Archive for September, 2014

Eosinophilic Esophagitis Causing Esophageal Dysmotility

We describe a case of eosinophilic esophagitis in a 38- year-old man with aspirin-sensitivity asthma which presented as noncardiac chest pain. Manometric mea­surements demonstrated tertiary contractions. Biopsies showed a dense eosinophilic infiltrate in the mucosa. There was no response to therapy for reflux. Symptoms quickly resolved with corticosteroid therapy. Subsequent manometric values recorded after corticosteroid therapy showed resolution of the dysmotility. Biopsies showed normal mucosa. Adult asthmatic subjects with noncardiac chest pain should receive further investigation if reflux therapy fails to resolve the symptoms.

The most common esophageal symptoms in asthmatic subjects are due to gastroesophageal reflux. Reflux may worsen the asthma, and control of the asthma may not occur until the reflux is adequately managed. Many medications used to treat asthma decrease lower esophageal sphincter tone. This may contribute to the reflux symptoms. Therefore, reflux is commonly seen in both children and adults with asthma, both as a cause of the asthma and as a consequence of treatment.

In this case report, we describe an asthmatic patient with a long history of reflux who develops a new chest pain syndrome related to, but distinct from, the reflux. Initial attempts to manage the reflux did not decrease the pain. A  diagnosis of dysmotility was made by esophageal manometric measurements. Mucosal biopsy demonstrated eosinophilic esophagitis. The patient promptly responded to corticosteroid treatment. 

Case Report

A 38-year-old man with asthma was seen for a 1-month history of atypical chest pain. The pain was substemal, squeezing, and did not radiate. The pain often awoke the patient at night. Sometimes the pain was preceded by heartburn. It was partially relieved by antacids and swallowing cold liquids. The episodes of pain would last from 15 min to several hours. There was no shortness of breath or diaphoresis. There was no exertional component. The chest pain was preceded by a 2-week history of increased nasal discharge. There were no new medications, new foods, or changes in diet.

Recently, it has become apparent that invasive thymoma is relatively sensitive to combination chemotherapy and that survival is relatively long. In two fairly large series using the РАСregimen or a combination of cisplatin, doxorubicin, vincristine, and cyclophosphamide, overall response rates ranged from 70 to 91.8%, with median durations of response averaging 11.9 months and median survival ranging from 15 to 37.7 months. Recendy, РАСwith etoposide and concurrent granulocyte colony-stimulating factor had been used for advanced thymoma or thymic cancer with a reported 42.9% response rate (all partial remissions) but with significant bone marrow toxicity. The РАСregimen was chosen for our patients because of the favorable response rates noted. We substituted carboplatin for cisplatin for easier outpatient administration. The concurrent use of oral prednisone in case 1 was not a likely confounding factor because his tumor progressed during low-dose steroid therapy.

Our patients developed progressive thymoma after ini­tially responding to combination chemotherapy consisting of cyclophosphamide, doxorubicin, and carboplatin. The standard treatment options for this situation, in order of decreasing effectiveness, are a subsequent surgical resection, radiotherapy, and corticosteroid use. There are reports of small prospective trials of second-line chemotherapy using various regimens (single or in combination) with disappoint­ing results.3 7 The role of low-dose oral etoposide in the management of recurrent thymoma has not been evaluated in clinical trials although there are reports of some efficacy as first-line therapy in combination with cisplatin. We elected to use the same chemotherapeutic regimen to treat our patients’ recurrences because their disease had re­sponded to the РАСregimen previously, because the disease-free interval was greater than 6 months, and because there was evidence that secondary responses occurred with the same regimen in lung, breast, and ovarian cancers as well as in Hodgkin’s lymphomas. Higher response rates were noted when the disease-free intervals were greater than 12 months in breast cancer, 24 months in epithelial ovarian cancer, and 12 months in Hodgkin’s lymphoma. The disease-free intervals in our patients were 14 and 60 months, respectively.  

