Treatment of Internal Hemorrhoids by Endoscopic Sclerotherapy with Aluminum Potassium Sulfate and Tannic Acid.

Objective. A new sclerosing agent for hemorrhoids, aluminum potassium sulfate and tannic acid (ALTA), is attracting attention as a curative treatment for internal hemorrhoids without resection. The outcome and safety of ALTA sclerotherapy using an endoscope were investigated in the present study. Materials and Methods. Subjects comprised 83 internal hemorrhoid patients (61 males and 22 females). An endoscope was inserted and retroflexed in the rectum, and a 1st-step injection was applied to the upper parts of the hemorrhoids. The retroflexed scope was returned to the normal position, and 2nd-4th-step injections were applied to the middle and lower parts of the hemorrhoids under direct vision. The effects of endoscopic ALTA sclerotherapy were determined by evaluating the condition of the hemorrhoids using an anoscope and interviewing the patient 28 days after the treatment. Results. A cure, improvement, and failure were observed in 54 (65.1%), 27 (32.5%), and 2 (2.4%) patients, respectively, treated with ALTA. Complications developed in 4 patients (mild fever in 3 and hematuria in 1). Recurrence occurred in 9.6%. Conclusions. The results of the present study suggest that endoscopic ALTA has the potential to become a useful and minimally invasive approach for ALTA sclerotherapy.

Molecular Cloning and Sequence Analysis of the cDNAs Encoding Toxin-Like Peptides from the Venom Glands of Tarantula Grammostola rosea.

Tarantula venom glands produce a large variety of bioactive peptides. Here we present the identification of venom components obtained by sequencing clones isolated from a cDNA library prepared from the venom glands of the Chilean common tarantula, Grammostola rosea. The cDNA sequences of about 1500 clones out of 4000 clones were analyzed after selection using several criteria. Forty-eight novel toxin-like peptides (GTx1 to GTx7, and GTx-TCTP and GTx-CRISP) were predicted from the nucleotide sequences. Among these peptides, twenty-four toxins are ICK motif peptides, eleven peptides are MIT1-like peptides, and seven are ESTX-like peptides. Peptides similar to JZTX-64, aptotoxin, CRISP, or TCTP are also obtained. GTx3 series possess a cysteine framework that is conserved among vertebrate MIT1, Bv8, prokineticins, and invertebrate astakines. GTx-CRISP is the first CRISP-like protein identified from the arthropod venom. Real-time PCR revealed that the transcripts for TCTP-like peptide are expressed in both the pereopodal muscle and the venom gland. Furthermore, a unique peptide GTx7-1, whose signal and prepro sequences are essentially identical to those of HaTx1, was obtained.

Characterization of voltage-dependent calcium channel blocking peptides from the venom of the tarantula Grammostola rosea.

Voltage-dependent calcium channel blocking peptides were purified and sequenced from the venom of the tarantula, Grammostola rosea. cDNAs encoding the peptide sequences were cloned from the venom gland cDNA library. The electrophysiological effects of the peptides on several types of voltage-dependent calcium channels were evaluated using a Xenopus laevis oocyte expression system. A peptide contained in one of the HPLC peak fractions inhibited P/Q type voltage-dependent calcium channels (Ca(v)2.1). The amino acid sequence of this peptide is identical to that of ω-grammotoxin SIA. A peptide from another discrete peak, which is identical to GsAFII except for one tryptophan residue in the C-terminus, inhibited L-type voltage-dependent calcium channels (Ca(v)1.2). A novel peptide, named GTx1-15 (Accession number, AB201016), shows 76.5% sequence homology with the sodium channel blocker phrixotoxin 3, however, GTx1-15 preferentially inhibited T-type voltage-dependent calcium channels (Ca(v)3.1). In silico secondary and tertiary structure prediction revealed that GTx1-15 and sodium channel blockers such as hainantoxin-IV, phrixotoxin 3, and ceratotoxin 2 show very similar ß-strand composition, distribution of Optimal Docking Areas (continuous surface patches likely to be involved in protein-protein interactions), and surface electrostatic potential. These findings suggest that these peptide toxins evolved from common ancestors by gene duplication to maintain surface atmospheres appropriate for interaction with low-voltage-dependent ion channels.

Sigmoid colon carcinoma that developed from a sessile-type cancer in a short period of time.

