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 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism is a clinical condition related to an excessive and abnormally regulated secretion of parathyroid hormone (PTH) from the parathyroid glands which is responsible for an alteration of the calcium and phosphorus metabolism. Parathyroid adenomas are the most important cause of primary hyperparathyroidism (80-85%). A case of parathyroid adenoma observed in a patient aged 47, admitted to the Emergency Medicine Department of our Hospital with a diagnosis of hypertensive crisis, cephalea, vomiting, and a clinical history of recurrent episodes of severe abdominal and renal pain, is presented. Lab data showed severe hypercalcemia and a progressive worsening of the renal function. A severe neurological involvement with stupor, derangement of mind, the arising of acute respiratory depression, lethargy compelled the colleagues to transfer him to the Intensive Care Unit; a neck ultrasonography showed a poor-echogenous area under the right thyroid inferior pole, with signs of vascularization. The suspect of a primary hyperparathyroidism related to a single adenoma of the parathyroid gland suggested a surgical treatment. A ''concise parathyroidectomy'' was performed. Our surgical approach was confirmed by the comparison of the preintervention and the post-intervention iPTH values: 2080 pg/mL (normal range: 12-65 pg/mL) before excision vs 101 pg/mL after the removal. The histologycal exam reported a parathyroid adenoma with large areas with haemorrage. Three days after surgery the patient was in good general conditions. Patients affected by primary hyperparathyroidism are often misdiagnosed because their clinical conditions can create differential diagnosis problems with other diseases. However the surgical option remains the gold standard treatment.
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PMID:Primary hyperparathyroidism related to a parathyroid adenoma: the dramatic clinical evolution of a misdiagnosed patient and its surgical solution. 1656 23

We report a case of bone pain associated with primary hyperparathyroidism in a patient with sickle cell disease. A 17-year-old girl with sickle cell disease (SS phenotype) was seen for bilateral knee and back pain. She had had recurrent severe vaso-occlusive crises and acute chest syndrome in the course of her disease. In the last 2 years, she had frequent visits to the emergency department for severe bone pain. She complained of long-standing fatigue and lethargy. Her physical examination was normal. Hydroxyurea treatment, as well as and long- and short-acting narcotics were given, with little improvement in symptoms. Poor compliance with medication, family dysfunction, and potential narcotic addiction were felt to be significant contributors to the patient's symptoms. She was incidentally found to have an extremely elevated total calcium level of 3.19 mmol/L (range: 2.25-2.76) with an ionized calcium level of 1.9 mmol/L (range: 1.15-1.35). Phosphorus level was 0.82 mmol/L (range: 0.90-1.50), alkaline phosphatase level was elevated at 519 U/L (range: 10-170), and parathyroid hormone level was extremely high at 1645 pg/mL (range: 10-60). Her renal function was normal. Ultrasonography of the neck and a Sestamibi scan revealed a single left inferior parathyroid adenoma adjacent to the thyroid lobe. There was no evidence of an underlying multiple endocrine neoplasia. The patient was diagnosed with primary hyperparathyroidism. Fluid hydration, hydrocortisone, calcitonin, and bisphosphonates were initiated for acute hypercalcemia management before surgical excision of the left parathyroid adenoma. On review of previous blood work, a borderline calcium level of 2.72 was present 18 months before this admission. Two years postsurgery, she has normal renal function, calcium, and parathyroid hormone levels. The weekly visits to the emergency department for pain episodes decreased to 1 every 2 months within the first few months after her surgery. The decrease in pain episodes, even if it coincided with the treatment of primary hyperparathyroidism, may still reflect the natural evolution of sickle cell disease in this patient. However, the high morbidity associated with primary hyperparathyroidism was successfully prevented in this patient. Primary hyperparathyroidism is rare in childhood. In a recent study, it occurred more commonly in female adolescents and was because of a single adenoma, as in our patient. Significant morbidity, mainly secondary to renal dysfunction, was because of the delay in diagnosis after the onset of symptoms (2.0-4.2 years), emphasizing the need for a rapid diagnosis. Sickle cell disease affects approximately 1 of every 600 blacks in North America. Acute episodes of severe vaso-occlusive crisis account for > 90% of sickle cell-related hospitalizations and are a significant cause of morbidity in patients. There is no known association between sickle cell disease and primary hyperparathyroidism, and this case is most probably a random occurrence. However, as emphasized by this case report, pain may also be a harbinger of other disease processes in sickle cell disease. Because management may vary, we suggest that care providers consider the diagnosis of vaso-occlusive crisis as the diagnosis of exclusion and that other etiologies for pain be envisaged in this patient population, especially in the presence of prolonged pain or unusual clinical, radiologic, or biological findings.
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PMID:Primary hyperparathyroidism mimicking vaso-occlusive crises in sickle cell disease. 1688 90

