Olmesartan-induced enteropathy

Strategies to Prevent Acute Diarrhea and Upper Respiratory Tract Infection among Disaster Relief Workers.

Introduction: Olmesartan-induced enteropathy is a rare but serious condition associated with the angiotensin receptor blocker olmesartan. It presents with chronic diarrhea, weight loss, and villous atrophy resembling celiac disease—but without improvement on a gluten-free diet. Early recognition is crucial for diagnosis and management. Case Description/Methods: A 71-year-old man presented with chronic diarrhea, nausea, vomiting, ∼100-pound weight loss, and profound weakness. Medications included olmesartan 40 mg daily. Symptoms began in June 2024 and persisted despite cholecystectomy for choledocholithiasis in October 2024 and after 3-week gluten-free diet failed to improved symptoms after an esophagogastroduodenoscopy (EGD) with duodenal biopsies in February 2025 showed villous blunting, lymphoplasmacytic infiltration, and rare PAS-positive macrophages. A few days after completing gluten-free diet trial, he presented to our hospital. Labs revealed anemia, elevated creatinine, hypercalcemia, and a gamma gap of 5.7. Celiac serologies, infectious stool studies, and HIV were negative. Initial concern was amyloidosis. Further testing showed low immunoglobulin A/immunolglobulin M, elevated immunoglobulin G and an M-protein on SPEP/UPEP. Bone marrow biopsy revealed plasma cell dyscrasia; skeletal survey showed calvarial lucencies. Repeat EGD showed erythematous gastric mucosa and mucosal changes in the duodenum. Duodenal biopsies again revealed villous blunting, lymphoplasmacytic infiltration, and rare PAS-positive macrophages; stains for AFB, Congo red, and Helicobacter pylori were negative. Gastric biopsies showed chronic atrophic gastritis with pyloric metaplasia. Given the failed gluten-free diet and histological findings on biopsy, olmesartan-induced enteropathy was favored over amyloidosis. Olmesartan was discontinued, and budesonide 3 mg three times a day was initiated. He was discharged on nasoduodenal tube feeds. One month later, he had gained 20 pounds, reported resolution of symptoms, and had the tube removed. Budesonide taper and repeat EGD were planned. He was referred to hematology for newly diagnosed multiple myeloma. Discussion: This case underscores the diagnostic challenge of olmesartan-induced enteropathy, especially with overlapping concern for amyloidosis. Despite initial suspicion for amyloid, histologic findings and clinical response to olmesartan cessation supported drug-induced enteropathy. Clinicians should consider olmesartan-induced sprue-like enteropathy in patients with unexplained malabsorptive symptoms and celiac-like histology unresponsive to dietary modification.

BackgroundChronic diarrhea in adults is a common symptom with a wide range of underlying etiologies. Although various strategies have been proposed for evaluation, there are still cases with undetermined origins even after extensive workup. Amyloidosis with gastrointestinal (GI) involvement is one of the causes that should be considered in adult patients with chronic diarrhea. We report a case of primary systemic amyloid light-chain (AL) amyloidosis, presenting initially as chronic diarrhea and weight loss.Case presentationA 43-year-old man with chronic diarrhea and weight loss was referred to our hospital. Prior to his presentation, extensive evaluation including an exploratory laparotomy was carried out and did not yield any valuable findings. An echocardiography performed after repeated episodes of orthostatic hypotension revealed infiltrative cardiomyopathy. Moreover, biopsies of the terminal ileum revealed amyloid deposition confirmed by Congo Red staining. Finally, a diagnosis of systemic AL amyloidosis was made after hematological workup. Anti-plasma cell therapy did ameliorate his GI symptoms.ConclusionAlthough amyloidosis with GI involvement is a rare cause of chronic diarrhea, it should be considered especially in patients with intestinal malabsorption and extra-GI manifestations, such as orthostatic hypotension. The delayed diagnosis in the present case highlights the importance of recognizing clinical “red flags” not seemingly related to one another, and underscores the need to get intestinal biopsies even with normal endoscopic appearance of the mucosa.

