OBJECTIVE: Aging is associated with elevated levels of glucose, insulin, and triglycerides. Our objective was to assess the effect of a nutritional program designed to reduce these correlates of aging. DESIGN: This is a retrospective chart review of patients attending an outpatient metabolic management program including a high-fat, adequate-protein, low-carbohydrate diet, nutritional supplementation and periodic individual visits. Outcomes measured at baseline and follow-up included body weight, fasting serum glucose, insulin, leptin, lipids, and thyroid hormone. RESULTS: Thirty-one patients were identified with complete information. The mean age of patients was 57.6 ± 2.4 consisting of 53% female and 47% male patients. The average duration between follow up visits was 91.5 ± 8.5 days. Of the parameters measured at the follow-up visit, body weight, serum leptin, insulin, fasting glucose, triglyceride, and free T(3) significantly decreased by 8.1 ± 0.8%, 48.2 ± 3.8%, 40.1 ± 4.7%, 7.6 ± 2.1%, 28.3 ± 5.7%, and 10.8 ± 1.8%, respectively. Furthermore, the triglyceride/high density lipoprotein ratio decreased from 5.1 ± 1.7 to 2.6 ± 0.5. CONCLUSIONS: In the context of an outpatient medical clinic, a high-fat, adequate-protein, low-carbohydrate diet with nutritional supplementation led to improvements in serum factors related to the aging process. Further research regarding this dietary approach and its relationship to aging is in order.
BACKGROUND: Cryptococcus neoformans is an encapsulated yeast that is an important cause of infection in patients with human immunodeficiency virus (HIV), lymphoid malignancies, and in those receiving corticosteroid therapy. The spectrum of diseases caused by C neoformans ranges from pulmonary infection to disseminated disease frequently involving the central nervous system, and occasionally skin and bone. Other extrapulmonary and extraneural sites of infection are less common. Cryptococcal peritonitis is an unusual entity, which is most often encountered in patients with end-stage renal disease undergoing ambulatory dialysis. CASE REPORT: We present a case of cryptococcal peritonitis which developed in a patient with hepatitis C-related cirrhosis. As little is know about the relationship between cirrhosis and cryptococcosis, we further reviewed the literature of this unusual but life-threatening relationship. DISCUSSION: Severe liver disease has not been fully recognized as a predisposing factor in the development of cryptococcal infection, particularly cryptococcal peritonitis, but the scattered case reports in the medical literature and our case report augment the association between the advanced liver disease and cryptococcal peritonitis. Therefore, cryptococcal infection should be considered in the evaluation of these patients with possible peritonitis.
BACKGROUND: Prostate cancer is the most common malignancy in men in the United States. Both at diagnosis and throughout the disease progression, it can metastasize to multiple organs, most commonly bone and lymph nodes. Effusions (either pleural or abdominal) are relatively uncommon. PATIENTS AND METHODS: We reviewed the medical literature including the case reports and post-mortem studies relating ascites to prostate cancer, identified through a MEDLINE search (human; all languages; 1969-2004). RESULTS: We found 12 published cases. Forty two percent of patients presented initially with ascites, in 50% ascites developed later with progressive disease, and 8% had ascites being the only site of recurrence. The response rate to endocrine therapy, including orchiectomy, was 25%. Ascites in these patients conferred a poorer prognosis. CONCLUSION: The development of ascites secondary to prostate cancer, either as an initial manifestation or recurrent disease, is not well known and may be unfamiliar to many physicians. If patients with history of prostate cancer develop malignant effusions, prostate specific antigen (PSA) immunohistostaining of the fluid can serve as a valuable adjunctive study for the diagnosis. This clinical situation becomes particularly important in patients with ascites with a carcinoma of unknown primary. Palliation can be achieved in patients with ascites secondary to prostate cancer using hormone manipulation. Lack of knowledge about this complication of prostate cancer may delay the diagnosis and treatment of this hormonally responsive malignancy.