Several investigators have reported cases of second-line chemotherapy using different regimens with mixed results. In three patients who had relapses following therapy with a regimen of combination cisplatin, doxorubicin, vincristine, and cyclophosphamide, treatment  with cisplatin, etoposide, and ifosfamide resulted in stable disease in two patients.3 Only one other report of a response to salvage chemotherapy with the same regimen was noted in the medical literature. Kosmidis et al reported a case of unresectable invasive thymoma treated with radiotherapy with an 80% response but 4 months later there was disease progression. Local recurrence was treated with cyclophosphamide, doxorubicin, and vincristine, which produced a partial response. The patient refused further treatment against medical advice. Nine months later, the patient presented with renal and abdominal lymph node metastasis. This was treated with the same combination of drugs, again producing a significant improvement consisting of a more than 50% reduction in tumor bulk, noted both clinically and radiographically. The patient eventually had a relapse 9 months after reinitiation of chemotherapy and died of renal failure.

A 54-year-old white man without any significant past medical history presented to our institution in June 1989 with a 4-year his­tory of vague anterior neck swelling and discomfort. A neck MRI at this time demonstrated a large solid soft-tissue mass in the lower area of the left side of the neck with mediastinal extension, tracheal deviation, and left innominate vein occlusion. A chest radiograph suggested a right pleural effusion. He was subsequently admitted to the hospital, and a needle biopsy of the neck mass demonstrated malignant thymoma. He received 3 courses (every 21 days) of cy­clophosphamide (500 mg/m ), doxorubicin (50 mg/m2), and cis- platin (50 mg/m2) from July 28 to September 20, 1989, resulting in a 50% reduction in the tumor size and resolution of the pleural ef­fusion. A thymectomy was performed in October of 1989 with re­section of all visible tumor. He had mediastinal radiotherapy (60 Gy) thereafter, completing treatment in December 1989. He did well for 5 years until February 1995 when he presented with cough and hoarseness. An ear, nose, and throat evaluation revealed left vocal cord paralysis, tracheal deviation to the right, and a palpable mass in the suprasternal notch adjacent to the left sternoclavicular joint. A CT scan of the neck and chest demonstrated an ill-defined 3.0×2.5-cm mass to the left of the trachea at the thoracic inlet and a 1.5×2.0-cm anterior mediastinal lymph node. Recurrent thymoma was confirmed by ultrasoundguided biopsy of the tumor. He began 4 courses (every 28 days) of carboplatin (300 mg/m2), doxorubicin (40 mg/m2), and cyclophosphamide (400 mg/m2) from Feb­ruary to June 1995. A postchemotherapy chest CT scan showed that the tumor and anterior mediastinal lymph node were no longer detectable. A positron emission tomography scan done 2 months later revealed no evidence of malignancy. He continues to do well and remains in remission as of February 1996, 8 months after his remission was noted.