This article describes the case of a 16-month-old Hispanic male toddler with cow's milk allergy living in northern California who was admitted to a children's hospital for weight loss and markedly elevated levels of serum alkaline phosphatase and parathyroid hormone. At a routine outpatient well-child visit, his mother expressed concern about a decrease in his appetite and activity level. A detailed diet history revealed that breast milk was his primary source of nutrition during his first year of life and he had not been given supplemental vitamins. With attempts to introduce cow's milk formula, he had developed a rash and swelling around the mouth. Shortly after his first birthday, his mother weaned him from breast milk and introduced unfortified rice milk as a palatable milk substitute. Upon admission he was pale and lethargic; his laboratory studies were remarkable for elevated serum alkaline phosphatase and parathyroid hormone and low levels of phosphorus, 25-hydroxy-vitamin D, and ferritin. Lower extremity radiographic studies were consistent with rickets. After 5 weeks of therapy with vitamin D(3) and iron, his serum 25-hydroxy-vitamin D level normalized. Within 12 weeks following therapy, the child demonstrated significant clinical improvement, with resolution of growth failure and bone reossification. His activity level had returned to normal. This case emphasizes the importance of adequate vitamin D intake for children with special attention to those who might have nutrition deficiencies attributable to milk allergy.
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PMID:Vitamin D--deficient rickets in a child with cow's milk allergy. 2809 94

Phosphorus is an essential substance in our body, and hypophosphataemia (HP) is well-described in rickets, refeeding syndrome, diabetic ketoacidosis (DKA), and in chronic alcohol-abuse. However, to our knowledge, HP among severely-malnourished children has not been studied in detail, and information on prevalence, severity, and treatment is scarce. Currently, there are only a few published case reports of HP. This case series describes three cases of HP that presented to Dhaka Hospital of the International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b). Our first case required mechanical ventilation for respiratory distress associated with severe hypokalaemia (K 1.1 mmol/L) and moderate hypophosphataemia (P 2.1 mg/dL). The second case presented with severe sepsis which was associated with symptomatic hypocalcaemia (Ca 1.68 mmol/L), hypokalaemia (K 1.82 mmol/L), and severe hypophosphataemia (P 0.9 mg/dL). The third case presented with pneumonia and sepsis which were complicated by hypokalaemia (K 2.05 mmol/L) and severe hypophosphataemia (P 1.1 mg/dL). Marked lethargy and severe hypotonia were associated with HP in all of these cases. Manifestations of HP are diverse and can occur in association with other electrolyte imbalances, especially among malnourished children. Malnutrition, combined with sepsis, is one of the major killers of children younger than 5 years of age, and both malnutrition and sepsis can cause HP. It is concluded that the underlying causes of morbidity, including HP, should be actively sought and treated to reduce the mortality of children aged below five years.
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PMID:Hypophosphataemia among severely-malnourished children: case series. 2330 16