This study was performed to better understand and more precisely quantify the amount and burden of illness caused by acute diarrhoea in the United States today. A telephone-based population survey was conducted between 1 July, 1996, and 31 June, 1997, in sites of the Foodborne Diseases Active Surveillance Network (FoodNet). The overall prevalence of acute diarrhoea in the 4 weeks before interview was 11%, giving a rate of 1.4 episodes of diarrhoea per person per year. The rate of diarrhoeal illness defined as a diarrhoeal episode lasting longer than 1 day or which resulted in significant impairment of daily activities was 0.7 per person per year. It can be concluded that acute diarrhoea is common and represents a significant burden of illness in the United States. Our data on self-reported diarrhoea, when generalized to the entire nation, suggests 375 million episodes of acute diarrhoea each year in the United States. Many of these episodes are mild. However, our data also indicate that there are approximately 200 million episodes of diarrhoeal illness each year in the United States.

Severe Spruelike Enteropathy Associated With Olmesartan

Introduction: Olmesartan has been implicated as an etiology of sprue-like enteropathy characterized by duodenal villous atrophy refractory to a gluten-free diet, negative celiac serologies, and resolution of symptoms following discontinuation of olmesartan. We present a series of 3 patients with olmesartan-associated enteropathy identified at our institution. Three patients were identified with olmesartan-associated enteropathy; all 3 were white females with a mean age of 64.7 years. All were taking olmesartan for several years prior to development of symptoms. Symptoms at presentation were characterized by chronic progressive diarrhea, weight loss, and abdominal pain. Celiac serologies including tissue transglutaminase IgA and quantitative IgA levels were normal. Upper endoscopy showed histologic findings suggestive of celiac disease, including severe duodenal villous atrophy and increased intra-epithelial lymphocytes in all patients. Colonoscopy with biopsies revealed microscopic colitis in 2 patients and was normal in the third. One patient was HLA-DQ2 heterozygote-positive and one patient was HLA-DQ8 heterozygote positive. Two patients were started on gluten-free diets without symptomatic improvement. All 3 patients were prescribed budesonide without symptomatic improvement. One patient was prescribed mesalamine while another was prescribed prednisone, which did not resolve symptoms. Complete symptom resolution was noted a mean of 5 weeks following discontinuation of olmesartan. No patient developed recurrent symptoms with alternative antihypertensive medications. This case series highlights the association of olmesartan and the development of sprue-like enteropathy, which may present years after initiation of olmesartan therapy. It corroborates previous findings with complete resolution of symptoms after discontinuation of olmesartan. Thus, in patients with seronegative villous atrophy and symptoms suggestive of celiac disease, clinicians should consider olmesartan as a potential cause of symptoms.

We report the case of a 45-yr-old white man, investigated for chronic diarrhea, malabsorption and weight loss associated with sicca syndrome. Endoscopic and x-ray examinations showed normal macroscopic mucosa in gastrointestinal tract (GIT). Immunohistochemistry showed diffuse polyclonal T cell lymphocytes infiltrating either epithelium and lamina propria in GIT. There was no villous atrophy in the jejunum and ileum. Corticosteroids, azathioprine, and cyclosporine failed to improve symptoms. Monthly intravenous cyclophosphamide administered over 1 yr, stopped the diarrhea and weight loss. The patient is free of symptoms up to a 5-yr follow-up.

When a patient presents with acute diarrhoea, the most important question is whether it represents the first episode of chronic inflammatory bowel disease (CIBD) or acute self-limited colitis (ASLC). The early changes in the rectal mucosa of patients with ASLC have been claimed to be highly diagnostic, the presence of an unspecific inflammatory infiltrate in the lamina propria and the absence of disturbances in the crypt architecture being the characteristic features. Thirty-two patients who in the period 1980-1984 presented with their first episode of acute diarrhoea and whose rectal mucosa showed these histologic features were followed up for 1.5-7 years. Forty-one per cent of the patients were finally classified as having ASLC and 28% as having diseases other than CIBD or ASLC. Thirty-one per cent eventually developed CIBD. Thus the features claimed to be diagnostic of ASLC could not predict the final outcome of the disease in patients presenting for the first time with acute diarrhoea. The histologic interpretation can provide significant information in these patients but should never replace a careful clinical judgement and, if doubt remains, further observation of the patients.