A 26-year-old Asian man was first seen at our institution in No­vember 1978 with a diagnosis of myasthenia gravis requiring ther­apy with prednisone and subsequently a thymectomy in December 1978. During the next decade, he suffered recurrent upper respiratory tract infections and myasthenic exacerbations. He was read­mitted to this hospital in May of 1992 for productive cough and fe­ver. A chest radiograph done at this time showed an anterior mediastinal mass, and a subsequent CT scan confirmed the presence of recurrent mediastinal thymoma with pleural metastasis which was later confirmed by mediastinoscopy and biopsy. In late May, an open thoracotomy was performed, which showed tumor involvement of the parietal pleura and both vagus and phrenic nerves, precluding complete resection of the tumor. The patient was therefore offered and agreed to treatment with chemotherapy consisting of four courses (every 21 days) of a combination of carboplatin at 300 mg/m2, doxorubicin at 50 mg/m2, and cyclophosphamide at 500 mg/m2 beginning on July 6, 1992. Prior to starting chemotherapy and throughout the treatment period, the patient received prednisone for myasthenia gravis and asthma with daily oral doses averaging 10 to 15 mg. The patient eventually completed chemotherapy on September 28, 1992. Chest radiographs taken immediately before and after chemotherapy revealed a reduction in size of the tumor from a 5×4-cm irregularly sized mass to an indistinct haziness over the left lung field. He continued to remain in clinical remission until December 1993 when he was readmitted for a malignant right-sided pleural effusion requiring chest tube drainage and pleurodesis. The chest radiograph at this time revealed a 6.5-cm pleural based mediastinal mass in the left hemithorax consistent with recurrent thymoma. A chest CT showed multiple large inhomogenous pleural-based soft tissue masses in the left hemithorax and the anterior mediastinum (Fig 1). At this time, the patient received another course of the РАСregimen at adjusted doses: carboplatin, 300 mg/m2; doxorubicin, 40 mg/m2; and cyclophosphamide, 400 mg/m2; the therapy was administered at 4-week intervals for a total of 4 cycles beginning in late December 1993. Another chest CT scan in April 1994 showed a reduction in the size of the mediastinal mass from 9×10 cm at the widest dimensions to 7×3 cm (Fig 2). By May of 1994, a month after the last cycle of therapy was administered, a chest CT scan revealed complete res­olution of the mass adjacent to the aortic arch. Throughout this time, he was receiving prednisone at an average dose of 2.5 mg daily for myasthenic symptoms. He remained in clinical remission for 6 months when recurrence of the tumor was noted over the anterior mediastinum and left hemithorax. His health progressively deteriorated until he died with severe pneumonia and progressive thymoma in June of 1995.

Invasive thymoma recently has been shown to be sen­sitive to combination chemotherapy and in some cases to be relatively indolent. Two cases of extensive thymoma which responded to primary treatment with a combination of a platinum compound (carboplatin or cisplatin), doxorubicin (Adriamycin), and cyclophos­phamide (or РАС) are described. Tumor progression occurred 14 (case 1) and 60 months (case 2) after completion of initial РАСtherapy and was treated with the same regimen resulting in a second remission, which lasted 6 months in case 1 and is continuing at 8 months in case 2. Similar reports of secondary re­sponses using the same chemotherapy have been de­scribed in breast, lung, and ovarian cancers, as well as in Hodgkin’s lymphomas. Our observations suggest that retreatment with the same platinum-based regimen should be considered in patients who have progressive thymoma following a previous chemotherapeutic response and a disease-free interval of greater than 12 months.

Thymomas are rare tumors of the anterior superior me­diastinum, accounting for about 15% of all mediastinal masses. Although thymomas are histologically benign and grow indolently, some invade the surrounding structures and behave as malignant tumors. Only 40% of thymomas are completely encapsulated, with no evidence of microscopic invasion. Traditional management of invasive thymomas generally involves surgical resection and radiotherapy, but recently cytotoxic chemotherapy, particularly regimens us­ing cisplatin, doxorubicin (Adriamycin), and cyclophosphamide (РАС), has been shown to produce response rates of 70 to 91.8%. In addition to being relatively sensitive to chemotherapy,5 it appears that invasive thymomas are somewhat indolent with some incurable patients surviving for years. Therefore, some patients who initially responded to chemotherapy will be candidates for salvage chemother­apy.

This is a report of two patients with unresectable invasive thymoma who initially responded to a course of a platinum compound, РАС, and whose recurrence again responded to  РАС. These appear to be the first reported cases of thymoma in which the same platinum-based regimen achieved a sec­ondary remission.

This mind workout is to deal with any bad past sex encounter that causes you anxiety and continues to live rent free in your persona. Desensitisation is a technique to face up to it and deal with it It is different from Mind Power I above because it deals with actual bad past sex encounters, not an attitude about yourself.

As much as you are a product of your past experiences, it is also true that your past cannot be changed. Past ED encounters would have left their mark on your persona and some of them may have been so hurtful as to qualify as Sexual Trauma which we listed as a possible source of ED in Step 3. You need to desensitise yourself from any such bad thoughts or trauma Canadian Sildenafil citrate so that they do not develop in your conscience. Covering them up or suppressing them increases your anxiety.

