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C S Pitchumoni

Publications and source records attributed to C S Pitchumoni.

At least 19 recordsLinked to original sources
PubMed2006

Pravastatin: a potential cause for acute pancreatitis.

Acute pancreatitis (AP) secondary to drugs is un-common, with an incidence ranging from 0.3% to 2.0% of AP cases. Drug-induced AP due to statins is rare, and only 12 cases have thus far been reported. In this case report, we report a case of a 50-year-old female on pravastatin therapy for 3 d prior to developing symptoms of AP. The common etiological factors for AP were all excluded. The patient was admitted to the intensive care unit secondary to respiratory distress, though she subsequently improved and was discharged 14 d after admission. Although the incidence of drug-induced AP is low, clinicians should have a high index of suspicion for it in patients with AP due to an unknown etiology. Clinicians should be aware of the association of statins with AP. If a patient taking a statin develops abdominal pain, clinicians should consider the diagnosis of AP and conduct the appropriate laboratory and diagnostic evaluation if indicated.

Acute Disease↗
PubMed2006

Clinical utility of wireless capsule endoscopy: experience with 200 cases.

GOALS: To evaluate the indications and diagnoses made with 200 small bowel capsule endoscopies in an academic medical center. BACKGROUND: Wireless capsule endoscopy (PillCam SB) has recently become available as a new tool in the evaluation of patients with small bowel diseases. Its impact on patient care and usefulness in clinical practice has steadily been gaining ground, yet there are few studies that evaluate large numbers of patients. METHODS: A retrospective review of wireless capsule endoscopies was performed between September 2003 and January 2005. Reviewed are the indications for the studies, number of complete and incomplete examinations, evaluation of gastric and small bowel transit times, findings made on examination, and the percent of diagnoses made and diagnoses suspected for each study indication. RESULTS: A total of 200 cases were reviewed. Indications included anemia (66% of cases), gastrointestinal hemorrhage (31% cases), abdominal pain (21% cases), diarrhea (11% cases), and other indications such as evaluation of abnormal radiographic findings or surveillance of inflammatory bowel disease (9% cases). The average patient age was 61.5 years (SD +/- 19.1 years). Males comprised 49% of patients. The wireless capsule endoscopy study completely evaluated the entire small bowel in 87% of cases. The most common cause for an incomplete examination was premature battery failure in 8% of cases. Only 9.5% of studies were normal without findings. Small bowel ulcerations were present in 38% of studies. Vascular ectasias were present in 23% of studies. Overall, a diagnosis was made in 23% of all studies, whereas a diagnosis was suspected based on the findings in an additional 31% of studies. The indication with the highest percentage of diagnoses made or suspected was gastrointestinal hemorrhage, with a diagnostic yield of 65%, followed by anemia 61%, diarrhea 36%, and pain 17%. CONCLUSIONS: Wireless capsule endoscopy is a valuable diagnostic tool in the evaluation of occult small bowel lesions, and was most effective in patients with gastrointestinal hemorrhage and anemia.

Endoscopes, Gastrointestinal↗
PubMed2005

Drug-induced pancreatitis: an update.