<h3></h3> Coeliac crisis is a medical emergency, rarely encountered in clinical practice. It may be a consequence of a delayed diagnosis of coeliac disease (CD). Diagnostic criteria for coeliac crisis include severe dehydration including orthostatic changes, renal dysfunction, neurological dysfunction, metabolic acidosis, abnormal electrolyte levels, hypoproteinaemia with Albumin below 3 g/dl and weight loss more than 4.5 kg. A diagnosis is made if more than 2 criteria are present.¹ We describe the case of a 4-year-old girl who presented with coeliac crisis as the first manifestation of undiagnosed coeliac disease, to raise awareness of the diagnostic criteria for coeliac crisis and consideration of this in unwell patients. Our patient presented with chronic diarrhoea, fatigue, and exhaustion. On admission she was not clinically dehydrated, had peripheral oedema, mildly distended abdomen with no signs of ascites. She had 20% weight loss, and her BMI was 13.23 (on 2d centile). A no-biopsy diagnosis of coeliac disease was made as she had IgA anti-tissue transglutaminase antibodies more than ten times the upper limit of normal and positive endomysium antibodies.⁵ Bloods showed compensated metabolic acidosis, with bicarbonate of 13, normal glucose at 4.1, low magnesium at 0.39 mmol/L, low albumin at 13 g/L. She required magnesium and albumin infusions for deficit correction. In addition, she had deranged PT/INR which normalised after two doses of intravenous Vitamin K. She also had transaminitis, and an extensive hepatitis screen. Autoimmune hepatitis was ruled out. An abdominal ultrasound showed fatty liver and normal elastography. Metabolic screen was normal. The levels of Vitamin D, folic acid, copper and zinc were low, and she had supplementation. Our patient met 4 out of the 7 criteria for coeliac crisis. She was commenced on gluten free diet, initially via nasogastric tube, then orally from day 4. She was monitored for refeeding syndrome and discharged following nutritional rehabilitation after 11 days. At her 2 months clinic follow up her bloods were normal; she has gained weight. Four months after her presentation her BMI improved to 17.7 (on 91st centile). Coeliac crisis was first described by Andersen and Di Sant’ Agnese in 1953 when they reported 35 patients with coeliac crisis, among which 3 were complicated by fatality.^{3 4} It is rarely encountered, probably due to better screening and early diagnosis; however, this can occasionally be the initial presentation of CD. The only effective treatment is a life-long gluten free diet. In coeliac crisis, the emergency treatment of electrolyte abnormalities is followed by gluten free diet and monitoring for refeeding syndrome. The role of corticosteroids in coeliac crisis is controversial but there are case reports of coeliac crisis with a good response to steroids, as they can reduce intestinal inflammation and restore the brush border enzymes.² Our patient did not require steroids and responded well to gluten free diet. This case highlights the importance of considering coeliac crisis in an acutely unwell patient with chronic diarrhoea, weight loss and metabolic derangements. <h3>References</h3> Mauro A, Casini F. Celiac crisis as the life-threatening onset of celiac disease in children: a case report. <i>Frontiers in Pediatrcs</i>. DOI 10.3389/fped.2023.1163765. Gupta S, Kapoor K. Steroids in celiac crisis: doubtful role. <i>Indian Pediatrics</i> 2014;<b>51</b>(9):756–757. Di Sant’ Agnese PA. Idiopathic coeliac disease. II. Course and prognosis. <i>Pediatrics</i> 1953 Mar;<b>11</b>(3):224–37. Andersen DH, Di Sant’ Agnese PA. Idiopathic coeliac disease. I. Mode of onset and diagnosis. <i>Pediatrics</i> 1953 Mar;<b>11</b>(3):207–23. Husby S, Koletzko S, Wessels M, <i>et al</i>. European society paediatric gastroenterology, hepatology and nutrition guidelines for diagnosing coeliac disease 2020. <i>JPGN</i> 2020;<b>70</b>:141–157.

