Diseases Health Symptoms

Can Ketamine Treat Depression?

Depression is a growing problem in the developed world. According to the Anxiety Disorders Association of America, approximately 40 million adults suffer from it. This is nearly one in five of all adults in the country. Many people use SSRIs and other medications. While these drugs can help many people, they are ineffective for others and carry unwanted side effects. Fortunately, there are other options worth considering. Ketamine is a natural supplement that can treat many mental health problems, such as depression.

Studies on Ketamine Effectiveness

There are a number of studies that prove that ketamine is a very effective way to treat depression. Here is an overview of some of the research on this groundbreaking treatment.

Icahn School of Medicine

The Icahn School of Medicine has conducted numerous trials on the effectiveness of ketamine. One of these studies used a group of ketamine patients and another group of lithium patients as a control group. The preliminary results showed that ketamine was an effective treatment for depression. They are still conducting further research, but the findings thus far have been encouraging.

National Institutes of Health Clinical Center

The National Institutes of Health Clinical Center is another organization that has funded research on the effectiveness of depression treatments. Their study Rapid Antidepressant Effects of Ketamine in Major Depression showed that patients could see remarkable improvement shortly after administering the supplement. Some patients so results within a few hours.

The organization funded another study called Antidepressant Efficacy of Ketamine in Treatment-Resistant Major Depression: A Two-Site Randomized Controlled Trial, which compared the effectiveness of ketamine with midazolam. The study found that 64% of patients that had failed to treat depression with other means noticed significant results. The reduction rate of patients in the midazolam group was less than half that.

When Should Patients Turn to Ketamine?

Recent research indicates that ketamine can be a very effective way to treat depression. The side effects of ketamine are mild for most people when taken in moderate quantities. As with any medication, it is still a good idea to make sure that it is the right treatment first. Patients should always consult with a doctor before trying it or any other treatment.

Patients should also try to learn as much as possible about the root cause of their depression. Patients that are feeling down after a major loss are most likely suffering from grief rather than depression. They should speak with a clinical psychologist that has experience dealing with grievances. This professional may let them know whether they should speak with a psychiatrist to see if a prescription is warranted.

Despite the limited side effects, ketamine should still be treated under the oversight of a doctor. If you feel that ketamine is the right treatment for you, then you can learn more at Ketamine Clinics. They have extensive experience helping patients treat pain and mental health problems with depression. 

Diseases Symptoms

Fibrodysplasia Ossificans Progressive Overview and Symptoms

Fibrodysplasia Ossificans Progressive (FOP) (MIM:1351000) is a rare disease that affects connective tissue. Its worldwide prevalence is 1:2,000,000 inhabitants. Although the transmission of Fibrodysplasia Ossificans Progressive is autosomal dominant, in most patients it is due to a new mutation in previously unaffected families. It is characterized by the formation of heterotopic bone in soft tissue, associated with different bone malformations. The most obvious characteristic is a deformation in the first toe of both feet (hallux valgus), which is present in 95% of cases.

Prevalence Statistics on Fibrodysplasia Ossificans Progressive

Fibrodysplasia Ossificans Progressive generally appears at an early age, with the first pockets of ossification appearing in the first decade of life and being difficult to diagnose in the early stages of the disease. The appearance of ossification foci can vary in different cases, although their distribution usually starts in a craniological way and from proximal to distal. The most frequently affected locations are the head, the neck and the back. This pathology occurs in outbreaks, which may be triggered by commonplace trauma, invasive procedures, infections or appear spontaneously.

The physiopathology of Fibrodysplasia Ossificans Progressive is not fully clarified, although an overexposure of bone forming protein (BMP) has been described, which could act as a signal for the formation of heterotopic bone.

The genetic alteration of Fibrodysplasia Ossificans Progressive is due to mutations in the ACVR1 gene located on chromosome 2q23-24, with most patients presenting the mutation p.Arg206His in heterozygosis. Publications describing new mutations in the ACRV1 gene associated with FOP are currently appearing.

Currently, no treatment has been shown to stop the disease.