We report a case of sigmoid colon carcinoma that developed from a sessile-type cancer in a short period of time. An 83-year-old man was found to have a round sessile polyp, about 2 cm in diameter, in the sigmoid colon. Because he had taken anticoagulants, immediate endoscopic mucosal resection and biopsy were not performed. Forty-three days later, the apical surface of the sessile polyp had become depressed and ulcerated, and we judged that an endoscopic resection was not indicated for this lesion. The histologic diagnosis of the biopsy specimens was a well-differentiated adenocarcinoma. We recommended surgical treatment; however, the patient was not in favor of surgical treatment and would not consent to surgery. Two more examinations were performed and the tumor was found to have developed into an invasive cancer with ulcerated, nodular margins involving 3/4 of the colonic lumen. At 271 days after the initial examination, the patient finally consented to surgery and a partial resection of the sigmoid colon was performed. The tumor was classified as stage I (T2N0M0). The several examinations performed from presentation within a short time span provide evidence of the morphologic changes that occur when a sessile-type cancer develops into an ulcerating invasive cancer. We hypothesize that remarkable configuration changes and development take place when a tumor becomes invasive in the muscularis propria from massive submucosal invasion. Our findings suggest that among the tumors discovered as typical ulcerating invasive type colon cancers are those that developed from protuberant tumors in a short period of time.

[A case of duodenal perforation during mFOLFOX6 treatment for metastatic sigmoid colon cancer].

We present a case of metastatic sigmoid colon cancer causing duodenal perforation during modified FOLFOX6 chemotherapy. The patient was a 68-year-old man who underwent sigmoidectomy for an advanced sigmoid cancer in September 2007. He has been received mFOLFOX6 chemotherapy for multiple liver metastases since January 2009. In March 2010, the patient complained of abdominal pain during the 24th course of chemotherapy, and was admitted to our hospital. On admission, his vital signs were normal, and abdominal findings revealed no peritonitis signs. An abdominal CT scan showed free air and fluid collection on the first day of admission. The patient was diagnosed with gastrointestinal perforation, and underwent emergency operation for abdominal drainage. The leakage of biliary fluids was recognized at the drain to the Winslow postoperatively. It ceased on the 25th admission day, and an upper gastrointestinal examination showed good passage of fluids and no leakage at the duodenum. However, the patient died 36 days after admission from remarkable pleural effusion and respiratory failure.

[A case of ascending colon cancer with unresectable distant metastases treated by systemic chemotherapy].

The patient, a male in his 70s, was referred to this hospital by his neighborhood doctor with what was said to be impaired hepatic function. Detailed examinations revealed a circumferential ascending colon cancer, diffuse hepatic metastases scattered over both liver lobes, and lymph node metastases in the left axilla. With the primary lesion-induced symptoms of stenosis controllable, the patient began systemic chemotherapy by mFOLFOX6 without a resection of the primary lesion. After completing a 10-course treatment, the patient underwent surgery to resect the primary lesion in preparation for bevacizumab treatment. In the postoperative systemic chemotherapy, FOLFIRI and mFOLFOX6 were administered concomitantly with bevacizumab. After a total of 19 courses, the patient's systemic condition gradually deteriorated. He eventually died of cancer one year and seven months after diagnosis of the primary lesion or one year and one month subsequent to the resection of the primary lesion. No consensus has been reached on the necessity to resect the primary lesion in patients with advanced colorectal cancer who also have unresectable distal metastases. Systemic chemotherapy, nevertheless, can provide tumor control on both primary and metastatic lesions and could become a treatment option in the future.

[A patient with recurrent rectal cancer in whom pulmonary metastasis disappeared by FOLFOX 4 therapy].

We performed FOLFOX 4 therapy in a patient with lung metastasis (a 62-year-old woman) after surgery for rectal cancer and observed both normalization of tumor markers and disappearance of the metastasis. Low anterior resection was performed for progressive rectal cancer, and treatment with UFT and folinate was started one month after surgery. However, tumor markers increased after 2 months of treatment and CT scans showed metastases to both lungs. FOLFOX 4 therapy was started, and tumor markers became normal after four courses, while the lung metastases disappeared after 10 courses. The dosage of FOLFOX 4 was reduced after three courses due to neutropenia and diarrhea. This treatment appeared to be effective for the inhibition of lung metastasis associated with colorectal cancer.

Massive melena caused by a carcinoid of the small intestine: report of a case.

We report a case of massive melena caused by a carcinoid of the small intestine. A 28-year-old woman was admitted to our department after presenting with massive melena. The source of the bleeding could not be localized by upper or lower gastrointestinal endoscopy, computed tomography (CT), or labeled red blood cell scintigraphy. Enteroscopy allowed visualization only up to the jejunum, and we could not localize the lesion. The melena subsided with conservative treatment, but the patient was readmitted 4 months later when she suffered another episode of massive melena. A contrast CT scan performed immediately showed extravascular leakage and the retention of contrast medium in the ileum. Thus, she underwent an emergency surgery, during which endoscopy confirmed a small ileal tumor accompanied by pulsating bleeding from the exposed blood vessels at its center. The small intestine was partially resected, including the swollen lymph nodes, the size of small beans. Pathological examination confirmed a carcinoid tumor 1 cm in diameter, with an arterial rupture at its center and lymph node metastasis.