A Trans-Disciplinary Approach to Weight Loss in the Super Super Morbidly Obese

Olmesartan-induced spruelike enteropathy is a rare clinical entity that is characterized by unexplained chronic diarrhea and weight loss. Prompt recognition of this adverse event may be challenging due to clinical and histologic similarities with other small intestinal pathologies. We hereby delineate the case of an elderly female with a 14-month clinical history of non-bloody diarrhea and weight loss. After extensive diagnostic workup and exclusion of probable etiologies, the patient was diagnosed with olmesartan-associated enteropathy. A dramatic clinical and histologic recuperation was achieved after discontinuation of olmesartan. This paper illustrates the overarching need for a detailed clinical history focusing on medication review in patients presenting with chronic diarrhea with no obvious cause. The spruelike enteropathy associated with olmesartan is an emerging cause of small bowel injury. Clinicians should maintain a high index of suspicion for this adverse drug reaction. Early and correct diagnosis carries paramount importance in sparing these patients from unnecessary diagnostic investigations and therapeutic delays.

Rationale:Asymptomatic Paget disease of bone (PDB) is mostly diagnosed by accidental finding of osteolytic lesion on the plain film. However, in elderly patient with chronic renal insufficiency and weight loss, it is crucial to differentiate PDB from metabolic and metastatic bone diseases for further treatment and better outcome.Patient concerns:An 80-year-old man with chronic kidney disease presented to our emergency department due to fever with chillness for a day, while the abdominal fullness, anorexia, and weight loss had been noted for 3 months. Mixed osteoblastic and lytic changes in the pelvic bone were accidentally found on the abdominal plain film.Diagnosis:The patient was diagnosed as asymptomatic PDB and urinary tract infection of Pseudomonas aeruginosa.Interventions and outcome:The patient received 7 days intravenous and followed by 7 days oral antibiotic treatment, which lead to clinical improvement of his urinary tract infection. No pharmacological treatment was initiated for the asymptomatic and localized PDB. The patient was discharged under stable condition afterward.Lessons:In patients with mixed osteolytic and blastic lesions, the differential diagnoses include metabolic and metastatic bone disease. Thorough understanding of the morphology of the bone lesions in high risk patient, not only helps to make differential diagnosis, but it also leads to precise treatment and better outcome.

