Kidney Failure, Chronic
Protein S Deficiency
Calcium use increases risk of calciphylaxis: a case-control study. (1/61)OBJECTIVE: To investigate the risk factors for the development of calciphylaxis in renal failure, a poorly understood and often fatal condition characterized by calcium deposition in tissues. DESIGN: Retrospective case-control study. SETTING: University hospital peritoneal dialysis center. PATIENTS: Eight continuous ambulatory peritoneal dialysis (CAPD) patients with calciphylaxis were identified in a 3-year period. We matched up to five controls for dialysis modality and length of time on dialysis with each case. STATISTICS: Multivariate conditional logistic regression analysis for matched case-controls. MAIN OUTCOME MEASURES: Laboratory data and demographics were collected as well as cumulative calcium and vitamin D ingestion over the year prior to disease onset. RESULTS: All the patients were female, versus only 38% (14/37) of controls (p < 0.0001). While not statistically significant, a majority of the patients were diabetic [62.5% (5/8) vs 32% (12/37)]. Peak and average levels of serum calcium, phosphate, calcium x phosphate product, parathyroid hormone (PTH), albumin, iron, total iron-binding capacity (TIBC), and ferritin were not significantly different in cases compared with controls. The use of calcitriol alone or with calcium carbonate was not found to be a significant risk factor for the development of calciphylaxis. In a multivariate analysis, iron intake seemed to be protective, contrary to previous reports, while the use of calcium carbonate was associated with a strong trend to increased risk of calciphylaxis development (odds ratio = 1.029/g and 1.011/g calcium ingested per month, at 1 and 2 - 3 months prior to calciphylaxis development; p = 0.0556 and 0.0565, respectively). CONCLUSION: These data, although limited by the small numbers of index cases, suggest that calcium ingestion is a risk factor for calciphylaxis. The increased use of calcium salts as a phosphate binder in recent years might explain the apparent increased incidence of calciphylaxis in our and other centers. The preponderance of female diabetics among cases reported elsewhere was confirmed in our study. (+info)
Cutaneous calciphylaxis. An underrecognized clinicopathologic entity. (2/61)Calciphylaxis (CPX), an uncommon syndrome characterized, in part, by progressive cutaneous vascular calcification, is seen principally in the setting of renal failure-associated hyperparathyroidism and is difficult to distinguish histologically from other microvasculopathies. We assessed histologic specimens from 13 cases of clinicopathologically classic CPX of the skin and reviewed documented histologic findings in the literature. Our series included 7 "early" and 6 "late" lesions (absence or presence of tissue necrosis, respectively). Histologically, early lesions were subtle and almost inapparent microscopically. Late lesions were easier to recognize because of obvious epidermal ulceration, dermal necrosis, and easily seen mural vascular calcification. The most common finding in both groups was acute and chronic calcifying septal panniculitis. Endovascular fibroblastic proliferation was more common in advanced lesions. Necrosis of dermal collagen was identified in only a few early lesions. Frank luminal vascular thrombosis was infrequent in both groups. The cited histologic findings largely were mirrored by those in the literature. Although they are relatively nonspecific when considered in isolation, the cited histopathologic features of cutaneous CPX allow for the diagnosis of this potentially lethal disorder when they are seen in combination with one another, particularly if detailed clinical data also are available. (+info)
Risk factors and mortality associated with calciphylaxis in end-stage renal disease. (3/61)BACKGROUND: We conducted a case control study to determine risk factors and mortality associated with calciphylaxis in end-stage renal disease. METHODS: Cases of calciphylaxis diagnosed between December 1989 and January 2000 were identified. Three controls were identified for each hemodialysis patient, with calciphylaxis matched to the date of initiation of hemodialysis. Laboratory data and medication doses were recorded during the 12 months prior to the date of diagnosis and at the time of diagnosis of calciphylaxis. Conditional logistic regression was used to identify risk factors for calciphylaxis. Cox proportional hazards models were used to estimate the risk of death associated