The technique is as follows:

1. Think back over your worse ED experiences. For each one describe and write down the following. Be as objective as possible:

a. The Situation: where, when, after what event, before what expected event, partner mood, partner look, partner as much of the Situation as you can recall.

b. Thoughts: What did you think to yourself? For example, your mind may have brought up: “My Dick is going to let me down again or, I shouldn’t have drank so much”……

c. Feelings: Describe how you felt: can you recall being embarrassed, angry with yourself, felt miserable, started lying ? How severe where the feelings?

2. Put yourself in that Situation and for each Thought and Feeling you have written down, suggest a positive correction. For example: ‘It happened, so what, I am not alone and I will plan another encounter with Jane when my USCFs are in my favour; or, I will have another encounter with Jane without so much alcohol so that I can enjoy her body..;

3. Have break for a few minutes doing something distractive. Have a coffee, listen to some music or just do the washing to impress your Jane.

4. Now go back to your list of Situations and recall each one. Apply the positive alternatives to each one and see if you feel the same upsetting feelings. The goal is to feel differently about each one. Not to feel upset in any way.

5. Repeat the process, at different times if possible, until you are comfortable and do not feel bad about each of the hurtful Situations.

Desensitisation has a cleansing effect and can also be done for any future bad sex encounters you may encounter.

Know Your Genes – The Genetics of Colon Cancer

Other men start to develop many colonic polyps, which eventually become cancerous, from the age of 30 onwards. Hence it is important to know your family history and get yourself properly checked out.

Ulcerative Colitis and Colon Cancer

Chronic ulcerative colitis is a condition that causes inflammation of the lining of the colon. Colon cancer is a recognised complication of chronic ulcerative colitis and is related to the location and the extent of the disease. Therefore, if you suffer from this condition, regular colonoscopies are recommended to look Sildenafil citrate Canadian for pre-cancerous changes.

Other Risk Factors for Colon Cancer

Cigarette smoking has been associated with an increased risk of colon cancer. Patients with diabetes are more likely to be diagnosed with colon cancer. Obesity is associated with an increased risk, as is having a beer belly. Excess alcohol (more than 4 units per day), particularly beer consumption, is an associated risk factor for colon cancer.

What Are the Symptoms of Colon Cancer?

Bowel symptoms may include some or all of the following:

  • A persistent change in bowel habit, such as constipation, diarrhoea or alternating constipation and diarrhoea
  • Bleeding from the back passage
  • Narrow stools
  • A feeling of incomplete emptying of the bowel when going to the toilet
  • A straining feeling or discomfort in the back passage
  • Abdominal pain, cramps or bloating

Colon cancer can be present for several years before symptoms develop. Other symptoms of colon cancer can include fatigue, nausea, weakness, loss of appetite and weight loss. Symptoms vary according to where in the large bowel the tumour is located. The right side of the colon is spacious, and cancers in this area can get big before they cause any abdominal symptoms. These cancers tend to cause iron deficiency anaemia due to the slow loss of blood over a long period of time. Iron deficiency anaemia causes fatigue, weakness and shortness of breath.

The left side of the colon is narrower than the right side and cancers here are more likely to cause partial or complete bowel blockage or obstruction. Cancers causing partial bowel obstruction can cause symptoms of constipation, narrowed stools, diarrhoea, abdominal pains, cramps and bloating. Bright red blood in the stool may also indicate a growth near the end of the left side of the colon or rectum.

If you have these symptoms you should see your doctor without delay. However, other conditions, such as irritable bowel syndrome (spastic colon), ulcerative colitis, Crohn’s disease, diverticulosis, and peptic ulcer disease, can all have symptoms that mimic colon cancer.

I have given you a lot of information and it can be confusing as to where to start and what to do. There are many directions you go in to work on your erectile issue. And what I’m about to suggest is just one direction. You can create your own plan using the information that I have given you here. But here is a summary of what has been said in this e-book.

If you have been having problems getting an erection for a few times this is not erectile dysfunction. For some reason you have lost confidence in producing a strong and hard erection and that should pass. But if it continues then, you can do some about it using this information.