A 6-year-old female alpaca (case 1) was examined at the George D. Widener Hospital for Large Animals of the University of Pennsylvania for evaluation of lethargy, diarrhea, and weight loss of 3 months' duration. A diagnosis of Mycoplasma haemolamae had initially been made by the referring veterinarian based on blood smear examination findings. The animal was treated with a long-acting form of oxytetracylinea (10 mg/kg sq q24h) for 10 days but its clinical signs failed to improve. Serial fecal floatations performed before referral showed no parasite ova. Additional treatments received before referral included ivermectin, fenbendazole, B vitamins, injectable iron, procaine penicillin, oral sulfadimethoxine, and oral electrolytes. As the diarrhea and weight loss persisted, the alpaca was referred for further evaluation. The animal was pregnant (approximately 155 days gestation) at the time of presentation. The animal was from a herd of 78 alpacas, and was pastured with a group of pregnant females and young animals. Routine vaccinations on the farm included rabies, Clostridium perfringens Types C and D, and tetanus. On presentation, the alpaca was quiet but responsive and in poor body condition (body condition score 3/10), weighing 60 kg. Rectal temperature, heart rate, and respiratory rate were 98.2°F, 56 beats per minute, and 20 breaths per minute, respectively. The alpaca appeared well hydrated with pale mucous membranes. It had green, watery feces, and a poor appetite. Initial laboratory abnormalities included mild nonregenerative anemia (PCV, 23%; reference interval, 25–46%), hypoproteinemia (total protein, 4.2 g/dL; reference interval, 4.6–6.9 g/dL), hypoalbuminemia (albumin, 1.40 g/dL; reference interval, 2.50–4.20 g/dL), and azotemia (serum creatinine concentration, 2.28 mg/dL; reference interval, 0.6–1.80 mg/dL). Blood smear examination was negative for Mycoplasma haemolamae organisms. Feces were submitted for fecal floatation, Mycobacterium avium spp. paratuberculosis (MAP) RT-PCR,b,c, b,c acid-fast staining for Cryptosporidium, fecal occult blood, and bacterial cultures. Blood was submitted for MAP antibody detection with ELISA.d No parasite ova were observed on fecal floatation, and the acid-fast staining was negative for Cryptosporidium organisms. The occult blood test result was negative. Fecal bacterial cultures were negative for Salmonella spp. and Clostridium spp. Fetal and abdominal ultrasound examinations were performed. The sonographic appearance of the visible gastrointestinal structures was within normal limits. Fetal sonographic evaluation detected an irregular heart rate, suggestive of fetal distress. Additional diagnostic tests performed during the hospital stay included determination of serum trace mineral concentrations (Cu, Fe, Se, and Zn), fecal coronavirus detection with electron microscopy, and bovine viral diarrhea (BVD) testing by PCR on the buffy coat. Serum trace mineral concentrations were within the reference range. Results of coronavirus and BVD tests later returned negative. The patient remained hospitalized for 5 days while awaiting diagnostic test results. During that time, supportive care in the form of IV fluids (Normosol-R, 1.5 mL/kg/h) and partial parenteral nutrition (1.5 mL/kg/h) were administered. Ranitidine (1.5 mg/kg IV q8h) was also administered for prevention of 3rd compartment ulceration. RT-PCR results for MAP detection identified a strong positive result with duplicate values of 17.43 and 17.79 cycles to positive threshold (CT). Because of the animal's advanced clinical signs and potential risk to the rest of the herd, permission was obtained for euthanasia. The alpaca was euthanized by administration of a barbiturate overdose and a postmortem examination performed. At necropsy, gross findings included emaciation, fluid intestinal contents, and markedly enlarged ileocecal lymph nodes. The uterus contained a 34-cm crown-to-rump length female fetus. No macroscopic lesions were observed in the bone marrow or intestine. An impression smear of an ileocecal lymph node disclosed acid-fast bacilli among numerous lymphocytes and macrophages (Fig 1). On histology, most of the bone marrow consisted of mature adipocytes, with occasional small foci of cellularity where all cell lines were represented. The ileocecal lymph nodes were expanded by infiltrating sheets of epithelioid macrophages, scattered multinucleate cells, and low to moderate numbers of eosinophils. The mucosa of the distal jejunum and ileum was markedly expanded by sheets of infiltrating macrophages (Fig 2). The villi were atrophied, and nodular infiltrates of macrophages surrounded the lymphatics. Sheets of macrophages also infiltrated the submucosal lymphoid tissue of the large intestine. A postmortem a diagnosis of severe chronic granulomatous enterocolitis and granulomatous lymphadenitis consistent with paratuberculosis was made. Samples of ileum, ileocecal junction, ileocecal lymph node, and feces were collected for mycobacterial culture with liquid media, and standard Herrold's Egg Yolk Medium (HEYM) according to methods described previously.1–3 In order to facilitate quantification of MAP growth, 4 serial 10-fold dilutions (1 : 10; 1 : 100, 1 : 1,000, and 1 : 10,000) were prepared from each original tissue and fecal samples. For each sample type, 100 μL of the original inoculum, and of each inoculum dilution, was added to 1 mycobacterial growth indicator tube (MGIT)e culture tube. Also, for each sample type, 100 μL of the original inoculum, and all but 2 dilutions (1 : 10 and 1 : 10,000), were added to 3 HEYM flasks. For liquid culture, time to positive was recorded in days for each inoculum, and the growth was confirmed as MAP by RT-PCR. For solid media culture, the total number of MAP colony forming units (CFU)/g of tissue or feces was estimated based on the sample weight, dilution factor, and the average number of colonies counted per flask. Oil immersion (100 ×) image of epithelioid macrophages stained by the Ziehl-Neelsen (“acid-fast” stain) method. Typical of herbivore Mycobacterium avium ssp. paratuberculosis enteric infections, the cytoplasm of many of macrophages is filled with brilliantly stained bacilli. Low magnification (10 ×) view of the distal jejunum on hematoxylin and eosin reveals sheets of epitheliod macrophages occupying the submucosa. Clusters of macrophages are also within the lamina of the mucosa. MAP was isolated from the fecal sample and all tissue samples obtained at necropsy. The estimated number of CFU/g of tissue was extremely high at 2,884,000 CFU/g, 10,500,000 CFU/g, and 1,813,000 CFU/g for ileum, ileocecal lymph node, and ileocecal junction, respectively. The estimated number of CFU/g of feces also was extremely high at 2,100,000 CFU/g. Genotyping of 1 of the isolates obtained from the alpaca was performed. The genotype was determined to be a cattle strain by IS1311 restriction endonuclease analysis and was confirmed as MAP by hsp65-PCR-REA and IS900 PCR.4 The patient was positive for MAP antibody detection with a commercial ELISA test kit (0.433 optical density [OD]; cutoff value, 0.190). After the animal's presentation to the university veterinary medical teaching hospital, individual blood and fecal samples were obtained from the remaining 77 herd animals. The individual samples were processed for MAP antibody detection with ELISA, fecal RT-PCR, and fecal cultures on HEYM. Pooled environmental fecal samples also were obtained from each of the farm's 3 pastures (pastures A, B, and C), and analyzed by RT-PCR. One alpaca had a positive ELISA, and 12 alpacas had positive fecal RT-PCR (including the ELISA-positive alpaca). None of the animals were positive on fecal culture. Of the 12 RT-PCR-positive animals, 5 had been pastured (pasture A) with the patient in the 8 months before testing. In addition, 4 of the 12 RT-PCR positive animals that were <12 months of age were kept on a pasture (pasture B) neighboring that of case 1. The remaining 3 RT-PCR positive animals had no known direct contact with the patient