with calciphylaxis. RESULTS: Nineteen cases and 54 controls were identified. Eighteen patients were hemodialysis patients, and one had a functioning renal allograft. Diagnosis was confirmed by skin biopsy in 16 cases. Women were at a sixfold higher risk of developing calciphylaxis (OR = 6.04, 95% CI 1.62 to 22.6, P = 0.007). There was a 21% lower risk of calciphylaxis associated with each 0.1 g/dL increase in the mean serum albumin during the year prior to diagnosis and at the time of diagnosis of calciphylaxis (OR = 0.79, 95% CI, 0.64 to 0.99, P = 0.037, and OR = 0.80, 95% CI, 0.67 to 0.96, P = 0.019, respectively). There was a 3.51-fold increase in the risk of calciphylaxis associated with each mg/dL increase in the mean serum phosphate during the year prior to diagnosis (95% CI, 0.99 to 12.5, P = 0.052). At the time of diagnosis of calciphylaxis, for each 10 IU/L increment in alkaline phosphatase, the risk of calciphylaxis increased by 19% (OR = 1.19, 95% CI, 1.00 to 1.40, P = 0.045). Body mass index, diabetes, blood pressure, aluminum, and higher dosage of erythropoietin and iron dextran were not independent predictors of calciphylaxis. Calciphylaxis independently increased the risk of death by eightfold (OR = 8.58, 95% CI, 3.26 to 22.6, P < 0.001). CONCLUSIONS: Female gender, hyperphosphatemia, high alkaline phosphatase, and low serum albumin are risk factors for calciphylaxis. Calciphylaxis is associated with a very high mortality. (+info)
Calciphylaxis. (4/61)The phenomenon of calciphylaxis is rare, but potentially fatal. It has been recognised for a long time in patients with chronic renal failure with secondary hyperparathyroidism. Disturbed calcium and phosphate metabolism can result in painful necrosis of skin, subcutaneous tissue and acral gangrene. Appearance of the lesions is distinctive but the pathogenesis remains uncertain. The beneficial effects of parathyroidectomy are controversial. However, correction of hyperphosphataemia or occasionally hypercalcaemia is imperative. Fulminant sepsis as a consequence of secondary infection of necrotic and gangrenous tissue is a frequent cause of patient morbidity and mortality. (+info)
Hyperbaric oxygen in the treatment of calciphylaxis: a case series. (5/61)BACKGROUND: Calciphylaxis, also referred to as calcific uraemic arteriolopathy, is a syndrome associated with end-stage renal disease (ESRD), and causes necrotic skin ulcers, often leading to a fatal outcome. Hyperbaric oxygen (HBO(2)) therapy has been used to enhance wound healing, but its role in the treatment of calciphylaxis is unclear. METHODS: We undertook a retrospective study of patients on renal replacement therapy with biopsy-proven calciphylaxis who were treated with HBO(2) between March 1997 and February 2000. RESULTS: Five patients were treated with HBO(2): three patients were on continuous ambulatory peritoneal dialysis (CAPD) and two were on chronic haemodialysis therapy. None of the patients had uncontrolled hyperparathyroidism and none underwent parathyroidectomy. The patients each received 25-35 treatments of HBO(2) at 2.5 atmospheres for 90 min per treatment. Two of these patients had complete resolution of extensive necrotic skin ulcers, with no adverse effects of HBO(2) therapy. Both had improvement in wound area transcutaneous oxygen pressure (P(tc)O(2)) with administration of 100% oxygen when measurements were taken at normobaric and hyperbaric pressures. In the other three patients receiving HBO(2), the skin lesions did not resolve. P(tc)O(2) was measured in two of these patients, neither of whom showed improvement with 100% oxygen administered at normobaric pressure. CONCLUSIONS: The data support a role for HBO(2) in the treatment of some patients with calciphylaxis, particularly as in the absence of uncontrolled secondary hyperparathyroidism there are few therapeutic options. (+info)
