levoleucovorin and Calcinosis

This study aimed to explore the correlation between survival and tumor calcification in patients with metastatic colorectal cancer who received cetuximab combined with chemotherapy. The study was a single-center retrospective analysis that enrolled 111 patients who had received therapy between April 2011 and October 2016. Tumor calcification and treatment efficacy were evaluated independently by radiologists on the basis of computed tomography scans. Clinical characteristics and follow-up data were collected from electronic medical records. Correlations between tumor calcification and clinical characteristics, tumor response rate, and patient survival were analyzed. Among the 111 enrolled patients, 27 had tumor calcification [27/111 (24.3%)]. The median progression-free survival was significantly longer for patients with tumor calcification than for those without calcification (9.3 vs. 6.2 months, P=0.022). Patients with tumor calcification also had a higher objective response rate (55.6 vs. 31%, P=0.021) and better overall survival (21.9 vs. 16.5 months, P=0.084). The correlation between calcification features and prognosis showed that patients with an increasing number of calcifications after treatment had a significantly longer median overall survival (22.9 vs. 9.1 months, P=0.033). Simultaneously, new liver metastases and multiple calcifications also showed a trend toward better overall survival. There were also no significant correlations between clinical characteristics (sex, age, gene mutation, primary tumor location, pathological type, blood test result) and survival (Supplementary Table 1, Supplemental digital content 1, http://links.lww.com/ACD/A280). Tumor calcification is associated with a better treatment outcome and is a potential prognostic marker.

Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Calcinosis; Cetuximab; Colorectal Neoplasms; Female; Fluorouracil; Follow-Up Studies; Humans; Irinotecan; Leucovorin; Liver Neoplasms; Male; Middle Aged; Oxaliplatin; Prognosis; Retrospective Studies; Survival Rate

Between December 1981 and May 1991, 44 infants and children with congenital toxoplasmosis were referred to our study group. A uniform approach to evaluation and therapy was developed and is described herein along with the clinical characteristics of these infants and children. In addition, case histories that illustrate especially important clinical features or previously undescribed findings are presented. Factors that contributed to the more severe disabilities included delayed diagnosis and initiation of therapy; prolonged, concomitant neonatal hypoxia and hypoglycemia; profound visual impairment; and prolonged, uncorrected increased intracranial pressure with hydrocephalus and compression of the brain. Years after therapy was discontinued, three children developed new retinal lesions (without loss of visual acuity when therapy for Toxoplasma gondii was initiated promptly), and three children experienced a new onset of afebrile seizures. Most remarkable were the normal developmental, neurological, and ophthalmologic findings at the early follow-up evaluations of many--but not all--of the treated children despite severe manifestations, such as substantial systemic disease, hydrocephalus, microcephalus, multiple intracranial calcifications, and extensive macular destruction detected at birth. These favorable outcomes contrast markedly with outcomes reported previously for children with congenital toxoplasmosis who were untreated or treated for only 1 month.

Topics: Animals; Calcinosis; Chemistry, Pharmaceutical; Child; Child, Preschool; Drug Administration Schedule; Drug Therapy, Combination; Feasibility Studies; Humans; Infant; Leucovorin; Magnetic Resonance Imaging; Neutropenia; Physical Examination; Pilot Projects; Prenatal Care; Pyrimethamine; Spiramycin; Sulfadiazine; Tomography, X-Ray Computed; Toxoplasma; Toxoplasmosis, Cerebral; Toxoplasmosis, Congenital; Toxoplasmosis, Ocular; Treatment Outcome

Topics: Antiprotozoal Agents; Brain; Calcinosis; Female; Humans; Infant; Leucovorin; Pyrimethamine; Sulfadiazine; Tomography Scanners, X-Ray Computed; Toxoplasma; Toxoplasmosis, Congenital

The significance of complete calcification of liver metastases on imaging is unknown. This study was conducted to determine whether complete calcification of liver metastases after chemotherapy, as assessed by imaging, was synonymous with sterilization of disease.. Imaging by triphasic contrast-enhanced helical CT scan and abdominal ultrasound showed complete calcification of eight liver metastases in four patients after systemic chemotherapy. All eight completely calcified liver metastases were resected within four weeks of imaging. Histological and surgical findings were analyzed to see whether there was any correlation between radiological and pathological status for completely calcified liver metastases.. The pretreatment median diameter at initial imaging of the eight liver metastases that became completely calcified after chemotherapy was 24 mm. In all eight resected calcified liver metastases, pathological examination showed the presence of residual viable tumor cells. Most of the tumor volume was occupied by calcification, necrosis and fibrosis; but small discrete islands of viable tumor cells were detected at the periphery of lesions.. This preliminary study shows that although imaging evidence of complete calcification of liver metastases may be a good indicator of chemotherapy response, it does not imply sterilization of the malignancy.