Gemcitabine (Gemzar) is the only chemotherapeutic agent approved by the U.S. Food and Drug Administration (FDA) for the treatment of advanced pancreatic cancer. Thromboembolism requiring anticoagulation is a common paraneoplastic complication in these patients. We report a case of patient with pancreatic cancer, complicated by gastrointestinal bleeding following therapy with concomitant gemcitabine-warfarin (Coumadin).The patient was a 65-year-old male with medical history notable for atrial fibrillation for which he was taking warfarin 57.5 mg/week (international normalized ratio [INR] 1.94). He received capecitabine-radiotherapy for locally advanced pancreatic cancer. Later, he developed multiple liver metastases. The patient was started on gemcitabine. At the end of first cycle, he experienced bright red blood per rectum. His platelet count was normal, but his INR was noted to be significantly elevated at 8.00. Esophagogastroduodenoscopy (EGD) revealed 2 antral ulcers and a duodenal ulcer. The patient was stabilized and recovered without further incident.Patients with pancreatic cancer who receive warfarin and gemcitabine should be monitored for any potential drug interactions. Weekly prothrombin time (PT)/INRs for anticoagulated patients receiving gemcitabine is suggested.
BACKGROUND: Serum alkaline phosphotase (ALP) levels are frequently elevated in patients with metastatic colorectal cancer (CRC). However, the significance of ALP in terms of detecting hepatic metastasis or prognosis is not well established. MATERIALS AND METHODS: Medical records of patients with CRC seen at University of Alabama at Birmingham (UAB) (1998-2002) were reviewed and statistical analysis was done to evaluate the significance of ALP as a prognostic tool. The normal range for ALP was quantified at 39 U/L to 117 U/L. Change in ALP levels over time (defined as time interval between two cycles; such as 4 weeks for Mayo regimen, 8 weeks for Roswell Park regimen and 6 weeks for IFL regimen) was categorized as large (120+ U/L), medium (20-119 U/L), and minimal (< 20 U/L). RESULTS: A total of 105 patients with eligible medical records were identified (Mean age: 59 yrs; 53% male; Staging: II: 43 patients, III: 31 patients, IV: 32 patients). Increasing ALP levels correlated with increasing stage (Mean: I = 116, II = 219, III = 302; P = 0.0003). ALP levels were elevated in 74% of patients with liver metastases (Mean, 290) and in 33% without liver metastases (Mean, 122) (P = 0.001). Patients with elevated ALP levels at the most recent time of progression were 5.7 (95% CI, 2.4-13.3) times more likely to have a liver metastases compared to patients with normal levels. Additionally, patients with elevated ALP levels at their most recent visit were 4.2 (95% CI, 1.7-10.7) times more likely to have a worse prognosis compared to patients with normal levels. However, after controlling for the effects of liver metastases, the association between elevated levels and prognosis was no longer significant. After controlling for the effects of age, sex, and liver metastases, large changes in AP levels were associated with a 4.4 (95% CI, 1.0-19.1) times greater odds of having a worse prognosis compared to patients with a minimal change. Patients with an ALP level greater than 160 were 12 (95% CI, 4.3-33.3) times more likely to have liver metastases than patients with an ALP level of less than 160. Mean CEA level was 78 for patients without liver metastases and 308 for patients with liver metastases. CEA levels were compared against ALP in a random sample of 18 patients, which revealed a correlation between increasing levels of CEA (.002) with increasing levels of ALP. CONCLUSION: Instead of the upper normal limit for ALP, our data shows that using an ALP cutoff of 160 U/L increases the sensitivity of liver metastases detection. Also, a change in ALP levels of greater than 120 U/L over four-to-six weeks may be indicative of disease progression. Monitoring ALP is a simple, low cost, and relatively sensitive screening tool. Prospective studies involving evaluation of ALP in addition to CEA in patients with CRC is indicated.