Healing of skin necrosis and regression of anticardiolipin antibodies achieved by parathyroidectomy in a dialyzed woman with calcific uremic arteriolopathy. (6/61)AIM: To present the impact of parathyroidectomy on the spontaneous healing of necrotic lesions of the skin of the lower leg and on anticardiolipin antibodies regression in a 68-year-old female dialyzed patient with hyperparathyroidism and calcific-uremic arteriolopathy (CUA). METHODS: After the occurrence of initial lesions of the lower leg skin, the intact parathyroid (iPTH) level, calcium (Ca) and phosphorus (P) product were measured, and on two occasions at 6-week intervals, the titer of anticardiolipin antibodies was determined, followed by a clinical monitoring of the progress of necrotic skin lesions. Two months after the occurrence of the skin lesions, the patient's right leg was amputated below the knee due to gangrene, and a histopathological analysis of the skin tissue sample of the amputated lower leg was made. After parathyroidectomy, iPTH, Ca x P product were measured, and on two occasions at 6 weeks' intervals, anticardiolipin antibodies titer was determined, followed by a clinical monitoring of lesions of the left lower leg skin. RESULTS: Before parathyroidectomy, iPTH level and Ca x P product were increased, as well as IgG anticardiolipin antibody titer measured on two occasions 6 weeks apart. The histopathological analysis of the skin tissue sample of the amputated right lower leg showed mural calcification of artery walls and thrombotic occlusions of small arteries, arterioles, and dermal capillaries, in addition to epidermolysis. A week after parathyroidectomy, iPTH level and Ca x P product were within normal range. Two measurements 6 weeks apart revealed no anticardiolipin antibodies. Eight weeks after parathyroidectomy, spontaneous healing of necrotic skin lesions of the left lower leg was observed. CONCLUSION: Regression of anticardiolipin antibodies, normalization of Ca x P product, and healing of the skin lesions after parathyroidectomy all pointed to the elevated PTH level as a crucial factor in the pathogenesis of CUA. (+info)
Calciphylaxis in a patient with end-stage renal disease secondary to systemic lupus erythematosus associated with acral gangrene and mesenteric ischemia. (7/61)A patient with end stage renal disease secondary to systemic lupus erythematosus (SLE) ultimately required amputation of the four extremities and developed mesenteric ischemia. The patient presented with widespread medial calcification involving various small to medium sized arteries, although no noticeable secondary hyperparathyroidism was observed. We speculated that SLE associated with systemic vasculitis and uremic milieu over a number of years may represent the perfect preexisting condition for calcific arteriolopathy to occur following which several factors including chronic administration of corticosteroids, photosensitivity in lupus, and significant weight loss may have contributed to acral gangrene and mesenteric ischemia. (+info)
Calciphylaxis is usually non-ulcerating: risk factors, outcome and therapy. (8/61)BACKGROUND: Calciphylaxis, historically considered rare, seems to be increasing in frequency. In our single center, 36 new cases have accumulated in seven years. The majority of these cases were non-ulcerating, which we believe to be early disease, in contradistinction to the vast majority of published cases that presented with ulcers. METHODS: Prospective data were collected on all patients with calciphylaxis. As well, a case control study, with two controls per patient, was performed on patients presenting with non-ulcerating plaques. RESULTS: The incidence of calciphylaxis in dialysis patients increased with a rate of 4.5/100 patient-years in the past three years. Eighty percent of cases presented with non-ulcerating subcutaneous plaques in the calves, easily confused with cellulitis. In those patients presenting with plaques only, the mortality rate was 33% at six months. Once ulceration develops, the mortality rate increased to above 80%. Bone scan was positive in 97% of patients. Steroid therapy appeared to be beneficial in some patients. Peritoneal dialysis, female sex and diabetes were risk factors. In the case control study of patients presenting with plaques only, serum phosphate (OR 2.6; 95% CI 1.05 to 6.45, P = 0.038) and Ca x P product (OR 1.46; 95% CI 1.02 to 20, P = 0.038) predicted the disease, as did being on calcium salts + vitamin D (OR 4.05; 95% CI 1.14 to 14.5, P = 0.03). CONCLUSIONS: Calciphylaxis is no longer rare. It is usually nonulcerating and can be diagnosed clinically in all patients. These patients have a high mortality, especially once ulceration occurs. Calcium salts plus vitamin D, as well as serum Ca x P product and high serum P increase the chance of the diseases. Therefore, the disease may be preventable. Steroids may be of benefit to some patients. (+info)
The condition is often seen in patients with long-standing ESRD, particularly those on hemodialysis. The exact cause of calciphylaxis is not well understood, but it is thought to be related to abnormal mineral metabolism, vascular inflammation, and oxidative stress.