before referral to the hospital. Both pastures A and B were positive for MAP on RT-PCR; pasture C was negative. Approximately 2 months after the patient's presentation to the veterinary medical teaching hospital, 2 additional alpacas from the same herd were submitted for postmortem examination. Both animals had been pastured with case 1. Case 2 was a 10-year-old female alpaca that was euthanized on the farm after complications from dystocia. At necropsy, a uterine prolapse associated with a vaginal laceration was found. No histologic evidence of paratuberculosis was detected but 2 of 8 (25%) intestinal tissue samples submitted for MAP culture on HEYM were positive. Interestingly, during the whole herd testing 2 months previously, case 2 was negative on fecal RT-PCR and ELISA. Case 3 was a 14-year-old female euthanized on the farm because of chronic weight loss. At necropsy, chronic peritonitis secondary to 3rd compartment ulcers was identified. Similar to case 2, no histologic evidence of paratuberculosis was detected in the intestinal tract but 18 of 28 (64%) intestinal tissue samples submitted for MAP culture on HEYM were positive. At the whole herd testing 2 months previously, case 3 was positive on fecal RT-PCR and was negative on ELISA. At that time, individual fecal samples were obtained from the herd animals that had previously tested positive on fecal RT-PCR. Of the 12 previously positive animals, 11 were available for follow-up testing (case 3 had been euthanized). Nine animals were now negative. Environmental samples were not obtained at the time. The MAP isolates obtained from all 3 cases were further genotyped with 2 short sequence repeat (SSR) segments by a technique described elsewhere.5 Three major genotypes were identified based on the combinations of numbers of repeats within each SSR locus. All genotyped isolates from cases 1 and 2 carried 12G residues and 5 GGT repeats. This strain was identified as a cattle strain. Three isolates from case 3 were identified as a 7G, 6 GGT genotype, while 1 additional isolate from case 3 was identified as a 7G, 5 GGT genotype, both of which were identified as sheep strains. Johne's disease (JD) or paratuberculosis previously has been reported in camelid species6,7 but disease prevalence in North American herds is unknown. Clinical signs of paratuberculosis in camelids are similar to those reported in cattle and small ruminant species and may include lethargy, chronic weight loss, and dependent edema. In contrast to cattle, but similar to small ruminants, not all camelids in advanced stage of disease will develop diarrhea or changes in fecal consistency. Case 1 had diarrhea for at least 3 months before presentation, but cases 2 and 3 did not. Two llamas from a previous report showed signs of weight loss associated with diarrhea.6 Another report on 10 alpacas described 5 animals that experienced diarrhea before death.7 The difference in the occurrence of diarrhea between cattle and camelids (and small ruminants) may be related to the latter's intestinal tract physiology and their ability to reabsorb water. Also in contrast with cattle, camelids and small ruminants affected with paratuberculosis can present with anemia of variable severity. The pathophysiology for the development of anemia in camelids and small ruminants with JD is unclear, but could be secondary to the chronicity of the disorder, especially when the anemia is classified as normocytic and normochromic.8 In addition, concurrent disease processes such as internal parasitism or infection with Mycoplasma haemolamae may contribute to the degree of anemia. The reported age at onset of clinical signs tends to be younger in camelids than in cattle. Three of the 10 alpacas reported before were between 11 and 14 months of age,6 and 1 of the 2 llamas in the other report was 16 months old.7 A possible explanation for this finding is that the incubation period for certain MAP strains is shorter in camelids than in other species, but this has not been proven. Case 1 had been purchased 3 years before becoming ill. Information regarding the JD status of the farm of origin was not available to the authors. During 3 years on the current farm, no contact with other domestic ruminants was identified. To the farm owner's knowledge, this was the 1st case of JD in the herd since it was established several years ago. For both cases 2 and 3, the lack of histologic findings consistent with paratuberculosis in the presence of positive tissue cultures was suggestive of early infection with MAP. The absence of histologic lesions in the face of positive tissue culture has been documented in short-term bovine experimental challenges with MAP.9 Furthermore, we hypothesized that case 1, which was shedding very high numbers of MAP in the feces, could have been the source of infection within the herd. However, genotyping of the MAP strains isolated from all 3 alpacas described here suggests that >1 strain of MAP was present in the herd and that case 1 was not solely responsible for the presence of additional positive animals within the herd. The MAP strain identified in cases 1 and 2 was reported as a cattle strain, whereas the 2 different MAP strains isolated from case 3 were identified as a sheep strains. Isolation of bovine-type strains in camelids affected by JD has been reported before,6,7 and most strains probably can infect across ruminant species lines.10 The practice of feeding bovine colostrum to neonatal crias is believed to be a possible source of MAP introduction within a herd. Cases 2 and 3 would have been 7 and 11 years old, respectively, when case 1 joined the herd. Traditionally, adult animals have been considered fairly resistant to infection with MAP, because the critical period for acquiring infection is during the neonatal period.11 Age resistance could have been overcome by the pressure of infection if the environment was highly contaminated by a high-shedding animal (case 1). Previous reports of JD in camelids have not included quantitative culture results for MAP on either tissues or feces. In this report, the number of MAP CFU/g was obtained from tissue samples (cases 2 and 3) or from both tissue and fecal samples (case 1). Although cases 2 and 3 had small to moderate numbers of CFU in their tissues, case 1 had extremely high numbers of MAP CFU/g of tissue and feces. Similar numbers (>10,000 MAP CFU/g) have been reported in cattle.12 These cows, shedding extremely large numbers of MAP in their feces, recently have been referred to as “super-shedders.”12 According to an arbitrary definition (> 10,000 MAP CFU/g feces), case 1 would fall into this category. In cattle, the presence of 1 or more high shedding cows in a herd has been considered as an important factor in the transmission and control of the disease.12 Because high-shedding animals can shed millions of MAP CFU daily, they represent a greater risk for the spread of the disease to herd mates. In addition, as demonstrated in this report, the presence of 1 or several animals shedding large numbers of MAP in their feces may contribute to “passive shedding” of MAP by herd mates. As MAP is deposited on pasture by the infected animals, it may be ingested by other animals and detected in their feces by RT-PCR. Follow-up fecal RT-PCR testing performed on the farm described here showed a decrease in the number of animals classified as positive after removal of case 1 from the herd, suggesting that these animals were passive shedders, and passive shedding ceased once the high-shedding animal was removed. To the authors' knowledge, this is the 1st description of MAP high shedding in an alpaca. Detection and culling of high-shedding animals within a herd is an important part of disease control. aLiquamycin, Pfizer Animal Health, New York, NY bVetAlert, Tetracore Inc, Rockville, MD cSmartCycler, Cepheid, Sunnyvale, CA dParachek, Biocor Animal Health Inc, Omaha, NE eMGIT, Bactec, BD Diagnostic Systems, Franklin Lakes, NJ The authors acknowledge Terry Fyock and Sue McAdams for their technical assistance.