BACKGROUND AND AIMS: Many frequently prescribed drugs are suspected to cause acute pancreatitis (AP). The goal of this paper is to bring to light the often occult but real problem of drug-induced pancreatitis (DIP). METHODS: We searched the National Library of Medicine/Pubmed for reported cases of DIP from 1966 to April 30, 2004. Medications implicated in AP are classified based on the strength of evidence into one of three classes of drugs associated with pancreatitis. We reviewed the top 100 prescription medications in the United States for their association with AP. RESULTS: Class I medications (medications implicated in greater than 20 reported cases of acute pancreatitis with at least one documented case following reexposure): didanosine, asparaginase, azathioprine, valproic acid, pentavalent antimonials, pentamidine, mercaptopurine, mesalamine, estrogen preparations, opiates, tetracycline, cytarabine, steroids, trimethoprim/sulfamethoxazole, sulfasalazine, furosemide, and sulindac. Class II medications (medications implicated in more than 10 cases of acute pancreatitis): rifampin, lamivudine, octreotide, carbamazepine, acetaminophen, phenformin, interferon alfa-2b, enalapril, hydrochlorothiazide, cisplatin, erythromycin, and cyclopenthiazide. Class III medications (all medications reported to be associated with pancreatitis). Of the top 100 most frequently prescribed medications in the United States, 44 have been implicated in AP, 14 of them fall into either Class I or II of medications associated with AP. CONCLUSIONS: Among adverse drug reactions, pancreatitis is often-ignored because of the difficulty in implicating a drug as its cause. The physician should have a high index of suspicion for DIP, especially in specific subpopulations such as geriatric patients who may be on multiple medications, HIV+ patients, cancer patients, and patients receiving immunomodulating agents.

Adolescent↗
PubMed2005

Factors influencing mortality in acute pancreatitis: can we alter them?

Severe acture pancreatitis (SAP), a multisystem disease, is characterized by multiple organ system failure and additionally by local pancreatic complications such as necrosis, abscess, or pseudocyst. The rate of mortality in SAP, which is about 20% of all cases of acute pancreatitis (AP), may be as high as 25%, as in infected pancreatic necrosis. The factors that influence mortality in different degrees are various. Etiology for the episode, age, sex, race, ethnicity, genetic makeup, severity on admission, and the extent and nature of pancreatic necrosis (sterile vs. infected) influence the mortality. Other factors include treatment modalities such as administration of prophylactic antibiotics, the mode of feeding (TPN vs. enteral), ERCP with sphincterotomy, and surgery in selected cases. Epidemiological studies indicate that the incidence of AP is increasing along with an increase in obesity, a bad prognostic factor. Many studies have indicated a worse prognosis in idiopathic AP compared to pancreatitis induced by alcoholism or biliary stone. The risk for SAP after ERCP is the subject of extensive study. AP after trauma, organ transplant, or coronary artery bypass surgery is rare but may be serious. Since Ranson reported early prognostic criteria, a number of attempts have been made to simplify or add new clinical or laboratory studies in the early assessment of severity. Obesity, hemoconcentration on admission, presence of pleural effusion, increased fasting blood sugar, as well as creatinine, elevated CRP in serum, and urinary trypsinogen levels are some of the well-documented factors in the literature. The role of appropriate prophylactic antibiotic therapy although still is highly controversial, in properly chosen cases appears to be beneficial and well accepted in clinical practice. Early enteral nutrition has gained much support and jejunal feeding bypassing the pancreatic stimulatory effect of it in the duodenum is desirable in selected cases. The limited role for endoscopic sphincterotomy in patients with demonstrated dilated CBD with impacted stone and evidence of impending cholangitis is well documented. Surgery in AP other than for removal of the gallbladder is often limited to infected pancreatic necrosis, pseudocysts, and pancreatic abscess and in some cases of traumatic pancreatitis with a ruptured duct system. The progress in the understanding of the role of cytokines will over us opportunities to use immunomodulatory therapies to improve the outcome in SAP.

Antibiotic Prophylaxis↗
PubMed2004

How often are liver function tests normal in acute biliary pancreatitis?