A 6-month-old infant, admitted to our hospital for urinary tract infection, with no family or personal history of interest, was diagnosed in one case study. Physical examination showed different skeletal malformations such as bilateral hallux valgus and clinodactyly of the first finger of both hands, which according to the mother were present from birth. Two subcutaneous tumours at cranial level (left parieto-temporal and right parieto-occipital), of stony consistency and of approximately 3-4cm in diameter, stood out (fig. 2). These had appeared a few months after birth, unrelated to any traumatic event. The rest of the exploration was normal. The haemogram, biochemistry and analysis of the phosphocalcic metabolism were normal. X-rays of the feet and hands showed bone malformation of the first toe of both feet and a shortening of the first metacarpal. A cranial CT scan was performed which was normal and showed no foci of heterotopic ossification. In the case of suspected FOP, a genetic study was requested, which showed in heterozygosis the mutation p.Arg206His (c.617G>A) of exon 7 of the ACVR1 gene, which confirmed the diagnosis. The patient completed the treatment for the urinary infection for which he had been admitted and was discharged. At present, he is still undergoing regular check-ups in our unit, having so far not presented any exacerbation of the disease.

Hallux valgus is characteristic sign of Fibrodysplasia Ossificans Progressive.

The rarity of Fibrodysplasia Ossificans Progressive means that most of the time it goes unnoticed or is misdiagnosed, despite the fact that the typical malformations are present from birth. One study showed that in up to 87% of published cases the initial diagnosis was not correct. This fact takes on special importance when it comes to avoiding invasive procedures that trigger new outbreaks of the disease and/or unnecessary treatments.

Although there is no curative treatment for Fibrodysplasia Ossificans Progressive, different publications suggest that the use of anti-inflammatory drugs can help reduce the intensity of outbreaks. Bisphosphonates are another therapeutic option, but should not be used routinely because of their side effects. We must emphasize both multidisciplinary management to help improve the quality of life and mobility of these patients, as well as preventive measures. New treatment modalities are currently being developed based on the use of monoclonal antibodies that inhibit BMP, which could provide a solution to this disease in the future.

Diseases Symptoms

Diagnosing the Symptoms of Von Hippel Lindau

You may have heard of Von Hippel Lindau disease and wondered what it means. What are the symptoms of Von Hippel Lindau? How can you protect yourself?

You need to know what Von Hippel Lindau is, how to diagnose it and how to treat it. Keep reading to learn more.

Overview and Symptoms of Von Hippel Lindau Disease

Von Hippel Lindau disease is a rare, hereditary, multisystemic disease characterized by the development, at an early age, of tumors in different locations: ocular, renal, adrenal gland, pancreas and central nervous system (system formed by the brain and spinal cord).

It was first described in 1895 by Eugene von Hippel, who described that retinal angiomas (tumors characterized by hyperplasia, excessive development of tissues, blood vascular tissue) were hereditary and later Arvin Lindau, in 1926, suspected that these tumors were part of a broader lesion of the central nervous system.

During the first decades of the 20th century, families were reported having not only angiomas in the retina or central nervous system, but also cysts (closed sac under the skin that may contain a liquid or semisolid content) and tumors of visceral organs, including the kidneys, adrenal glands, pancreas, and epididymis (set of seminal vessels located above the testicle).

These tumors specifically include clear cell renal carcinoma, pancreatic cystadenomas, pancreatic islet tumors, and pheochromocytomas.

In 1964 Melmon and Rosen coined the term Von Hippel Lindau and proposed a diagnostic definition of this disease as follows: a hemangioblastoma associated with a typical visceral tumor, or a hemangioblastoma or characteristic tumor associated with a family history of Von Hippel Lindau.

The estimated prevalence (number of cases of a disease in a population) is 1/35,000. Almost all cases occur before age 65, although the disease is usually diagnosed at an average age of 26.

Von Hippel Lindau disease is due to a genetic defect. The normal Von Hippel Lindau gene acts as a “tumor suppressor gene,” whose function is to suppress tumor formation. For a tumor to form, both copies of the gene, one from the father and one from the mother, must be inactivated.

In an individual who does not have the hereditary alteration in the Von Hippel Lindau gene, both copies need to be mutated for a tumour to form, due to the inactivation of the Von Hippel Lindau gene.

In the case of people who inherit one defective copy of the gene, only the deactivation of the remaining copy is sufficient for the tumor to form. Tumours therefore form earlier and in more organs than in normal people, as all the cells in the individual’s body have an altered copy of the gene from birth.

Those affected have one or more characteristic tumours, and/or a concomitant family history.