Hypothyroidism is considered by many as a “great mimicker” of many common complaints in the emergency department (ED). Thyroid disorders pose a significant threat when prolonged or in the acute presentation, and are potentially serious disorders with symptoms that range from non-specific constitutional to subtle or frank neuropsychiatric symptoms. Untreated disease can lead to myxedema crisis or coma, a life-threatening presentation that is rarely identified in young male patients and carries by itself a high risk of mortality, even in cases that undergo proper medical management. We present a case of a 26-year-old non-smoker Hispanic man with a medical history of hypothyroidism since the age of 13, and bronchial asthma. In a period of 3 - 4 months, he developed generalized malaise, fatigue, cold intolerance and unintentional weight loss. He visited the ED after developing acute abdominal pain associated with non-bloody watery diarrheas. At the initial evaluation, vital signs revealed hypotension, borderline low heart rate, and hypoglycemia. On physical examination, he looked pale, appeared lethargic, with facial puffiness, macroglossia and bilateral hyporeflexia with delayed relaxation on muscle stretch reflexes. The laboratory results showed a thyroid stimulating hormone (TSH) of 314.75 uIU/mL. There was also low sodium and elevated creatinine and hepatic enzymes levels. Abdominopelvic CT scan incidentally revealed a large pericardial effusion that was later confirmed with echocardiogram. A diagnosis of myxedema crisis was established, prompt initiation of intravenous hydrocortisone, levothyroxine and triiodothyronine therapy was administered, and he was transferred to another institution for management of the pericardial effusion. This case raised concerns about the incidence where thyroid disease presentations are not identified and where patients fail to receive adequate medical therapy. We as primary care physicians should encourage patients to adhere to medical therapy and the recommended follow-up instructions to avoid catastrophic complications such as myxedema crisis. J Med Cases. 2017;8(12):404-406 doi: https://doi.org/10.14740/jmc2942w