BACKGROUND: The biochemical markers of a biliary etiology of acute pancreatitis (AP) include an ALT elevation of more than 3 times the upper range of normal (ULN) and a serum total bilirubin greater than 3 mg%. OBJECTIVES: To analyze the frequency of normal LFTs (Bilirubin, ALP, ALT, and AST) in patients with biliary AP. DESIGN: In this prospective study data collected for other ongoing studies on AP in the division of Gastroenterology in the last 20 years were analyzed. MATERIAL AND METHODS: Serum total Bilirubin, AST, ALT, and ALP levels in 269 patients with biliary AP out of 728 cases of AP of various etiologies were analyzed. The biliary etiology was confirmed on the basis of gallstones documented by transabdominal US or at surgery. RESULTS: We noted normal bilirubin, AST, ALT, and ALP levels in 14.5%, 12.3%, 11.2%, and 26.4% of cases of acute biliary pancreatitis respectively. When all the 4 laboratory tests were considered collectively, the incidence of normal values was 10.4%. We also noted an ALT elevation of <3 x ULN in 16.7% of cases of biliary AP and 43.5% of cases had a T. Bilirubin level of less than 3 mg %. CONCLUSIONS: Almost 15 to 20% of patients with biliary AP manifest with normal LFTs. The clinician should not exclude a biliary etiology solely on the basis of normal LFTs.

Acute Disease↗
PubMed2003

Issues in hyperlipidemic pancreatitis.

Hypertriglyceridemia (HTG) is a rare cause of pancreatitis. Pancreatitis secondary to HTG, presents typically as an episode of acute pancreatitis (AP) or recurrent AP, rarely as chronic pancreatitis. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is an identifiable risk factor. The typical clinical profile of hyperlipidemic pancreatitis (HLP) is a patient with a preexisting lipid abnormality along with the presence of a secondary factor (e.g., poorly controlled diabetes, alcohol use, or a medication) that can induce HTG. Less commonly, a patient with isolated hyperlipidemia (type V or I) without a precipitating factor presents with pancreatitis. Interestingly, serum pancreatic enzymes may be normal or only minimally elevated, even in the presence of severe pancreatitis diagnosed by imaging studies. The clinical course in HLP is not different from that of pancreatitis of other causes. Routine management of AP caused by hyperlipidemia should be similar to that of other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. Reduction of TG levels to well below 1,000 mg/dL effectively prevents further episodes of pancreatitis. The mainstay of treatment includes dietary restriction of fat and lipid-lowering medications (mainly fibric acid derivatives). Experiences with plasmapheresis, lipid pheresis, and extracorporeal lipid elimination are limited.

Acute Disease↗
PubMed2003

Tropical chronic pancreatitis: an update.

Tropical chronic pancreatitis represents a juvenile nonalcoholic form of chronic pancreatitis prevalent in many tropical developing countries. Tropical chronic pancreatitis differs from temperate zone pancreatitis in its younger age of onset, more accelerated course, higher prevalence of pancreatic calculi and diabetes, and greater propensity to pancreatic malignancy. The diabetic stage of the disease is referred to as fibrocalculous pancreatic diabetes. The diabetes is severe and insulin requiring although ketosis resistant. Diabetic complications occur in fibrocalculous pancreatic diabetes just like in other primary forms of diabetes. The etiology of tropical chronic pancreatitis remains unclear, although malnutrition along with dietary cyanogen toxicity, antioxidant deficiency, and a genetic predisposition have been proposed. In the last few decades, the prognosis has markedly improved as a result of better management of diabetes. Yet a better understanding of the pathogenesis of tropical chronic pancreatitis could further improve treatment options and offer an opportunity for prevention of this disorder, which leads to severe morbidity in a large proportion of affected patients.

Adult↗
PubMed2002

A critical evaluation of laboratory tests in acute pancreatitis.