There are differences in renal anatomy and physiology between rabbits and other domestic species. Neurogenic renal ischemia occurs readily. Reversible prerenal azotemia may be seen in conjunction with gut stasis. Potentially fatal acute renal failure may be due to structural kidney damage or post-renal disease. Chronic renal failure is often associated with encephalitozoonosis. Affected rabbits cannot vomit and often eat well. Weight loss, lethargy, and cachexia are common clinical signs. Polydypsia/polyuria may be present. Derangements in calcium and phosphorus metabolism are features of renal disease. Radiography is always indicated. Urolithiasis, osteosclerosis, aortic and renal calcification are easily seen on radiographs.
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PMID:Diagnosis of renal disease in rabbits. 2334 42

A commercial diet fed to a colony of inbred strain 13 guinea pigs for approximately 6 weeks was subsequently recalled for excessive levels of vitamin D. Twenty-one of 62 animals exhibited clinical signs, including anorexia, lethargy, and poor body condition. Nine affected and 4 clinically normal animals were euthanized for further evaluation, including serum chemistry, urinalysis, and gross and/or histopathology. Macroscopic findings included white discoloration in multiple organs in 8 animals, and microscopic evaluation confirmed multiorgan mineralization in tissues from 7 animals. Serum 25-hydroxyvitamin D levels were elevated in 10 animals. Serum inorganic phosphorus and alkaline phosphatase levels were increased in all exposed animals; however, total calcium and ionized calcium levels were not significantly higher in exposed animals than in control strain 13 guinea pigs from a different institution. The data support a diagnosis of hypervitaminosis D with metastatic calcification. Following the diet recall, the remaining guinea pigs increased their food intake and regained body condition. Diagnostic testing of 8 animals euthanized approximately 3 months after returning to a normal diet demonstrated that serum parathyroid hormone remained significantly lower, and ionized calcium and ionized magnesium were significantly higher, in recovered animals compared to controls and exposed animals. These results indicate that diagnostic tests other than serum calcium are necessary for a diagnosis of hypervitaminosis D in guinea pigs.
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PMID:Hypervitaminosis D and Metastatic Calcification in a Colony of Inbred Strain 13 Guinea Pigs, Cavia porcellus. 2528 51

A 7-yr-old male Major Mitchell's cockatoo (Lophochroa leadbeateri) presented with a recent history of lethargy and anorexia. Physical examination revealed poor body condition and cloacal prolapse. Abnormalities on serum chemistry included severe hyperuricemia and hyperphosphatemia with a low calcium-to-phosphorus ratio. Symptomatic treatment was initiated including intravenous fluids and antibiotics. The bird continued to decline and died within a few days. Visceral gout and renal and cloacal pathology were observed on gross necropsy. Histopathology revealed chronic inflammation within the kidney, ureter, and cloaca in association with protozoal organisms and an invasive cloacal adenocarcinoma tumor. The location and morphology was consistent with Cryptosporidium sp., confirmed by immunohistochemistry and molecular testing. Direct sequencing identified Cryptosporidium avian genotype V. To the author's knowledge, this is the first reported infection of Cryptosporidium avian genotype V associated with clinical disease in birds and the first renal Cryptosporidium infection in a psittacine.
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PMID:RENAL AND CLOACAL CRYPTOSPORIDIOSIS (CRYPTOSPORIDIUM AVIAN GENOTYPE V) IN A MAJOR MITCHELL'S COCKATOO (LOPHOCHROA LEADBEATERI). 2666 55