Bilateral asynchronous adrenocortical adenoma in a girl with beckwith-wiedemann syndrome.

We report a case of asynchronous occurrence of bilateral adrenocortical adenoma in a 13-yr-old girl with Beckwith-Wiedemann syndrome. A right virilizing adrenal adenoma was surgically removed at age 6, following clinical manifestation of virilization such as acne, voice change, clitoris hypertrophy and overgrowth. Histopathological examination of the resected specimen revealed an adrenocortical adenoma predominantly composed of eosinophilic tumor cells expressing all the steroidogenic enzymes. High serum levels of DHEA-S (6,380 ng/ml) and testosterone (547 ng/dl) were noted prior to the operation. Postoperative course was unremarkable. Menstruation started at age 11, with a regular interval. At the age of 13 yr old, a high serum level of DHEA-S (8,250 ng/ml) was detected. In contrast to the episode of virilization at age 6, however, the serum testosterone level was not so high (122 ng/dl), and no clinical symptoms of virilization were apparent. Abdominal ultrasonography demonstrated the presence of a left adrenocortical adenoma. Pathological examination of the resected specimen revealed a circumscribed and well encapsulated tumor with essentially the same histological features as the tumor previously removed, except that the tumor cells showed a more prominent morphological similarity to the fetal adrenal cortex and did not express 3ß HSD. The absence of virilization at the second episode was due to the relatively low serum level of testosterone compared with that of DHEA-S.

Retrospective analysis of infants designated as positive on mass-screening for congenital hypothyroidism at kagoshima university.

Mass-screening for congenital hypothyroidism has identified cases of mild hypothyroidism, transient hypothyroidism, and transient hyperthyrotropinemia as well as typical hypothyroidism. In this paper, we examine the clinical data of the cases found positive in the screening test at our hospital. From 1989 to 1999 there were 72 patients with positive screening tests who started levothyroxine sodium (l-T4; Thyradin-S) as supplement therapy. At the age of 3 to 4 yr the patients were re-evaluated to determine whether treatment should be continued. Thyroid scintigraphies were done at the same time. We divided these cases into 4 groups. Those in group 1A started l-T4 in early infancy without a TRH test because of obvious clinical evidence of hypothyroidism, and treatment was continued after re-evaluation (n=37). Those in group 1B also started treatment in early infancy without a TRH test, but treatment was discontinued after re-evaluation (n=20). Patients in group 2A started l-T4 after evaluation by a TRH test and treatment was continued after re-evaluation (n=14), while those in group 2B started treatment after a TRH test, but after re-evaluation, treatment was discontinued (n=1). In group 2A, only a low dose of l-T4 was needed, and a slightly elevated TSH and slightly decreased free T4 (FT4) were observed after the drug washout period. However, these patients had an exaggerated response to the TRH test at re-evaluation. These findings indicate that this group, forming not a small part of whole screening-positive subjects, had mild hypothyroidism. Such patients require careful follow-up and repeated evaluation to determine whether treatment should be continued.

A case with hyperthyroidism who had been treated with thyroid hormone because of congenital hypothyroidism.

We encountered a case with hyperthyroidism at the age of 14 who had been diagnosed with congenital hypothyroidism (CH) and had received thyroid hormone replacement therapy. At the age of 16 d, the patient was referred to our hospital because of positive results at neonatal screening for CH. Serum level of TSH was 91.0 µU/ml and serum level of T4 was 6.9 µg/dl. The patient was diagnosed as having hypothyroidism, and hormone replacement therapy was started. Thereafter the dosage of thyroid hormone was adjusted and increased gradually as he grew to a maximum dose of 110 µg/day at the age of 11. Until the age of 13, the patient's serum levels of TSH were within the normal range; then, at the age of 13 yr and 4 mo, his serum level of TSH dropped to a level below the detectable range. The dosage of administered thyroid hormone was tapered off and eventually eliminated at the age of 14. A thyroid scan and a radioactive iodine uptake test demonstrated a diffuse goiter with homogeneous uptake of radioactive iodine; the uptake rate was 60% at 24 h, and the serum level of TSH receptor antibody (TRAb) was 62.5% at that time. Administration of an antithyroid drug was started after confirmation that our patient had developed hyperthyroidism. There have been no case reports similar to our case.