The causes of impotence are varied but there are the areas that you need to work on:

-Bad habits that create cardiovascular disease
-Alkaline body for normal health and to eliminate illness
-Brain stimulus to improve your libido or sexual desire
-Blood circulation to improve the flow of blood to your penis
-Nitric oxide to promote hardness
-Nerve function to stimulate your sexual centers
-Hormonal balance to normalize your sexual secretions Bad Habits

I have listed which bad habits you need to change. These include smoking, using medical drugs, using over-the-counter remedies Sildenafil citrate Canada, drinking alcohol, and a few others. If you are not able make these changes then, this health program will not be as effective.

The reason you have hardness problems is because of the lifestyle you are living and if you want to improve your hardness then you need to make some drastic changes.

You don’t have to make these changes all of a sudden. You need to withdraw from them slowly by decreasing your dependence on them weekly and by reduce the quantity you use.

Alkaline Body

You need to change your body condition from acid to alkaline. Having an acid body is a major reason why some many people are sick with a variety of deadly diseases. You can recover your health by creating an alkaline body.

Next you need to follow the body cycles. The eating patterns suggested here are so that you can help your body eliminate toxins. These toxins make your body malfunction and keep your body acidic.

Evidence suggests that it is possible to shield vulnerable organs such as the ovaries from the damaging effects of cancer treatments Viagra pharmacy in Canada. The ovaries can be surgically moved out of the direct path of radiation exposure. Ovarian transposition can be to an alternative location in the abdomen or to a heterotopic site such as the forearm. While this ovarian transposition has been used in adults with limited success, it is not a long-term solution for the preservation of fertility in younger patients.

An alternative protective approach, which is suitable for girls, is based on the idea that the pre-pubertal ovary is relatively quiescent and can be pharmacologically protected from the cytotoxic effects of medical therapies that destroy rapidly dividing cells. The drugs that can be used to limit the gonadal toxicity of otherwise successful treatments include gonadotrophin-releasing hormone (GnRH) agonists and antagonists. These synthetic hormones are based on the endogenous brain peptide GnRH and are routinely used in reproductive medicine to reversibly shut down ovarian function and induce a hypogonadotrophic2 state. In the context of shielding the ovary of a young patient, the GnRH analogue would be administered before the start of chemo- or radiotherapy to suppress the release of the follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the brain. FSH and LH normally drive cell division and pro-mote growth in ovarian follicles. If the cells in the follicle are actively dividing, they are more vulnerable to the cytotoxic damage by chemo- or radiotherapy treatments. Administration of drugs such as GnRH agonists during treatment would therefore be expected to protect the ovaries by inhibiting the later stages of follicle growth. In support of this idea, Ataya et al. demonstrated in primates that GnRH-agonist co-treatment protected the Rhesus monkey from cyclophosphamide (an alkylating agent) induced ovarian damage. These findings are supported by several clinical studies. For example, co-treatment with GnRH agonist during chemotherapy resulted in premature ovarian failure in only 2.3 per cent of patients compared with 58 per cent in the group treated with chemotherapy only. GnRH agonist administration to adolescents during chemotherapy has also been shown to confer some degree of protection on the ovary. While these studies are encouraging, conflicting evidence raises doubts as to the benefit of this approach and for the most part the data remain unconvincing.

Programmed cell death by apoptosis has been identified as the mechanism responsible for both the loss of oocytes that occurs during the normal process of oogenesis (the process by which mature ova are produced in the ovary) and for oocyte loss induced by anti-cancer therapies. Preliminary evidence has implicated sphingosine3-based lipid signalling molecules such as ceramide and sphingosine-1-phosphate (SIP) as key mediators of cellular growth, differentiation and apoptosis in postnatal ovaries. This observation has opened new avenues for protecting the ovaries of patients from possible side-effect damage. Treatment of mouse ovaries in vitro with SIP resisted the apoptosis induced by anticancer therapy, whereas in vivo injection of SIP into the ovarian bursa of mice completely prevented radiation-induced oocyte loss. Further research is required to explore the potential protective effect of small lipid molecule therapy on the ovaries of young patients.