Topics: Adenocarcinoma; Aged; Antineoplastic Combined Chemotherapy Protocols; Calcinosis; Camptothecin; Colorectal Neoplasms; Female; Fluorouracil; Hepatectomy; Humans; Leucovorin; Liver Neoplasms; Male; Middle Aged; Neoadjuvant Therapy; Organoplatinum Compounds; Tomography, Spiral Computed; Treatment Outcome; Ultrasonography

To determine the natural history of intracranial calcifications in infants with treated congenital toxoplasmosis.. Between January 1982 and March 1994, cranial computed tomography was performed in 56 infants with treated congenital toxoplasmosis when they were newborns and approximately 1 year old. Locations and sizes of intracranial calcifications were noted.. Forty newborns had intracranial calcifications. By 1 year of age, calcifications diminished or resolved in 30 (75%) and remained stable in 10 (25%) of these treated infants. Ten (33%) of the 30 infants whose calcifications diminished versus seven (70%) of the 10 infants with stable calcifications received less intensive antimicrobial treatment than the other treated infants. In contrast, a small number of infants who were untreated or treated 1 month or less had intracranial calcifications that increased or remained stable during their 1st year of life.. Diminution or resolution of intracranial calcifications was an unexpected and remarkable finding in infants with treated, congenital toxoplasmosis, consonant with their improved neurologic functioning.

Topics: Anti-Infective Agents; Brain; Calcinosis; Follow-Up Studies; Humans; Infant; Infant, Newborn; Leucovorin; Pyrimethamine; Sulfadiazine; Time Factors; Tomography, X-Ray Computed; Toxoplasmosis, Cerebral; Toxoplasmosis, Congenital

Hyperphenylalaninemia in infants and children may be caused by a deficiency of dihydropteridine reductase (DHPR). Recommended therapy includes folinic acid as a source of tetrahydrofolate, a phenylalanine-restricted diet, and both dopamine and serotonin precursors. We report a child with progressive basal ganglia and other subcortical calcifications prior to the use of folinic acid. Six other reported cases of DHPR deficiency demonstrated similar calcifications prior to folinic acid therapy. Since this pattern of calcification also resembles that seen in CNS folate deficiency caused by both congenital folate deficiency and that which is methotrexate-induced, we propose that intracranial calcification in DHPR deficiency is caused by inadequate CNS tetrahydrofolate and may be prevented by the use of folinic acid. Our patient achieved excellent seizure control following the use of folinic acid, suggesting either a direct or indirect anticonvulsant effect of this compound in patients with DHPR deficiency.

Topics: Brain; Brain Diseases; Calcinosis; Female; Humans; Infant, Newborn; Leucovorin; NADH, NADPH Oxidoreductases; Phenylketonurias; Seizures; Tomography, X-Ray Computed

A 10-year-old girl with aplastic anemia developed seizures and a mild hemiparesis following a bone marrow transplant. Based on serologic evidence and a computed tomography scan, which showed a left parietal lucency with ring enhancement, a diagnosis of toxoplasmosis was considered. A brain biopsy of the lucent area demonstrated the inflammation and necrosis but no organisms were seen. During a six-week course of pyrimethamine, sulfadiazine, and folinic acid therapy there was clinical and neuroradiologic resolution. The short course of therapy as well as the inadvertent substitution of folic acid for folinic acid and trimethoprim-sulfamethoxazole for sulfadiazine resulted in the reappearance of neurologic deficits. Reinstitution of appropriate therapy produced gradual improvement over a nine-month period. Serial computer tomography scans correlated with the clinical course. In the immunologically compromised host CNS toxoplasmosis should be considered in the differential diagnosis of an evolving CNS syndrome. Early detection and prolonged therapy with appropriate drugs can result in a favorable outcome. Computed tomography scanning may be helpful in diagnosis and follow-up.

Topics: Anemia, Aplastic; Bone Marrow; Bone Marrow Transplantation; Calcinosis; Child; Drug Therapy, Combination; Female; Humans; Immunosuppression Therapy; Leucovorin; Neurologic Examination; Pyrimethamine; Sulfadiazine; Thalamus; Tomography, X-Ray Computed; Toxoplasmosis