The symptoms of calciphylaxis can vary depending on the severity of the condition, but may include:
* Skin lesions or ulcers
* Painful muscle weakness
* Difficulty moving or contracting muscles
* Numbness or tingling in the affected areas
* Decreased blood flow to organs and tissues
Calciphylaxis can be diagnosed through a combination of physical examination, laboratory tests, and imaging studies such as X-rays or CT scans. Treatment is primarily focused on managing the underlying causes of the condition, such as controlling blood pressure, correcting mineral imbalances, and addressing any infections or inflammation. In severe cases, surgical interventions such as bypass grafting or angioplasty may be necessary.
Overall, calciphylaxis is a rare and debilitating condition that can significantly impact the quality of life of patients with ESRD. Early detection and aggressive management are critical to preventing complications and improving outcomes.
Some common penile diseases include:
1. Erectile Dysfunction (ED): The inability to achieve or maintain an erection sufficient for satisfactory sexual performance.
2. Premature Ejaculation (PE): Ejaculation that occurs before or shortly after penetration, with minimal sexual stimulation and before the person wishes it.
3. Penile Cancer: A type of cancer that affects the skin or tissue of the penis.
4. Phimosis: A condition in which the foreskin cannot be retracted over the head of the penis.
5. Paraphimosis: A condition in which the foreskin becomes trapped behind the head of the penis and cannot be returned to its normal position.
6. Balanitis: Inflammation of the glans (head) of the penis.
7. Posthetic Syndrome: Pain or discomfort after surgery on the penis.
8. Priapism: A persistent and usually painful erection that lasts for more than four hours and is not relieved by sexual activity or orgasm.
9. Urethritis: Inflammation of the urethra, which can be caused by bacterial or viral infections.
10. Proctitis: Inflammation of the rectum, which can be caused by bacterial or viral infections.
These diseases can be diagnosed through physical examination, medical history, and diagnostic tests such as blood tests or imaging studies. Treatment options vary depending on the underlying cause of the disease and can include antibiotics, medications, surgery, or lifestyle changes.
It is important to seek medical attention if symptoms persist or worsen over time, as some penile diseases can lead to complications such as scarring, loss of sensation, or erectile dysfunction if left untreated. It is also important to practice safe sex and take steps to prevent the transmission of sexually transmitted infections (STIs) to help prevent the development of penile diseases.
There are different types of gangrene, including:
1. Wet gangrene: This type of gangrene is caused by bacterial infection and is characterized by a foul odor. It is often associated with diabetes, peripheral artery disease, and other conditions that affect blood flow.
2. Dry gangrene: This type of gangrene is not caused by infection and is often associated with circulatory problems or nerve damage. It does not have a foul odor like wet gangrene.
3. Gas gangrene: This type of gangrene is caused by the bacterium Clostridium perfringens and is characterized by the presence of gas in the tissue.
4. Necrotizing fasciitis: This is a serious and potentially life-threatening condition that occurs when bacteria infect the tissue under the skin, causing widespread damage to the skin and underlying tissues.
The signs and symptoms of gangrene can vary depending on the type and location of the affected tissue, but they may include:
* Pain or tenderness in the affected area
* Swelling or redness in the affected area
* A foul odor in the case of wet gangrene
* Weakness or numbness in the affected limb
Gangrene is diagnosed through a combination of physical examination, medical history, and imaging tests such as X-rays, CT scans, or MRI scans. Treatment for gangrene depends on the underlying cause and may include antibiotics, surgical debridement (removal of dead tissue), and amputation in severe cases.
Prevention measures for gangrene include:
* Proper wound care to prevent infection
* Keeping blood sugar levels under control in people with diabetes
* Avoiding smoking and other unhealthy lifestyle habits that can increase the risk of infection and circulatory problems
* Getting prompt medical attention for any injuries or infections to prevent them from spreading and causing gangrene.
Prognosis for gangrene depends on the severity of the condition and the underlying cause. In general, early diagnosis and treatment improve the outlook, while delayed treatment or the presence of underlying health conditions can increase the risk of complications and death.
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
Symptoms of leg ulcers may include:
* Pain or tenderness in the affected area
* Redness or swelling around the wound
* Discharge or oozing of fluid from the wound
* A foul odor emanating from the wound
* Thickening or hardening of the skin around the wound
Causes and risk factors for leg ulcers include:
* Poor circulation, which can be due to conditions such as peripheral artery disease or diabetes
* Injury or trauma to the lower leg
* Infection, such as cellulitis or abscesses
* Skin conditions such as eczema or psoriasis
* Poorly fitting or compression garments
* Smoking and other lifestyle factors that can impair healing
Diagnosis of a leg ulcer typically involves a physical examination and imaging tests, such as X-rays or ultrasound, to rule out other conditions. Treatment may involve debridement (removal of dead tissue), antibiotics for infection, and dressing changes to promote healing. In some cases, surgery may be necessary to remove infected tissue or repair damaged blood vessels.