A 6-year-old female spayed Domestic Shorthair cat was presented with acute lethargy, dehydration, marked azotemia, metabolic acidosis, left-sided renomegaly, and bilateral hydronephrosis. Ureterolithiasis and ureteral obstruction were suspected based on further diagnostics including abdominal sonography. Medical treatment was not successful. Fluoroscopically guided antegrade pyelography confirmed the diagnosis of bilateral ureteral obstruction due to ureterolithiasis. Subcutaneous ureteral bypass (SUB) devices were placed bilaterally, followed by close patient monitoring. Frequent reassessment of patient parameters and blood work served to adjust the fluid needs of the patient and to ensure proper hydration, correction of azotemia at an appropriate rate, and cardiovascular stability. After significant improvement of all patient parameters within 5 days, the patient was discharged from the hospital. Treatment included a dietary change to reduce the risk of stone formation as well as a phosphorus binder. Clinical and clinicopathologic parameters were unchanged at the 1- and 4- and 7-month rechecks (consistent with IRIS CKD stage II-NP-AP0), and both SUB devices continued to provide unobstructed urine flow. Bilateral placement of subcutaneous ureteral bypass devices may be a safe and potentially effective treatment option for acute bilateral ureteral obstruction in cats with ureterolithiasis. Strict patient monitoring and patient-centered postoperative treatment decisions are crucial to successful treatment outcomes.
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PMID:[Subcutaneous ureteral bypass devices as a treatment option for bilateral ureteral obstruction in a cat with ureterolithiasis]. 2689 28

This study evaluates the clinical findings obtained in routine screening examinations in cats with obstructive feline lower urinary tract disease at the time of service. Twenty-six cats with urethral obstruction were assessed by physical examination, blood pressure, electrocardiogram, and laboratory tests. Cats with signs of obstruction less than 36 hours before the service were in a state of alert, with body temperature and heart rate higher compared with cats in lethargy and stupor, obstructed up to 36 hours. The results revealed that 30.76% of the cats were hypertensive (>140mmHg). Arrhythmias were found in 15.38% of the cats with potassium >8.5mEqL. Creatinine, phosphorus, magnesium, potassium, and lactate concentrations were higher in cats obstructed more than 36 hours. All these data claim that a protocol of examinations should be established for obstructed cats, principally to stabilize the cat before the anesthesia for unobstruction.
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PMID:Routine Screening Examinations in Attendance of Cats With Obstructive Lower Urinary Tract Disease. 2831 15

Chronically debilitated loggerhead sea turtles (Caretta caretta) (DT) are characterized by emaciation, lethargy, and heavy barnacle coverage. Although histopathological findings associated with this condition have been reported, only limited data is available on health variables with clinical application. The objectives of this study were to 1) to compare morphometrics, clinicopathological variables, and immune functions of DTs to a group of apparently healthy loggerhead turtles to better understand the pathophysiology of the condition and 2) to assess health parameters in live debilitated turtles as they recovered during rehabilitation in order to identify potential prognostic indicators. We examined and sampled 43 DTs stranded from North Carolina to Florida for 47 health variables using standardized protocols to further characterize the condition. DTs were grouped into categories of severity of the condition, and those that survived were sampled at four time points through rehabilitation. All groups and time points were compared among DTs and to clinically healthy loggerhead turtles. Compared to healthy turtles, DTs had significantly lower body condition index, packed cell volume (PCV), total white blood cell (WBC) count, lymphocytes, glucose (Glc), total protein, all protein fractions as determined by electrophoresis, calcium (Ca), phosphorus (P), Ca:P ratio, potassium (K), lymphocyte proliferation, and greater heterophil toxicity and left-shifting, uric acid (UA), aspartate aminotransferase, creatine kinase, lysozyme, and respiratory burst. From admission to recovery, hematology and plasma chemistry data improved as expected. The most informative prognostic indicators, as determined by correlations with a novel severity indicator (based on survival times), were plastron concavity, P, albumin, total solids, UA, lymphocyte proliferation, WBC, K, Glc, Ca:P, and PCV. The results of this study document the wide range and extent of morphometric and metabolic derangements in chronically debilitated turtles. Monitoring morphometrics and clinicopathological variables of these animals is essential for diagnosis, treatment, and prognosis during rehabilitation.
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PMID:Chronic debilitation in stranded loggerhead sea turtles (Caretta caretta) in the southeastern United States: Morphometrics and clinicopathological findings. 2999 Mar 25


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