An ideal laboratory test in the evaluation of a patient with acute pancreatitis (AP) should, in addition to accurately establishing the diagnosis of AP, provide early assessment of its severity and identify the etiology. None of the tests available today meet all these criteria, and presently there is no biochemical test that can be considered the "gold standard" for the diagnosis and assessment of severity of AP. In the diagnosis of AP, serum amylase and lipase remain important tests. Advantages of amylase estimation are its technical simplicity, easy availability, and high sensitivity. However, its greatest disadvantage is its low specificity. A normal amylase would usually exclude the diagnosis of AP, with the exception of AP secondary to hyperlipidemia, acute exacerbation of chronic pancreatitis, and when the estimation of amylase is delayed in the course of the disease. The major advantage of lipase is an increased sensitivity in acute alcoholic pancreatitis and in patients who initially present to the emergency room days after the onset of the disease, as lipase remains elevated longer than amylase. Although once considered to be specific for AP, nonspecific elevations of lipase have been reported in almost as many disorders as amylase, thus decreasing its specificity. Simultaneous estimation of amylase and lipase does not improve the accuracy. Other enzymes for the diagnosis of AP--pancreatic isoamylase, immunoreactive trypsin, and elastase--are more cumbersome and expensive and have no clear role in the diagnosis of AP. No enzyme assay has a predictive role in determining the severity or etiology of AP. Once the diagnosis of AP is established, daily measurements of enzymes have no value in assessing the clinical progress of the patient or ultimate prognosis and should be discouraged. A host of new serological and urinary markers have been investigated in the last few years. Their main use is in predicting the severity of AP. At present, serum C-reactive protein at 48 h is the best available laboratory marker of severity. Urinary trypsinogen activation peptides within 12-24 h of onset of AP are able to predict the severity but are not widely available. Serum interleukins 6 and 8 seem promising but remain experimental.

Acute Disease↗
PubMed2002

Serum and liver micronutrient antioxidants and serum oxidative stress in patients with chronic hepatitis C.

OBJECTIVES: The exact pathogenesis of liver injury and fibrosis in chronic hepatitis C (CHC) is unclear. Free radicals play a role in CHC liver damage. Antioxidants (AO) (enzymatic and nonenzymatic) scavenge free radicals and prevent tissue injury. The aims of our study were to estimate serum levels of malondialdehyde (MDA), serum and liver levels of nonenzymatic fat-soluble AO, and to correlate the liver AO levels with the degree of inflammation and fibrosis on biopsy. METHODS: AO levels were estimated by high-pressure liquid chromatography in the pretreatment serum and liver biopsy specimen of 20 treatment-naïve patients with CHC who were not on vitamin supplements. Serum levels of MDA were measured as a marker of increased oxidative stress. Twenty-two healthy individuals with no history of vitamin supplementation served as controls. AO analyzed were: retinol, alpha- and gamma-tocopherol, lutein, beta-cryptoxanthin, lycopene, and alpha- and beta-carotene. RESULTS: Twenty CHC patients (11 men, nine women, mean age 48.5 +/- 7.9 yr) were studied. Patients and controls were comparable in age and sex. Serum MDA levels were significantly higher in CHC patients compared with controls (1.62 +/- 0.57 vs 0.23 +/- 0.15 micromol/L, p = < 0.0000). Serum levels of all AO except lutein were significantly decreased in CHC patients, and their levels were two to ten times lower than serum levels in controls. Liver levels of alpha-carotene (p = 0.0004), beta-carotene (p = 0.006), and lutein (p = 0.002) correlated with the serum levels, whereas the levels of retinol, alpha-tocopherol, lycopene, and beta-cryptoxanthin showed no correlation. Serum MDA levels were significantly higher in patients with moderate-to-severe inflammation or fibrosis compared with those with mild inflammation or fibrosis. The levels of all liver AO except alpha-carotene were significantly lower in patients with moderate-to-severe fibrosis. The severity of inflammation (portal or lobular) did not affect liver AO levels. CONCLUSIONS: Our findings suggest that increased oxidative stress is present in patients with CHC. Micronutrient AO are severely depleted in serum and liver tissue of patients with CHC, and liver levels of some AO appear to reflect serum levels. Increasing fibrosis is associated with decreased liver AO levels indicating that severe disease may be a consequence of AO depletion or decreased liver storage resulting from fibrosis.

Adult↗
PubMed2002

Geriatric medicine programs in India: has the time arrived?