Prevention is key in managing leg ulcers. This includes maintaining good circulation, protecting the skin from injury, and managing underlying conditions such as diabetes or peripheral artery disease. Compression stockings and bandages can also be used to help reduce swelling and promote healing.
Prognosis for leg ulcers varies depending on the severity of the wound and underlying conditions. With proper treatment and care, many leg ulcers can heal within a few weeks to months. However, some may take longer to heal or may recur, and in severe cases, amputation may be necessary.
Overall, managing leg ulcers requires a comprehensive approach that includes wound care, debridement, antibiotics, and addressing underlying conditions. With proper treatment and care, many leg ulcers can heal and improve quality of life for those affected.
Examples: Some examples of catastrophic illnesses include:
1. Cancer: Especially aggressive forms such as pancreatic, lung, and brain cancer.
2. Neurodegenerative diseases: Conditions such as Alzheimer's disease, Parkinson's disease, and motor neuron disease that can lead to cognitive decline, memory loss, and difficulty with movement and communication.
3. Organ transplant: The need for an organ transplant, particularly if the patient has end-stage renal disease or liver failure, can be catastrophic due to the high cost of medical care and the risk of complications.
4. Severe burns: Burns that cover a large portion of the body can require prolonged hospitalization, multiple surgeries, and rehabilitation, resulting in significant financial and emotional burden on the patient and their family.
5. Traumatic brain injury: A severe head injury can lead to long-term cognitive impairment, memory loss, and difficulty with communication and mobility, which can be catastrophic for the affected individual and their family.
6. Rare genetic disorders: Conditions such as Huntington's disease, cystic fibrosis, and sickle cell anemia are rare and can have a significant impact on the patient's quality of life, requiring extensive medical care and financial resources.
Impact on patients and families: Catastrophic illnesses can have a profound impact on both the patient and their family members. The physical and emotional toll of these conditions can lead to significant stress, anxiety, and depression. Additionally, the financial burden of medical care can result in bankruptcy, loss of employment, and other social and economic challenges.
Insurance coverage: To address the financial burden of catastrophic illnesses, many insurance plans offer catastrophic coverage, which provides a high level of coverage for expensive medical services and procedures. However, these policies often have high deductibles and co-payments, making them unaffordable for some families.
Government assistance: Governments around the world provide various forms of assistance to individuals with catastrophic illnesses. For example, in the United States, Medicare and Medicaid offer coverage for certain medical services and prescription drugs, while Social Security Disability Insurance (SSDI) provides financial support for individuals who are unable to work due to a disabling condition.
Charitable organizations: Many charitable organizations provide financial assistance and other resources to individuals with catastrophic illnesses and their families. For example, the Ronald McDonald House Charities provides housing and other support services to families of children receiving medical treatment for serious illnesses.
Research and development: Research into new treatments and therapies is ongoing for many catastrophic illnesses. Stem cell research, gene therapy, and other innovative approaches hold promise for improving outcomes and quality of life for individuals with these conditions.
Conclusion: Catastrophic illnesses are a significant challenge to the healthcare systems around the world. These illnesses can have a profound impact on the lives of patients and their families, both in terms of medical costs and quality of life. However, there are many resources available to help manage the financial burden of these conditions, including government assistance programs, charitable organizations, and research into new treatments and therapies. By leveraging these resources and working together to address the challenges posed by catastrophic illnesses, we can improve outcomes and quality of life for those affected by these conditions.
The main difference between primary hyperparathyroidism (HPT) and secondary HPT is the underlying cause of the disorder. In primary HPT, the overactive parathyroid glands are due to a genetic mutation or an autoimmune response, while in secondary HPT, the overactivity is caused by another condition or medication that affects vitamin D levels.