Although members of a family group may develop a similar pattern of tumours, the expression of the disease is characteristically variable in each case.

Thus, first-degree relatives may develop tumours in different organs, in varying numbers and aggressiveness and with different complications for otherwise similar tumours.

Few patients develop the full range of possible manifestations and about 50% of those affected present only one manifestation of Von Hippel Lindau.

Many affected people do not develop expressions of the disease until an advanced age.

The most frequent initial manifestation is angiomatosis in the retina and hemangioblastomas in the cerebellum, with subsequent appearance of tumors in the brain, spinal cord, pheochromocytoma in the adrenal glands, microcystic serous cystoadenoma in the pancreas and renal cell carcinomas.

Angiomatous lesions in the liver, kidney, pancreas, lung, skin and epididymis have also been described.

Von Hippel Lindau disease is classified into two types based on the presence or absence of pheochromocytomas

Type 1: those that do not present pheochromocytomas, account for about 80% of cases.

Type 2: with the presence of pheochromocytomas, approximately 20% of the cases, with a worse prognosis than type 1.

Type 2A: characterized by the absence of renal cell carcinomas and pancreatic cysts.

Type 2B: with the presence of renal cell carcinomas and pancreatic cysts, which is the group with the highest mortality and worst prognosis.

Von Hippel Lindau disease presents a great clinical variability and symptoms depend on the size and location of the tumors. Thus: Angiomatosis in the retina can cause retinal detachment, bleeding and eventually blindness. Hemangioblastomas of the central nervous system produce various symptoms such as: headache, unsteadiness in walking, vomiting, balance disorders and weakness in upper and lower extremities.


Assessing the Symptoms and Prognosis of Hutchinson-Gilford Progeria Syndrome

HGPS (Hutchinson-Gilford Progeria syndrome) is a rare, autosomal dominant inherited disease with an estimated incidence of 1:4 million live births. It was first discovered by Jonathan Hutchinson in 1886. In 1904, Hastings Gilford coined the term progeria, derived from the Greek pro=early and geras=old.

Symptoms and Prognosis for People with Hutchinson-Gilford Progeria

In most cases, clinical manifestations are evident after the first year of life, with an average age at diagnosis of 2.9 years. The appearance of infants with Hutchinson-Gilford Progeria at birth is normal. However, a major decrease in growth occurs during the first year. They present craniofacial dysmorphism with prominent eyes, hooked nose, thin lips, abnormal dentition, micrognathia, prominent ears with absence of earlobes, alopecia, prominent cranial veins, loss of subcutaneous fat, joint stiffness, bone changes and skin changes, which are apparent during the second to third year of life. Death usually occurs in adolescence, secondary to cardiovascular complications. In 2003, Ericksson et al identified mutations in the lamina A gene in 20 of 23 patients with HGPS. Sandre-Giovannoli et al identified mutations in the same gene in 2 patients with Hutchinson-Gilford Progeria.

A 2-year old male patient of mixed race and urban origin was sent to pediatric endocrinology because of short stature, alopecia and dry skin.

He is the product of a second pregnancy complicated by threatened abortion in the first trimester and polyhydramnios without fetal morphological alterations in the second trimester. Delivery was by cesarean section at 39 weeks of gestational age. Birth weight and height were 3,400g and 52cm, respectively. The Apgar test score was 7/7 and the physical examination was normal. It was clear at a later date that he had Hutchinson-Gilford Progeria.

A few days after birth, dry, stiff skin with lesions on the trunk and extremities was observed, and from 2 months onwards, growth retardation (weight and height) and mild hypotonia.

In the physical examination at 2 years the following characteristics were observed in the infant later diagnosed with Hutchinson-Gilford Progeria: weight of 8kg (<3%), height of 77cm (<3%) and a body mass index of less than 3%. Craniofacial features were disproportionate head, micrognathia, prominent scalp veins, generalized alopecia, prominent eyes, sparse eyelashes and eyebrows, pointed and sculpted nose tip, thin lips, prominent ears, absence of earlobes, high-pitched voice, delayed teething. The chest was pyriform; the exploration showed rhythmic heart sounds without murmurs and good air intake in both lung fields. The skin was thin, tight, dry, wrinkled, with hyperpigmented lesions and had loss of subcutaneous fat. The extremities were thin with riding posture and joint stiffness (fig. 1). Neurological and psychomotor developmental examinations were normal. Phenotype progression is evident in figure 2. In laboratory studies, a skin biopsy was performed with evidence of scleroderma. The rest of the studies were normal (duodenal biopsy, digestive endoscopy, thyroid profile, serum electrolytes, renal function tests, karyotype, echocardiogram, abdominal ultrasound, chest X-ray, blood glucose and carpogram). The clinical diagnosis of Hutchinson-Gilford Progeria was reached. Molecular confirmation was made by finding a mutation defined as c.1824 C>T (p. Gly608Gly) in exon 11 of the LMNA gene.

