No reports on granulocyte colony-stimulating factor-producing lung cancer associated with antiphospholipid antibody syndrome. A 73-year-old man was referred to our department to undergo surgery for lung cancer in the right upper lobe. His examination results suggested that his condition was caused by an elevated white blood cell count and an increased inflammatory response due to granulocyte colony-stimulating factor production. The presence of antiphospholipid antibody syndrome was suspected, and the decrease in coagulation factors was considered to be inhibited by the lupus anticoagulant. Perioperatively, the patient was treated with heparin and steroids, and a thoracoscopically assisted right upper lobectomy was performed. Postoperatively, histopathological examination revealed pleomorphic carcinoma, and the patient tested negative for anticardiolipin IgG antibodies. In lung cancer patients with elevated white blood cell counts, fever, and an inflammatory response, granulocyte colony-stimulating factor-producing lung cancer is an important differential diagnosis. Additionally, when coagulation abnormalities are observed preoperatively, a thorough examination is necessary to prepare for perioperative management.

Estimating impact of the various product-related variants and impurities on a biotherapeutic\'s safety and efficacy is an essential requirement in the quality by design paradigm. In view of the limited role that clinical studies offer in this regard, we demonstrate a preclinical approach to achieve this for granulocyte colony-stimulating factor (GCSF). While our repeated-dose toxicity data suggest that these variants do not elicit any adverse effects or histopathological changes, aggregated GCSF impurity caused sluggishness in animal behavior manifested by a possible muscular injury. Cell assay data revealed that the cys-64-cys74 disulfide bond in reduced GCSF imparts stabilization in absence of the cys-36-cys42 bond. PK data demonstrate variability in half lives of different species when compared to the native GCSF. PD data along with differential expression of JAK-2 and STAT5a genes show that all the tested variants triggered the required signal transduction pathways for neutrophil proliferation and activation.

•Granulocyte-colony stimulating factor (GCSF) secretion by gynecologic tumors is rare.•Elevations in serum GCSF can be seen in the absence of tumor GSCF secretion.•Extreme leukocytosis is associated with autocrine tumor growth and poor prognosis.

The biosimilar industry is witnessing an unprecedented growth with the newer therapeutics increasing in complexity over time. A key step towards development of a biosimilar is to establish analytical comparability with the innovator product, which would otherwise affect the safety/efficacy profile of the product. Choosing appropriate analytical tools that can fulfil this objective by qualitatively and/or quantitatively assessing the critical quality attributes (CQAs) of the product is highly critical for establishing equivalence. These CQAs cover the primary and higher order structures of the product, product related variants and impurities, as well as process related impurities, and host cell related impurities. In the present work, we use such an analytical platform for assessing comparability of five approved Granulocyte Colony Stimulating Factor (GCSF) biosimilars (Emgrast, Lupifil, Colstim, Neukine and Grafeel) to the innovator product, Neupogen(®). The comparability studies involve assessing structural homogeneity, identity, secondary structure, and product related modifications. Physicochemical analytical tools include peptide mapping with mass determination, circular dichroism (CD) spectroscopy, reverse phase chromatography (RPC) and size exclusion chromatography (SEC) have been used in this exercise. Bioactivity assessment include comparison of relative potency through in vitro cell proliferation assays. The results from extensive analytical examination offer robust evidence of structural and biological similarity of the products under consideration with the pertinent innovator product. For the most part, the biosimilar drugs were found to be comparable to the innovator drug anomaly that was identified was that three of the biosimilars had a typical variant which was reported as an oxidized species in the literature. But, upon further investigation using RPC-FLD and ESI-MS we found that this is likely a conformational variant of the biotherapeutic been studied.

Achromobacter xylosoxidans is an aerobic, motile, oxidase and catalase positive, non-fermenting, gram negative bacillus. It is an opportunistic pathogen which is responsible for various nosocomial and community-acquired infections. However, there are only very few reports of pulmonary infections caused by this bacterium in cancer patients. We are presenting a case of a patient with carcinoma of epiglottis, who developed pulmonary infection caused by Achromobacter xylosoxidans. According to the available literature, this is the first case of pulmonary infection caused by Achromobacter xylosoxidans, which was detected in a cancer patient in India. Since Achromobacter xylosoxidans demonstrates resistance to many classes of antimicrobials, vigilant and efficient microbiological work-ups and surveillances are needed, to diagnose infections caused by this rare pathogen in clinical settings.

Febrile neutropenia is an oncologic emergency that can result in serious consequences. Granulocyte colony stimulating factors (G-CSFs) are often used as prophylaxis for febrile neutropenia. Bone pain is the most notorious adverse effect caused by G-CSFs. Specifically, with pegfilgrastim (Neulasta(®)), the incidence of bone pain is higher in practice than was observed during clinical trials. Traditional analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs) and opioids, can be ineffective in severe pegfilgrastim-induced bone pain. With the high frequency of this adverse effect, it is clear that health practitioners need additional treatment options for patients who experience severe pegfilgrastim-induced bone pain. The mechanisms of bone pain secondary to G-CSFs are not fully known, but research has shown that histamine release is involved in the inflammatory process. There is scant previous clinical data on antihistamine use in the management of G-CSF-induced pain. We present the first case report in which loratadine prophylaxis completely alleviated NSAID-resistant severe pain secondary to pegfilgrastim. The result showed that loratadine may be a promising option for severe, resistant pegfilgrastim-induced bone pain. Further clinical studies are warranted and ongoing.