The symptoms of SHPT are similar to those of primary HPT and may include:
* Bone pain or weakness
* Osteoporosis or osteopenia
* Kidney stones or other kidney problems
* High blood pressure
* Nausea or vomiting
* Increased urination
SHPT can be diagnosed with a combination of physical examination, laboratory tests, and imaging studies such as ultrasound or CT scans. Treatment typically involves addressing the underlying cause of the condition and replacing vitamin D deficiency with supplements. In some cases, surgery may be necessary to remove part or all of the parathyroid glands.
While SHPT is rare, it is important for healthcare providers to be aware of this condition in patients who present with symptoms suggestive of HPT but have normal imaging studies and no family history of the condition. Early diagnosis and treatment can help prevent complications and improve quality of life for affected individuals.
In summary, secondary hyperparathyroidism is a rare endocrine disorder caused by a deficiency in vitamin D that leads to overactive parathyroid glands and an imbalance in calcium levels. It can cause a range of symptoms, including bone pain, osteoporosis, high blood pressure, and kidney problems. Treatment involves addressing the underlying cause of the condition and replacing vitamin D deficiency with supplements. Early diagnosis and treatment can help prevent complications and improve quality of life for affected individuals.
Livedo reticularis is a condition characterized by a bluish-purple discoloration of the skin, particularly on the extremities such as the hands and feet. It is also known as "livedo racemosa" or "purpura of pregnancy." The condition is caused by a variety of factors, including hormonal changes during pregnancy, taking certain medications, and certain medical conditions such as anemia and hypothyroidism.
The symptoms of livedo reticularis can vary in severity and may include:
* Bluish-purple discoloration of the skin, particularly on the hands and feet
* Small, flat spots or patches on the skin that are darker than the surrounding area
* Thread-like vessels visible just beneath the skin
* Coldness and numbness in the affected areas
* Pain or tenderness in the affected areas
Livedo reticularis is usually a harmless condition, but it can be a sign of an underlying medical condition. Treatment depends on the underlying cause and may include addressing any underlying medical conditions, stopping certain medications, and managing hormonal changes during pregnancy. In some cases, no treatment may be necessary and the condition will resolve on its own over time.
In summary, livedo reticularis is a condition characterized by bluish-purple discoloration of the skin, typically on the extremities, caused by a variety of factors including hormonal changes during pregnancy, medications, and certain medical conditions. Treatment depends on the underlying cause and may include addressing any underlying medical conditions, stopping certain medications, and managing hormonal changes during pregnancy.
There are several types of ulcers, including:
1. Peptic ulcer: A type of ulcer that occurs in the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are caused by excess acid production and are often associated with stress, spicy foods, and certain medications.
2. Stomal ulcer: A type of ulcer that occurs in the stoma (the opening) of a surgically created ostomy (a procedure that creates an artificial opening in the abdominal wall).
3. Pressure ulcer: A type of ulcer that occurs as a result of prolonged pressure on the skin, often seen in people who are bedridden or have mobility issues.
4. Venous ulcer: A type of ulcer that occurs on the legs and is caused by poor blood flow and increased pressure in the veins.
5. Diabetic foot ulcer: A type of ulcer that occurs on the feet of people with diabetes, often as a result of nerve damage (neuropathy) and poor blood flow.
The symptoms of an ulcer can vary depending on its location and severity, but may include:
* Pain or discomfort in the affected area
* Redness and swelling around the ulcer
* Discharge or pus from the ulcer
* Fever or chills
* Difficulty healing
Treatment for an ulcer will depend on its cause and severity, but may include:
* Antibiotics to treat any underlying infections
* Medications to reduce acid production or protect the stomach lining
* Wound care and dressing changes to promote healing
* Surgery to close the ulcer or remove any dead tissue
* Changes to diet and lifestyle to manage underlying conditions such as diabetes or high blood pressure.
Types of Skin Ulcers:
1. Pressure ulcers (bedsores): These occur when pressure is applied to a specific area of the skin for a long time, causing the skin to break down. They are more common in people who are bedridden or have mobility issues.
2. Diabetic foot ulcers: These are caused by nerve damage and poor circulation in people with diabetes, which can lead to unnoticed injuries or infections that do not heal properly.
3. Venous ulcers: These occur when the veins have difficulty returning blood to the heart, causing pressure to build up in the legs and feet. This pressure can cause skin breakdown and ulceration.