PURPOSE: To report our clinical experience with 25 patients receiving concurrent capecitabine and irradiation in the treatment of locally advanced or resected pancreatic cancer. METHODS AND MATERIALS: We reviewed the medical records of patients with pancreatic cancer who received treatment with capecitabine and irradiation for pancreatic cancer and received capecitabine 1200 to 1600 mg/m(2) orally twice daily Monday through Friday with concurrent radiation (5040-5400 cGy, 180 cGy, 5 days/week), followed by a 4-week rest, then 6 to 8 cycles of capecitabine alone 2000 to 2500 mg/m(2) twice daily for 14 days every 3 weeks (surgically resected), and capecitabine 2000 to 2500 mg/m(2) BID for 14 days every 3 weeks until progressive disease (unresected). RESULTS: The population consisted of 14 females and 11 males, with a median age of 64 years (range 37-80 years). Histology was adenocarcinoma in 23 patients and neuroendocrine tumor in 2 patients. One patient had resected tumor, 3 patients were resected with positive margins, 1 patient was resectable with poor performance status prohibiting resection, and 20 patients had unresected locally advanced disease. Median dose of capecitabine concurrent with radiation was 1500 mg/m(2)/day (600-1600 mg/m(2)/day) given orally in two divided doses, 5 days per week on days of treatment with radiation therapy. Patients received a median total radiation dose of 5040 cGy (4500-5040 cGy) over 6 weeks. Eleven patients were continued on capecitabine cycles after treatment with concurrent capecitabine and irradiation. The median number of cycles completed was 3, with one patient completing 8 cycles. Median survival was 14 months, with 18 patients surviving through the end of the study period. Median overall primary tumor response over the study period was -2% (-100%-100%). Five patients were taken to laparotomy after treatment based on radiographic response and two patients were successfully resected. By the end of the study period, there were 4 complete remissions, 2 partial remissions, 6 stable disease, and 13 progressive disease. Grade 3 or 4 toxicity was observed mainly with gastrointestinal symptoms including nausea, vomiting, diarrhea, and anorexia. Three patients had G3 hand-foot syndrome, 1 patient had G3 peripheral neuropathy, 1 patient had G4 gastrointestinal bleed, and 1 patient had G3 radiation enteritis. There was one death directly related to treatment secondary to uncontrolled GI bleeding. CONCLUSION: In patients with locally advanced pancreatic cancer, concurrent capecitabine and radiation had good survival response in patients and good tumor response. Toxicity of oral capecitabine was well tolerated.
Oxaliplatin has become an integral part of the standard treatment for advanced colorectal cancer. While oxaliplatin has only mild hematologic and gastrointestinal side effects, its dose-limiting toxicity is a cumulative sensory neurotoxicity. Oxaliplatin causes a unique, but frequent, acute sensory neuropathy that is triggered or aggravated by exposure to cold but is rapidly reversible, without persistent impairment of sensory function. Various strategies have been proposed to prevent or treat oxaliplatin-induced neurotoxicity. One such strategy is the "Stop-and-Go" concept, which uses the reversibility of neurologic symptoms to aim at delivering higher cumulative oxaliplatin doses, as long as the therapy is still effective and the other is the administration of neuromodulatory agents (ie, calcium-magnesium infusions, carbamazepine, gabapentin, amifostine, alpha-lipoic acid, and glutathione) that could limit the neurotoxic effects of oxaliplatin. Among all of the agents, intravenous calcium and magnesium have shown the most promise in prophylaxis and treatment of oxaliplatin-induced neurotoxicity. We report a case of a patient, in which oral calcium supplements not only were successful in treating his neurotoxicity, but we also were able to administer a cumulative dose of 2500 mg/m(2) (990 mg/m(2) with oral calcium). Although the current recommendations for the management of the acute and cumulative neurotoxicity from oxaliplatin with the use of infusion of Ca/Mg remain valid, our case is the first report demonstrating the role of oral minerals in ameliorating neurotoxicity from oxaliplatin. Future studies to evaluate the role of oral Ca/Mg are warranted, since they could prove to be an effective, less expensive and more convenient way to treat and prevent oxaliplatin-associated toxicity.
