale and cachexic with stable vitals. Generalized lymphadenopathy was present. Fundus examination revealed bilateral papilledema. Multiple, nodular, rubbery, and firm swellings of varying sizes ranging from two to seven centimeters (in greatest dimension) were seen conglomerated over the posteromedial aspect of left leg, highly suggestive of neurofibromas. Other neurocutaneous markers for neurofibromatosis such as cafe-au-lait spots, shagreen's patch, and ash-leaf macules were absent. Slit-lamp examination did not reveal lisch nodules or posterior subcapsular cataract. Nervous system examination revealed positive neck rigidity and Kernig's sign. On further survey, lower motor neuron type of weakness was present in left upper limb and bilateral lower limbs with sparing of right upper limb. Areflexia and impaired vibration and position sense was present in involved limbs. Cranial nerves, autonomic, and cerebellar function tests were normal, and bilateral plantar response was flexor. Chest examination revealed trachea to be deviated to left with signs suggestive of volume loss in left apical lobe. Other systemic examinations revealed no abnormality. Blood investigations revealed anemia (62 gm/L), high alkaline phosphatase (3506 IU/L), and serum PSA of 1.51 mcg/L. Chest radiograph revealed old healed pulmonary tuberculosis of left upper lobe with osteosclerotic metastasis to humerus (Figure 2).
 Initially, we were mislead by the lesions in the leg considering it to be the primary, but histopathological evaluation of the biopsy specimen revealed atypical neurofibroma. When subjected to immunohistochemical studies, the specimen stained positive for S-100 but negative for calretinin, confirming the diagnosis of neurofibroma. Sonography of abdomen was normal. CT of thorax revealed diffuse, osteoblastic metastasis to sternum, vertebrae, ribs, and humerus. Bone marrow aspirate revealed cells with round to oval nuclei, fine granular chromatin with single large central prominent nucleoli and abundant pale eosinophilic to vacuolated cytoplasm with acini formation suggestive of adenocarcinoma (Figures 3(a) and 3(b)).
MRI of brain and spinal cord with contrast revealed diffuse metastatic deposits over leptomeninges in the brain and spinal cord causing nerve root compression. CSF examination for malignant cytology showed large cells with high nucleus to cytoplasm ratio suggestive of malignant cells (Figure 4). 
Gastroscopy was conducted which showed an ulceroinfiltrative growth from cardia involving the whole of corpus which on biopsy revealed diffuse adenocarcinoma stomach. Histopathological study of biopsy specimen of the growth revealed poorly differentiated adenocarcinoma with architectural disarray and signet-ring cells (Figures 5(a) and 5(b)) which are characteristic finding of diffuse variety of adenocarcinoma stomach.
We planned palliative management for our patient due to his poor Karnofsky's performance status of 10. Treatment was given with intrathecal methotrexate at a dose of 10 mg/m2 twice weekly, systemic corticosteroid as intravenous dexamethasone at a dose of 4 mg every 8 hourly, systemic chemotherapy using 5-FU at a dose of 200 mg/m2 as intravenous infusion weekly for 6 weeks, folinic acid at a dose of 500 mg/m2 as intravenous infusion weekly for 6 weeks 2 hours prior to 5-FU, and cisplatin at a dose of 50 mg/m2 as infusion twice weekly were given after premedication with pheniramine, hydrocortisone, and ondansetron. 5-FU and cisplatin were not given on the same day. Patient showed significant improvement in his complaints, but we lost the patient to followup.