4. Arterial ulcers: These are caused by poor circulation due to blockages or narrowing of the arteries, which can lead to a lack of oxygen and nutrients to the skin.
5. Traumatic ulcers: These are caused by injuries or surgery and can be shallow or deep.
Symptoms of Skin Ulcers:
2. Redness around the wound
4. Discharge or pus
5. A foul odor
6. Increased pain when touched or pressure is applied
7. Thick, yellowish discharge
8. Skin that feels cool to the touch
9. Redness that spreads beyond the wound margins
10. Fever and chills
Treatment for Skin Ulcers:
1. Debridement: Removing dead tissue and bacteria from the wound to promote healing.
2. Dressing changes: Applying a dressing that absorbs moisture, protects the wound, and promotes healing.
3. Infection control: Administering antibiotics to treat infections and prevent further complications.
4. Pain management: Managing pain with medication or other interventions.
5. Offloading pressure: Reducing pressure on the wound using specialized mattresses, seat cushions, or orthotics.
6. Wound cleansing: Cleaning the wound with saline solution or antimicrobial agents to remove bacteria and promote healing.
7. Nutritional support: Providing adequate nutrition to promote wound healing.
8. Monitoring for signs of infection: Checking for signs of infection, such as increased redness, swelling, or drainage, and addressing them promptly.
9. Addressing underlying causes: Managing underlying conditions, such as diabetes or poor circulation, to promote wound healing.
10. Surgical intervention: In some cases, surgery may be necessary to promote wound healing or repair damaged tissue.
Prevention of pressure sores is always preferable to treatment, and this can be achieved by taking steps such as:
1. Turning and repositioning regularly: Changing positions regularly, at least every two hours, to redistribute pressure.
2. Using pressure-relieving support surfaces: Using mattresses or cushions that reduce pressure on the skin.
3. Keeping the skin clean and dry: Ensuring the skin is clean and dry, especially after incontinence or sweating.
4. Monitoring nutrition and hydration: Ensuring adequate nutrition and hydration to support healing.
5. Managing underlying conditions: Managing conditions such as diabetes, poor circulation, or immobility to reduce the risk of pressure sores.
6. Using barrier creams or films: Applying barrier creams or films to protect the skin from moisture and friction.
7. Providing adequate cushioning: Using cushions or pillows that provide adequate support and reduce pressure on the skin.
8. Encouraging mobility: Encouraging regular movement and exercise to improve circulation and reduce immobility.
9. Monitoring for signs of pressure sores: Regularly checking for signs of pressure sores, such as redness, swelling, or pain.
10. Seeking medical advice if necessary: Seeking medical advice if pressure sores are suspected or if there are any concerns about their prevention or treatment.
Protein S is a vitamin K-dependent protein that is produced in the liver and circulates in the blood. It works by inhibiting the activity of thrombin, a clotting factor that helps to form blood clots. In people with protein S deficiency, there may be an overactivation of thrombin, leading to an increased risk of blood clots forming.
Protein S deficiency can be caused by several factors, including genetic mutations, vitamin K deficiency, and certain medical conditions such as liver disease or cancer. It is usually diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies.
Treatment for protein S deficiency typically involves replacing the missing protein with intravenous immune globulin (IVIG) or recombinant human protein S. In some cases, medications that inhibit thrombin activity, such as heparins or direct thrombin inhibitors, may also be used to reduce the risk of blood clots forming.
Preventing protein S deficiency involves ensuring adequate intake of vitamin K through dietary sources or supplements, managing underlying medical conditions, and avoiding factors that can increase the risk of bleeding or thrombosis, such as smoking, obesity, and inactivity.
In summary, protein S deficiency is a condition characterized by low levels of protein S, which increases the risk of developing blood clots. It can be caused by several factors and treated with replacement therapy or medications that inhibit thrombin activity. Prevention involves ensuring adequate vitamin K intake and managing underlying medical conditions.