Aging trends in India and the world over are burdening society with the health care and economic problems resulting from an older population. With this in mind, countries are preparing themselves to face the challenges of meeting this burden. India with its huge population and improving life-expectancy should be no exception. The task involves preparation in healthcare to take care of the elderly and train a new generation of physicians in geriatric medicine. The review attempts to address some of these issues and makes pertinent recommendations, based on the author's own experiences in developing a large geriatric program with all necessary components in the last decade.

Aged↗
PubMed2001

Pathogenesis of alcohol-induced chronic pancreatitis: facts, perceptions, and misperceptions.

The pathogenesis of chronic pancreatitis secondary to chronic alcoholism is not fully understood. A major hurdle in the understanding of the pathogenesis is the inability to study early lesions of the pancreas and the sequential changes. Facts are few; observations are many. Each new hypothesis argues against all previous hypotheses; however, clinical chronic pancreatitis is initiated by one or more of the mechanisms. Good experimental models for alcoholic pancreatitis are not available, limiting the ability to study the pathogenesis. Additional studies on genetic markers and immunologic mechanisms might explain acinar cell injury, which seems to be the earliest lesion in most, if not all, types of chronic pancreatitis. Opie's common channel and obstruction regurgitation theories seem unrelated to chronic pancreatitis. Although biochemical changes of the pancreatic secretion in alcoholic patients promote protein-plug formation, evidence is too weak to consider protein plug as the earliest change. The theory of necrosis of the acinar cell by some unknown mechanism, subsequently leading to fibrosis, is gaining support; however, it is clear that the pathogenesis of alcoholic pancreatitis is not yet fully understood.

Humans↗
PubMed2001

Histopathology and immunohistochemistry of pancreatic islets in fibrocalculous pancreatic diabetes.

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.

Adolescent↗
PubMed2001

Intraabdominal vancomycin-resistant enterococcus infections: the new threat.

GOALS: To determine the clinical course and outcome in patients with intraabdominal vancomycin-resistant enterococcus infections (VRE-A) and to identify probable risk factors for VRE-A. BACKGROUND: Vancomycin-resistant enterococcus is one of the most notable nosocomial emerging pathogens. The incidence is increasing, especially in the abdominal surgery setting. STUDY: A comparative study of patients with VRE-A and VRE infection in other sites (VRE-O) who were hospitalized for over 1 year. Fisher exact test and Student t test were used; a two-tailed p value of less than 0.05 was considered to be significant. RESULTS: Of 89 nine patients with VRE, six had VRE-A, 24 had VRE-O, and 59 had VRE colonization. The VRE-A group was comprised of one patient with an inoperable Klatskin tumor and biliary sepsis, one with acquired immune deficiency syndrome and an infected pancreatic pseudocyst, two with fecal peritonitis, and two with biliary sepsis after surgery for common bile duct stones. All six patients with VRE-A had recent surgery before VRE isolation, as compared with three in the VRE-O group (p = 0.0001). Despite adequate treatment with intravenous chloramphenicol, resulting in eradication of VRE in all six VRE-A cases, the mortality rate remained high at 50%. CONCLUSIONS: Vancomycin-resistant enterococcus should be recognized as an emerging nosocomial pathogen that causes potentially fatal intraabdominal infections in the postsurgical setting. However, the impact of treatment on ultimate outcome needs further evaluation.

Abdomen↗
PubMed2001

Percutaneous endoscopic gastrostomy and outcome in dementia.

The use of percutaneous endoscopic gastrostomy for the administration of food and medications in patients with dementia has been on an increase. Many studies have failed to demonstrate the positive outcome expected of this feeding modality for the indications that required tube placement. Hence, the concept of feeding through gastrostomy tubes has become the subject of much discussion and controversy in recent times. We have reviewed the literature with regard to outcome in older patients with dementia and percutaneous endoscopic gastrostomy with respect to nutritional parameters, quality of life, and survival. A brief discussion on ethical and legal aspects is included. Much of the data do not suggest that outcome in dementia is favorably improved after percutaneous gastrostomy.

Aged↗