Hospital readmission within thirty days is common among Medicare beneficiaries, but the relationship between rehospitalization and subsequent mortality in older adults is not known. To compare one-year mortality rates among community-dwelling elderly hospitalized Medicare beneficiaries who did and did not experience early hospital readmission (within 30 days), and to estimate the odds of one-year mortality associated with early hospital readmission and with other patient characteristics. A cohort study of 2133 hospitalized community-dwelling Medicare beneficiaries older than 64 years, who participated in the nationally representative Cost and Use Medicare Current Beneficiary Survey between 2001 and 2004, with follow-up through 2006. One-year mortality after index hospitalization discharge. Three hundred and four (13.7 %) hospitalized beneficiaries had an early hospital readmission. Those with early readmission had higher one-year mortality (38.7 %) than patients who were not readmitted (12.1 %; p<0.001). Early readmission remained independently associated with mortality after adjustment for sociodemographic factors, health and functional status, medical comorbidity, and index hospitalization-related characteristics [HR (95 % CI) 2.97 (2.24-3.92)]. Other patient characteristics independently associated with mortality included age [1.03 (1.02-1.05) per year], low income [1.39 (1.04-1.86)], limited self-rated health [1.60 (1.20-2.14)], two or more recent hospitalizations [1.47 (1.01-2.15)], mobility difficulty [1.51 (1.03-2.20)], being underweight [1.62 (1.14-2.31)], and several comorbid conditions, including chronic lung disease, cancer, renal failure, and weight loss. Hospitalization-related factors independently associated with mortality included longer length of stay, discharge to a skilled nursing facility for post-acute care, and primary diagnoses of infections, cancer, acute myocardial infarction, and heart failure. Among community-dwelling older adults, early hospital readmission is a marker for notably increased risk of one-year mortality. Providers, patients, and families all might respond profitably to an early readmission by reviewing treatment plans and goals of care.