Here is the phenotype of a toddler with Hutchinson-Gilford Progeria at 2 years of age. A) Low size at 24 months of age. B, C and D) Prominent alopecia and cranial vasculature, absence of ear lobes. E) Sclerotic skin. F) Drummer stick fingers. G) Prominent knees.

Understanding the Progression of Hutchinson-Gilford Progeria

Phenotype at 2 years of age. A) Low size at 24 months of age. B, C and D) Prominent alopecia and cranial vasculature, absence of ear lobes. E) Sclerotic skin. F) Drummer stick fingers. G) Prominent knees.

Phenotype progression. A) 2 months. B) 4 months. C) 9 months. D) 15 months. E) 24 months F) 29 months.

HGPS belongs to a group of disorders associated to mutations in the LMNA gene or “laminopathies”, including Emery-Dreyfuss muscular dystrophy, dilated cardiomyopathy, Charcot-Marie-Tooth disease type 2B, waist muscular dystrophy type 1B and Dunnigan type partial family lipodystrophy.

Apps Health Lifestyle

3 Great iPhone Apps to Take Your Temperature with

In 2013, Engadget published an interesting article on using your iPhone to take your temperature. At the time, this was a cutting-edge article that was talking about a disruptive new technology. Today, this technology is commonplace.

Here are some iPhone apps that you can use to take your temperature.


Kickstarter continues to be an inexhaustible source of good ideas. Of these ideas was designed to improve iOS devices and increase their usability to take temperatures. It is known as Thermodo and first reached the market in 2013. It is a tiny thermometer that we can take everywhere.

The idea is simple. Thermodo can be carried on our keychain. When you need to measure the temperature of a particular place, you just take it out of its capsule and insert it into the 3.5-millimeter jack of the iPhone. You can take your own temperature or the temperature of a room. Its data usage is so small that it can be run through your iPhone connection. This is something we have already seen with IRDA emitters as well.

In order to operate effectively, an application will need to send an audio signal through the temperature sensor. This sensor will attenuate the amplitude of the signal depending on the ambient temperature. This attenuation will be detected by the microphone of the terminal. The data collected is processed and analyzed by the Thermodo application to show the actual temperature on the screen. Although it is a somewhat complex process, the temperature reading is done instantly.


Although Kinsa has been developed to make temperature measurements and observe its evolution through the representation of graphs, the creators will launch an API so that other programmers can implement the application. This offers a much greater range of possibilities.

Kinsa costs just $20 (plus another $10 for shipping and handling). Although it may not seem like cutting edge technology, Thermodo has already managed to reach the $35,000 needed for the project to go ahead and there are still 33 days left until its promotion at Kickstarter.


iCelsius Pro is an accessory capable of expanding the functions of your iPhone by converting your device into a thermometer to measure the temperature and perform various functions. Thanks to a compatible application and the new iCelsius Pro, you will be able to turn your iPhone into a thermometer with which you can measure the temperature of where you are, create graphics and program different alerts.

The application can be configured so that degrees can be expressed in Celsius and Fahrenheit. Also, once you make your graphs, you can save it as an image or send it by email in a simple way. To make everything very accurate, manufacturers ensure that when there’s a change in temperature, the iCelsius Pro detects it instantly and accurately.

The iCelsius Pro can measure temperatures from -30°C to 150°C as it is made of stainless steel with a highly sensitive tip.

The standard version of iCelsius is free. However, you can get greater functionality with the premium version.

As we have already mentioned, to read all this information you need an application available for free in the App Store. The iCelsius Pro is priced at $49.99 and is available at the Amazon store.

Take Your Temperature with the Best iPhone Apps

There are a lot of iPhone apps that you can use to take your temperature with. You want to make sure you choose the best apps, so the results will be accurate without paying an arm and a leg.