Sodium thiosulfate (medical use)
Chronic kidney disease
Deaths in October 2022
Vitamin and mineral management for dialysis
Coronary artery disease
List of diseases (C)
List of skin conditions
List of MeSH codes (C18)
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- On further questioning, patient was found to have a history of IgA nephropathy with end-stage renal disease , secondary hyperparathyroidism and calciphylaxis . (bvsalud.org)
Morbidity and morta2
- It was hypothesized that in calciphylaxis and calcinosis, ongoing inflammatory activity contributes to the calcium deposition in the media of small arteries, as well as perivascular and periarticular tissues. (northwestern.edu)
- Calciphylaxis is a systemic disease , characterized by high levels of calcium and progressive calcification of the vascular medial layer leading to ischemia . (bvsalud.org)
- We also discuss the unique histopathological features of calciphylaxis and contrast it with those of other forms of general vessel calcification. (wustl.edu)
- Calciphylaxis should be considered in the differential diagnosis of BRAO, BRVO, PAMM or any ophthalmic vascular manifestation in patients with end-stage renal disease . (bvsalud.org)
- Calciphylaxis is a condition where small cutaneous blood vessels become calcified, leading to acute, painful necrosis and ulceration of the skin. (slideshare.net)
Associated with chronic1
- Calciphylaxis is a life-threatening complication most often associated with chronic kidney disease that occurs as a result of the deposition of calcium in dermal and adipose microvasculature. (wustl.edu)
- Conclusion and importance Clinical manifestations of calciphylaxis are variable and a detailed clinical history is important to suspect calciphylaxis . (bvsalud.org)
- Here, we review the literature on uremic calciphylaxis with a focus on its pathophysiology, clinical presentation, advances in diagnostic tools, and treatment strategies. (wustl.edu)
- However, calciphylaxis remains a diagnosis that may be clinically challenging to make. (wustl.edu)
- This review emphasizes the need for multidisciplinary collaboration including nephrology, dermatology, and palliative care to ultimately provide the best possible care to patients with calciphylaxis. (wustl.edu)
- Calciphylaxis treatment should include a multimodal approach with a focus on supportive care, infection prevention, pain management, and wound healing. (medicalbag.com)
- To report a case of branch retinal artery occlusion (BRAO) followed by branch retinal vein occlusion (BRVO) and paracentral acute middle maculopathy (PAMM) in a patient with confirmed calciphylaxis . (bvsalud.org)
- The first patient was on haemodialysis and developed severe calciphylaxis with large ulcers and tissue necrosis. (northwestern.edu)
- 16. Calciphylaxis in primary hyperparathyroidism: a case report and brief review. (nih.gov)
- Zembowicz A, Navarro P, Walters S, Lyle SR, Moschella SL, Miller D. Subcutaneous thrombotic vasculopathy syndrome: an ominous condition reminiscent of calciphylaxis: calciphylaxis sine calcifications? (medscape.com)
- BACKGROUND: Calciphylaxis is a thrombotic vasculopathy characterized by painful necrotic ulcerations. (bvsalud.org)
- Baig MA, Aksoy T, McClain D, Fomberstein B. Calciphylaxis in a hemodialysis patient on corticosteroids and etanercept for psoriatic arthritis. (medscape.com)
- Association of warfarin with calciphylaxis has been reported in the literature, but, to the authors' knowledge, there are no literature reports of patients with CKD who were not on dialysis or warfarin developing calciphylaxis. (medscape.com)
- The authors report an unusual case of calciphylaxis in a patient with stage 3 CKD who was not on dialysis, warfarin, or insulin. (medscape.com)
- Association between calciphylaxis and inflammation in two patients on chronic dialysis. (medscape.com)
- Revascularization surgery for penile calciphylaxis. (nih.gov)
- Calciphylaxis cutis: a case report and review of literature. (medscape.com)
- Ortiz A, Ceccato F, Roverano S, Albertengo A, Paira S. Calciphylaxis associated with rheumatoid arthritis: communication of the second case. (medscape.com)
- Calciphylaxis mimicking penile gangrene: a case report. (nih.gov)
- This case illustrates that early diagnosis, intervention, and a multidisciplinary approach are of utmost importance in the management of calciphylaxis. (medscape.com)
- [ 1 ] Implying a systemic anaphylactic or hypersensitivity reaction, the term calciphylaxis is actually a misnomer. (medscape.com)
- Penile calciphylaxis: 5-year experience and literature review]. (nih.gov)
- Calciphylaxis, or calcific uremic arteriolopathy, is a rare, life-threatening disease characterized by vascular calcifications. (medscape.com)
- Penile calciphylaxis: a conservative approach. (nih.gov)