Publications

A 54-year-old male observed change in his bowel function in September 2002. He experienced constipation and difficulties in emptying, as well as pain in the left side of his pelvis. Ultrasonographic exam detected a pathological mass in the descendent colon. Colonoscopy revealed a tumor that nearly occluded the lumen of the colon at the junction of the sigmoid and descendent colon. Upon tumor biopsy, histology confirmed adenocarcinoma stage III, T3N1MX, Dukes C1. Segmental resection of the colon was performed at the end of October 2002. In November 2002, 12 cycles of adjuvant chemotherapy were initiated using the DeGramont protocol. This therapy continued until April 2003.

In April 2004, the patient presented with a sudden rise in blood pressure. Abdominal computed tomography scan and renal scintigraphy diagnosed hydronephrosis carotis verte. Subsequently, a laparoscopic left-sided nephrectomy was performed. In the middle of August 2004, elevated CEA (4.2ng/ml) was detected, although abdominal and chest computed tomography scans found no abnormalities.

In mid-July 2005, a PET-CT scan detected a 10mm diameter focal FDG accumulation at the level of the 12^th thoracic vertebra. Several 8-30mm diameter focal FDG accumulations were also detected paraaortically between the lumbar 2-5 vertebrae. About 2/3^rd of the oral section of the ascendant colon showed intense FDG accumulation, while the rest of the intestines showed normal accumulation. These observations indicated recurrent, disseminated disease with retroperitoneal involvement.

In early August 2005, a colonoscopy discovered numerous pea-sized thickenings of the mucosal surface at a height of 30cm in the colon. A diagnosis of diverticulosis was made. Subsequent computed tomography scan detected the in 10^th segment of the lung a subpleural focus 9mm in diameter that was a metastasis. Wall thickness of the rectal and a 13cm long section of the sigmoid colon varied from 8-11mm, suggesting a pathological mass.

In mid-September 2005, 5 cycles of chemotherapy were initiated using the FOLFIRI protocol. At the end of October 2005, a computed tomography scan detected a 7mm diameter focus subpleurally in the 9^th segment of the right lung, and below that another 3mm size focus. These were pulmonary metastases. Progression of the previously described abdominal lymph node metastases was also observed.

Progression of the disease required a change in the chemotherapy protocol to the FOLFOX regime (6 cycles). Computed tomography scan at the end of February 2006 demonstrated further progression of the retroperitoneal metastases. Despite its lack of efficacy, continuing the same chemotherapy protocol was recommended. At that point, the patient decided to pursue an alternative solution, and in the mid-April 2006 began taking our MSQ 15D dietary composition, 2tbsp TID.

At the end of July 2006, the patient presented with a severe Salmonella infection after eating an infected egg and was hospitalized for 5 days. After completing a course of antibiotic therapy, he continued to have difficulties with food intake for another two weeks, experiencing a weight loss of 15kg during this episode. He was taking probiotics and received injections of Vitamins B6 and B12, Vitamin C and Vitamin E from his general practitioner. He was unable to take the MSQ 15D during this period.

In early August 2006, a computed tomography scan found no progression of the retroperitoneal lesions, while some of them were already undergoing calcinosis. There was no change in the status of the lungs. In mid-August 2006, the patient was admitted to the hospital and presented with difficulties with swallowing and vomiting. Oesophago-gastro-duodenoscopy exam found an obstruction in the jejunum that was biopsied. Braun anastomosis was subsequently performed to open up the passage. The jejunal obstruction was possibly a consequence of the inflammation caused by the Salmonella infection.

Restoring passage through the anastomosis required reoperating, followed by a nearly month-long period of recovery. The patient began using the MSQ 15D again in early October 2006, and shortly afterwards regained 4kg of weight. In mid-October 2006, a computed tomography scan demonstrated no disease progression in the abdomen and calcification of some of the retroperitoneal lymph nodes. There was no change in the status of the lungs.

During November 2006, the patient’s weight gain continued (6kg gain). His energy returned and he resumed working, initially with a light workload. He continued to recover through the rest of the year, with a weight gain of 7kg. In early January 2007 the patient was hospitalized with passage disturbance, and was released following day after his passage resumed.

In early February 2007, a computed tomography scan showed some calcified retroperitoneal lymph nodes. No tumor was detected in the abdomen or the chest. The patient was carrying a full workload at that time and pursuing normal activities. On March 10, 2007, a Friday night, the patient felt abdominal pain after consuming a heavy meal, and reported to the hospital. Ultrasonongraphic scan detected ileus, and the patient was admitted to the ICU. No surgical team was on call for the weekend in the small town hospital. By Monday, the patient was septic and expired. Autopsy revealed that the obstruction in the small intestine was caused by adhesions; no tumors were found in the abdomen.